Information

Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?

Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?



We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

I read these two from various books, and got confused. The confusion is -

Reticulospinal tracts control gamma motor neurons. Gamma motor neurons control tone of muscle. In decerebrate rigidity, the reticulospinal tracts are cut, so the gamma motor neurons start firing excessively, and SPASTICITY develops. I understood this part and why Decerebrate Rigidity is a misnomer as it is actually spasticity.

Question is, in decorticate rigidity, the cerebral cortex is damaged. The basal ganglia are intact. One explanation I found is that the basal ganglia keep the reticulospinal tract activated so gamma motor neuron is under control. But if basal ganglia have no direct communication with brainstem or spinal cord, and their efferents pass through cerebral cortex, then even in decorticate rigidity, the reticulospinal tract should not be working, and thus the gamma motor neurons should fire excessively, in which case the decorticate rigidity also becomes a spasticity.

Am I missing anything? I am keeping red nucleus and vesticular nuclei out of this just to make matter simple. My question is about activity of gamma motor neurons in these two conditions. I hope you got the question. Thank you.


1)

a. Decorticate posturing means rubrospinal tract is the dominant output to the motor neurons of the body… maybe dominant is the wrong word, I am not all that knowledgable on this subject, but it is certainly altering the standard reticulospinal tract based extensor posturing.

http://en.wikipedia.org/wiki/Rubrospinal_tract

It is responsible for the strange flexion of upper limbs (aka arms). I say strange because when you think coma you think extension, not flexion. The lower limbs (aka legs), as always is extensor. Why the upper limb but not the lower limb? The red nucleus may play an additional role in controlling muscles of the shoulder and upper arm via projections of its magnocellular part.

b. In decerebrate posturing the rubrospinal tract is also cut, since the lesion is below the red nucleus. In this scenario the reticular activating system (aka reticulospinal tract) is the dominant output to the motor neurons of the body. Here you get the classic extensor pose, for both upper and lower limbs…

The point is: Rubrospinal tract was what you were missing. The red nucleus is the specific part of the basal ganglia that is involved…


2) the difference between spasticity vs rigidity:

  • spasticity is an increased resistance to the passive movement of a joint due to abnormally high muscle tone (hypertonus) which varies with the amplitude and speed of displacement of a joint.
  • rigidity is an increased resistance to the passive movement of a joint which is constant throughout the range of joint displacement and not related to the speed of joint movement.

your supposed to test this out on patients to get a feel for what's the difference.

spaciticity is the case for upper motor neurons lesions (ex. stroke), since the spinal reflexes are not being inhibited from above…

an example of rigidity in neurology is Parkinson's disease, which is the loss of the substantial nigra, which like the red nucleus is also in the midbrain… while the the substantial nigra and basal ganglia loop do influence the motor control of the body… they are not upper motor neurons. Upper motor neuron is specific to the corticospianl tract, it is the neuron going from cortex to anterior horn of spinal cord. Basal ganglia does influence the motor cortex but it isn't part of the corticospinal tract, hence not an upper motor neuron lesion.


3) Role of muscle spindles in spasticity from upper motor neuron lesions:

I am using this website for this part of my answer:

http://www.d.umn.edu it's from university of minnisota, which is funny because their acronym is UMN

high resistance to stretch occurs when the spindles are overactive (usually due to high rate of gamma motor neuron discharge) --> HYPERTONIC (SPASTIC)

removing inhibitory inputs to the gamma motor neurons increases their discharge rate, and increases spindle output

this can happen when there is an UPPER MOTOR NEURON lesion

It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes are intact so the a/g-motor neurons should relax, since only UMN damaged and not any part of the reflex arc. I seem to be missing something here.

I'm calling for back up, someone please help!


Not sure if this helps but its what i know after reading my class notes on reticular formation.This may not help but as I trying to learn also I will share.

Decorticate - The motor part way/Rubrospinal no longer has the influence of the higher centers such as the corticospinal - Flexor Response

Decerebrate - The lesion happens below the red nucleus therefore the rubrospinal spinal tract is not functioning - Extensor Response


Since in decorticate posture the lesion is at the level of neurons which originate from cortexand relay in the basal ganglia… but since basal ganglia are still intact they do influence in controlling increased discharge rates of gamma motor neuron. Moreover red nucleus is dominant here since no input from motor cortex flexor posture is present that too in upperlimbs since rubrospinal tract ends in cervical spinal cord.

Decerebrate means no rubro no cortex no basal ganglia… so gamma motor neuron are like "yay, i'm free now" so they keep increasingly discharging causing spastic extensor response…


Reticular formation

The reticular formation is a set of interconnected nuclei that are located throughout the brainstem. It is not anatomically well defined, because it includes neurons located in different parts of the brain. The neurons of the reticular formation make up a complex set of networks in the core of the brainstem that extend from the upper part of the midbrain to the lower part of the medulla oblongata. [2] The reticular formation includes ascending pathways to the cortex in the ascending reticular activating system (ARAS) and descending pathways to the spinal cord via the reticulospinal tracts. [3] [4] [5] [6]

Neurons of the reticular formation, particularly those of the ascending reticular activating system, play a crucial role in maintaining behavioral arousal and consciousness. The overall functions of the reticular formation are modulatory and premotor, [A] involving somatic motor control, cardiovascular control, pain modulation, sleep and consciousness, and habituation. [7] The modulatory functions are primarily found in the rostral sector of the reticular formation and the premotor functions are localized in the neurons in more caudal regions.

The reticular formation is divided into three columns: raphe nuclei (median), gigantocellular reticular nuclei (medial zone), and parvocellular reticular nuclei (lateral zone). The raphe nuclei are the place of synthesis of the neurotransmitter serotonin, which plays an important role in mood regulation. The gigantocellular nuclei are involved in motor coordination. The parvocellular nuclei regulate exhalation. [8]

The reticular formation is essential for governing some of the basic functions of higher organisms and is one of the phylogenetically oldest portions of the brain. [ citation needed ]


"Storming" (Dysautonomia)

Dysautonomia (dys-auto-nomia) is a syndrome that is also referred to, among many other names, as storming or autonomic dysfunction syndrome. It is caused by an injury to the upper portions of the brain stem or the hypothalamus, responsible for the autonomic nervous system (ANS - see site encyclopaedia). Severe hypoxia or anoxic brain injury can cause the ANS to become hypersensitive and to lose control. This lack of control presents itself in the form of an 'excitatory' response within the brain by discharging massive amounts of neurotransmitters such as adrenaline into the central nervous system (CNS).

The symptoms observed are described 'as frightening as a tornado to the untrained eye'. The signs of dysautonomia are high blood pressure (hypertension), rapid heart beat (arrhythmia), accelerated metabolism, abnormal high body temperature above (hyperthermia) above 105 degrees F), dilated pupils, cognitive impairment, changes in level of awareness/alertness, rapid breathing (tachypnea), poor eye tracking, abnormal profuse sweating and posturing (decerebrate or decorticate) and agitated or irritable behaviour. Not all those symptoms are necessarily present in people suffering from the syndrome.

Dysautonomia happens spontaneously and is unpredictable and uncontrolled. The brain becomes 'hyperactive' but the EEG and MRI/CT scans show no abnormality. It should not be mistaken for seizures. One should, however, be on the lookout for triggers. Those can include infection, nerve pain, psychological stress and undue environmental over-stimulation such as noise or medical/nursing procedures such as suctioning, turning or bathing. The treatment of dysautonoia is symptomatic, that is, by treating the presenting symptoms such as ventilatory management and medication (such as beta-blockers, morphine derivatives and bromocriptine), to reduce the neurological symptoms.

A quick response is necessary for controlling the storming episodes. Dysautonomia can become serious and even fatal, if not treated speedily, at worst leading to heart damage, cerebral haemorrhage, brain herniation and even malignant hypertension. Extreme hyperthermia and abnormally raised metabolic rate can also lead to further episodes of hypoxia, an increase in the risk of secondary brain injury and possible cell death, so treatment and monitoring of blood glucose, cooling down the body core temperature, increasing nutrition and hydration and management of contractures and spasms are also essential to avoid weight loss, skin breakdown and muscle wastage.

Needless to say, the impact of storming on the family is chaotic, stressful and distressing. Both family education and participation are important. Doctors and nursing staff should actively involve the family in all aspects of monitoring and managing dysautonomia by reviewing the causes, symptoms, duration, management and treatment of the storming episodes. Good treatment and management will reduce the need to admit the person to ICU care and the family have a big role to play in the symptom monitoring, identifying triggers or treating an episode. The family will gain the sense of security and control by helping in the care of their loved one. The family have a lot to offer by carrying out tasks such as putting a cool cloth on the forehead, turning the fan on or removing the covers, aiding in bathing, helping their loved one to relax, identifying triggers and monitoring their response to medication.

Faith is not believing that God can. It is knowing that God will.

Aug 09, 2006 #2 2006-08-09T18:44

Neurogenic storming is also known medically by many other names, the current one being Paroxysmal Autonomic Instability With Dystonia (PAID).

A complication of severe brain injury, regardless of etiology, but happens frequently following anoxic brain injury, it is a syndrome of marked agitation, excessive perspiration (diaphoresis), unusually high body temperature(hyperthermia), high blood pressure (hypertension), rapid heart rate (tachycardia) and rapid breathing (tachypnea) accompanied by increased muscle tension (hypertonia) and extensor posturing where the arms are extended by the sides, the head is arched back, and the legs are extended.

Usually episodic, it first appears in the intensive care setting but may persist into the rehabilitation phase for weeks, months or years after injury in individuals who remain in a low-response state. The syndrome engenders alarm because it may be difficult to distinguish from life-threatening conditions such as sepsis, impending herniation, or epileptic seizure. These manifestations could lead to secondary hypertensive or hyperthermic encephalopathy and even death.

The review article below may be of interest to those whose loved ones have experienced neurogenic storming or PAID. Just go to:

Faith is not believing that God can. It is knowing that God will.

Aug 09, 2006 #3 2006-08-09T18:57

Paroxysmal Autonomic Instability With Dystonia After Brain Injury
James A. Blackman, MD, MPH Peter D. Patrick, PhD Marcia L. Buck, PharmD Robert S. Rust, Jr, MD

A complication of severe brain injury is a syndrome of intermittent agitation, diaphoresis, hyperthermia, hypertension, tachycardia, tachypnea, and extensor posturing. To capture the main features of this syndrome, derived through literature review and our own case series, we propose the term paroxysmal autonomic instability with dystonia. We reviewed reports of autonomic dysregulation after brain injury and extracted essential features. From the clinical features, consistent themes emerge regarding signs and symptoms, differential diagnosis, and pharmacological therapies. We used these findings to make recommendations regarding diagnosis and treatment. Paroxysmal autonomic instability with dystonia appears to be a distinctive syndrome after brain injury that can mimic other life-threatening conditions. Early recognition may lead to fewer diagnostic tests and a rational approach to management. Prospective trials of specific drugs are needed to determine optimal efficacy.

INTRODUCTION
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

A complication of severe brain injury, regardless of etiology, is a syndrome of marked agitation, diaphoresis, hyperthermia, hypertension, tachycardia, and tachypnea accompanied by hypertonia and extensor posturing. Usually episodic, it first appears in the intensive care setting but may persist into the rehabilitation phase for weeks to months after injury in individuals who remain in a low-response state. The syndrome engenders alarm because it may be difficult to distinguish from life-threatening conditions such as sepsis, impending herniation, or epileptic seizure. These manifestations could lead to secondary hypertensive or hyperthermic encephalopathy and even death.

Various labels have been applied to this phenomenon, such as paroxysmal sympathetic storms, diencephalic seizures, or midbrain dysregulatory syndrome. However, the syndrome remains poorly understood and underrecognized, despite its distinctive and characteristic features. The lack of a standardized nomenclature is a major problem with research into this condition.1 Based on a review of limited existing literature, generally consisting of reports of a single or only a few cases, and of our own case series, we propose the following name for this syndrome: paroxysmal autonomic instability with dystonia (PAID). We will define its characteristics as precisely as possible, provide guidelines for distinguishing it from other conditions with similar characteristics, and suggest a rational treatment approach.

The pathophysiology of PAID can be best explained by dysfunction of autonomic centers in the diencephalon (thalamus or hypothalamus) or their connections to cortical, subcortical, and brainstem loci that mediate autonomic function. Bullard2 suggested a release phenomenon in which loss of cortical and subcortical control of vegetative functions occurs, including regulation of blood pressure and temperature. Boeve et al3 expanded this concept by speculating that the mechanism likely involves activation (or disinhibition) of central sympathoexcitatory regions such as the paraventricular hypothalamic nucleus, lateral periaqueductal gray substance, lateral parabrachial nucleus, or rostral ventricular medulla. Cortically provoked release of adrenomedullary catecholamines during PAID episodes may contribute to the rise in blood pressure as well as tachycardia and tachypnea.4-5

Thermoregulatory dysfunction may also be produced by hypothalamic dysfunction, as has been demonstrated experimentally6 and clinically. The temperature elevations associated with PAID may also be explained, at least in part, by the hypermetabolic state that accompanies sustained muscular contractions.

Rigidity and decerebrate posturing are seen experimentally and clinically with lesions in the midbrain, blocking normal inhibitory signals to pontine and vestibular nuclei.7 This allows these nuclei to become tonically active, transmitting facilitatory signals to the spinal cord control circuits. Spinal reflexes become hyperexcitable, evoked by sensory input signals that are usually below the threshold for excitation of a motor response.


LITERATURE REVIEW
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

Episodic agitation, diaphoresis, hyperthermia, tachycardia, tachypnea, and rigid decerebrate posturing after severe brain injury were first noted in a report by Strich in 1956.8 He called these events brainstem attacks. Subsequently, this constellation of clinical signs has received a variety of labels, including autonomic dysfunction syndrome, fever of central origin, neurostorming, acute midbrain syndrome, hypothalamic-midbrain dysregulation syndrome, hyperpyrexia associated with sustained muscle contractions, dysautonomia, sympathetic storms, paroxysmal sympathetic storms, acute hypothalamic instability, and diencephalic seizures.

Table 1 provides a summary of the clinical features of relevant case reports. We have included a series of our own patients. Permission was obtained from the Human Investigation Committee, University of Virginia, Charlottesville, to review patient records for this report. Because some of these patients received intensive care at other hospitals and their daily nursing and physician notes were not available, it was not possible to determine the time of initial onset of PAID signs or their total duration.


View this table:
[in this window]
[in a new window]
Table 1. Reports of Patients With Paroxysmal Autonomic Instability With Dystonia


Although some heterogeneity in manifestations has been noted, there is a sufficient degree of uniformity to justify viewing these cases as a syndrome. The cases have in common autonomic dysregulation and rigidity due to dystonia (involuntary sustained muscle contraction and extensor posturing). The PAID syndrome has been reported in children and adults. Traumatic and hypoxic brain injury account for most cases, but some were due to tumors, intracranial hemorrhage, or hydrocephalus. It is most likely to be encountered after processes that produce diffuse axonal or brainstem injury.

The onset of PAID signs often occurs in the first week after severe brain injury, when differential diagnosis is most difficult, and continues for weeks to months, in some cases for longer than 1 year. We have found that the episodes tend to persist the longest in patients with brain injury due to anoxia. Early diagnosis is challenging because the various constituent parts of the syndrome may be caused by a wide variety of processes that may occur in these very ill patients, including seizures, infection, the effects of drugs, withdrawal from drug therapy, pain, or agitation. PAID signs occur at a time when the patient's mental status is abnormal, and tests such as electroencephalography may be difficult to obtain or coordinate with the intermittent phenomena. These signs invariably include temperature elevation (as high as 41C), increases in heart and breathing rates, hypertension, diaphoresis, agitation, and extensor posturing. Creatine kinase levels are rarely reported in one case these values were within the reference range, and in another, elevated.

The most commonly used drugs for treatment of PAID are morphine sulfate, bromocriptine mesylate, propranolol hydrochloride, clonidine hydrochloride, lorazepam, and dantrolene sodium. Each one of these drugs is rational and addresses a component of the PAID syndrome (Table 2).


View this table:
[in this window]
[in a new window]
Table 2. Drugs Commonly Used for Paroxysmal Autonomic Instability With Dystonia


Opioid receptors are found in brain cardiovascular nuclei, the heart, and blood vessels.20 Opiates such as morphine, when peripherally injected into healthy animals, produce hypotension.21 Morphine induces analgesia, respiratory depression, and bradycardia. Its analgesic properties may interfere with pain as an inciting factor, and its sedative effects may counter the tachycardia and tachypnea. Constipation is a problematic adverse effect of morphine and narcotic dependency. Withdrawal from opiate therapy may provoke signs that falsely suggest PAID.

The use of dopamine antagonists or the withdrawal of dopamine agonist therapy may also result in neuroleptic malignant syndrome (NMS), the clinical features of which suggest PAID. Thus, it is not surprising that the use of bromocriptine, a dopamine agonist, has been found to be helpful in PAID.

Because excitation of the sympathetic nervous system appears to be a major feature of PAID, the uses of -adrenergic blockade, such as propranolol (nonselective -adrenergic blockade) or labetalol hydrochloride (nonselective - plus 1-adrenergic blockade), are logical choices and have proven clinically useful in the amelioration of some of the most important clinical signs (eg, hypertension), but not cholinergic signs (eg, diaphoresis) of PAID. In the experience of Do et al,9 1-adrenergic selective antagonists (eg, metoprolol or atenolol) are not effective, as in mitigating autonomic dysregulation.

Clonidine, an 2-adrenergic agonist, reduces blood pressure, has a behavior-stabilizing effect, and causes sedation. These features treat the sympathetic signs and may interrupt feedback into the system that otherwise would perpetuate the cycle of autonomic dysregulation.

The benzodiazepines, such as lorazepam, have anxiolytic and sedating effects and muscle relaxant properties that may account for benefits observed in treatment of PAID.

In addition to its direct muscle relaxant properties, dantrolene may diminish fever due to prolonged muscle contraction and may also reduce the somatosympathetic spinal reflexes that contribute to sympathetic excitation.


DIFFERENTIAL DIAGNOSIS
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

The following clinical entities have features in common with PAID and may share underlying pathophysiological mechanisms (Table 3).


View this table:
[in this window]
[in a new window]
Table 3. Comparison of Clinical Signs in Conditions That Mimic PAID After Traumatic Brain Injury


Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome is a severe disturbance of motor tone seen in patients taking dopamine receptorblocking agents, ie, phenothiazines such as thioridazine hydrochloride (Mellaril) and prochlorperazine (Compazine) and butyrophenones such as haloperidol (Haldol). This syndrome consists of fever, muscle rigidity, autonomic instability, alteration of consciousness, and elevation of serum creatine phosphokinase levels. Formerly, neuroleptics such as haloperidol were frequently used to treat agitation in brain-injured patients. The decline in this practice has diminished the occurrence of NMS in such patients. Because a considerable number of safer agents are now available, the use of neuroleptics in this setting is generally considered to be contraindicated.

Several cases have been reported with withdrawal of dopamine agonists (levodopa/carbidopa22 and amantadine hydrochloride.23 Numerous reports also associate the syndrome with the use of the dopamine receptor antagonist metoclopramide hydrochloride (Reglan),24-27 a drug commonly used to stimulate gastric emptying and reduce aspiration risk in patients with brain injury. Two case reports implicating metoclopramide involved children,28-29 and in 1 case symptoms were likely triggered by metoclopramide but did not reach their full manifestation until after the therapy was discontinued.30

Neuroleptic malignant syndrome apparently results from deficient compensatory mechanisms after blockade of dopaminergic regulation of muscle tone and autonomic function.31 Neuroleptic malignant syndrome occurs in only 1% of individuals taking neuroleptics. The incidence of NMS is likely lower than this with the newer antipsychotic drugs. Cases have been reported in children as young as 1 year after a single accidental dose.32 Symptoms usually occur 3 to 9 days after starting therapy. Extrapyramidal signs may be associated with other NMS clinical features. With early recognition and appropriate treatment, mortality due to NMS is low. Treatment includes stopping the neuroleptic therapy and providing supportive care.

Malignant hyperthermia (MH) is a disease of skeletal muscle characterized by hypermetabolism that occurs with exposure to a triggering agent such as inhalational anesthetic agents or depolarizing muscle relaxant drugs (eg, succinylcholine chloride), usually during induction or sometimes within 2 to 3 hours and rarely more than 24 hours later. After surgery, MH has been reported to occur in the absence of administration of a known triggering agent and may continue for several days.33

Malignant hyperthermia may also follow head injury without any exposure to anesthesia or surgery.34 A 21-year-old man became agitated and diaphoretic 36 hours after head injury. His temperature rose to 42.3C he was tachycardic, hypotensive, tachypneic, and displayed decerebrate posturing. Rhabdomyolysis and renal and liver failure developed. Results of a muscle biopsy confirmed the diagnosis of MH, including a characteristically abnormal response of muscle to halothane in vitro.

Malignant hyperthermia tends to occur most commonly in younger persons 52% were younger than 15 years in 1 case series.35 Inheritance of MH is primarily autosomal dominant, although it may also be autosomal recessive, polygenic (genes on chromosomes 3, 17, and 19 have been implicated), or sporadic.36-39

Abnormal calcium regulation appears to be the basic underlying defect resulting in tonic muscle contraction with production of excessive heat, resulting in a rise in body temperature to as high as 44C. Skeletal muscle rigidity can be local or diffuse, and is often first observed in the masseter muscles, extremities, and chest. Damaged muscles release large amounts of tissue thromboplastin, leading to coagulopathy, and myoglobin, leading to myoglobinuria and acute tubular necrosis.

Apart from discontinuing the triggering agent, if known, the use of dantrolene is the only effective treatment for MH. Dantrolene blocks calcium release from the sarcoplasmic reticulum causing muscle relaxation, and has reduced mortality due to MH dramatically.

The PAID syndrome frequently has been termed and confused with true diencephalic seizures. In 1929, Penfield40 described a 41-year-old women with a tumor of the third ventricle who displayed paroxysmal discharges of the vegetative nervous system that he described as autonomic epilepsy. Subsequent case reports of episodes characterized by irregular respirations, altered heart rate, labile blood pressure, hypothermia, and diaphoresis were associated with neoplasms of the diencephalon,41 agenesis of the corpus callosum,42-44 trapped third ventricle,45 and a suprasellar arachnoid cyst. The key features of hypothermia and profuse sweating generally responded to anticonvulsants, although electroencephalographic studies did not typically show epileptiform discharges. One case of periodic hypothermia, described as diencephalic epilepsy, responded only to total sympathectomy.46

Several cases of what appears to us to be the PAID syndrome have been described in the literature as diencephalic seizures.2-3 Goh et al10 described a 7-year-old child with repeated episodes of sympathetic hyperactivity due to a midbrain glioma as having a variant of diencephalic seizures. They acknowledged in the discussion that the term seizure is a misnomer, because there has never been a demonstration of an epileptogenic focus during a PAID episode, and most patients with PAID do not benefit from antiepileptic medications. Thus, diencephalic seizures constitute a syndrome distinct from PAID.

Autonomic dysreflexia (AD) occurs in individuals with spinal cord injury at the level of T6 through T8 or above. Any noxious stimulus below this level, such as a distended bladder, may initiate reflexive sympathetic activity resulting in life-threatening hypertension uncontrolled by feedback parasympathetic activity.47 Other manifestations of AD include headache, flushing and sweating of the face and upper torso, and apprehension. Removing the inciting stimulus relieves AD. Patients with spinal cord injury may have brain injuries as well, predisposing them to sympathetic dysregulation at the spinal cord and brain levels.

Fever is common after central nervous system trauma.48 Causes include wound infection, meningitis, blood in the cerebrospinal fluid, drug fever, and pneumonia/atelectasis. Central fever is a diagnosis of exclusion, attributed to trauma if it affects the base of the brain or the hypothalamus. The fever, often very high and persisting for weeks after injury, is relatively resistant to antipyretic therapy and occurs in the absence of perspiration.

The clinical sign that is probably most often confused with PAID is simple agitation. After emergence from true coma (return of sleep/awake cycles) with returningalbeit sometimes very slowlyarousal and awareness, the patient typically becomes agitated with extensor posturing and thrashing about the bed. The following tabulation shows the levels of cognitive functioning of the Rancho Los Amigos Scale49:

If the patient is at level II, there may be no purposeful movements. The lack of autonomic instability (ie, excessive rise in temperature and blood pressure) distinguishes agitation from PAID. Pain or discomfort from any source (eg, musculoskeletal, visceral, or headache) can produce agitation. When purposeful movements are observed with agitation, such as pulling out tubes or hitting, as seen at Rancho Los Amigos levels III and IV, PAID is clearly not the cause of agitation. Another possible cause of agitation is narcotic withdrawal, as almost all patients with severe brain trauma accompanied by other injuries such as fractures receive narcotics in the intensive care setting, and they are weaned from the drugs as they progress toward rehabilitation.

In acute brain injury, the pathophysiology of PAID may be similar in some ways to that of NMS or MH. Drug exposure or withdrawal or even stress may initiate aspects of these conditions, confusing the diagnosis. Any of the single features of PAID, such as hypertension, agitation, or hypertonia, could stimulate the full-blown syndrome. This might explain why a single drug that addresses 1 feature (eg, dantrolene for hypertonia) could interrupt and perhaps abort the process, especially if therapy is initiated early. Four cases of posttraumatic dysautonomia successfully treated with intrathecal baclofen, a muscle relaxant, illustrate this point.11 Most often, more than 1 drug is required for control.

It is clear that PAID is not associated with seizure activity and, thus, the term diencephalic or hypothalamic seizure is not appropriate to describe this condition. Unless there are comorbid seizures, antiepileptic drugs for PAID are not a rational choice except for use as mood stabilizers, possibly treating the agitation feature.


CRITERIA FOR PAID
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

It seems useful clinically and for future research to establish a single name that encompasses and clearly denotes the main features of the clinical phenomena described in this report. Paroxysmal autonomic instability with dystonia appears to accomplish this. Based on the literature review and our own experience, we propose specific criteria for the PAID syndrome. Within the clinical setting of traumatic brain injury, signs of PAID syndrome include (1) severe brain injury (Rancho Los Amigos level, IV), (2) temperature of at least 38.5C, (3) pulse of at least 130 beats/min, (4) respiratory rate of at least 140 breaths/min, (5) agitation, (6) diaphoresis, and (7) dystonia (ie, rigidity or decerebrate posturing). The duration is at least 1 cycle per day for at least 3 days. Finally, other conditions must be ruled out. In addition to recognizing consistent features of PAID, it is as important to recognize signs of other diseases or conditions that require prompt attention and a different diagnostic or treatment approach.


ASSESSMENT AND TREATMENT
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

Differential diagnosis is challenging, especially in the phase of acute brain injury. Because patients may be heavily sedated for ventilation or pain management, temperature elevation is usually the first concern, prompting body fluid cultures, leukocyte counts, and various imaging studies to rule out sepsis. If these test results are negative, fever may be attributable to noninfectious causes.

As sedation and analgesia are withdrawn, more typical cycles of PAID may become evident. Typically, the next sign of concern is elevated blood pressure, leading to the initiation of antihypertensive therapy. Gradually, the cyclical nature of the PAID signs becomes evident with episodes daily or several times daily and with the return of vital signs to normal between episodes.

Before accepting PAID as a diagnosis, alternative causes of autonomic dysregulation should be considered, especially treatable intracranial abnormalities such as hydrocephalus, increased intracranial pressure, or extra-axial blood or fluid accumulation. Other treatable irritants, such as dehydration, constipation, fracture site pain, or uncomfortable casts must be alleviated. Drugs or anesthetics that might precipitate or exacerbate PAID should be avoided, and caution should be used in the sudden withdrawal of dopamine agonist therapy.

As described earlier, a finite number of drugs have been used singly or in combination to alleviate PAID. No clear evidence suggests that one medication regimen is superior to another, and drugs seem to work well for some patients but not others. The goal is to maximize effectiveness while minimizing adverse effects. For example, sedation medications that are administered as needed, like narcotics or benzodiazepines, may quiet an episode but depress arousal and awareness between episodes. Clonidine will reduce blood pressure effectively, but also is sedating. Dantrolene as a muscle relaxant may be preferable to baclofen because it does not sedate however, its use may be limited by toxic effects to the liver. -Blockers will lessen sympathetic features, but should be used with caution in patients with asthma or diabetes.

A logical approach is to choose target signs, consider safety of particular drugs for the individual, and set a time frame for determination of efficacy before a drug is changed or a second drug is added. In our center, we try to devise a regimen that will prevent or ameliorate rather than rely on as-required drugs that may overtreat the condition.

Greater awareness of PAID and appropriate early intervention may minimize repetitive and expensive tests (eg, sepsis workups), ease nursing management, avoid pharmacological excess, prevent secondary injury, and allay the anxiety of parents and health care workers observing repeated episodes.

Further research is needed to evaluate individual or combination pharmacotherapy for PAID. A clearer definition of this syndrome may facilitate cross-institutional studies.


AUTHOR INFORMATION
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

Corresponding author and reprints: James A. Blackman, MD, MPH, Kluge Children's Rehabilitation Center, University of Virginia, 2270 Ivy Rd, Charlottesville, VA 22903 (e-mail: [email protected]).

Accepted for publication October 29, 2003.

Author contributions: Study concept and design (Drs Blackman and Patrick) acquisition of data (Dr Blackman) analysis and interpretation of data (Drs Blackman, Buck, and Rust) drafting of the manuscript (Drs Blackman and Rust) critical revision of the manuscript for important intellectual content (Drs Blackman, Patrick, Buck, and Rust) administrative, technical, and material support (Drs Blackman, Buck, and Rust) study supervision (Dr Blackman).

From the Kluge Children's Rehabilitation Center, Department of Pediatrics (Drs Blackman, Patrick, and Buck), and the Division of Pediatric Neurology, Department of Neurology (Dr Rust), University of Virginia, Charlottesville.


REFERENCES
Jump to Section
Top
Introduction
Literature review
Differential diagnosis
Criteria for paid
Assessment and treatment
Author information
References

1. Baguley IJ. Nomenclature of "paroxysmal sympathetic storms" [letter]. Mayo Clin Proc. 199974:105. PUBMED
2. Bullard DE. Diencephalic seizures: responsiveness to bromocriptine and morphine. Ann Neurol. 198721:609-611. ISI | PUBMED
3. Boeve BF, Wijdicks EFM, Benarroch EE, Schmidt KD. Paroxysmal sympathetic storms ("diencephalic seizures") after severe head injury. Mayo Clin Proc. 199873:148-152. ISI | PUBMED
4. Nosuka S. Hypertension induced by extensive medial anteromedian hypothalamic destruction in the rat. Jpn Circ J. 196630:509-523. PUBMED
5. Reis DJ, Gauthier P, Nathan MA. Hypertension, adrenal catecholamine release, pulmonary edema, and behavioral excitement elicited from the anterior hypothalamus in rat. In: Usdin E, Kvetnansky R, Kopin I, eds. Catecholamines and Stress. Elmsford, NY: Pergamon Press Inc 1976:195-206.
6. Kupferman I. Hypothalamus and limbic system, II: motivation. In: Kandel ER, Schwartz JH, eds. Principles of Neuroscience. New York, NY: Elsevier Science Publishers 1985:626-635.
7. Guyton AC, Hall JE. Textbook of Medical Physiology. Philadelphia, Pa: WB Saunders Co 2000:622.
8. Strich SJ. Diffuse degeneration of the cerebral white matter in severe dementia. J Neurol Neurosurg Psychiatry. 195619:163-185. ISI
9. Do D, Sheen VL, Bromfield E. Treatment of paroxysmal sympathetic storm with labetalol. J Neurol Neurosurg Psychiatry. 200069:832-833. FREE FULL TEXT
10. Goh KYC, Conway EJ, DaRosso RC, Muszynski CA, Epstein FJ. Sympathetic storms in a child with midbrain glioma: a variant of diencephalic seizures. Pediatr Neurol. 199921:742-744. FULL TEXT | ISI | PUBMED
11. Cuny E, Richer E, Castel JP. Dysautonomia syndrome in the acute recovery phase after traumatic brain injury: relief with intrathecal baclofen therapy. Brain Inj. 200115:917-925. FULL TEXT | ISI | PUBMED
12. Thorley RR, Wertsh JJ, Klingbeil GE. Acute hypothalamic instability in traumatic brain injury: a case report. Arch Phys Med Rehabil. 200182:246-249. FULL TEXT | ISI | PUBMED
13. Scott JS, Ockey RR, Holmes GE, Varhese G. Autonomic dysfunction associated with locked-in syndrome in a child. Am J Phys Med Rehabil. 199776:200-203. FULL TEXT | ISI | PUBMED
14. Sneed RC. Hyperpyrexia associated with sustained muscle contractions: an alternative diagnosis to central fever. Arch Phys Med Rehabil. 199576:101-103. ISI | PUBMED
15. Meythaler JM, Stinson AM III. Fever of central origin in traumatic brain injury controlled with propranolol. Arch Phys Med Rehabil. 199475:816-818. ISI | PUBMED
16. Pranzatelli MR, Paviakis SG, Gould RJ, De Vivo DC. Hypothalamic-midbrain dysregulation syndrome: hypertension, hyperthermia, hyperventilation, and decerebration. J Child Neurol. 19916:115-122. ISI | PUBMED
17. Rossitch E Jr, Bullard DE. The autonomic dysfunction syndrome: aetiology and treatment. Br J Neurosurg. 19882:471-478. PUBMED
18. Talman WT, Florek G, Bullard DE. A hyperthermic syndrome in two subjects with acute hydrocephalus. Arch Neurol. 198845:1037-1040. ABSTRACT
19. Klug N, Hoffman O, Zierski J, Buss K, Laun A, Agnoli AL. Decerebrate rigidity and vegetative signs in the acute midbrain syndrome with special regard to motor activity and intracranial pressure. Acta Neurochir (Wein). 198472:219-233. PUBMED
20. Siren A-L, Feuerstein G. The opioid system in circulatory control. News Physiol Sci. 19927:26-30. FREE FULL TEXT
21. Holaday JW. Cardiovascular effects of endogenous opiate systems. Annu Rev Pharmacol Toxicol. 198323:541-594. FULL TEXT | ISI | PUBMED
22. Friedman JH, Feinberg SS, Feldman RG. A neuroleptic malignantlike syndrome due to levodopa therapy withdrawal. JAMA. 1985254:2792-2795. ABSTRACT
23. Toru M, Matsuda O, Makiguchi K, Sugano K. Neuroleptic malignant syndromelike state following a withdrawal of antiparkinsonian drugs. J Nerv Ment Dis. 1981169:324-327. ISI | PUBMED
24. Donnet A, Harle JR, Dumont JC, Alif CA. Neuroleptic malignant syndrome induced by metoclopramide. Biomed Pharmacother. 199145:461-462. FULL TEXT | ISI | PUBMED
25. Bakri YN, Khan R, Subhi J, Kawi Z. Neuroleptic malignant syndrome associated with metoclopramide antiemetic therapy. Gynecol Oncol. 199244:189-190. ISI | PUBMED
26. Patterson JF. Neuroleptic malignant syndrome associated with metoclopramide. South Med J. 198881:674-675. ISI | PUBMED
27. Friedman LS, Weinrauch LA, D'Elia JA. Metoclopramide-induced neuroleptic malignant syndrome. Arch Intern Med. 1987147:1495-1497. ABSTRACT
28. Shaw A, Matthews EE. Postoperative neuroleptic malignant syndrome. Anaesthesia. 199550:246-247. ISI | PUBMED
29. Brower RD, Dreyer CF, Kent TA. Neuroleptic malignant syndrome in a child treated with metoclopramide for chemotherapy-related nausea. J Child Neurol. 19894:230-232. PUBMED
30. Le Couteur DG, Kay T. Delayed neuroleptic malignant syndrome following cessation of prolonged therapy with metoclopramide [letter]. Aust N Z J Med. 199525:261. ISI | PUBMED
31. Pearlman CA. Neuroleptic malignant syndrome: a review of the literature. J Clin Psychopharmacol. 19866:257-273. ISI | PUBMED
32. Klein SK, Levinsohn MW, Blumer JL. Accidental chlorpromazine ingestion as a cause of neuroleptic malignant syndrome in children. J Pediatr. 1985107:970-973. ISI | PUBMED
33. Pollock N, Hodges M, Sendall J. Prolonged malignant hyperthermia in the absence of triggering agents. Anaesth Intensive Care. 199220:520-523. ISI | PUBMED
34. Feuerman T, Gade GF, Reynolds R. Stress-induced malignant hyperthermia in a head-injured patient: case report. J Neurosurg. 198868:297-299. ISI | PUBMED
35. Strazis KP, Fox AW. Malignant hyperthermia: a review of published cases. Anesth Analg. 199377:297-304. ABSTRACT
36. Britt BA, Kalow W. Malignant hyperthermia: a statistical review. Can Anaesth Soc J. 197017:293-315. ISI | PUBMED
37. Kalow W, Britt BA, Terreau ME, Haist C. Metabolic error of muscle metabolism after recovery from malignant hyperthermia. Lancet. 19702:895-898. PUBMED
38. Isaacs H, Barlow MB. The genetic background to malignant hyperpyrexia revealed by serum creatine phosphokinase estimations in asymptomatic relatives. Br J Anaesth. 197042:1077-1084. ISI | PUBMED
39. McPherson E, Taylor CA Jr. The genetics of malignant hyperthermia: evidence for heterogeneity. Am J Med Genet. 198211:273-285. ISI | PUBMED
40. Penfield W. Diencephalic autonomic epilepsy. Arch Neurol Psychiatry. 192922:358-374.
41. Solomon GE. Diencephalic autonomic epilepsy caused by a neoplasm. J Pediatr. 197383:277-280. ISI | PUBMED
42. Shapiro WR, Williams GH, Plum F. Spontaneous recurrent hypothermia accompanying agenesis of the corpus callosum. Brain. 196992:423-436. ISI | PUBMED
43. Carr-Locke D, Millac P. Diencephalic epilepsy in a patient with agenesis of the corpus callosum confirmed by computerized axial tomography. J Neurol Neurosurg Psychiatry. 197740:808-814. ISI | PUBMED
44. LeWitt PA, Newman RP, Greenberg HS, Rocher LL, Calne DB, Ehrenkranz JR. Episodic hyperhidrosis, hypothermia, and agenesis of corpus callosum. Neurology. 198333:1122-1129. ABSTRACT
45. Darnell RB, Arbit E. Reversible diencephalic dysfunction: episodic hyperhidrosis due to a trapped third ventricle. Neurology. 199343(3, pt 1):579-582. ABSTRACT
46. Fox RH, Wilkins DC, Bell JA, et al. Spontaneous periodic hypothermia: diencephalic epilepsy. BMJ. 19732:693-695. ISI | PUBMED
47. Lee BY, Karmaker MG, Herz BL, Sturgill RA. Autonomic dysreflexia revisited. J Spinal Cord Med. 199518:75-87. PUBMED
48. Cunha BA, Tu RP. Fever in the neurosurgical patient. Heart Lung. 198817(6, pt 1):608-611. ISI | PUBMED
49. Hagen C, Malkmus D, Durham P. Levels of Cognitive Functioning. Downey, Calif: Rancho Los Amigos Hospital 1979.


What to know about opisthotonos

Opisthotonus is a type of abnormal posture where the back becomes extremely arched due to muscle spasms.

The condition is usually a sign of serious brain conditions, such as meningitis, tetanus, and trauma.

Share on Pinterest A painting by Sir Charles Bell from 1809 of opisthotonos.

Opisthotonos is a specific abnormal posture associated with conditions and injuries that impair brain and muscle function. The characteristic symptoms of opisthotonos are a severely arched or curved spine and head and heels that tilt backward.

Though relatively rare, the condition is usually a symptom of severe neurological conditions that are life threatening and require medical care.

Opisthotonos mostly impacts infants and young children, though it can occasionally affect adults.

Opisthotonos causes the back to become extremely rigid and curved or arched. The heels and head usually bend or flex backward as far as possible in response.

If someone is on their back, they will arch upwards, forming an n-shape. In this position, the back usually lifts the back off floor or mattress to some extent.

The arms also bend towards the body. In some cases, the head and lower body may be the only part of the body to keep in contact with the ground.

If someone is on lying on their stomach when opisthotonos occurs, they will bend inward creating a u-shape. The legs and arms usually reach backward and upward.

If the condition occurs when someone is lying on their side, the arching will form a c-shape. The person’s knees bend, and their arms either bend in or extend straight out. In this position, the backward arching of the neck may be more noticeable or severe.

Aside from these postural symptoms, the signs of opisthotonos vary depending on the cause.

People should seek medical attention anytime severe muscle spasms occur. Opisthotonos is considered life-threatening and is associated with serious health complications.

Symptoms that may accompany opisthotonos and require emergency care include:

  • trouble breathing
  • difficulty swallowing
  • rapid heart rate
  • a bluish tone in the fingers and toes
  • stiff jaw, neck, and abdominal muscles
  • extreme pain and soreness in the neck, shoulders, and muscles that surround the spine
  • high fever
  • convulsions
  • uncontrollable vomiting
  • reduced alertness or response time
  • dilated pupils or vision problems
  • extreme and unexplainable exhaustion

Because the condition mostly affects infants and young children, these symptoms may be harder to pinpoint. Uncontrollable, persistent crying with muscle spasms may be a sign of opisthotonos.

Infants may sleep more than usual but are restless, continually waking to adjust or find a more comfortable position.

Meningitis: When an infection causes inflammation of the tissues that surround the brain and spinal chord. The majority of cases in the United States are viral, but bacteria and fungi can also cause the condition.

Tetanus: Caused by toxins produced by the bacteria Clostridium tetani, which damage the nervous system and brain tissue. Tetanus is often called lockjaw because its most common symptoms are a locked jaw, stiff neck, and trouble swallowing.

Poisonings or overdoses: Young children are at a greater risk of accidental poisoning. Consuming strychnine, a chemical found in rodent poisons, pesticides, and insecticides can also cause the condition.

Cerebral palsy: When brain damage that occurs during fetal development causes a range of symptoms related to muscle dysfunction.

Phenothiazines: These are drugs commonly used to treat certain mental health conditions, such as schizophrenia. Opisthotonos is a rare side effect, and symptoms usually go away once the person has stopped taking the drugs.

Krabbe disease: An inherited condition that mostly impacts infants, young children, and young adults. Krabbe disease causes loss of muscle control and seizures that do not respond to treatment and can lead to premature death.

Gaucher disease: Fat-filled cells build up in organs, especially the liver and spleen, causing them to swell fat cells also affect the bone marrow, causing bone pain. One severe form of Gaucher disease can cause opisthotonus in infants, but this is rare.

Bilirubin encephalopathy, or kernicterus: A brain dysfunction that can potentially cause irreversible brain damage. Newborns and adults with pre-existing liver conditions have a higher risk of bilirubin encephalopathy.

Infant alcohol withdrawal: This occurs when a pregnant woman drinks excessive amounts of alcohol while pregnant. Infant alcohol withdrawal can cause reduced or uncontrollable muscle function. It rarely causes opisthotonos, however.

Other causes include conditions that involve increased cranial pressure, such as:

  • Brain hemorrhage or bleeding: This occurs when injury, disease, congenital disabilities, or blood vessels in the brain rupture, causing blood to accumulate and put pressure on brain tissues.
  • Hydrocephalus: Congenital disability, injury, or disease cause cerebral spinal fluid (CSF) to accumulate, putting pressure on the brain.
  • Subarachnoid hemorrhage: This happens when bleeding occurs between the brain and the tissues surrounding it.
  • Brain tumor: An abnormal, often uncontrollable cellular growth that can put pressure on the brain tissues and disrupt nerve function.
  • Chiari malformation: Part of the lower brain pushes out through the spinal canal, increasing pressure on the spine, brain, and often interfering with fluid flow causing hydrocephalus. Only some types of Chiari malformation do this.

Doctors diagnose opisthotonos by observing the posture when it is happening. Doctors are usually more focused on identifying and quickly treating the underlying cause than confirming opisthotonos.

Tests used to diagnosis the causes of opisthotonos include:

  • complete blood and urine tests
  • magnetic resonance imagining (MRI) of the brain
  • electrolyte tests
  • lumbar puncture (spinal tap)
  • cerebrospinal fluid (CSF) culture test
  • computed tomography (CT) scan

Treatment options depend on the underlying cause of opisthotonos. Commonly used treatment plans include:

  • Antibiotics for bacterial based infections, such as meningitis and tetanus. Antibiotics are also prescribed to prevent infection or further bacterial infections after surgery.
  • Over-the-counter pain medications, increased fluid intake, and rest are recommended for most cases, especially viral infections, such as meningitis.
  • Intravenous fluids are usually given in severe cases and to counteract bronchodilator overdoses.
  • Surgery is often necessary in cases of trauma, bleeding, and Chiari malformation to reduce pressure on the brain.
  • Antitoxin injections or medications are often given to those with tetanus to limit excess tissue damage associated with severe infection.
  • Ventilator and oxygen may be used when breathing is limited, labored, or difficult.

There are vaccines that offer protection against some of the conditions that cause opisthotonos, such as tetanus and some types of bacterial meningitis.


We found at least 10 Websites Listing below when search with decorticate posturing vs decerebrate quizlet on Search Engine

Decorticate vs decerebrate Flashcards Quizlet

Quizlet.com DA: 11 PA: 49 MOZ Rank: 60

  • Start studying Decorticate vs decerebrate
  • Learn vocabulary, terms, and more with flashcards, games, and other study tools.

Decerebrate and Decorticate Posturing and

Quizlet.com DA: 11 PA: 50 MOZ Rank: 62

  • Start studying Decerebrate and Decorticate Posturing and Cranial Nerves
  • Learn vocabulary, terms, and more with flashcards, games, and other study tools.

Decorticate or decerebrate Flashcards Quizlet

Quizlet.com DA: 11 PA: 50 MOZ Rank: 63

  • Better prognosis (b/c not in brainstem) decerebrate
  • Lesion below the rubral (red) nuclei in the brainstem = "cutting" of the rubrospinal tract
  • Vestibulospinal tract goes "unchecked" = LE extension
  • "pons" part of reticular nucleus goes "unchecked" = …

Decerebrate+posturing Flashcards and Study Sets Quizlet

Quizlet.com DA: 11 PA: 33 MOZ Rank: 47

  • Learn decerebrate+posturing with free interactive flashcards
  • Choose from 15 different sets of decerebrate+posturing flashcards on Quizlet.

Peds ATI ch 14 Flashcards Quizlet

Quizlet.com DA: 11 PA: 37 MOZ Rank: 52

COMA SYNDROMES Flashcards Quizlet

Quizlet.com DA: 11 PA: 38 MOZ Rank: 54

½ decerebrate and ½ decorticate posturing indicates what cause n o Uncal herniation (unilateral so only 1 side of BS effected) Methods used to rapidly drop ICP in herniation coma 5

Exam 2 (quick study guide) Flashcards Quizlet

Quizlet.com DA: 11 PA: 47 MOZ Rank: 64

  • A speech disorder caused by a weakness or incoordination of the muscles used in speech
  • Dyskinetic (cerebral palsy) abnormal involuntary motion
  • Early signs of increased intracranial pressure (14) -headache
  • -vomiting (poss projectile) -blurred or double visions (diplopia) -dizzy

Decerebrate vs. Decorticate Mnemonic and Review

  • These two types of posturing are ABNORMAL and are associated with a brain injury.
  • Let’s look at the differences between the two: De cor ticate
  • This is a type of flexed posturing and can indicate damage to the cerebral hemispheres.
  • There will be adduction and flexion of the arms and the hands will be closed shut (flexed).

Difference Between Decerebrate And Decorticate Rigidity

  • How to remember decorticate vs decerebrate
  • Decorticate and decerebate) can be elicited by noxious (adversive) stimulation
  • Is that decorticate is to peel or remove the bark, husk, or outer layer from something while decerebrate is to remove the cerebrum in …

What is the Difference Between Decorticate and Decerebrate

  • Decorticate posturing is when the patient’s back arches backwards and flexes the arms, where as decerbrate posturing is where the patietn arches the back (like in decorticate posturing) but then extends the arms out parallel to the body
  • Both decorticate posturing and decerebrate posturing are indicative of serious head injuries with

Decerebrate And Decorticate Posturing

  • Synonymous terms for decerebrate posturing include abnormal extension, decerebrate rigidity, extensor posturing, or decerebrate response
  • There is a criticism within the literature of the use of the terms decorticate and decerebrate posturing in clinical contexts due to their association with discrete anatomical locations that, in reality, may

Decorticate and decerebrate posturing causes & treatment

Healthjade.net DA: 14 PA: 13 MOZ Rank: 38

  • Decorticate vs Decerebrate posturing
  • Decerebrate posturing is an abnormal body posture and it is defined the arms and legs being held straight out, the toes being pointed downward, and the head and neck being arched backward 3)
  • Decerebrate posturing usually means there has been severe damage to the brain.

Decorticate posture : introduction , causes & diagnosis

  • Decorticate posture — a sign of severe damage to the brain — is an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight
  • The arms are bent in toward the body and the wrists and fingers are bent and held on the chest
  • This type of posturing is a sign of severe damage in the brain.

Decorticate vs Decerebrate Posturing

  • Decorticate and/or decerebrate posturing exhibited in coma patients due to external stimuli can be indicative of intracranial pressure, along with damage to the brain stem, cerebellum, and midbrain
  • They can occur in adults as well as infants as a result of illnesses such as malaria, Creutzfeldt–Jakob disease, and cerebral hypoxia, among others.

Decorticate Posturing: Symptoms and Causes

Healthline.com DA: 18 PA: 29 MOZ Rank: 61

  • Decorticate posturing — a sign of severe damage to the brain — is a specific type of involuntary abnormal posturing of a person

Simultaneous decerebrate and decorticate posteuring EMTLIFE

Emtlife.com DA: 11 PA: 50 MOZ Rank: 76

  • Decerbrate is a midbrain, cerebellum and / or stem injury while decorticate implies a motor neuron disfunction affecting the lateral corticospinal tract
  • Both can be present at the same time

NeuroLogic Examination Videos and Descriptions: Motor

  • A UMN lesion above the level of the red nucleus will result in decorticate posture (thumb tucked under flexed fingers in fisted position, pronation of forearm, flexion at elbow with the lower extremity in extension with foot inversion) while a lesion below the level of the red nucleus but above the level of the vestibulospinal and reticulospinal nuclei will result

Decerebrate vs Decorticate Posturing Rigidity Mnemonic

Youtube.com DA: 15 PA: 6 MOZ Rank: 38

Decerebrate and decorticate posturing rigidity NCLEX review with mnemonic and pictures on how to tell the difference between the two conditions.Decorticate v


7 - Cerebral malaria

This chapter discusses diagnosis, clinical features, management, prognosis, and antimalarial chemotherapy of cerebral malaria. In cerebral malaria, mild hyponatremia and hypocholeremia are common. The blood urea is often elevated because of dehydration, but some degree of renal impairment is common. Abnormal liver function tests are also common, but difficult to interpret because of the coexisting hemolysis and release of muscle enzymes. The alanine aminotransferase value is usually proportionately lower than the corresponding aspartate aminotransferase or lactate dehydrogenase values, and the alkaline. The essentials of management are prompt administration of effective schizonticidal antimalarial drugs, intensive care of the unconscious patient and early detection or, where possible, avoidance of life-threatening complications, such as acute pulmonary edema, metabolic acidosis, renal failure, bacterial septicemia and aspiration pneumonia. If the clinical presentation and background are suggestive of cerebral malaria, then after a brief clinical examination, intravenous antimalarial should be given in case of pending results of the routine baseline hematological and biochemical tests. A finger prick stick test is useful in the diagnosis and monitoring of hypoglycemia. It should be remembered that false low readings may be obtained with old or damp strips.


II. Clinical and Hematological Features of Malaria

Climent Casals-Pascual, MB, MSc, and David J. Roberts, *

Blood Research Laboratory, National Blood Service - Oxford Centre, John Radcliffe Hospital, Headington, Oxford, OX3 9DU, United Kingdom

Acknowledgments: The work of Dr. Roberts is supported by the National Blood Service and the Howard Hughes Medical Institute. The work of Dr. Casals-Pascual is supported by the University of Oxford. We thank Professors Marsh, Snow, Warrell, and White and Drs. Newton, English, Crawley, Krishna, and colleagues in Oxford for very many helpful discussions.

Malaria is a major public health problem in tropical areas, and it is estimated that malaria is responsible for 1 to 3 million deaths and 300-500 million infections annually. The vast majority of morbidity and mortality from malaria is caused by infection with P. falciparum, although P. vivax, P. ovale, and P. malariae also are responsible for human infections. This review will focus on the principal clinical and hematological features of falciparum malaria and also highlight some of the particular problems faced by those managing patients and potential carriers of malaria in nonendemic areas.

Clinical Features of Malaria

The signs and symptoms of malaria infection in humans are caused by the asexual blood stage of the parasite. The ratio of numbers of deaths to infections from malaria suggests that infection with blood stage parasites may result in a wide range of outcomes and pathologies. Indeed, the spectrum of severity ranges from asymptomatic infection to rapidly progressive, fatal illness. The clinical presentation of malaria infection is particularly influenced by host age, by immune status with respect to malaria and pregnancy, and by the species, genotype, and perhaps the geographical origin of the parasite. The characteristics of falciparum malaria have been most extensively studied in African children, and it is most appropriate to begin by describing the features of malaria in this group.

Malaria in African Children

Symptoms may appear on average 12 days (but occasionally 6 months or more) after inoculation of sporozoites into the bloodstream. An infection may be asymptomatic in those with acquired or innate immunity to malaria others with no or partial immunity may suffer from a severe acute illness.

Uncomplicated or mild malaria

Prodromal symptoms of malaria include headache (which is often severe and dominates the presenting complaint), myalgia, and coughing that precede the typical sequence of shaking chills, fever, and sweating associated with a paroxysm of fever. The erythrocytic cycle in falciparum malaria is usually synchronized so, in the initial stages of infection, fever occurs on days 1 and 3 (and thus is a tertian fever). In advanced infections the pattern of fever becomes less regular, even continuous. Nausea, vomiting, diarrhea, and abdominal pain may accompany fever. In an uncomplicated infection, signs are few, with the notable absence of lymphadenopathy or rash, but include splenomegaly and mild jaundice. If the course of treatment is incomplete or if the parasites are resistant to the treatment given, then parasites may recrudesce and once more cause a patent infection. Follow-up of treated cases is therefore essential.

Severe malaria

In some children, malaria causes more serious disorders. They may present with prostration or inability to take oral fluids or, in younger children, inability to suckle. As disease progresses they may exhibit a number of syndrome(s) of severe disease including coma, respiratory distress, anemia, and hypoglycemia and may also have a high rate of bacteremia. 1 On admission, children usually give a history of only a few days’ illness.

Exclusion of intercurrent diseases may be difficult. The parasitemia is an unreliable guide to the disease severity, and severe disease may occur in the face of undetectable parasitemia where the parasites are sequestered and their growth cycle is tightly synchronized. Thus, clinical assessment must always seek to exclude other illnesses, in particular acute respiratory infection, bacterial meningitis, encephalitis, Reye’s syndrome and septicemia which may mimic respiratory distress, coma, and/or multisystem disease due to malaria.

Cerebral malaria. The cardinal signs of ‘cerebral malaria’ are reduced consciousness and coma. A core of patients have signs consistent with a diffuse metabolic encephalopathy, although patients who present with reduced consciousness may have other distinct pathophysiological disturbances including seizures, metabolic acidosis, and hypoglycemia. The pathology of ‘cerebral malaria’ is linked with the sequestration of parasitized erythrocytes in postcapillary venules of the cerebral circulation, although the functional disturbance(s) that lead to an encephalopathy are poorly understood. 2, 3

The depth of coma can be measured at the bedside using a simplification of the Glasgow coma scale devised initially in Blantyre, Malawi. 4 As unconsciousness deepens, the patient fails to localize pain and may demonstrate abnormal posturing (decorticate rigidity, decerebrate rigidity, and opisthotonus), pupillary changes, absent corneal reflexes, and abnormal respiratory patterns including hypoventilation and periodic breathing. 5 Retinal hemorrhages are common.

Seizures are a prominent feature of cerebral malaria. Children may suffer simple febrile seizures, have prolonged or multiple seizures, or have features suggesting a focus of epileptic activity, including localized motor seizures. Status epilepticus and prolonged post-ictal periods are not uncommon. Interestingly, simultaneous EEGs and video recordings of comatose clinical patients have shown that generalized seizures may occur with minimal physical signs, such as twitching of finger(s), conjugate or nystagmoid deviation of the eyes, or hypoventilation with excessive salivation. 6 Such patients may recover consciousness after anticonvulsant therapy. Similarly, children presenting with metabolic acidosis and/or hypoglycemia may recover after appropriate treatment.

The progression of signs in cerebral malaria is variable, but sometimes a cephalo-caudal progression of signs is seen including isolated cranial nerve palsies and brain stem signs culminating in respiratory arrest. This sequence of events and direct measurement of cerebrospinal fluid (CSF) pressure in children presenting in a coma has suggested that, unlike nonimmune adults with cerebral malaria, at least some children with cerebral malaria may have intracranial hypertension. 7 This has led to re-evaluation of the risk of early lumbar puncture in excluding meningitis in parasitemic, comatose children, and now some clinicians suggest delaying lumbar puncture and commencing empirical antibiotic treatment, to cover bacterial meningitis, with concurrent antimalarial treatment. 8

Children who recover from cerebral malaria usually do so within 48 hours, although a significant minority suffers from neurological sequelae. Up to 15% of children may have hemiplegia, ataxia, dysphasia, hearing difficulty, visual problems including cortical blindness, or epilepsy. Over half of these children make a full recovery, but there is a residue of serious disability caused by cerebral malaria, including abnormal cognitive function and behavior. 8, 9

Anemia. The blood stage of falciparum malaria may cause life-threatening anemia, and hemoglobin of less than 5 g/dL is considered to represent severe disease. Anemia may become worse after treatment begins, particularly if the parasitemia is high. The anemia is typically normocytic and normochromic, with a notable absence of reticulocytes, although microcytosis and hypochromia may be present due to the very high frequency of alpha and beta thalassemia traits and/or iron deficiency in many endemic areas. 10 However, difficulties in assessing, not only the absolute, but also the ‘functional’ iron stores complicate the diagnosis and treatment of iron deficiency in the context of acute malaria infection. In such circumstances the only diagnostic test of iron deficiency may be the response to iron supplementation. The indication(s) for and duration of treatment have not, however, been established. Although chronic hemolysis may increase folate requirements, a frank deficiency is uncommon in children presenting with acute malaria, at least in East Africa.

The pathophysiology of severe anemia is a complex but relatively neglected area of study. Certainly, malaria gives ample reasons for both increased destruction and reduced production of red cells. Red blood cells are destroyed as parasites complete their growth cycle, although some parasites may be removed from erythrocytes as immature ring forms by phagocytic cells. 11 Infected erythrocytes may also be phagocytosed by macrophages following opsonization by immunoglobulins and/or complement components. Other effector cells and mechanisms are less well defined but may include antibody-dependent cytotoxicity and natural killer (NK) cells.

The survival of uninfected erythrocytes is also reduced. The activity and the number of macrophages are increased in malarial infection. Moreover, the signals for recognition of uninfected erythrocytes for removal by macrophages are enhanced. Uninfected erythrocytes bind increased amounts of immunoglobulin and/or complement as detected in the direct antiglobulin test (DAT or Coomb’s Test). 12, 13 The specificity of the immunoglobulins on the surface of the red cells has remained controversial. These antibodies do not have a particular specificity but are more likely to represent immune complexes absorbed onto the surface of red blood cells by complement receptors including CR1 (CD35). 14

No discussion of the pathology of malarial anemia is complete without consideration of ‘blackwater fever.’ The sudden appearance of hemoglobin in the urine indicating severe intravascular hemolysis leading to hemoglobinemia and hemoglobinuria received particular attention in early studies of anemia in expatriates living in endemic areas. There was an association between blackwater fever and the irregular use of quinine for chemoprophylaxis. This drug can act as a hapten and stimulate production of a drug-dependent complement-fixing antibody. Recent studies of sudden intravascular hemolysis have shown it is rare in Africa, but more common in Southeast Asia and Papua New Guinea, where it is associated with G6PD deficiency and treatment with a variety of drugs including quinine, mefloquine, and artesunate. 15

Reticulocytopenia has been observed in numerous clinical studies of malarial anemia. The histopathological study of the bone marrow of children with malarial anemia shows erythroid hyperplasia, with dyserythropoiesis, cytoplasmic and nuclear bridging, and irregular nuclear outline. 16 The functional abnormality has not been defined, but an increased proportion of the erythroid progenitors are found in the G2 phase compared with normal controls.

The prime candidates for the host factors mediating dyserythropoiesis have been growth factors and cytokines. Serum erythropoietin (Epo) was appropriately raised in a study of African children with malarial anemia. However, other studies in adults from Thailand and Sudan have concluded that the Epo concentration, although raised, was inappropriate for the degree of anemia.

The concentrations of tumor necrosis factor α (TNF-α) and interferon (IFN)-γ have been correlated with the severity of the disease, 17 and high levels of TNF-α have been shown to suppress erythropoiesis. These cytokines may also contribute to reduced production of Epo and to increased erythrophagocytosis.

The possibility has been raised that high levels of the Th2-type cytokine interleukin-10 (IL-10) might prevent the development of severe malarial anemia. Low levels of IL-10 have been described in African children with severe malarial anemia. 18 However, the mechanism of protection from anemia by IL-10 is unclear.

The hypothesis that parasite products directly stimulate the production of inflammatory cytokines, including TNF-α, has been widely promoted. The glycosylphosphatidylinositol (GPI) anchor of malarial membrane proteins may cause cellular dysfunction, but a role for this toxin in dyserythropoiesis remains to be established. 19 Other toxic products may exist. During its blood stage, the malaria parasite proteolyses host hemoglobin, releasing heme as a by-product. β-Hematin forms as a crystalline cyclic dimer of oxidized heme and is complexed with protein and lipid products as malarial pigment or hemozoin. The function of monocytes and macrophages is severely inhibited after ingestion of hemozoin. Here, the biologically active moieties may be lipoperoxides such as 4-hydroxynonenal (4-HNE) and 15(R, S) hydroxyeicosatetraenoic acid (HETE) produced by oxidation of membrane lipids (reviewed in 20 ). Their effect on other cellular functions, such as erythropoiesis, has not been established.

Anemia in falciparum malaria is clearly multifactorial and there is a strong argument that erythrocyte destruction and ineffective erythropoiesis play equal parts in the etiology of malarial anemia.

Respiratory distress and metabolic acidosis. Respiratory distress is common in severe disease and has been shown to be an independent predictor of poor outcome. 21 It is defined by tachypnea, by deep, gasping breathing, and by use of the secondary muscles of respiration and usually represents metabolic acidosis, although acute respiratory infection must be carefully excluded. 22, 23 Acidosis is largely due to excessive lactic acid although other anions may contribute to the anion gap. Salicylate toxicity can also cause a metabolic acidosis when inappropriate home treatment with aspirin occurs. Some children presenting with respiratory distress are dehydrated and may be resuscitated with saline. However, the majority of children presenting with respiratory distress are severely anemic, have a metabolic acidosis secondary to reduced oxygen-carrying capacity, and respond to rapid transfusion of fresh blood (reviewed in 24 ). However, in pregnant women with malaria and nonimmune adults with malaria, transfusion must be given with careful hemodynamic monitoring (see below).

A minority of children with respiratory distress does not respond to appropriate resuscitation. They probably represent a heterogeneous clinical group and may have renal failure, systemic bacterial infection, or a more profound syndrome of systemic disturbance due to malaria parasites.

Hypoglycemia. Hypoglycemia is most common in children and in pregnant women with severe disease. 4, 25, 26 Hypoglycemia may be evident at presentation or may occur during treatment and sometimes in the face of glucose infusions. In children, insulin levels are appropriate and hypoglycemia appears more likely to follow impaired hepatic gluconeogenesis and increased consumption of glucose in peripheral tissues and by parasites. 27 In adults, hypoglycemia has been associated with hyperinsulinemia, and it has been postulated that malaria-derived products and/or quinine directly or indirectly stimulate the beta cells of the pancreatic islets. 25 Whatever the pathogenesis of the condition, it is clear that all severely ill patients with malaria should be carefully monitored and aggressively treated for hypoglycemia.

Outcome of malaria infection

The prognosis of severe falciparum malaria is poor, with a case fatality rate of 15-20% in African children. Mortality is higher when multiple syndromes of severe disease are present (Figure 4 ). A number of clinical and laboratory parameters have been associated with poor outcomes, including deep coma, respiratory distress, hypoglycemia (blood or plasma glucose < 2.2 mM), metabolic acidosis (lactate > 5 mM), raised CSF lactate, renal failure (creatinine > 265 μmol), hyperparasitemia, appearance of pigmented parasitized erythrocytes, and leucocytosis. 4, 21, 22, 28 Severe malaria in nonimmune adults also has a high case-specific mortality, and here the rate is probably dependent on the availability of critical care facilities to support multiorgan failure (Table 1 ).

Syndromes of Severe Malaria at Different Ages

One unexplained but consistent feature of the epidemiology of clinical malaria is the age distribution of syndromes of severe disease. Children born in endemic areas are protected from severe malaria in the first 6 months of life by the passive transfer of maternal immunoglobulins and by expression of fetal hemoglobin. Beyond infancy, the presentation of disease changes from predominantly severe anemia in children aged between 1 and 3 in areas of high transmission to predominantly cerebral malaria in older children in areas of lower transmission. 29 In this light, the picture of cerebral malaria with multisystem disease in nonimmune adults represents an extreme end of the spectrum in the relationship between age, transmission, and syndrome of severe disease. The reasons for this pattern are unknown but probably include age-specific responses to malaria and also cross-reactive responses activated during infection in older children.

Malaria in Nonimmune Adults

Many travellers (and returning residents with significant levels of clinical immunity) present with what is effectively mild malaria as seen in African children. However, in nonimmunes, severe disease can progress very rapidly and cause life-threatening illness. In this group, multiorgan failure is more prominent than in children with malaria, and some features of the syndromes of malaria differ from those described above for African children (Table 1). 30

Cerebral malaria

Coma is a very prominent feature of severe illness in nonimmunes, although neurological sequelae are recorded less frequently. However, epilepsy and psychiatric disturbances have been found at increased frequency in a large series of Vietnam veterans who suffered from cerebral malaria. 31

Respiratory failure

Deteriorating respiratory function with widespread pulmonary edema may develop during the disease and carries a very poor prognosis. Some cases of pulmonary edema may be secondary to fluid overload and/or rapid correction of dehydration. However, other patients have adult respiratory distress syndrome (ARDS) with a normal pulmonary wedge pressure, suggesting that the primary abnormality is endothelial damage and excessive permeability. The primary causes of endothelial damage are unknown. 32

Renal failure

Renal impairment is common in severe malaria in nonimmune adults, and the microscopic pathology is acute tubular necrosis: glomerulonephritis is rare. 33 In some cases acute tubular necrosis may be precipitated by intravascular hemolysis. The pathogenesis in other cases is unclear. Patients may require short-term dialysis for acidosis, fluid overload, hyperkalemia, or rapidly rising creatinine.

Bleeding disorders

Disordered coagulation and clinical evidence of bleeding are not infrequent in adults, and patients may present with bleeding at injection sites, gums, or epistaxis.

Other complications

Hemoglobinuria secondary to intravascular hemolysis and jaundice are more common in adults than in children. As in children, concurrent bacteremia is common.

Malaria in Pregnancy

During pregnancy, women are both more susceptible to malaria infection and also more likely to develop hypoglycemia and pulmonary edema. In pregnant women, malaria infection, often without fever, may nevertheless cause anemia and placental dysfunction. This effect is greatest in primigravidae and has been attributed to the adhesion of parasitized erythrocytes to chrondrotin sulfate A and hyaluronic acid in the placenta. Fetal growth is impaired and babies born to women with placental malaria are on average 100 g lighter than controls born to women without malaria. The subsequent contribution of malaria to infant mortality is substantial. 34

Features of P. vivax, P. ovale, and P. malariae Infection

In P. vivax and P. ovale malaria high parasitemias are rare, as invasion of erythrocytes is limited to reticulocytes. The parasites do not appear to sequester in the peripheral circulation or cause organ-specific syndromes. Mortality is limited to occasional deaths from splenic rupture or from intercurrent illnesses in already weakened individuals. Nevertheless, P. vivax malaria has been clearly associated with anemia during pregnancy and with low birth weight in children of affected mothers. In these cases, cytokines or other inflammatory mediators appear to cause placental dysfunction. 35 P. malariae infection is also rarely fatal but is distinguished by the persistence of blood-stage parasites for up to 40 years. It can, however, cause a progressive and fatal nephrotic syndrome.

White Cell, Platelet, and Coagulation Changes in Acute Malaria Infection

Changes in leucocyte and platelet counts are present in malaria. In addition, there are significant effects on leucocyte function.

White cells

Malaria is accompanied by a modest leucocytosis, although leukopenia may also occur. Occasionally, leukemoid reactions have been observed. Leukocytosis has been associated with severe disease. 4 A high neutrophil count may also suggest intercurrent bacterial infection. Monocytosis and increased numbers of circulating lymphocytes are also seen in acute infection, although the significance of these changes is not established. 36 However, malarial pigment is often seen in neutrophils and in monocytes and has been associated with severe disease and unfavorable outcome. 37

There is a significant dysfunction of myeloid cells in malaria. The adhesive phenotypes expressed by falciparum-infected erythrocytes were previously thought simply to permit sequestration of parasites in the peripheral circulation. Recent work has illuminated how malaria-infected erythrocytes may modulate the function of macrophages and myeloid dendritic cells through the adhesion of malaria-infected cells to CD36 and/or CD51 on host cells (for review, see Urban and Roberts 20 ). Furthermore, the function of monocytes and macrophages may be inhibited by the action of hemozoin from digested hemoglobin. 38 These observations suggest that the inhibition of phagocytosis and of other inflammatory responses, mediated by adhesion of infected erythrocytes to myeloid cells and by ingestion of hemozoin, may influence the outcome of infection and facilitate survival of both parasite and host.

Platelets

Thrombocytopenia is almost invariable in malaria and so may be helpful as a sensitive but nonspecific marker of active infection. However, severe thrombocytopenia (< 50 × 10 9 l 1 ) is rare. Increased removal of platelets may follow absorption of immune complexes, but there is no evidence for platelet-specific alloantibodies. By analogy with erythropoiesis, there may be a defect in thrombopoiesis but this has not been established.

Thrombocytopenia is not associated with disease severity, although, somewhat paradoxically, platelets have been shown to contribute to disease pathology in animal and in human malaria. 39 Moreover, in human infections, platelets may form ‘clumps’ with infected erythrocytes. 40 Therefore, one explanation of this paradox could be that low levels of platelets may not only be a marker of parasite burden but may also be protective from severe disease.

Coagulation

Abnormalities of laboratory tests of hemostasis, suggesting activation of the coagulation cascades, occur in acute infection, particularly in adults. Patients may present with bleeding at injection sites or mucous membranes. However, histological evidence of intravascular fibrin deposition is notably absent in those dying from severe malaria. 2 However, Factor XIII, normally responsible for cross-linking fibrin, is inactivated during malaria infection, and these data may explain low levels of fibrin deposition in the face of increased procoagulant activity. 41

Chronic Malaria Infection and the Transmission of Malaria by Transfusion

One of the outstanding problems for those managing the blood supply in nonmalaria endemic countries is the prevention of the transmission of malaria by blood transfusion. In nonimmunes, falciparum malaria would almost invariably develop within 3 months of return from a malaria-endemic area. Furthermore, the infection is symptomatic at very low levels of parasitemia. Nonimmune potential blood donors could be safely excluded from transmitting P. falciparum if they remain asymptomatic 6 months after return from the tropics, although the exact time limits for exclusion of donors who have returned from the tropics are widely debated.

However, malaria is readily transmissible by blood transfusion from semi-immune donors harboring an asymptomatic infection several years after return from a malaria-endemic area. 42, 43 These donors can in principle be identified by the presence of high titer antibodies against blood-stage antigens. 42 Previously, blood donors who were semi-immune to malaria and carrying asymptomatic infection were identified by an ELISA test to detect anti-blood-stage malaria antibodies, using an extract of blood-stage parasites grown in Aotus monkeys. However, the sensitivity of the test, latterly supplied commercially using a stock of antigen derived from the original preparation, declined until it was insufficiently reliable for use in the National Blood Service in the UK.

Commercial tests for the detection of antimalarial antibodies using recombinant malarial antigens are under evaluation. The antigens used in these kits are vaccine candidates and are proteins expressed on the surface of the invasive blood stages of the malaria parasites. However, these same proteins are targets of protective immune responses and are therefore antigenically diverse and elicit highly variable natural antibody responses. It remains to be seen if kits based on antigenically diverse antigens will detect antimalarial antibodies from prospective blood donors with sufficient sensitivity.

Diagnosis

In spite of the distinct clinical syndromes of severe disease, malaria is often misdiagnosed outside endemic areas as the initial signs of disease are nonspecific. Examination of traditional Giemsa-stained thick or thin films will in most cases confirm the diagnosis. The distinctive features of the different types of malaria are described in standard texts. 44 Examination of thick films for malaria parasites is a skill honed by regular practice and probably requires specific training for those working in nonendemic areas. Occasionally, severe disease from malaria can be present without detectable parasites in the peripheral circulation, and empirical therapy should be commenced if the patient is seriously ill and there is clinical suspicion of malaria infection.

The traditional methods of diagnosis have been challenged but not superseded by the application of modern methods. Microscopy with fluorescent stains (QBC), polymerase chain reaction assays, and some automated blood cell analyzers offer new approaches, but these are not in wide use. 45 More recently, dipstick tests for the detection of parasite antigens HRP2 and pLDH have been developed (Parasight-F [Becton Dickinson, Cockeysville, MD, USA], ICT [ICT Diagnostics, Sydney, Australia], and OptiMAL [Flow Inc., Portland, OR, USA]). These methods may be a useful adjunct in a busy lab, but the tests lose sensitivity at low parasitemias (< 10,000/μL) and have not been licensed for use by the Food and Drug Administration. 46

Treatment

Malaria requires urgent effective chemotherapy to prevent progression of disease such chemotherapy may be the most crucial public health intervention to reduce global mortality from malaria. In severely ill patients, good nursing care is vital. Monitoring and treatment of fits and hypoglycemia are essential and antipyretics should be given. 47

Chemotherapy

The drug treatment of malaria must take account of the expected pattern of drug resistance in the area where the infection was contracted, the severity of clinical disease, and the species of parasite. The spread of drug-resistant parasites and the optimal use of affordable, effective drugs are of continual concern, and these topics have been reviewed recently. 48, 49

Transfusion

Blood transfusion is in principle a straightforward solution to the treatment of severe malarial anemia, although controversy exists over the trigger for transfusion and the rate of administration of blood. The standard regimes of cautious and slow delivery of blood have been challenged by the demonstration that rapid initial flow rates may correct lactic acidosis. However, in nonimmunes and pregnant women, blood transfusion must be accompanied by careful hemodynamic monitoring to avoid precipitating or exacerbating pulmonary edema.

No formal controlled trials for the transfusion of patients with malaria have been performed. Whatever clinical guidelines emerge, blood transfusion in the heartland of malaria endemic areas is beset by many practical and theoretical problems, including the absence of well-characterized donor panels and the residual risk of HIV transmission in the serological window of infectivity without detectable antibodies (estimated at 1 in 2000). At a practical level, positive indirect antiglobulin tests in acute infection may make the exclusion of alloantibodies difficult. Depending on the clinical urgency and transfusion history, the least serologically incompatible blood may have to be given.

Exchange transfusion

One therapeutic option available in North America and in Europe for the urgent treatment of nonimmune patients with severe disease would be exchange blood transfusion. This procedure removes nonsequestered, infected erythrocytes and possibly circulating ‘toxins.’ In the absence of evidence from trials for the use of exchange transfusion in malaria, some have suggested that this treatment could be given for hyperparasitemia (> 20%) in severely ill nonimmune patients. 8, 50

Conclusion

The clinical features of malaria are diverse in severity and syndrome and include coma, severe anemia, and respiratory distress. In nonimmunes, severe disease may include renal and/or respiratory failure. Emerging themes in clinical management include the management of seizures and of respiratory distress. No reliable nonmicroscopic methods are available for the detection of low parasitemia or of those potential blood donors who may be harboring asymptomatic infection. The optimal chemotherapy regimes for endemic areas and for nonimmune patients are under continuous review as drug-resistant parasites emerge, but there is no specific adjunctive treatment for established disease. However, our understanding of both the parasitological and clinical aspects of pathophysiology is fragmentary, and a detailed description of the pertinent disease processes may lead to novel approaches to treat or to prevent malaria.


Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer? - Biology

Search for a word or term

Measure of molecular weight or mass the atomic mass unit a measure of mass for atoms and subatomic particles. One hydrogen atom has mass of 1 Da. Proteins and other macromolecule molecular weights are usually measured in kDa or kD (kiloDaltons) - 1000 Da.

Daughter cell

A cell that is the offspring of a cell that has undergone mitosis or meiosis.

Darwinian fitness

A measure of the relative contribution of an individual to the gene pool of the next generation. The true measure of evolutionary change of an organism. Darwinian fitness refers to the numerical advantage of having offspring. The individual with the most offspring has the higher fitness. The reasons can be chance or natural selection and are not important to measure fitness. It is often equated with survival of the fittest, which is often meant to be the strongest or best adapted individual. However, this interpretation is wrong, if it does not explain why a certain individual has the most offspring. Overall, the genetic variation of the individuals with the most offspring will dominate the gene pool of a population. The change in genetic variability in a population from generation to generation is the true measure of (micro-)evolution.

Digital audio tape. A high density storage medium.

Data compression

Large amounts of data can create enormous problems in storage and transmission. Data compression is the term to describe a variety of techniques to compress the volume of data, e.g., to represent large images with as few bits as possible, but to do so with minimum loss of information, according to some fidelity criterion
The widespread, consumer-market use of information in the form of images has contributed much to the development of data compression techniques. All image compression techniques try to get rid of the inherent redundancy, which may be spatial (neighbouring pixels), spectral (pixels in different spectral bands in a colour image) or temporal (correlated images in a sequence, e.g. television).
There are lossless methods, which are reversible, viz. do not sacrifice any information, and lossy methods which may be used if the quality of a compression-decompression sequence is judged by general criteria, like unchanged quality for the human visual system. Note that in image processing jargon, ``lossless'' is sometimes used in the sense of ``no visible loss''.
Examples of lossless methods are run-length coding, Huffman coding , or the Lempel-Ziv-Welsh (LZW) method. In run-length coding one replaces runs , sequences of equal greyvalues, by their lengths and the greyvalues. Huffman and LZW coding are approximations to entropy encoding, i.e. frequently used sequences are replaced by short codes, rare sequences by longer codes. In Huffman coding, sequences are single greyvalues, for LZW they are strings of greyvalues.
Of the many lossy coding techniques the simplest may be thresholding, applicable in some situations the most important ones are predictive and transform coding. In predictive coding, one removes the correlation between neighbouring pixels locally, and quantizes only the difference between the value of a sample and a predicted value (Quantization). Transform coding decorrelates the whole signal, e.g. a block of 8x8 pixels in an image, as a unit, and then quantizes the transform coefficients, viz one sets insignificant coefficients to zero. Only complete sets of unitary transforms are considered, i.e. transforms with the property of equal energy in the spatial domain and in the transform domain. This compression works well if the energy is clustered in a few transform samples. One talks of zonal coding, if certain coefficients are systematically set to zero (e.g. frequencies in the Fourier domain), and of adaptive coding, if coefficients are set to zero according to some threshold criterion of significance ( e.g. rank reduction in principal component analysis)
The following sets of unitary transforms are usually described in the literature:

  • Karhunen-Loeve or principal component analysis,
  • Discrete cosine transform,
  • Fourier transform,
  • Hadamard transform,
  • Slant transform,
  • Haar transform.

They are listed above in order of decreasing energy compaction and computer time used. The popular JPEG algorithm for compression of colour images uses essentially the discrete cosine transform (DCT), followed by quantization and Huffman coding (JPEG, short for the original committee ``Joint Photographic Experts Group'', is a widely used compression standard for still images).

Data normalization

A scaling process for numbers in a data array
In normalization, typically data points in a set are divided by a reference value, to reduce any systematic error in data. Normalization is used where there is such great spread in the data as to render difficult any standard statistical analysis. The transformation of the data results in a new distribution of numbers that are more homogeneously spread within a defined range.
The need for data normalization is determined by the user and depends on the application. Data are often normalized before any application processing and therefore data normalization is usually referred to as data pre-processing.
The purpose of data normalization depends on the proposed data application and methodological approach. It includes the use of linear scaling to compress a large dynamic range, scaling the values to correct for large variations or for handling obscuring variations, removing systematic errors in data, or efficiently removing redundancy in non-linear models.
Some data normalization methods include:
Mean-corrected data (Covariance matrix): The mean value is subtracted from each data point to produce a new array of normalized data.
Normalization by a maximum value: In this procedure, all un-normalized data are scaled so that they range between zero and one, with the maximum data point scaled to be one and the minimum to be zero and the other data points distributed between these end points.
Normalization by standard deviation: Each data point is normalized by dividing the standard deviation of the data set.
Logarithmic normalization: Each data point is divided by the mean value for that data set. Then the logarithm to base-two (log2) is calculated for that resultant value. The consequence of this logarithmic transformation is that there is a decrease in the variance of values as the transformation reduces the high values faster than the low ones.
Unit total probability mass normalization (Total intensity normalization): Each data point is divided by the sum of all data points, and then multiplied by the mean for that data set.
Standardizing data: Dividing the mean subtracted data (mean-corrected data see above) by the standard deviation of the data set.

The term dataset or "data set" is used in specific ways in different contexts.

  • ICPSR defines a dataset as "a collection of data records" and uses this term to encompass a file or group of files associated with one part of a study. Files associated with a dataset might include a data file, a machine- readable codebook , SPSS control cards, and other files related to the data file. Examples: The files associated with California might be considered one dataset in the 1990 Census of Population and Housing STF 1A study the files associated with the First Congress, House of Representatives, in the study "Congressional Roll Call Voting Records."

SAS. In the SAS statistical software, a SAS "data set" is the internal representation of data. Raw data when read by SAS command statements is converted into a SAS Data Set before SAS can use the data. SAS Data Sets have specific filename extensions for different operating systems e.g., a SAS 6.12 Data Set created in Unix has the filename extension ".ssd01" and in Windows, ".sd2".

Dauermodification

The persistence for several generations of an environmentally induced trait.

Daughter cells

The products of cell division of protists.

Death phase

Occurs when cells are being inactivated or killed because conditions no longer support growth or survival. Some environmental factors such as temperature can cause acute inactivation. Others may cause mild inactivation as with growth in the presence of organic acids.

Decay constant

A constant unique to each radioactive nuclide which represents the proportion of the atoms in a sample of that radionuclide undergoing decay in unit time. The decay constant of a nuclide is related to the nuclide's half-life.

Decay series

Most radioisotopes do not decay into a stable daughter element in one single decay but through a series of radioactive intermediaries.

Decerebrate rigidity (also known as Decerebate posture)

Exaggerated posture of extension as a result of a lesion to the prepontine area of the brain stem, and is rarely seen fully developed in humans. A spasticity resulting from functional disruption of brain stem activities at the mid-collicular level. In reporting, it is preferable to describe the posture seen.

Decorticate Posture (Decorticate Rigidity)

Exaggerated posture of upper extremity flexion and lower extremity extension as a result of a lesion to the mesencephalon or above. In reporting, it is preferable to describe the posture seen.

A decibel (abbreviated dB) is a unit used to record the level of sound.
A decibel is one-tenth of a bel and, since a bel is a logarithm to base 10, a decibel is a logarithm to base 100.1, i.e. a logarithm to base 1.259 (rounded to 3 decimal places).

An increase in the intensity of sound of 1.259 times represents an addition of one decibel. A doubling of intensity represents an addition of 3 decibels [because 2 = (1.259)3] a tripling of intensity represents an addition of about 5 decibels [because 3 = (1.259)5]. Ten times the intensity adds 10 decibels one thousand times the intensity adds 30 decibels [because 1000 = (1.259)30]. The important thing to realise is that just a few extra decibels makes a substantial difference to the intensity of sound to which a person is exposed. Because decibels convert a multiplication to an addition, you can&rsquot add decibels in the usual way, e.g. 85dB + 85dB = 88dB (not 170dB).

dB Sound Pressure Level (dB SPL): Measuring the level of a sound relative to a base level, set to be 20 μPascals (by convention worldwide):

dB Sound Hearing Level (dB HL): Measuring the hearing sensitivity of a subject expressed relative to normal hearing sensitivity in a large normative database. Here thresholds from a large normal-hearing young population have been measured at each of a number of standard audiometric frequencies at each frequency the mean value (in dB SPL) is then expressed as 0 dB HL. Then someone with a hearing level 20 dB worse than normal mean hearing sensitivity at (say 1 kHz) is said to have a hearing threshold of 20 dB HL at 1 kHz, etc.

Decimal numbers

The numbers in the base 10 number system.

Declarative memory (Episodic memory & Semantic memory)

The type of memory used when recalling (or declaring) facts or experiences, as opposed to skills.
Episodic memory: The type of declarative memory used when one talks about events in one&rsquos life (includes time, place and emotions).
Semantic memory: The type of declarative memory used when talking about facts and concepts.
Both semantic and episodic memories are declarative memories and can easily be forgotten.

Decomposition of movement

Lack of fluidity in movement characterized by the breaking down of composite movements into their component parts, a symptom of cerebellar disease

Decreasing function

A function is considered to be decreasing if f(b) < f(a) when b > a.

Decubitus ulcer (More commonly called a "pressure sore")

Pressure area, bed sore, skin opening, skin breakdown. A discolored or open area of skin damage caused by pressure. Common areas most prone to breakdown are buttocks or backside, hips, shoulder blades, heels, ankles and elbows. A breakdown of skin tissue caused by pressure on the skin, especially around bony areas (knees, heels, buttocks), when a person remains in one position for a long period of time, especially without padding friction under a brace moisture from perspiration moisture and chemicals from incontinence. A pressure sore, which begins as a red spot on the skin, can progress to an open wound with very serious medical complications. It is necessary to establish a daily routine for prevention which includes periodic pressure relief (e.g. by changing position) and the use of appropriate cushions.

Decussation

The crossing of a neural pathway in the spinal cord or brainstem from one side of that structure to the opposite side.

A conclusion arrived at by reasoning.

Deep vein thrombosis (DVT)

A blood clot (thrombus) in a deep vein in the thigh or leg. The clot can break off as an embolus and make its way to the lung, where it can cause respiratory distress and respiratory failure.

Definite integral

The definite integral of f(x) between a and b represents the area under the curve y = f(x) , above the x - axis, to the right of the line x = a, and to the left of the line x = b.
The definite integral of f(x) = F(b) - F(a) where F is an antiderivative function for f(x).

Degenerate code

A code in which several code words have the same meaning. The genetic code is degenerate because there are many instances in which different codons specify the same amino acid. A genetic code in which some amino acids may each be encoded by more than one codon.

Unit of measure of an angle. 1/360 of a full rotation. There are 360 degrees in a circle.

Degrees Brix

Measure of the density of a solution. (see Brix hydrometer scale)

Degrees of freedom

An estimate of the number of independent categories in a particular statistical test or experiment.

Deglutition

Swallowing
Consists of three phases:
The buccal phase occurs voluntarily in the mouth when the tongue forces the food bolus back into the pharynx.
The pharyngeal phase occurs involuntarily when food enters the pharynx, as follows:

  • The soft palate and uvula fold upward and cover the nasopharynx to prevent the passage of food up and into the nasal cavity.
  • The epiglottis, a flexible cartilaginous flap at the top of the larynx, folds down as the larynx rises. As a result, the opening to the larynx is covered, and food can pass only into the esophagus.

The esophageal phase occurs involuntarily in the esophagus. The esophageal sphincter, normally closed, opens to allow food to pass when the larynx rises during swallowing. When food reaches the lower end of the esophagus, the cardiac sphincter opens to allow the food to enter the stomach.

Degrees of freedom

The degrees of freedom of a statistical group are the number of values in the group which are free to vary. This number is usually one less than the sample size, the number of items in the group.A degree of freedom accounts for an independent variable in a system. Independent variables allow for changes within a system. For instance, the movement of two atoms in a gas is independent of each other assigning the distance between two atoms one degree of freedom. Two atoms covalently linked together within a molecule (a chemical bond) are also described by the same degree of freedom, also their movements are usually coupled. While this is true for the movement of the entire molecule, the length of the chemical bond is not static, but vibrates at very short time ranges measured in femto seconds to pico seconds (one trillionth to one billionth of a second). How many degrees of freedom a system has depends on the number of components and their interactions.

Breaking open at maturity, along a definite line, to release materials (e.g., seeds, spores).

The state a substance is in when moisture has been removed from it. Too much heat can dehydrate the body.

Dehydration reaction

A chemical reaction in which two molecules covalently bond to one another with the removal of a water molecule.

Deionized water

Water that has had the ions removed. Used in laboratories for making reagents.

Delayed language

A language disorder in which there is a noticeable slowness in the development of the vocabulary and grammar necessary for expressing and understanding thoughts and ideas.

Delayed speech

Failure of speech to develop at the expected age. More specifically: A deficit in speaking proficiency where the person performs like someone much younger.

Deletion (in genetics)

Loss of a DNA (chromosome) segment from a chromosome:
(1) A deficiency in a chromosome resulting from the loss of a fragment through breakage.
(2) A mutational loss of one or more nucleotides from a nucleic acid sequence (a gene).
Deletions are recognised genetically by:
Absence of reverse mutation
Presence of a deletion loop at meiosis that is isualized cytologically
Revealing of recessive lethals
pseudodominance
Hence a deletion chromosome = a chromosome containing a deletion.

An acute organic mental disorder characterized by confusion and altered,
possibly fluctuating consciousness due to an alteration of cerebral metabolism which may include delusions, illusions and/or hallucinations. The condition is reversible except when followed by dementia or death. Often emotional changes, typically appearing as anxiety and agitation, are present.

Delirium tremens

An acute and sometimes fatal brain disorder (in 10-15% of untreated cases) caused by total or partial withdrawal from excessive alcohol intake.Usually develops in 24-96 hours after cessation of drinking. Symptoms include fever, tremors, ataxia and sometimes convulsions, frightening illusions, delusions and hallucinations. The condition is often accompanied by nutritional deficiencies.

An organic mental disorder in which there is a deterioration or previously acquired intellectual abilities of sufficient severity to interfere with social or occupational functioning. Memory disturbance is the most prominent symptom. In addition, there is impairment of abstract thinking, judgment, impulse control and/or personality change.Dementia may be progressive, static or reversible, depending on the pathology with the availability of effective treatment.

Living on or near the bottom of a body of water.

A voice resonance problem that occurs when too little air passes through the nasal cavity.

Denaturation

1)The separation of the two strands of a DNA double helix, or
2) The severe disruption of the hydrogen bonded structure of any complex molecule without breaking the covalent bonds of its chains The loss of the native configuration of the macromolecule, such as the unfolding of the tertiary structure of an antibody protein.
Denaturation usually results in the loss of the macromolecule's biological or immunological reactivity or solubility.
For proteins, a process in which a protein unravels and loses its native conformation, thereby becoming biologically inactive. For DNA, the separation of the two strands of the double helix. Denaturation occurs under extreme conditions of pH, salt concentration, and temperature.
See Denatured

Denaturation map

A map of a stretch of DNA showing the locations of local denaturation loops, which correspond to regions of high AT content.

Denaturing gradient gel electrophoresis (DGGE)

A method for separating DNA fragments according to their variable mobilities under increasingly denaturing conditions (usually increasing formamide/urea concentrations).A method for separating species using their DNA. Abbreviated to DGGE.

Denaturing high-performance liquid chromatography (DHPLC)

Large scale chromatographical method to detect sequence polymorphisms.

Loss of natural configuration (of a molecule) through heat or other treatment, resulting in a loss of biologically activity of the molecule.
Fully denatured DNA is single-stranded.

One of usually numerous, short, highly branched processes of a neuron that conveys nerve impulses toward the cell body.

Denervation hypersensitivity

Elevated response of a nerve or muscle membrane receptor to a transmitter following resection or removal of its afferent nerve supply.After a nerve or nerves o a target structure has been cut or removed, there is often a hypersensitivity of that target structure to applications of the neurotransmitter that used to be released by the cut nerves. Thus, the target structure that has been denervated has become hypersensitive.

Denhardt's solution

A solution commonly used during probe hybridizations that involve filters (such as Southern, Northern, or Western blots).

Denitrifcation

The process by which certain bacteria living in poorly aerated soils break down nitrates, using the oxygen for their own respiration and releasing nitrogen back into the atmosphere.

Denominator

The bottom part of a fraction.

Mass per unit volume. Usually expressed as a body&rsquos specific gravity

Density-dependent factor

Any factor influencing population regulation that has a greater impact as population density increases.

Density-dependent inhibition

The phenomenon observed in normal animal cells that causes them to stop dividing when they come into contact with one another.

Density-dependent factors

Any factor influencing population regulation that acts to reduce population by the same percentage, regardless of size.

Density-gradient centrifugation

A method of separating macromolecules by their
(1) differential rate of sedimentation in a centrifugal gradient
(2) differential bouyancy in a density gradient.

Dentatorubro-pallidoluysian atrophy (DRPLA)

A C-A-G trinucleotide repeat disorder that is characterized by abrupt muscle jerking, involuntary movements, and eventual dementia.

Deoxyribonuclease

A class of enzymes which digest DNA. The most common is DNase I, an endonuclease which digests both single and double-stranded DNA.

Deoxynucleotide

Components of DNA, containing the phosphate, sugar and organic base. When in the triphosphate form, they are the precursors required by DNA polymerase for DNA synthesis (i.e., ATP, CTP, GTP, TTP).

Deoxyribonuclease (dnase)

An enzyme that degrades DNA to nucleotides.

Deoxyribonucleic acid (DNA)

The nucleic acid molecule consisting of deoxyribonucleotide building blocks that encode genetic information. An antiparallel double helix of nucleotides (having deoxyribose as their sugars) linked by phosphodiester (sugar-phosphate) bonds to adjacent nucleotides in the same chain and by hydrogen bonds to complementary nucleotides in the opposite chain.
The fundamental substance of which genes are composed. The genome of most organisms is contained in a double-stranded, double-helical form held together with chemical bonds between each strand of complementary nucleotide base pairs.
Deoxyribose = The sugar component of DNA, having one less hydroxyl group than ribose, the sugar component of RNA.
DNA is a double-stranded molecule held together by weak bonds between base pairs of nucleotides. The four nucleotides in DNA contain the bases: adenine (A), guanine (G), cytosine (C), and thymine (T). In nature, base pairs form only between A and T and between G and C thus the base sequence of each single strand can be deduced from that of its partner.

Deoxy-ribonucleotide triphosphate (dNTP)

A generic term referring to the four deoxyribonucleotides: dATP, dCTP, dGTP and dTTP.

Deoxyribose

The sugar component of DNA, having one less hydroxyl group than ribose, the sugar component of RNA.

Dependent variable

The output of a function. In an experiment, the dependent variable is the factor that responds when another factor is manipulated.

Depolarisation

A reduction in the polarity (charge) found across a cell membrane at rest an electrical state in an excitable cell whereby the inside of the cell is made less negative relative to the outside than at the resting membrane potential.Cell membranes are able to separate charge because of their selective permeability to ions. This charge separation is found even at rest, is known as the Resting Membrane Potential (RMP or EM), is typically such that the inside of the cell membrane is negatively charged compared to the outside. When a stimulus or some other event causes inward currents carried by Na+ and Ca++ ions this difference in charge moves towards 0 (i.e., a lesser difference in charge), this is called depolarization. In many cells, the depolarization can actually overshoot 0 and attain some positive value depending on what ions are permeating the cell and causing the depolarization.

A type of bipolar disorder characterized by lowered mood, slowed thinking, decreased movement or agitation, loss of interest, guilt, lowered self-esteem, sleep disturbance and decreased appetite.

Derepressed

The condition of an operon that is transcribing because repressor control has been lifted. May apply more generally to any gene being transcribed.

The rate of change of a function. The derivative at x of f(x) is the slope of the tangent line at (x, f(x)). y' = f ' (x) = [f(x + delta x) - f(x)] / delta x.

Describes a character state that is present in one or more subclades, but not all, of a clade under consideration. A derived character state is inferred to be a modified version of the primitive condition of that character, and to have arisen later in the evolution of the clade. For example, "presence of hair" is a primitive character state for all mammals, whereas the "hairlessness" of whales is a derived state for one subclade within the Mammalia.

The inner of the two layers of skin. The dermis is a connective tissue layer under the epidermis containing elastic and collagen fibers, capillary networks, and nerve endings that signal somatic information such as nociceptive (painful) and temperature sensations.

Desalination

The removal of salts from saline water to provide freshwater. This method is becoming a more popular way of providing freshwater to populations.

An enzyme (group) "family" that is present within the soybean plant and other oilseed crops (e.g., sunflower, canola, corn/maize).One or more desaturases is involved in the synthesis "pathway" via which oilseed crops produce unsaturated fatty acids (e.g., linoleic acid). A desaturase is also involved in production of beta carotene (in some plants).

Descriptor culling

Reducing the number of descriptive terms used in descriptive analyses to a practical or manageable number for analysis or interpretation.

Desensitisation

Designer foods

Foods that are enriched with nutraceuticals, antioxidants, and secondary metabolites to improve the physical performance of the body.

A type of intercellular junction in animal cells that functions as an anchor.

Detector (in assays)

An analytical instrument which is capable of measuring the amount of tracer label in an immunoassay sample, such as scintillation counters, microplate readers, and automated immunoassay analyzers.

Detector data (in assays)

The initial sample measurement(s) recorded by the detector instruments which is converted into the raw data.
The raw data are then transmitted from the detector instrument.

Determinant

The determinant | a b | = ad - bc.
| c d |

Determinate cleavage

A type of embryonic development in protostomes that rigidly casts the developmental fate of each embryonic cell very early.

Determinate growth

A type of growth characteristic of animals, in which the organism stops growing after it reaches a certain size.

Determination (of cells)

The process of commitment of cells to particular fates. The progressive restriction of developmental potential, causing the possible fate of each cell to become more limited as the embryo develops.

Deterministic

Events that have no random or probabilistic aspects but proceed in a fixed predictable fashion.

Detritivore

An organism that eats detritus. Fragments of dead plant and animal material before, during and after breakdown by agents of decay. May incorporate inorganic matter (such as mud).

Development

The process by which a multicellular organism is produced from a single cell. The progressive production of the phenotypic characteristics of a multicellular organism, beginning with the fertilization of an egg.

Developmental aphasia

A language disorder in children, caused by brain damage, characterized by complete or partial impairment of language comprehension, formulation, and use.

Developmental labeling approach

An approach to labeling that is based on deviations in the course of development from what is considered normal.

Temperature to which the air must be cooled to reach saturation (assuming air pressure remains the same). The dew point is a direct measure of the amount of moisture present in the air, and directly affects how you feel or in other words measures the amount of humidity in the air. The temperature never drops below its dew point, but can drop to it.

Diabetes Insipidus

This condition is a result of missing antidiuretic hormone (ADH). This hormone is made by the pituitary gland and helps the kidneys balance the fluid in the body. A person with this condition may have a large amount of urine each day and be very thirsty. If untreated, this condition can lead to dehydration, problems with growth, weight gain and appetite.

Diabetes Mellitus, Types I and II

A disorder associated with defects in insulin action. Type I diabetes is characterized by inadequate insulin secretion Type II diabetes is characterized by impaired insulin secretion in response to elevated blood glucose levels or by loss of sensitivity to insulin by target cells.

The line segment connecting two nonadjacent vertices in a polygon.

Diagnostic and Statistical Manual of Mental Disorders

A classification system for mental illnesses developed by the American Psychiatric Association.

1 The nature of a disease the identification of an illness. 2 A conclusion or decision reached by diagnosis. The diagnosis is rabies . 3 The identification of any problem. The diagnosis was a plugged IV.

Removal of small molecules from a solution of a macromolecule, by allowing them to diffuse through a semipermeable membrane into water or buffer.
The process carried out at the kidney.

The line segment joining two points on a circle and passing through the center.

A sheet of muscle that forms the bottom wall of the thoracic cavity in mammals active in ventilating the lungs.

Excessive bowel movements of loose, watery stools, which can be acute or chronic.
Chronic diarrhea may lead to nutrient deficiencies because food may be passing through the intestinal tract too quickly for nutrients to be absorbed.
Acute diarrhea may lead to electrolyte imbalances and dehydration which can be life threatening.

A loss of function due to depression of activity at some distance from a lesion.

The stage of the heart cycle in which the heart muscle is relaxed, allowing the chambers to fill with blood..

Diastolic pressure

The pressure in an artery during the ventricular relaxation phase of the heart cycle.

Production of male and female reproductive elements at different times by a hermaphroditic organism in order to ensure allogamy.

Dichotomous tree

A tree where all branching points are dichotomies. That is, a tree is dichotomous if at each branch point there are only two immediate descendents. This is in contrast to a polytomous tree.

Dichotomy (Plural = Dichotomies)

A branch point on a tree that has two immediate descendents.

Dictionary file

A special form of machine-readable codebook that contains information about the structure of a data file and the locations and, often, the names of variables variables in the data file.
Typically, you use a dictionary file and a data file together with statistical software the statistical software uses the dictionary so that you may specify variables by name, rather than having to specify their locations in the file.

Dideoxy method

A method of DNA sequencing that uses chain-terminating (dideoxy) nucleotides.

Dideoxynucleotides (didN)

Chain-terminating precursors of DNA synthesis that block further polymerization when added to the end of the DNA strand by DNA polymerase.
These nucleotides lack a 3'-OH (hydroxyl) group necessary for continued 5'-to-3' DNA synthesis. Dideoxynucleotides are used in molecular biology for Sanger-type DNA sequencing, and in medicine as anti-retroviral drugs for the treatment of HIV infection (e.g., ddI, ddC, and AZT).

Dielectric constant

Property of a material representing the ability to store electromagnetic energy.

Dielectirc loss

Property of a material representing the ability to dissipate electromagnetic energy as heat.

The result of subtracting two numbers.

Difference threshold (successive)

The minimum increase in stimulus intensity required to produce a perception of a change in the stimulus.

Differential RNA synthesis

Concept that cells are different from each another because they turn on (transcribe mRNAs from) different sets of genes thus each cell makes different proteins appropriate to its particular function.

Differentiable

A function is differentiable over an interval if it is continuous over the interval and if the derivative exists everywhere on the interval.

Differential

An infinitesimally small change in a variable, represented by d, as in dx, or dy.

Differentiaton

1. In embryology The process whereby an unspecialized embryonic cell acquires the features of a specialized cell such as a heart, liver, or muscle cell.
2. In mathematics: The process of finding a derivative.
Differentiation is controlled by the interaction of a cell's genes with the physical and chemical conditions outside the cell, usually through signaling pathways involving proteins embedded in the cell surface.

Differentiaton pathways

The chemical/gene expression pathways responsible for causing a single type of cells (e.g., stem cells, embryonic stem cells, etc.) to become multiple, different types of (specialized) cells.Expression of each of the specific genes responsible for (i.e., the genes that code for the particular proteins which cause) differentiation is itself controlled by exquisite methylation and acetylation of the histone proteins adjacent to those genes.

Diffraction

The deviation in the path of a wave that encounters the edge of an obstacle. e.g., The bending of light as it passes through a small slit or opening

Diffusion feeding

Feeding strategy in which the predator relies on the movements of the prey to make contact - as in heliozoa and suctoria.

Diffuse Axonal Injury (DAI)

A shearing injury of large nerve fibers (axons covered with myelin) in many areas of the brain. It appears to be one of the two primary lesions of brain injury, the other being stretching or shearing of blood vessels from the same forces, producing hemorrhage

Diffuse Brain Injury

Injury to cells in many areas of the brain rather than in one specific location.

The spontaneous movement of substances from a region of high concentration (high chemical potential) to a region of low concentration (low chemical potential)Molecules undergo spontaneous Brownian motion, which is dependent on the temperature (the higher the temperature, the greater the Brownian motion). In regions of high concentration of a molecule, the chances of colliding with other molecules are therefore higher than in regions of low concentration of that molecule. In turn this means that there is greater chance of &ldquobouncing off&rdquo after collisions with each other from a region of high molecule concentration to a region of low concentration.Diffusion governs the movement of many substances in the body, especially across the cell membrane. The structure of the cell membrane confers selective permeability whereby the cell can regulate what substances can move across from one side of the cell membrane to the other side.

Diffusion coefficient (D)

The diffusion coefficient D describes the relationship between a concentration gradient DC/Dx and the flow of matter per unit area (flux rate J).

DiGeorge syndrome (Also known as Shprintzen, velo-cardio-facial, and 22q11.2 deletion syndrome.)

A genetic disease caused by a missing piece of chromosome material on chromosome #22 that results in many different health problems, and affects the normal fetal development of the heart, thymus, and parathyroid glands.

The ten symbols, 0, 1, 2, 3, 4, 5, 6, 7, 8, and 9 are digits. Example: the number 365 has three digits: 3, 6, and 5.

Digital mammography

A technique for recording x-ray images in computer code instead of on x-ray film, as with conventional mammography.
The images are displayed on a computer monitor and can be enhanced (lightened or darkened) before they are printed on film. From the patient&rsquos perspective, the procedure for a mammogram with a digital system is the same as for conventional mammography. Digital mammography may have some advantages over conventional mammography. The images can be stored and retrieved electronically, which makes long-distance consultations with other mammography specialists easier. Because the images can be adjusted by the radiologist, subtle differences between tissues may be noted. The improved accuracy of digital mammography may reduce the number of follow-up procedures. Despite these benefits, studies have not yet shown that digital mammography is more effective in finding cancer than conventional mammography.

The process of breaking down food into molecules small enough for the body to absorb.

A drug commonly used to treat congestive heart failure and certain heartbeat irregularities that is obtained from leaves of the Foxglove (digitalis) plant.

A hybrid individual that is heterozygous for two genes or two characters.

Dihybrid cross

A breeding experiment in which parental varieties differing in two traits are mated.

Having two different and distinct nuclei per cell found in the fungi. A dikaryotic individual is called a dikaryon.

A dilution is the ratio of the volume of pure specimen to the total volume of specimen plus a diluent such as buffer.Dilutions are expressed as the number of parts of pure specimen, a colon, and the total number of parts in the solution. The number of parts of diluent are determined by subtracting the number of pure specimen parts from the total. A dilution of 1:10 contains one part pure specimen and nine parts diluent. A dilution factor is the total number of parts with the volume of pure specimen being one part

The dimension of a space is the number of coordinates needed to identify a location in that space.

Dimerization

The chemical union of two identical molecules.

Displaying two separate growth forms.

Compound consisting of two amino acid units joined together, linking the amino (-NH2) group of one with the carboxylic acid group (-COOH) of the other.

Paralysis that affects both sides of the body, due to injury of both hemispheres of the brain. More commonly affects the legs more than the arms.

A serious bacterial infection which can cause pneumonia, heart failure, nerve damage, or death by suffocation. Immunization with the Diphtheria-Tetanus-Pertussis (DTP) vaccine protects against this disease.

Having two different sets of chromosomes in the same nucleus of each cell A full set of genetic material, consisting of paired chromosomes one chromosome from each parental set. The state of having each chromosome in two copies per nucleus or cell.
A cell having two chromosome sets, or an individual having two chromosome sets in each of its cells. Diploid organisms have diploid cells. Diploid cells have two copies of each chromosome.
The amount of DNA in diploid cells defines the normal DNA content for the species Most metazoans and plants are diploid. Most animal cells except the gametes have a diploid set of chromosomes. The diploid human genome has 46 chromosomes.

Diploid life cycle

Occurs when the only multicellular stage in an organism's life cycle is diploid.

Double vision, or the simultaneous awareness of two images of the same object.
Results from a failure of the two eyes to work in a coordinated fashion Covering one eye will erase one of the images.

1. A molecule having both partial positive (d+) and partial negative (d+) charges.
2. For oscillating magnetic fields, a magnetic particle that contains a *north* and *south* magnetic pole.

Dipole-dipole interaction

A weak intermolecular force of attraction between a partial positive (d+) charge on one particle and a partial negative (d+) charge on a second particle.

Computer-fitting of binding data (either saturation or competition data) to the logistic equation:

where b = concentration of ligand bound to the receptor, [L] = conc. of free ligand, K is the dissociation constant for the ligand and n is a constant which should equal 1 if the assumptions in kinetics of binding are valid (it can represent the number of ligand molecules which bind to each receptor). When saturation or competition data are directly fitted to a logistic equation in this way, the Hill plot becomes unnecessary, since the calculated value of n is equivalent to the slope of the Hill plot.

Directed differentiation

The manipulation of stem cell culture conditions to induce differentiation into a particular cell type.

Directed molecular evolution

A laboratory version of evolution at the molecular level that can produce "designer molecules."A large starting population of molecules (typically nucleic acids) that varies randomly in base sequence and shape is subjected to replication with variation, followed by selection. After several cycles of replication and selection, the population of molecules will evolve toward one containing a high proportion of molecules well adapted to the selection criterion applied.

Directed mutagenesis

Altering some specific part of a cloned gene and reintroducing the modified gene back into the organism.

Direct fluorescent antibody test (DFA)

A test that uses a fluorescent antibody to directly detect an antigen.

Directional cloning

DNA insert and vector molecules are digested with two different restriction enzymes to create non-complementary sticky ends at either end of each restriction fragment.
This allows the insert to be ligated to the vector in a specific orientation and prevent the vector from self-ligation.

Directional selection

Natural selection that favors individuals on one end of the phenotypic range.
Selection leading to a consistent directional change in any character of a population through time, for example selection for larger eggs.

Directly proportional

y is directly proportional to x if y = kx

Disaccharide

A class of sugars composed of two monosaccharide units joined together (by dehydration synthesis). The best known example is sucrose, which is composed of a glucose molecule joined with a fructose molecule. Likewise, lactose is composed of a glucose unit with a galactose unit, and maltose is a disaccharide composed of two joined glucose units.

The volume of water that passes a given location within a given period of time. Usually expressed in cubic feet per second.

Discontinuous replication

Replication of DNA in short 5' to 3' segments using the 5' to 3' strand as a template while going backward away from the replication fork.

Discriminability index (d&rsquo)

A measure of the separation between two distributions, and thus the ability to discriminate between the two distributions. The difference in means of two distributions divided by their standard deviations. It is a poor measure of performance when the amount of data in the distributions is low or when the two distributions are widely separated.

Discriminance analysis

Multivariate statistical analysis method
A dependent variable Y and several independent X. Can the combination of several X terms explain product differences Y?

Discriminant

The discriminant tells how many roots there are for the equation and the nature of the roots.
The discriminant of a quadratic equation, ax2 + bx + c = 0 is b2 - 4ac.

Disinhibition

Inability to suppress (inhibit) impulsive behavior and emotions. Generally occurs after frontal lobe damage.

Disintegrations Per Minute (DPM)

The number of radioactive disintegrations which actually occurred during one minute.The DPM of a sample is usually determined by dividing the number of disintegrations which were recorded by the efficiency of the detector instrument under the same conditions, particularly the amount of quenching, as were present in the measured sample.

Having no elements in common.

Disjunction

Disorientation

Not knowing where you are, who you are, or the current date. Health professionals often speak of a normal person as being oriented "times three" which refers to person, place and time.

Disorganized schizophrenia (Also known as"hebephrenic")

Characterized by disorganized thinking, shallow and inappropriate affect, inappropriate giggling, silly and regressive behavior and mannerisms and frequent hypochondriacal complaints. Delusions and hallucinations are usually bizarre and disorganized.

The scattering of organisms of a species, often following a major reproductive event.
Spores and larvae are commonly dispersed into the environment. Pollen or gametes may also be dispersed, but in this case the intent is to target another individual so that reproduction may occur. Organisms may disperse as spores, seeds, eggs, larvae, or adults.

Dispersive replication (of DNA)

A proposed model of DNA replication. This model involves the breaking of the parental DNA strands during replication, and somehow, a reassembly of molecules that were a mix of old and new fragments on each strand of DNA. (see Conservative replication and Semiconservative replication)

Disruptive selection

Selection favouring individuals that deviate in either direction from the population average. Selection favours individuals that are larger or smaller than average.

Dissociation constant

(1) An equilibrium constant (Kd) for the dissociation of a complex of two or more biomolecules into its components for example, dissociation of a substrate from an enzyme.
(2) The dissociation constant of an acid (Ka) or base (Kb), describing its dissociation into its conjugate base and a proton or conjugate acid and a hydroxide ion.

Dissociation disorder

A mental condition in which ideas or desires are separated from the mainstream of consciousness or from one's personality to a degree that they are no long accessible to memory or consciousness. The person has difficulty or is unable to perceive things or situations as a whole, but instead tends to respond to stimuli in terms of parts or segments.

Away from. Contrast with Proximal.

Distal tubule

The section of the renal tubule where tubular secretion occurs. Tubular secretion is the process in which ions and other waste products are transported into the distal tubules of the nephron.

Distortion (in speech)

An articulation error in which there are inaccurate productions of phonemes that resemble the target form. Some examples of these distortions are the lisps (lateral and dental), palatal distortions (where the wrong part of the tongue is used to form s, z, sh, and zh sounds), and the retroflex distortions (too much curling of the tip of the tongue).

Distributive property

A drug used to increase urine formation and output. Diuretics are prescribed for the treatment of edema (the accumulation of excess fluids in the tissues of the body), which often occurs as the result of disease of the kidneys, liver, lungs, or heart. Diuretics are also used to treat hypertension (high blood pressure).

Having a period or cycle that is a full tidal day Being active during the daytime rather than at night. Involving a 24-hour period that includes a day and the adjoining night.

Divergent series

A series whose sum is infinite.

Diverticulosis/diverticulitis

Small pouches may form along the walls of the large intestine called diverticuli which if symptomatic, causing discomfort to the patient, is called diverticulosis. These abnormal outpocketings may collect and not be able to empty fecal material which can lead to inflammation, diverticulitis

Term used to describe numbers of taxa, or variation in morphology.

Diversifying selection

Natural selection that favors extreme over intermediate phenotypes.

The number being divided. In a / b = c, a is the dividend.

The number doing the dividing. In a / b = c, b is the divisor.

Long molecule in the nucleus of cells, shaped like a double-helix, contains the genetic information that determines the development and functioning of an organism's cells. See Deoxyribonucleic acid

Storage of DNA, which may or may not be the complete genome, but should always be accompanied by inventory information.

DNA-DNA hybridization

When DNA is heated to denaturation temperatures to form single strands and then cooled double helices will re-form (renaturation) at regions of sequence complementarity. This technique is useful for determining sequence similarity among DNAs of different origin and the amount of sequence repetition within one DNA.

DNA fingerprint

A technique for identifying individual organisms based upon the uniqueness of their DNA pattern.The largely individual-specific autoradiographic banding pattern produced when DNA is digested with a restriction endonuclease that cuts outside a family of VNTRs, and a Southern blot of the electrophoretic gel is probed with a VNTR-specific probe.The technique has applications in forensics, paternity testing, anthropology, conservation biology and ecological research.

The ratio of GO/G1 peak channel in a DNA histogram of an experimental sample to the GO/G1 peak channel of a reference sample, when normal human diploid cells or nuclei are the reference. This is a measure of DNA aneuploidy, or abnormal DNA content.

An enzyme that rejoins cut pieces of DNA. A linking enzyme essential for DNA replication catalyzes the covalent bonding of the 3' end of a new DNA fragment to the 5' end of a growing chain.

Small DNA fragment used to locate a specific base sequence within a larger fragment
Any unique DNA sequence which can be used in DNA hybridization, PCR or restriction mapping experiments to identify that sequence.

DNA methylation

The addition of methyl groups (&ndashCH3) to bases of DNA after DNA synthesis may serve as a long-term control of gene expression.

DNA polymerase

An enzyme that catalyzes the elongation of new DNA at a replication fork by the addition of nucleotides to the existing chain.

DNA polymorphism

One of two or more alternate forms (alleles) of a chromosomal locus that differ in nucleotide sequence or have variable numbers of repeated nucleotide units.

A single-stranded piece of DNA that binds specifically to a complementary DNA sequence. A chemically synthesized, radioactively labeled segment of nucleic acid used to find a gene of interest by hydrogen-bonding to a complementary sequence.
The probe is labeled (e.g., with a fluorescent or radioactive tag or enzyme) in order to detect its incorporation through hybridization with DNA in a sample.

DNA replication

The process of making an identical copy of a section of duplex (double-stranded) DNA, using existing DNA as a template for the synthesis of new DNA strands. In humans and other eukaryotes, replication occurs in the cell nucleus.

DNA-RNA hybridization

When a mixture of DNA and RNA is heated to denaturation temperatures to form single strands and then cooled RNA can hybridize (form a double helix) with DNA that has a complementary nucleotide sequence. Useful for determining relationships between DNAs and RNAs.

DNA sequencing

Procedures for determining the nucleotidesequence of a DNA fragment.

DNA Synthesizer

A machine which automatically makes short, artificial polynucleotides or oligonucleotides with any desired sequence of nucleotide bases.

Docking protein

Responsible for attaching (docking) a membrane-bound vesicle (e.g., a ribosome or transmitter-containing vesicle) to a membrane by interacting with a signal particle attached to a the structure destined to be membrane bound.

1. In molecular biology: A discrete portion of a protein with its own function.
2. In mathematics and logic: The set of all possible values of the argument of a function.
The combination of domains in a single protein determines its overall function.

Domestic water use

water used for household purposes, such as drinking, food preparation, bathing, washing clothes, dishes, and dogs, flushing toilets, and watering lawns and gardens. About 85% of domestic water is delivered to homes by a public-supply facility, such as a county water department. About 15% of the Nation's population supply their own water, mainly from wells.

Dominance hierarchy

A linear "pecking order" of animals, where position dictates characteristic social behaviors.

Dominant allele

In a heterozygote, the allele that is fully expressed in the phenotype.

A period of suspended growth and metabolic activity. Many plants, seeds, spores, and some invertebrates become dormant during unfavorable conditions. Many animals hibernate during winter, a form of dormancy. A period during which growth ceases and metabolic activity is greatly reduced dormancy is broken when certain requirements, for example, of temperature, moisture, or day length, are met.

Pertaining to or situated near the back opposite of ventral.

Dorsiflexion

Backward flexion of a foot or hand, or of their digits. That is, bending fingers or toes backwards towards the upper surface of the foot or hand.When applied to the ankle, the ability to bend at the ankle, moving the front of the foot upward. (see Plantar flexion)

Dose-Response Relationship

The relationship between (1) the dose, actually based on "administration dose" ( i.e. exposure) rather than actual absorbed dose, and (2) the extent of therapeutic or toxic effect produced by the xenobiotic.

Dot blotting

A technique for measuring the amount of one specific DNA or RNA in a complex mixture. A method for detecting proteins by the specific binding of an antibody or binding molecule to a sample spot on nitrocellulose paper.
The samples are spotted onto a hybridization membrane (such as nitrocellulose or activated nylon, etc.), fixed and hybridized with a radioactive probe. The bound sample is visualized using an enzymatic or fluorimetric reporter conjugated to the probe. The extent of labeling (as determined by autoradiography and densitometry) is proportional to the concentration of the target molecule in the sample. Standards provide a means of calibrating the results.
Used for blotting cloned DNA without prior restriction digestion and electrophoresis. Autoradiography reveals dots indicating probe hybridization.

A two parameter data graph used for acquisition and analysis. Each dot on the display represents one event that the flow cytometer analyzed.

Double bond

The sharing of four electrons between two atoms.

Double blind study

A clinical trial or experiment in which neither the investigators nor the patients know which treatment has been administered.

Double circulation

A circulation scheme with separate pulmonary and systemic circuits, which ensures vigorous blood flow to all organs.

Double digest

The product formed when two different restriction endonucleases act on the same sample of DNA.

Double fertilization

A mechanism of fertilization in angiosperms, in which two sperm cells unite with two cells in the embryo sac to form the zygote and endosperm.

Double helix

The normal structural configuration of DNA consisting of two adjacent helices (of polynucleotide strands) winding about the same axis.
The interlocking helices are joined by hydrogen bonds between paired bases.

Double hemiplegia

Paralysis that involves both sides of the body, with one side being more greatly affected.

Double infection

Infection of a bacterium with two genetically different phages.

Double membrane

In mitochondria and plastids, there is a two-layered membrane which surrounds the organelle. This is believed to be the result of endosymbiosis, with the outer membrane coming from the eukaryotic cell, and the inner membrane belonging to the original prokaryote which was "swallowed".

Two particles stuck together, which a flow cytometer records as one larger event. Particles may also occur in triplets and higher associations.

Down syndrome

A condition resulting from a chromosomal abnormality, primarily the presence of an extra (or part of) a chromosome (specifically chromosome 21) , characterized by mental retardation and heart and respiratory defects. Characteristic features include mental retardation of varying degrees, epicanthal folds, oval-shaped eyes, thicker tongue, short neck. microcephaly, looseness of the joints, flat bridge of nose, etc.

Downstream (in genetics)

A convention used to describe features of a DNA sequence, gene or mRNA related to the position and direction (5' to 3') of transcription by RNA polymerase or translation by the ribosome. Downstream (or 3' to) is in the direction of transcription (or translation) whereas upstream (5' to) is in the direction from which the polymerase (or ribosome) has come. Conventionally DNA sequences, gene maps and RNA sequences are drawn with transcription (or translation) from left to right and so downstream is towards the right.

Drainage basin

land area where precipitation runs off into streams, rivers, lakes, and reservoirs. It is a land feature that can be identified by tracing a line along the highest elevations between two areas on a map, often a ridge. Large drainage basins, like the area that drains into the Mississippi River contain thousands of smaller drainage basins. Also called a "watershed."

lowering of the ground-water surface caused by pumping.

Drip irrigation

a common irrigation method where pipes or tubes filled with water slowly drip onto crops. Drip irrigation is a low-pressure method of irrigation and less water is lost to evaporation than high-pressure spray irrigation

Driving force

A terminology used in thermodynamics expressing the availability of energy to 'drive' a process such as mechanical work or chemical synthesis. Driving forces exist where a potential gradient exist. A potential gradient can be in form of a temperature gradient causing heat to flow, an electrical gradient causing electrons or ions to flow, or a concentration gradient causing diffusion.

Dropping point

Temperature at which a sample of fat becomes sufficiently fluid to flow under the conditions of the test. A portion of molten fats introduced into a sample cup, crystallized and then heated at a constant rate. The temperature at which the sample is able to flow through the orifice in the bottom of the cup is the end point.

Dual energy X-ray absorptometry (DEXA or DXA)

A technique for scanning bone and measuring bone mineral density (BMD).
A DXA scanner produces 2 X-ray beams, each with different energy levels. One beam is high energy while the other is low energy. The amount of x-rays that pass through the bone is measured for each beam. This will vary depending on the thickness of the bone. Based on the difference between the 2 beams, the bone density can be measured. DXA is relatively easy to perform and the amount of radiation exposure is considered low.

Duchenne muscular dystrophy

A lethal muscle disease in humans caused by mutation in a huge gene coding for the muscle protein dystrophin inherited as an X-linked recessive phenotype. The most common and severe form of muscular dystrophy. Dystrophic muscles are fragile, prone to injury, regenerate poorly after damage, and susceptible to Ca2+-overload and degeneration. Defective Ca2+ regulation has been implicated in these processes and it is widely accepted that dystrophic muscles have an elevated cytosolic [Ca2+] even at rest. DMD is an X-linked neuromuscular disease affecting

1 in 3500 live born males from early childhood. It is caused by a variety of mutations and deletions in the dystrophin gene on chromosome Xp21. The disease is progressive and eventually affects all muscles such thatpatients become dependent on a wheelchair, usually before their teens, and have only 25% of the muscle mass of healthy children. The relentless muscle wasting leads to premature death from respiratory or cardiac failure. The primary abnormality is the absence of the dystrophin protein, which normally links the actin cytoskeleton to laminin in the extracellular matrix through the dystrophin associated protein complex (DAPC). The DAPC stabilises the membrane against shear stresses and plays a protective role against muscle damage caused by &ldquoeccentric&rdquo (lengthening) actions. In addition to its mechanical functions, dystrophin has been suggested to play a role in intracellular processes such as Ca2+ regulation and signal transduction. There is no cure and existing therapies are ineffective.

Ductal lavage

An investigational technique for collecting samples of cells from breast ducts for analysis under a microscope. A saline solution is introduced into a milk duct through a catheter inserted into the opening of the duct on the surface of the nipple. Fluid, which contains cells from the duct, is withdrawn through the catheter. The cells are checked microscopically to identify changes that may indicate cancer that may increase the risk for breast cancer. The usefulness of ductal lavage is still under study.

The first section of the small intestine, where acid chyme from the stomach mixes with digestive juices from the pancreas, liver, gallbladder, and gland cells of the intestinal wall.

Duplication

An aberration in chromosome structure resulting from an error in meiosis or mutagens duplication of a portion of a chromosome resulting from fusion with a fragment from a homologous chromosome.

Dura mater (Latin for tough mother)

One of the three layers of meninges that cover and protect the brain and spinal cord. The dura mater is the thick and tough outer membrane lying just inside the skull and vertebrae, and close to the cranium and vertebrae.Separated from the arachnoid mater by the subdural space. In the brain, there are channels within the dura mater, the dural sinuses, which contain venous blood returning from the brain to the jugular veins.In the spinal cord, the dura mater is often referred to as the dural sheath. Here the inner and outer layers of the dura mater are separated by the extradural space. This fat-filled space between the dura mater and the vertebrae acts as a protective cushion to the spinal cord. (see Arachnoid mater, Meninges, Pia Mater)

D-value, decimal reduction time

Time required for a one-log cycle reduction in the microbial population, at a specific temperature, pressure, or electric field intensity. For the D-value to be meaningful, the semi logarithmic survivor curve must be a straight line.

A device that creates electricity by turning around a magnet near a coil of wire.

Dynamic compression

The compression of a fracture by weight bearing and/or muscle contraction. Fracture fixations that employ dynamic compression include dynamic hip screws, anti-glide plates, dynamized tibial and femoral nails, and tension band wiring.

A microtubule-dependent motor protein A large contractile protein forming the sidearms of microtubule doublets in cilia and flagella. Cytoplasmic dyneins work in organelle transport and mitosis, whereas the closely related ciliary dyneins are attatched to outer doublet microtubules in a cilium or flagellum, providing sliding/bending force used in (for example) sperm propulsion

A group of speech problems where sounds may be slurred, and speech may be slow or effortful Difficulty in forming words or speaking them.
Changes in pitch, loudness, rhythm, and quality of speech may also be noticed. Such problems are due to paralysis, weakness, or incoordination of muscles used in speaking. Arises because of weakness of muscles used in speaking or because of disruption in the neuromotor stimulus patterns required for accuracy and velocity of speech Dysarthria occurs in both children and adults, and is associated with neuromuscular diseases such as cerebral palsy, parkinsonism, Lou Gehrig's disease, or later stages of multiple sclerosis. It can also occur from stroke, brain injury, and tumors.

Dyscalculia

Lack of ability to perform mathematical functions, usually associated with neurological dysfunction or brain damage.

Dys-diadochokinesia.

Impairment of ability to perform rapid alternating movements, a symptom of cerebellar disease

Dysesthesia.

A persistent, painful sensation, produced by gentle stimulation, that often occurs after destruction of CNS pathways.

Extremely poor handwriting or the inability to perform the motor movements required for handwriting. The condition is often associated with neurological dysfunction.

Impairment of the ability to move resulting in fragmentary or incomplete movements. Caused by partial impairment of the coordination of voluntary muscles, which results in obvious clumsy movements and poor physical control.

A type of learning disability where, despite conventional classroom experience, a person may have problems remembering and recognizing written letters, numbers, and words, might read backwards, and have poor handwriting. The term is frequently used when neurological dysfunction is suspected as the cause of the reading disability.

Dyslipidemia

A disorder of the amount of lipids in the blood.A primary risk factor for the development of atherosclerosis and subsequent cardiovascular diseases.

A difficulty in learning, especially in learning language

Dyspepsia (indigestion)

A functional disorder of the gastrointestinal tract. Symptoms of dyspepsia as originating from the upper gastrointestinal tract, primarily the stomach and first part of the small intestine. These symptoms include: upper abdominal pain (above the navel), belching, nausea (with or without vomiting), abdominal bloating (the sensation of abdominal fullness without objective distention), early satiety (sensation of fullness after a very small amount of food), and, possibly, abdominal distention (swelling as opposed to bloating).
Most dyspepsia (not due to non-gastrointestinal diseases or drugs) is believed to be due to abnormal function (dysfunction) of the muscles of the organs of the gastrointestinal tract or the nerves controlling the organs.
Many gastrointestinal diseases have been associated with dyspepsia. However, many non-gastrointestinal diseases also have been associated with dyspepsia, e.g., diabetes, thyroid disease, hyperparathyroidism (overactive parathyroid glands), and severe kidney disease. It is unclear, however, how these non-gastrointestinal diseases might cause dyspepsia.
A second important cause of dyspepsia is drugs, e.g., nonsteroidal anti-inflammatory drugs (NSAIDs such as ibuprofen), antibiotics, and estrogens). In fact, most drugs are reported to cause dyspepsia in at least some patients.

Difficulty in swallowing. A swallowing disorder characterized by difficulty in oral preparation for the swallow, or in moving material from the mouth to the stomach. This also includes problems in positioning food in the mouth.

An unpleasant mood, such as depression, anxiety, or irritability.

Inability to perform coordinated movements, especially speech, with no apparent problem in the muscles or nerves.

Dyssynergia

Disturbance of coordination in closely related muscles.

Acute tonic muscular spasms, often of the tongue, jaw, eyes, and neck, but sometimes of the whole body. Sometimes occurs during the first few days of antipsychotic drug administration.

Protein in skeletal muscle. It makes up only 0.002% of all protein in skeletal muscle but appears to be vital for proper functioning of the muscle. Sufferers of muscular dystrophy appear to lack dystrophin.


Further reading

Thwaites GE, van Toorn R, Schoeman J. Tuberculous meningitis: more questions, still too few answers. Lancet Neurol 201312:999–1010. Find this resource:

Change in personality.

Confusion, psychiatric disturbance, or altered level of consciousness.

Headache, fever, and some neck stiffness: meningism is usually not prominent—some individuals have meningoencephalitis.

Focal neurological signs: hemiparesis or memory loss (usually indicative of temporal lobe involvement) is not uncommon.

Seizures: are common some are complex partial in nature.

Raised ICP and signs of brain shift ( Examination of brainstem function 3, pp. [link]– [link]).

Predisposing factors: immunocompromised patient.

For autoimmune and paraneoplastic encephalitis, see Box 6.5.

Box 6.5 Autoimmune and paraneoplastic encephalitis

• A group of conditions due to antibodies against cell surface markers or immune responses against intracellular targets that tend to be subacute (over weeks) and can mimic infectious encephalitis.

• Symptoms are broad and include psychiatric manifestations (psychosis, catatonia), seizures, amnesia, altered consciousness, dysautonomia, and movement disorders.

• MRI brain, CSF (possible mild lymphocyte and protein rise). Antibodies (e.g. VGKC associated antibodies, NMDA) in serum or CSF.

• Treat with IV immunoglobulin or steroids. May be paraneoplastic, so search for cancer and treat appropriately.

Box 6.6 Management key points: viral encephalitis

Antiviral therapy: aciclovir without waiting for confirmation of HSV—10mg/kg IV infused over 60min tds (reduced dose in renal insufficiency) for 10–14 days. Ganciclovir if CMV is a possible pathogen (renal transplant patients or in AIDS).

Antibiotics: if there is any suspicion of meningitis. Do not delay treatment because of investigations (i.e. CT and LP).

If there is any suspicion that the illness is meningitis, start antibiotics ( Acute bacterial meningitis: immediate management, pp. [link]– [link]). It is not necessary to await CSF analysis.

2. Specific antiviral therapies

Aciclovir has dramatically reduced mortality and morbidity in HSV encephalitis. Most clinicians therefore give it in suspected encephalitis, without waiting for confirmation that the pathogen is herpes simplex.

Aciclovir 10mg/kg IV (infused over 60min) every 8h (reduced dose in renal insufficiency) is given for 10–14 days.

Ganciclovir 2.5–5.0mg/kg IV (infused over 60min) every 8h should be given if CMV is a possible pathogen (more likely in renal transplant patients or those with AIDS). Treatment is usually for 14–28 days, depending upon the response.

3. CT scan: scan all patients prior to LP

In a patient with focal neurological signs, focal seizures, or signs of brain shift, a CT scan must be arranged urgently. CT may not demonstrate any abnormalities. In herpes simplex encephalitis, there may be low-attenuation areas, particularly in the temporal lobes, with surrounding oedema. MRI is more sensitive to these changes.

Measure opening pressure. CSF pressure may be raised (>20cm CSF), in which case the patient must be observed closely at 15-min intervals.

Analysis of CSF usually reveals lymphocytic leucocytosis (usually 5–500/mm 3 ) in viral encephalitis, but it may be entirely normal. The red cell count is usually elevated. PCR on CSF is sensitive and specific. CSF protein is only mildly elevated, and glucose is normal.

Serology: save serum for viral titres (IgM and IgG). If infectious mononucleosis is suspected (see Fig. 6.2), a monospot test should be performed.

EEG: should be arranged, even in those without seizures. There may be generalized slowing, and in herpes simplex encephalitis, there may be bursts of periodic high-voltage slow-wave complexes over the temporal cortex.

Fig. 6.2 Acute papilloedema (e.g. DM Chapter 9).

Reproduced from Easty D, et al. Oxford Textbook of Ophthalmology, 1999, with permission from Oxford University Press.

Neurological observations should be made regularly. Two complications may require urgent treatment.

Raised ICP due to cerebral oedema may require treatment with dexamethasone ( Intracranial space-occupying lesion, pp. [link]– [link]). In the acute situation, if there is evidence of brain shift, mannitol may be used ( Measures to reduce ICP, p. [link]). Another cause of raised ICP is haemorrhage within necrotic tissue. Perform a CT scan if there is any deterioration in the patient, and discuss with neurosurgeons.

Seizures may be difficult to control but are treated as seizures of any other aetiology.

For symptoms following a head injury, see Box 6.7.

• Varies from transient ‘stunning’ for a few seconds to coma.

• A fraction of patients who attend A&E need to be admitted for observation (indications for admission are given in Box 6.12).

Box 6.7 Symptoms following head injury


Metabolic Encephalopathies

Metabolic encephalopathy describes a clinical state of heterogeneous etiology wherein, cerebral activity is impaired in the absence of parenchymal inflammation or gross structural abnormalities. Metabolic encephalopathy is not a diagnosis but a state of global cerebral dysfunction induced by systemic stress, and can vary in clinical presentation from mild executive dysfunction, to an agitated delirium, to deep coma with decerebrate posturing. This chapter focuses on common causes of metabolic encephalopathy, and outlines the epidemiology, clinical presentation, laboratory and imaging findings, and management. The chapter gives an account for hepatic encephalopathy, uremic encephalopathy, posterior reversible leukoencephalopathy syndrome, pulmonary encephalopathy, pancreatic encephalopathy, and Hashimoto's encephalopathy. Thyroid hormones also act at the level of the mitochondrion to stimulate oxidative metabolism. They also act on the cell membrane to affect the sodium–potassium pump. Adrenal failure is a medical emergency related to a deficiency of adrenal cortical hormones. Electrolyte disturbances are common causes of metabolic encephalopathy. The chapter also describes encephalopathies related to the disruption of sodium, calcium, magnesium, phosphate, and glucose homeostasis.


Watch the video: Identify the lesion in CNS #Decorticate #Decerebrate #Rigidity #Posturing #Opisthotonus (August 2022).