One would expect the prefrontal cortex to be implicated in such a disinhibitory syndrome but what data exist have been complex and difficult to interpret allergy medicine and mucinex cheap allegra 120mg visa. Another approach to understanding the process has been to study a strain of mice that have been genetically altered to eliminate a dopamine transporter gene allergy medicine zyrtec coupons buy allegra us. Most of these are duplications or dele tions that congregate on chromosomes 15 and 16 allergy testing while on xolair purchase allegra without prescription. An observant psychologist allergy medicine safe for pregnancy and breastfeeding buy cheapest allegra and allegra, in performing intelligence tests, notes distractibility and difficulty in sustaining any activity. Erratic performance that is not the result of a defect in comprehension is also characteristic. The Vanderbilt Assessment Scale is a checklist that is com pleted with parents or teachers. If the child is hyperactive and inattentive mainly in school and less so in an unstruc tured environment, it may be that mild developmental delay or a specific cognitive deficiency or dyslexia, which prevents scholastic success, is a source of frustration and boredom. The child then turns to other activities that may happen to disturb the classroom. Or the hyperactive child may have failed to acquire self-control because of a disorganized home life, and the overactivity may be but one manifestation of anxiety or intolerance of constraint. For overactive children of normal intelligence who have failed to control their impulses, who at all times have boundless energy, require little sleep, exhibit a wrig gling restlessness (the "choreiform syndrome" of Prechtl and Stemmer), and manifest incessant exploratory activ ity that repeatedly gets them into mischief, even to their own dismay, medical therapy is justified. Paradoxically, stimulants have a quieting effect on these children, whereas sedatives may do the opposite. Methylphenidate is the drug most widely used and its use has been validated in several studies. Children weighing less than 30 kg are given 5 mg each morning on school days for 2 weeks, after which the dose can be raised to 5 mg morning and noon. Children weighing more than 30 kg can be given a single 20-mg sustained release tablet each morning. If methylphenidate proves ineffective after several weeks or cannot be tolerated, dextroamphetamine 2. Atomoxetine, a norepinephrine inhibitor, is also effective and is not classified as a stimulant but has caused a few cases of liver failure. It is not clear if there should be a long-term concern about hyperten sion, but the blood pressure is not generally measured at frequent intervals. If stimulants are ineffective, tricy clic antidepressants, particularly desipramine, may be tried. Classroom behavioral conditioning techniques and psy chotherapy may be needed for brief periods but are not as effective as medication. Ad u lt Atte nti o n -Deficit D i s o r d e r Certainly this disease i s a lifelong problem for a propor tion of children, although it is just as clear that many "outgrow" the hyperactivity and attention deficit. Hill and Schoener estimate that there is a 50 percent decline in prevalence with each 5 years that pass. These and other abnormalities of bladder function in the enuretic child, as well as treatment, are also discussed Chap. The efficacy and safety of stimulant drugs in the adult group are not known with certainty, but this class of medica tions has been tried with some benefit according to many patients. Some data have emerged that the cardiovascular risks are greater in adults than in children; reports of anx iety and palpations, as well as elevations in blood pres sure, are common among adults taking the medications. Many such individuals are of above-average intel ligence and have attained high degrees of professional success, perhaps as a result of strategies developed implicitly over the years, such as note taking, organizers, mental reminders to focus, etc. These same adjustments can be quite useful to others who are struggling with the disorder so that medication is not the only alternative to surmount the cognitive problem. The complete detachment of the child with psychosis, the amorality of the constitutional sociopath, the major dis turbances in thinking of the schizophrenic, and the mood swings of the bipolar also express themselves in many, if not most, instances by adolescence and sometimes by late childhood. Here one confronts a key problem in psychiatry-the extent to which sociopathy has its roots in genetically determined personality traits or in derange ments in the affective and social life of the individual con sequent to a harmful environment. The answers to these questions cannot be given with finality but most clinicians believe that genetic factors are more important than envi ronmental ones. Our general clinical experience suggests that these additional problems do not arise in the great major ity of such children. Recent studies have been reassur ing in X chromosome of paternal origin is another example. Furthermore, there is no critical evidence to show that deliberate alteration of the familial and social environmental measures now so popular have ever prevented sociopathy. It is during the period of late childhood and adoles cence, when the personality is evolving and least stable, that transient symptoms resembling the psychopatho signs of schizophrenia or bipolar disease. But many of these traits have logic states of adult life are most frequent and difficult to interpret. Some of these disorders represent the early this regard, but the concern regarding tics has remained. E n u resis Voluntary sphincteric control develops according to a predetermined time scale. Usually normal children stop soiling themselves before they can remain dry, and day control precedes night control. Some children are toilet trained by their second birthday, but many do not acquire full sphincteric control until the fourth year. Constant dribbling usually indicates spina bifida, another form of dysraphism, or a tethered cord, but in the boy, one must look also for obstruction of the bladder neck, and in the girl, for an ectopic ureter entering the vagina. When a child have a way of disappearing as adult years are reached so that one can only surmise that they represented either a matu rational delay in the attainment of mature social behavior or were expressions of adolescent turmoil, or what has been called "adolescent adjustment reaction.
The level of blood pressure rises early in the course of the hemorrhage but the preceding chronic hypertension is usually of the "essential" type allergy testing victoria australia discount generic allegra uk. Nonetheless allergy forecast new orleans generic 120mg allegra mastercard, causes of hypertension must always be considered-renal disease allergy treatment home remedies india discount allegra 120 mg without prescription, renal artery sto sis allergy testing scottsdale buy allegra us, eclampsia, pheochromocytoma, hyperaldosterorusm, adrenocorticotropic hormone or corticosteroid excess and, of course, sympathetically active drugs as mentioned. In the series reported by Brott and colleagues, 25 percent were found to have enlarged in the first hour and another 12 percent in the first day. Blod m cee bral tissue is absorbed slowly over months durmg which time symptoms and signs recede. The main types and locations of cerebral hemor rhage are described below and shown in. Chronic hypertension is associated with bleeding into the putamen, thalamus, pons, and cerebellum. H e m o r r h a g e the most common syndrome i s the one caused b y putam ina/ hemorrhage with extension to the adjacent internal capsule. Neurologic symptoms and signs vary slightly with the precise site and size of the extravasation, but hemiplegia from interruption of the capsule is a consistent feature of medium-sized and. With large hem orrhages, patients lapse almost immediately into a tupor with hemiplegia and their condition visibly detenorates as the hours pass. Within a few minutes or less the face sags on one side, speech becomes slurred or aphasic, the arm and leg weaken an are flaccid, an d. These events, occurring gradually over a penod of several minutes or more, are strongly suggestive of intracerebral bleeding. More advanced stages are charac terized by signs of upper brainstem comprssion (coa); bilateral Babinski signs; irregular or interrmttent resprra tion; dilated, fixed pupils, first on the side of the clot; and decerebrate rigidity. Neuroirnaging has disclosed the frequent occr rence of many smaller putaminal hemorrhages, which in former years would have been misdiagnosed as embolic or thrombotic strokes. With hemorrhages con fined to the anterior segment of the putamen, the hemi plegia and hyperreflexia tend to be less severe and o clear more rapidly according to Caplan (1993). With small posterior lesions, weakness is also mild and is attended by sensory loss, hemianopia, impaired visual pursuit to the opposite side, Wernicke-type aphasia (left-sided lesions), and anosognosia (right-sided). Those extending laterally and posteriorly into the internal capsule behav much like. Those exten mg medially into the lateral ventricle give rise to drowsmess, stupor, and either confusion and underactivity or restlessness and agitation. T h a l a m i c H e m o rr h a g e the central feature here i s severe sensory loss o n the entire contralateral body. If large or moderate in size, thalamic hemorrhage also produces a helniplegia or hemiparesis by compression or destruction of the aj cent internal capsule. The sensory defiCit involves all of the opposite side including the trunk and may exceed the motor weakness. Thalamic hemorrhage, by virtue of its extension into the subthalamus and high midbrain, may also cause a series of ocular disturbances-pseudoabducens palsies with one or both eyes turned asymmetrically inward and slightly downward, palsies of vertical and lateral gaze, forced deviation of the eyes downward, inequality of pupils with absence of light reaction, skew deviation with the eye ipsilateral to the hemorrhage assuming a higher position than the contralateral eye, ipsilateral ptosis and miosis (Horner syndrome), absence of con vergence, retraction nystagmus, and tucking in (retrac tion) of the upper eyelids. Compression of the adjacent third ventricle leads to enlargement of the lateral ventricles that may require temporary drainage. Small and moderate-sized hemorrhages that rupture into the third ventricle have been associated with fewer neurologic deficits and better outcomes, but early hydrocephalus is common. Pont i n e H e m o rr h a g e Hemorrhage into the pons i s almost invariably associated with deep coma within a few minutes; the remainder of the clinical picture is dominated by total paralysis with bilateral Babinski signs, decerebrate rigidity, and small (1-mm) pupils that react to light. Lateral eye movements, evoked by head turning or caloric testing, are impaired or absent. Death usually occurs within a few hours, but there are exceptions in which consciousness is retained and the clinical manifestations indicate a smaller lesion in the tegmentum of the pons (disturbances of lateral ocu lar movements, crossed sensory or motor disturbances, small pupils, and cranial-nerve palsies) in addition to signs of bilateral corticospinal tract involvement. In a series of 60 patients with pontine hemor rhage reviewed by Nakajima, 19 survived (8 of whom had remained alert). Louis reported that 21 percent made a good recovery-mostly those who were awake on admission. Cerebe l l a r H e m o rr h a g e this usually develops over a period o f 1 o r more hours, and loss of consciousness at the onset is unusual. Repeated vomiting is a prominent feature, with occipital headache, vertigo, and inability to sit, stand, or walk. Often these are the only abnormalities, making it imperative to have the patient attempt to ambulate; otherwise the examination may erroneously seem to be normal. In the early phase of the illness other clinical signs of cerebellar disease are usually minimal or lacking; only a minority of cases show nystagmus or cerebellar ataxia of the limbs, although these signs must always be sought. A mild ipsilateral facial weak ness, diminished corneal reflex, paresis of conjugate lateral gaze to the side of the hemorrhage, or an ipsilateral sixth-nerve weakness occur with larger hemorrhages that compress the pons or extend into the cerebellar peduncle. Other infrequent ocular signs include blepharospasm, involuntary closure of one eye, skew deviation, "ocular bobbing," and small, often unequal pupils that continue to react until very late in the illness. Contralateral hemiplegia and ipsilateral facial weakness occur if there is marked displacement and com pression of the medulla against the clivus. Occasionally at the onset there is a spastic paraparesis or a quadriparesis with preservation of consciousness. Louis and colleagues, patients with verm ian clots and hydrocephalus were at the highest risk for rapid deterioration. As the hours pass, and occasionally with unanticipated suddenness, the patient becomes stu porous and then comatose or suddenly apneic as a result of brainstem compression, at which point reversal of the syndrome, even by surgical therapy, is seldom success ful. As discussed further on, cerebellar hemorrhage is the most amenable to surgical evacuation with good results. Lo b a r H e m o rr h a g e Bleeding in areas other than those listed above, specifically in the subcortical white matter of one of the lobes of the cerebral hemisphere, is not associated strictly with hyper tension. Any number of other causes are usually respon sible, the main ones being anticoagulation or thrombolytic therapy; acquired coagulopathies, cranial trauma, arterio venous malformation (discussed further on), trauma, and, in the elderly, amyloidosis of the cerebral vessels. The role of antiplatelet agents in precipitating intracerebral hemor rhage has been a matter of contention with numerous sur veys and studies giving divergent results regarding larger, expanding or more clinically destructive hematomas.
Ce re b ra l Fat E m bo l i s m widespread petechial hemorrhages and small infarctions allergy sore throat discount allegra 120mg online, involving both white and gray matter and a few larger infarcts allergy medicine generic list generic allegra 120mg free shipping. Most patients with fat embolism recover sponta neously in 3 or 4 days allergy testing frequency cheap allegra 180mg visa, although a mortality rate of up to 10 percent is cited allergy treatment wiki discount allegra 120mg otc, usually related to underlying systemic and bony injuries. It is usually pos sible to categorize the patient by assessing the mental and neurologic status when first seen and at intervals after the accident. The Glasgow Coma Scale is used as a rapid refer ence to accomplish this purpose (Table 35-1) but does not substitute for a fuller neurologic examination. The scale registers three aspects of neurologic function: eye opening, verbal response, and motor response to various stimuli. This sequence is a result of systemic fat embolism, first of the lungs and then of the brain. In some cases the onset of pulmonary symptoms is associated with a petechial rash over the thorax, especially in the axillae and also in the conjunctivea and 1 in 3 cases is said to show fat globules in the urine. Respiratory distress is the most important and often the only feature of the fat embolism syndrome, evident in the chest film as fluffy infiltrates in both lungs. Roughly, two degrees of disturbed function can be rec ognized within this category. This is underscored by the results of a study of In one, the patient was not 215 children with minor head trauma unconscious at all but only stunned momentarily, "saw stars," or was briefly disoriented. This injury is insig nificant when judged in terms of life or death and brain damage, although, as we point out further on, there is still the small possibility of a skull fracture or the later devel opment of an epidural or subdural hematoma. Moreover, some patients are liable to a troublesome posttraumatic syndrome consisting of headache, giddiness, fatigability, insomnia, and nervousness that can appear soon after or within a few days of the injury. In the instance of consciousness that was temporarily abolished for a few seconds or minutes, recovery may already be complete, or the patient may be in one of the stages of partial recovery described earlier. Even though mentally clear, there is amnesia for events immediately preceding and following the injury. The latter produces a circumscribed confusional state that is usually confined to inattention and may be ongoing when the patient is first examined. It is characterized by a dazed appearance and repetitive questions from the patient about the circumstances that led to his being found. They include features that are sensitive but not spe cific for intracranial injury, such as age above 60 years, intoxication, more than 30 min of retrograde amnesia, suspected skull fracture, seizure, anticoagulation, and dangerous mechanism of injury, (see Smits et al and Stiell et al). Whether to obtain imaging of the head routinely in such patients is an unresolved problem. If there is no subarachnoid blood (a common finding) or intraparenchymal clot or contusion, and the patient is mentally clear there is little chance of developing an extradural hemorrhage. The presence of a fracture may increase these odds but most studies, such as the one by Lloyd and colleagues have found that the presence of a skull fracture in children proves to be a relatively poor indicator of intracranial injury. The exception is a fracture through the squamous bone and the groove of the middle meningeal artery, which represents a risk for arterial bleeding and epidural hemorrhage. Minor and seemingly trivial head injuries may sometimes be followed by a number of puzzling and worrisome clinical phenomena, some insignificant, oth ers serious and indicative of a pathologic process other than concussion. Delayed Hemiplegia the main causes of delayed hemiplegia are a late-evolving epidural or subdural hematoma and, in more severe injuries, an intracerebral hemorrhage. Most of these are associated with a dimi nution in the level of consciousness from the outset but there are exceptions. Drowsiness, Headache, and Confusion these symp toms occur most often in children, who, minutes or hours after a concussive head injury, seem not to be themselves. They lie down, are drowsy, complain of headache, and may vomit-symptoms that suggest the presence of an intracranial hemorrhage. There is usually no skull Dissection of the internal carotid artery should always be considered in cases of delayed hemiplegia the dis section may occur in the extracranial or the intracranial portion of the carotid artery and should be sought by vas cular imaging study if the hemiparesis has no other expla nation. In other instances, the hemiplegia has no clear explanation other than the blow to the head, perhaps related to the migraine phenomenon described earlier. Serious Cerebra l Da mage Following a Lucid I nterva l this group is smaller than the other two but is of impor tance because it includes a disproportionate number of patients who are in urgent need of surgical treatment. The initial loss of consciousness from concussion may have lasted only a few minutes or, exceptionally, there may have been no period of unresponsiveness at all, in which instance one might wrongly conclude that there was no concussion and little possibility of traumatic hemor rhage or other type of brain injury. Patients who display this sequence of events, in the past referred to vividly as "talk and die" by Marshall and associates (1983), have late deterioration because of the expansion of a subdural hematoma, worsening brain edema around a contusion, or the delayed appearance of an epidural clot. The symptoms subside after a few hours, attesting to the benign nature of the condition in most cases but some form of cerebral imaging is required. Transient Paraplegia, Blindness, and Migrainous Phenomena With falls or blows on top of the head, both legs may become temporarily weak and numb, with wavering bilateral Babinski signs and sometimes with sphincteric incontinence. It seems possible that these transient symptoms represent a direct localized concussive effect, caused either by indentation of the skull or by impact on these parts of the brain against the inner table of the skull, but a vascular mechanism cannot be excluded. The blindness and paraplegia are usually followed by a throbbing, vascular type of headache. Transient migrain ous visual phenomena, aphasia, or hemiparesis, followed by a headache, are observed sometimes after minimal concussion in athletes who participate in competitive contact sports. Possibly all of these phenomena are the result of an attack of migraine induced by a blow to the head. These focal syndromes can be perplexing for a few hours, especially if it is the first such attack of migraine in a child. Possibilities to be remembered, particularly in cases of acute quadriplegia, is traumatic cord compres sion or the rarer cartilaginous embolism of the cervical cord (see "Fibrocartilaginous Embolism" in Chap. A concussion of the cervical portion of the spinal cord is another potential mechanism of transient paraplegia.
Repeated observation may bear out the exis tence of an anxiety state or gloomy mood allergy shots weight gain allegra 120 mg online. Reassurance in combination with a therapeutic trial of antidepressant drugs may suppress symptoms of which the patient was barely aware allergy quick relief generic 120mg allegra with visa, thus clarifying the diagnosis allergy forecast ragweed allegra 120 mg otc. A few patients with chronic fatigue exhibit the psychologic disorder related to litigation ("compensa tion neurosis") allergy testing taunton purchase 180mg allegra. Noteworthy is the frequency with which a similar syndrome has become the basis of court action against employers or claims against the government, as in the "building-related illness" (formerly "sick-building syndrome"). As alluded to earlier, attribution of fatigue to Lyme disease and obscure infections or allergies should be made cautiously if there is no firm evidence. In intractable cases, tuberculosis, brucellosis, Lyme disease, hepatitis, bacterial endocarditis, mycoplasmal B, and other viral infections, and malaria, hookworm, giardiasis, and other parasitic infections need to be con sidered in the differential diagnosis, and an inquiry made for their characteristic symptoms, signs, and when appro priate, laboratory findings; however, such infections are infrequently found. There should also be a search for as temporal arteritis and polymyalgia rheumatica (sedi mentation rate); an endocrine survey (thyroid, calcium, and cortisol levels) and an evaluation for an occult tumor are also in order in obscure cases. It must be remembered that chronic intoxication with alcohol, barbiturates, or other sedative drugs, some of which are given to suppress nervousness or insomnia, may contribute to fatigability. The rapid and recent onset of fatigue should always sug gest the presence of an infection, a disturbance in fluid balance, gastrointestinal bleeding, or rapidly developing circulatory failure of either peripheral or cardiac origin. The features that suggest sleep apnea have been men tioned above and are discussed further in Chap. Auden referred to his era as "the age of anxiety," and little has changed since then. Medical historians have identified comparable peri ods of pervasive anxiety dating back to the time of Marcus Aurelius and Constantine, when societies were undergo ing rapid and profound changes, and individuals were assailed by an overwhelming sense of insecurity, personal insignificance, and fear of the future (Rosen). Like lassitude and fatigue, nervousness, irritability, and anxiety are among the most frequent symptoms encountered in office and hospital practice. Finally, it bears repeating that lassitude and fatigue must be distinguished from genuine muscular weakness. The demonstration of reduced power, reflex changes, fasciculations, and atrophy sets the case analysis along different lines, bringing up for particular consideration diseases of the peripheral nervous system or of the mus culature. Rare, difficult-to-diagnose diseases that cause 40 percent of the population, at one time or another, experienced symptoms of severe anxiety, and approximately 5 percent suffered from life long anxiety states (Lader). Of course, any person facing a challenging or threatening task for which he may feel unprepared and inadequate experiences some degree of nervousness and anxiety. Anxiety is then not abnormal, and the alertness and attentiveness that accompany it may actually improve performance up to a point. Barratt and White found that mildly anxious medical students performed better on examinations than those lacking in anxiety. As anxiety increases, so does the standard of performance, but only to a point, after which increasing anxiety causes a rapid decline in performance (Yerkes-Dodson law). If worry or depression stands in clear relation to seri ous economic reverses or loss of a loved one, the symptom is also usually accepted as normal, but no less worthy of emotional support. Only when it is excessively intense or prolonged or when accompanying visceral derangements are prominent do anxiety and depression become matters of medical concern. Admittedly, the line that separates normal emotional reactions and pathologic ones is not sharp. Chapter Most often nervousness represents no more than a transient psychic and behavioral state in which the per son is maximally challenged or threatened by difficult personal problems. Some persons claim to have been ner vous throughout life or to be nervous periodically for no apparent reason. In these instances, the symptoms blend imperceptibly with those of anxiety disorder or depres sion, described below. We use the term anxieh to denote an emotional state; characterized by subjective feelings of nervousness, irri tability, uneasy anticipation, and apprehension, often but by no means always with a definite topical content and the physiologic accompaniments of strong emotion, i. The vasomotor and visceral accompaniments are mediated through the autonomic nervous system, particularly its sympathetic part, and involve also the thyroid and adrenal glands. Pa n i c Attacks the symptoms of anxiety may be manifest either in acute episodes, each lasting several minutes or up to an hour, or as a protracted state that may last for weeks, months, or years. In the panic attack, the patient is suddenly over whelmed by feelings of apprehension, or a fear that he may lose consciousness and die, have a heart attack or stroke, lose his reason or self-control, become insane, or commit some horrible crime. These experiences are accompanied by a series of physiologic reactions, mainly sympathoadrenal hyperactivity, resembling the "fight-or flight" reaction. Breathlessness, a feeling of suffocation, dizziness, sweating, trembling, palpitation, and pre cordial or gastric distress are typical but not invariable physical accompaniments. As a persistent and less-severe state, the patient experiences fluctuating degrees of ner vousness, palpitation or excessive cardiac impulse, short ness of breath, light-headedness, faintness, easy fatigue, and intolerance of physical exertion. Attacks tend to occur during periods of relative calm and in nonthreatening circumstances. Usually, the appre hension and physical symptoms escalate over a period of minutes to an hour and then abate over Anxiety Reactions and Pan i c Attacks There is no unanimity among psychiatrists as to whether symptoms of nervousness, irritability, anxiety, and fear comprise a single emotional reaction, varying only in its severity or duration, or a group of discrete reactions, each with distinctive clinical features. In some writings, anxiety is classified as a form of subacute or chronic fear but there is reason to question this assumption. Anxious patients, when frightened under experimental conditions, state that the fear reaction differs in being more overwhelming. The exceedingly frightened per son is "frozen," unable to act or to think clearly, and his responses are automatic and sometimes irrational. The fear reaction is characterized by overactivity of both the sympathetic and parasympathetic nervous systems, and the parasympathetic effects (bradycardia, sphincteric relaxation) may predominate, unlike anxiety, in which sympathetic effects are the more prominent ones. Long ago, Cicero distinguished between an acute and transient attack of fear provoked by a specific stimulus (angor) and a protracted state of fearfulness (anxietas).
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But a few years later allergy treatment rash cheap 180mg allegra fast delivery, Erdheim recognized that the same syndrome could be a manifestation of a lesion (a suprasellar cyst in his case) involving or restricted to the hypothalamus allergy shots benadryl purchase allegra on line. Later it was determined that obesity and hypogonadism could occur together or separately and were often combined with a loss of vision and unprovoked rage allergy symptoms during pregnancy buy genuine allegra online, aggression allergy medicine nasal spray prescription safe 120 mg allegra, or antisocial behavior. In some patients, the clinical state is characterized by abulia, apathy, and reduced verbal output. The usual causes of the Froehlich syndrome are craniopharyngioma, adamantinoma, and glioma, but many other tumors have been reported (pituitary adenoma, cholesteatoma, lipoma, meningioma, glioma, angiosarcoma, and chordoma). The condition bears clinical similarities to the Prader-Willi syndrome, in which hypothalamic abnormalities are not found, as discussed in Chap. H y p o t h a l a m i c D i s o r d e rs A lterations i n We i g ht As s o c i a t e d With Fai l u re of Pu berty Several genetic conditions can lead to failure of puberty. Kallman syndrome is a type of hypogonadotropic hypogo nadism that is associated with anosmia. Several causative X-linked and autosomal dominant gene muta tions have been discovered. The Bardet-Biedl syndrome is a heterogenous disorder affecting multiple organ systems. Variable growth retardation, obesity, and dia betes mellitus are seen, along with hypogonadism and anosmia. Neuroanatomic studies have localized a satiety center in the ventromedial nucleus of the hypothalamus and an appetite center in the ventrolateral nucleus. Lesions in the lateral hypothalamus may result in a failure to eat and, in the neonate, failure to thrive; lesions in the medial hypothalamus may result in overeating and obesity. Bray and Gallagher, who analyzed 8 cases of the latter type, concluded that the critical lesion was bilateral destruction of the ventromedial regions of the hypothalamus. Most of the reported cases of this type have been caused by tumors, particularly craniopharyn gioma, and some to trauma, inflammatory disease, and hydrocephalus (Suzuki et al). In a case that was subject to clinicopathologic correlation, Reeves and Plum found that a hamartoma had destroyed the medial eminence and the ventromedial nuclei bilaterally but spared the lateral hypothalamus. Hyperphagia and rage reactions were the main clinical features; the associated polydipsia and polyuria were due to extension of the tumor to the anterior hypothalamus. It is evident that in only a tiny fraction of people can obesity be traced to a hypothalamic lesion. Of overriding importance are genetic factors, such as the number of lipocytes that one inherits and their abil ity to store fat. Progressive and ultimately fatal emaciation (failure to thrive), despite normal or near-normal food intake, in an otherwise alert and cheer ful infant is the main clinical feature. The lesion has usu ally proved to be a low-grade astrocytoma of the anterior hypothalamus or optic nerve (Burr et al). Extrahypothalamic parts o f the brain, if diseased, may also be associated with increased food-seeking behavior, food ingestion, and weight gain. A n o rexi a N e rvosa and B u l i m i a the special syndromes called anorexia nervosa and bulimia have been difficult to classify and are mentioned in this chapter only because they are associated with alterations in several hypothalamic functions, including appetite, temperature control, and menstruation. In all likelihood, these alterations are not the result of a primary dysfunc tion of hypothalamic nuclei but are secondary to the extreme weight loss, which is the primary feature of the disease. However, a causal link between these idiopathic diseases and hypothalamic dysfunction has been sug gested by the rare patients with an anorexia nervosa syndrome who were later found to have hypothalamic tumors (Bhanji and Mattingly; Berek et al; and Lewin et al). Anorexia nervosa and bulimia are probably best regarded as disorders of behavior, in this case an obses sion with thinness; consequently, they are discussed with the psychiatric disorders (see Chap. Many patients with the more severe forms of mental retardation are subnormal in height and weight, but the explanation for this has not been ascer tained. The hormone effects a spurt in growth during the first year of its administration, but whether it significantly influences growth in the long term is still under investigation. There is concern about the risk of transmitting prion or viral diseases through administra tion of the biologically derived hormone; this problem is obviated if a genetically produced hormone is used. Bilateral lesions in the anterior parts o f the hypothala mus, specifically of temperature-sensitive neurons in the preoptic area, may result in hyperthermia. The heat dissipating mechanisms of the body, notably vasodilata tion and sweating, are impaired. This effect has followed operations or other trauma in the region of the floor of the third ventricle but we have seen it most often after mas sive rupture of an anterior communicating artery aneu rysm. Acetylsalicylic acid has little effect on central hyperthermia; the only way to control it is by active evaporative cooling of the body while administering sedation. A less-dramatic example of the loss of natural circadian temperature patterns is seen in patients with postoperative damage in the supra chiasmatic area (Cohen and Albers) and suprachiasmatic metastasis (Schwartz et al). These types of lesions are invariably associated with other disorders of intrinsic rhythmicity, including sleep and behavior. It should be emphasized, however, that instances of "central fever" are rare, and unexplained fever of moderate degree should not be attributed to an existing or putative brain lesion. Hyperthermia is also part of the malignant hyperther mia syndrome, in which, in a limited number of cases, there is an inherited (autosomal dominant) susceptibility to develop hyperthermia and muscle rigidity in response to inhalation anesthetics and skeletal muscle relaxants ("Malignant Hyperthermia" in Chap 54). In some of these instances, it has been found to be caused by a defective ryanodine receptor.
