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Moreover pregnancy first trimester purchase generic nolvadex from india, the volume of blood injected women's health clinic lansing mi nolvadex 10mg discount, usually about 20 mL womens health 06484 order nolvadex without prescription, is not related to menopause urinary problems order nolvadex online the chances of success. The mechanism of this rapid improvement may not simply be the plugging of a dural leak. A number of patients fail to benefit or have only transient effects; it is then unclear whether repeating the procedure is helpful. The administration of caffeine-ergotamine preparations or intravenous caffeine may also have a salutary though temporary effect on the headache. The addition of analgesic medication is required if the patient must get up to care for himself or to travel. In protracted cases, patience is called for, since most headaches will resolve in 2 weeks or less. As to mechanism, Panullo and colleagues have shown that there is a downward displacement of the upper brainstem and posterior fossa contents when the patient assumes the upright position; but, as pointed out in Chap. These give rise to some of the most intractable low-pressure syndromes and must be investigated by radiologic and nuclide studies in order to establish the site of leakage. Several such leaks in our experience have been intermittent, adding to the difficulty in diagnosis. The point being made here is that these structures may also be involved in a number of noninfective processes, some of obscure origin. The lower spinal roots or spinal cord alone may be implicated in "spinal arachnoiditis. This may be accompanied by a pachymeningitis, and the latter may also be restricted to the cervical dura, also discussed below. A predominant localization to these basal or cervical structures may be apparent even in cases of diffuse cerebrospinal meningeal reactions, perhaps because of an uneven concentration of the noxious agent. In other instances, the primary disease appears to have arisen in the dura, with extension only to the adjacent piaarachnoid. In yet other instances, the ependyma of the aqueduct or fourth ventricle is primarily involved. The mechanisms by which these meningeal reactions affect parenchymal structures (brain, cord, and nerve roots) are not fully understood. Progressive constriction of nerve roots and spinal cord, literally a strangulation of these structures, is another plausible mechanism, but it is difficult to separate vascular factors from mechanical ones. Since any toxic agent introduced into the subarachnoid space has free access, via VirchowRobin spaces, to the superficial parts of the brain and spinal cord, direct parenchymal injury may follow. Perivascular reactions of subpial vessels, as in infectious processes, would be a plausible mechanism of injury to optic nerves and spinal cord, where long stretches of myelinated fibers abut the pia. Regional Arachnoiditis Arachnoiditis limited to the lumbosacral roots has followed ruptured discs, myelograms, and spinal surgery. Usually, there is sciatica and chronic neuropathic pain in the back and lower extremities, but sensorimotor and reflex changes in the legs are variable. The etiologic factors have been singularly elusive although in the past it followed the instillation of iophendylate (Pantopaque) for myelography and corticosteroids (for pain or multiple sclerosis) and other irritative agents. The condition may be accompanied by cranial basilar meningeal fibrosis with optic nerve involvement and hydrocephalus (see below), or it may occur in isolation. The most familiar form of spinal arachnoiditis was, in the past, that which followed the use of chemically contaminated spinal anesthetics. Our colleagues saw more than 40 cases of this type, now rare, dating from the time when vials of anesthetic were stored in detergent sterilizing solutions. Instillation of the anesthetic agent was followed immediately by back pain and a rapidly progressive lumbosacral root syndrome (areflexic paralysis, anesthesia of the legs, and paralysis of sphincters). Several cases have, in our more recent experience, followed prolonged spinal anesthesia with the patient in a decubitus position, usually for orthopedic procedures, but the resulting myelopathy or cauda equina radiculopathy is then difficult to separate from a direct toxic effect of the anesthetic. In other instances, protracted back pain lasting days to weeks is the only effect but is followed, after a period of months or years, by a progressive myelopathy. This takes the form of some combination of spinal arachnoiditis with ataxic paraparesis and sensory disturbance, hydrocephalus, or opticochiasmatic arachnoiditis. The point to be made is that there is always some risk attached to the subarachnoid instillation of any foreign agent. Opticochiasmatic Arachnoiditis this condition was well known to neurologists during the period when neurosyphilis was a common disease. It occurs after years of chronic syphilitic meningitis, sometimes in conjunction with tabes dorsalis or meningomyelitis. However, there were always nonsyphilitic cases, the cause of which was never ascertained. A constriction of visual fields, usually bilateral and asymmetrical (rarely scotomas), developed insidiously and progressed. Pathologically, the optic nerves were found to be enmeshed in thickened, opaque pia-arachnoid. Pachymeningitis the term pachymeningitis refers to a chronic, circumscribed, inflammatory thickening of the dura. The term is somewhat confusing insofar as the pia and arachnoid are usually equally involved in the inflammatory thickening and all three membranes are bound together by dense fibrous adhesions. This type of meningeal reaction, which is now exceedingly uncommon, was first described by Charcot and Joffroy. It occurred mainly in the cervical region (hence the name pachymeningitis cervicalis hypertrophica) and was attributed to syphilis. Involvement of cervical roots and compression of the spinal cord gave rise to variable degrees of paraparesis in association with root pain, paresthesias, sensory loss, and amyotrophy of the upper limbs. In the modern era, rheumatoid arthritis, sarcoidosis, and chronic local infection (fungal, tuberculous) have been the main causes, but some of the cases remain unexplained. Idiopathic instances continue to be reported; a summary of published cases and two personally studied ones is given by Dumont and colleagues. The subdural space and dura can be involved by extension of a pathologic process from the arachnoid, especially in infants and children, in whom subdural hygromas regularly follow meningitis. The fibrous connective tissue of which the dura is composed may also undergo pronounced thickening in the course of a mucopolysaccharidosis, especially in cases where fibroblasts are implicated. Other Abnormalities of the Ependyma and Meninges Although the ependyma may be involved as part of any chronic meningeal reaction, it may also be the site of a relatively isolated process. In experimental animals, Johnson and colleagues found that the mumps virus could localize in and destroy ependymal cells. This results in activation of subependymal astrocytes, which may bury the remaining ependymal cells and, by overgrowth, narrow the aqueduct of Sylvius. Ependymitis with similar consequences may be the dominant change in infantile toxoplasmosis and cytomegalic encephalitis. Spinal fluid and meningeal reactions to degradation products released from tumors that are in contact with the cerebrospinal spaces, particularly dermoid and craniopharyngioma, are discussed in Chap. Hemosiderosis (Superficial Siderosis) of the Meninges Sometimes mistaken by neuropathologists for hemochromatosis, which has entirely different effects on the nervous system, hemosiderosis is clearly the consequence of repeated contamination of the menin- ges by blood (McDougal and Adams; Fishman). An oozing vascular malformation or tumor has been the usual cause in our experience, although there have been instances in which the source of the blood could not be found. As a result, the surface of the cerebellum, spinal cord, hippocampi, and olfactory bulbs are stained orange-brown. Iron pigments and ferritin, which are toxic, gradually diffuse through the pia into superficial parts of the cerebellum, eighth cranial nerve, and spinal cord, destroying nerve cells and exciting a glial reaction. In microscopic sections stained for iron, the histiocyte-microglial cells contain iron and ferritin, and particles of iron can be seen studding nerve and glial cells for a distance of several millimeters beneath the pia. The clinical syndrome of siderosis of the meninges consists essentially of a progressive ataxia and nerve deafness; sometimes a spastic paraparesis is added and, rarely, mental impairment. Koeppen and associates attributed the vunerability of the acoustic nerves to their extended meningeal exposure before acquiring a fibroblastic perineurium and epineurium. There is no treatment other than finding the source of the meningeal blood and preventing further hemorrhage and treating hydrocephalus if it is present. Their importance derives from the facts that they occur in great variety; produce numerous neurologic symptoms because of their size, location, and invasive qualities; usually destroy the tissues in which they are situated and displace those around them; are a frequent cause of increased intracranial pressure; and, most of all, are often lethal. Slowly this dismal state of affairs is changing, as a result of advances in anesthesiology, stereotactic and microneurosurgical techniques, radiation therapy, and the use of chemotherapeutic agents.

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By 4 years breast cancer 14 buy nolvadex 10 mg on line, the child is normally capable of telling stories women's health center bismarck nd order 20 mg nolvadex otc, but with little distinction between fact and fancy womens health 092012 order 20mg nolvadex fast delivery. Also by that age menopause 3 months no period cheap nolvadex 20mg overnight delivery, children can indicate spatial and temporal relationships and start to inquire about causality. Here there must be an association of graphic symbols with the auditory, visual, and kinesthetic images of words already acquired. Usually the written word is learned by associating it with the spoken word rather than with the seen object. Writing is learned soon after reading, the audiovisual symbols of words being linked to cursive movements of the hand. The tradition of beginning grade school at 6 years is based not on an arbitrary decision but on the empirically determined age at which the nervous system of the average child is ready to learn and execute the tasks of reading, writing, and- soon thereafter- calculating. Once language is fully acquired, it is integrated into all aspects of complex action and behavior. Every plan for the solution of a problem must be cast into language, and the final result is analyzed in verbal terms. Anthropologists see in all this a grander scheme wherein the individual recapitulates the language development of the human race. They point out that in primitive peoples, language consisted of gestures and the utterance of simple sounds expressing emotion and that, over periods of time, movements and sounds became the conventional signs and verbal symbols of objects. Historically, signs and spoken language were the first means of human communication; graphic records appeared much later. Native Americans, for instance, never reached the level of syllabic written language. Writing commenced as pictorial representation and only much later were alphabets devised. For further details concerning communicative and cognitive abilities and methods of assessment, the reader should consult the monograph by Minifie and Lloyd. A more ambiguous meaning has been proposed by some psychologists, for whom the term is equated with all growth and development, the experience of pleasure, and survival. Much of Freudian psychoanalytic theory centers on the sexual development of the child and- on the basis of questionable observations- espouses the view that repression of the sexual impulse and the psychic conflicts resulting therefrom are the main sources of neurosis and possibly psychosis. Prepubertal In this period, attachments formed with older person of same sex (girlhood crushes); in boys, attachments to members of same sex (gang formation). Adolescence Emergence of increasing display of heterosexual behaviors in school, at dances, and in other social activities. In later childhood, erection is self-initiated and still later is carried to the point of ejaculation and orgasm (masturbation). The timetable of the menarche and other aspects of sexual development is not uniform; and there is considerable variation. If sexuality is not allowed natural expression, it often becomes a source of worry and preoccupation. Homosexuality the homosexual is motivated in adult life by a preferential erotic attraction to members of the same sex. Most psychiatrists exclude from the definition of homosexuality those patterns of behavior that are not motivated by specific preferential desire, such as the incidental homosexuality of adolescents and the situational homosexuality of prisoners. According to the early reports of Kinsey and colleagues, approximately 4 percent of Sexual Development the terms sexual and sexuality have several meanings in medical and nonmedical writings. More recent estimates, both in men and women, range from 1 to 5 percent (see LeVay and Hamer). These widely variable figures share a problem with all estimates derived from surveys and questionnaires: they cannot count people who do not wish to be counted. We favor the hypothesis that differences or variations in genetic patterning of the immature nervous system (probably of the hypothalamus) set the sexual predilection during early life. Swaab and Hofman have reported that the preoptic zone is three times larger in heterosexual males than it is in females, but it is about the same size in homosexual males as it is in females. If confirmed, these findings, which have been disputed by Byne, would support the view that homosexuality has a biologic basis. Pooled data from five studies in men have shown that about 57 percent of identical twins (and 13 percent of brothers) of homosexual men are also homosexual. The inheritance pattern of male homosexuality comes from the maternal side, implicating a gene on the X chromosome (LeVay and Hamer). The most widely held current view is that homosexuality is not a mental or a personality disorder, though it may at times lead to secondary reactive neurotic disturbances. The studies of Kinsey and colleagues indicate that a homosexual orientation cannot be traced to a single social or psychologic root. Instead, as indicated above, homosexuality seems to arise from a deep-seated predisposition, probably biologic in origin and as ingrained as heterosexuality. One has but to observe the resemblances between parent and child to confirm this view. Just as no two persons are physically identical, not even monozygotic twins, so too do they differ in any other refined quality one chooses to measure. These differences, together with certain predilections to disease, explain why any one person may have an unpredictable reaction to a pathogenic agent. Strictly speaking, the normal person is an abstraction, just as is a typical example of any disease. However, it is in other, seemingly nonphysical attributes that individuals display the greatest differences. Here reference is made to their variable place on a scale of energy, capacity for effective work, sensitivity, temperament, emotional responsivity, aggressivity or passivity, risk-taking, ethical sense, flexibility, and tolerance to change and stress. In the formation of personality, especially the part concerned with feeling and emotional sensitivity, basic temperament surely plays a large part. By nature, some children from the beginning seem to be happy, cheerful, and unconcerned about immediate frustrations; others are the opposite. By the third month of life, Birch and Belmont recognized individual differences in activity-passivity, regularity-irregularity, intensity of action, approach-withdrawal, adaptivity-unadaptivity, high-low threshold of response to stimulation, positive-negative mood, high-low selectivity, and high-low distractibility. Ratings at this early age were found to correlate with the results of examinations made at 5 years. Kagan and Moss recognized the trait of timidity as early as 6 months of age and noted that it persists lifelong. The strong genetic influence on personality development has also been demonstrated by Scarr and associates. Disorders of personality and the genetic predisposition to certain personality traits are discussed further in Chap 56. Social behavior, like other neurologic and psychologic functions in general, depends to a great extent on the development and maturation of the brain. Involved also are genetic and environmental factors, for one cannot adapt to society except in the presence of other people; i. The roots of social behavior are traceable to certain instinctive patterns that are progressively elaborated by conditioned emotional reactions. The sources of these social reactions are even more obscure than those of temperament, character, and intelligence. In children, difficulty in social adaptation tends first to be manifest by an inability to take their places in a classroom. However, the greatest demands and frustrations in social development are likely to occur in late childhood and adolescence. The development of adult gonadal function and the further evolution of psychosexual impulses create a bewildering array of new challenges in social adaptation. As social roles change, as intellectual and physical capacities first advance and later recede, new challenges demand new adaptations. The most severe forms of delayed motor development, associated with spasticity and athetosis, are usually manifestations of particular prenatal and paranatal diseases of the brain; these are discussed in Chap. In assessing developmental abnormalities of the motor system in the neonate and young infant, the following maneuvers, which elicit certain postures and reflexive movements, are particularly useful: 1. A loud noise, slapping the bed, or jerking one leg will have the same effect- causing an elevation and abduction of the arms followed by a clasping movement to the midline.

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This reaction is analogous to zoladex menstrual cycle order nolvadex 10mg on-line the tonic reflexes described by Magnus in decerebrate animals pregnancy outside the uterus buy discount nolvadex line. In some patients with the foregoing postural changes the lesions are clearly in the cerebral white matter or basal ganglia women's health center newport news va purchase 20 mg nolvadex free shipping, which is difficult to women's health center rochester ny 20mg nolvadex amex reconcile with the classic physiologic explanation of decerebrate posturing; presumably there is a functional derangement of structures in the midbrain. Decerebrate posturing, either in experimental preparations or in humans, is usually not a persistent steady state but an intermittent and transient one. Hence the term decerebrate state, as suggested by Feldman, is preferable to decerebrate rigidity, which implies a fixed, tonic extensor attitude. Decorticate rigidity, with arm or arms in flexion and adduction and leg(s) extended, signifies lesions at a higher level- in the cerebral white matter or internal capsule and thalamus. Forceful extensor postures of the arms and weak flexor responses of the legs are probably due to lesions at about the level of the vestibular nuclei. Lesions below this level lead to flaccidity and abolition of all postures and movements. Only in the most advanced forms of intoxication and metabolic coma, as might occur with anoxic necrosis of neurons throughout the entire brain, are coughing, swallowing, hiccoughing, and spontaneous respiration all abolished. Tendon reflexes are usually preserved until the late stages of coma due to metabolic disturbances and intoxications. In coma due to a large cerebral infarct or hemorrhage, the tendon reflexes may be normal or only slightly reduced on the hemiplegic side and the plantar reflexes may be absent or extensor. Plantar flexor responses, succeeding extensor responses, signify ether a return to normalcy or, in the context of deepening coma, a transition to brain death. This phenomenon has been attributed to isolation of the brainstem respiratory centers from the cerebrum, rendering them more sensitive than usual to carbon dioxide (hyperventilation drive). It is postulated that as a result of overbreathing, the blood carbon dioxide drops below the concentration required to stimulate the centers, and breathing gradually stops. Carbon dioxide then reaccumulates until it exceeds the respiratory threshold, and the cycle then repeats itself. It may occur during sleep in elderly individuals and can be a manifestation of cardiopulmonary disorders in awake patients. Only when it gives way to more irregular respiratory patterns that implicate structural damage of the brainstem is the patient in imminent danger, as discussed below. A number of other aberrant breathing rhythms occur with brainstem lesions (these are reviewed in Chap. The more conspicuous respiratory arrhythmias are associated with brainstem lesions below the level of the reticular activating system and are therefore found in the late stages of brainstem compression or with large brainstem lesions such as infarction, primary hemorrhage, or infiltrating tumor. This disorder is characterized by an increase in the rate and depth of respiration to the extent that respiratory alkalosis results. It must be distinguished from hyperventilation caused by medical illnesses, particularly pneumonia and acidosis. Mild degrees of hyperventilation are common after a number of acute neurologic events, notably head injury. However, North and Jennett, in a study of respiratory abnormalities in neurosurgical patients, found no consistent correlation between tachypnea and the site of the lesion. With lesions of the dorsome- dial part of the medulla, the rhythm of breathing is chaotic, being irregularly interrupted and each breath varying in rate and depth (Biot breathing; also called "ataxia of breathing"- not an appropriate term. Probably all of these erratic patterns of breathing are interrelated in some manner; Webber and Speck have shown that apnea, Biot breathing, and gasping could be produced in the same animal with lesions in the dorsolateral pontine tegmentum by altering the depth of anesthesia. Rapidly evolving lesions of the posterior fossa may cause sudden respiratory arrest without any of the aforementioned abnormalities of breathing; presumably this results from fulminant pontomedullary compression by the cerebellar tonsils. Papilledema develops within 12 to 24 h in cases of brain trauma and hemorrhage, but if it is pronounced, it usually signifies brain tumor or abscess- i. Increased intracranial pressure produces coma by impeding global cerebral blood flow; but this occurs only at extremely high levels of pressure. High pressure within one compartment produces shifts of central structures and a series of "false localizing" signs due to lateral displacements and herniations, as noted in the above discussion of herniation. The syndrome of acute hydrocephalus, most often from subarachnoid hemorrhage or from rapid obstruction of the ventricular system by a tumor in the posterior fossa, induces a state of abulia (page 359) followed by stupor and then coma with bilateral Babinski signs the pupils are small and tone in the legs is increased. Laboratory Procedures Unless the diagnosis is established at once by history and physical examination, it is necessary to carry out a number of laboratory procedures. If poisoning is suspected, aspiration and analysis of the gastric contents is sometimes helpful, but greater reliance should be placed on chromatographic analysis of the blood and urine ("toxic screen"). A specimen of urine is obtained by catheter for determination of specific gravity and for glucose, acetone, and protein content. Proteinuria may also be found for 2 or 3 days after a subarachnoid hemorrhage or with high fever. Urine of high specific gravity, glycosuria, and acetonuria occur almost invariably in diabetic coma; but transient glycosuria and hyperglycemia may result from a massive cerebral lesion. Blood counts should be obtained, and in malarial districts a blood smear should be examined for parasites. Neutrophilic leukocytosis occurs in bacterial infections and also with brain hemorrhage and infarction, although the elevation of leukocytes in the latter conditions rarely exceeds 12,000/mm3. This is the only way to reveal nonconvulsive status epilepticus as the cause of a stupor. Diseases that cause no focal or lateralizing neurologic signs, usually with normal brainstem functions. Metabolic disturbances: anoxia, diabetic acidosis, uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypo- and hypernatremia, hypoglycemia, addisonian crisis, profound nutritional deficiency, carbon monoxide, thyroid states including Hashimoto encephalopathy (Chaps. Severe systemic infections: pneumonia, peritonitis, typhoid fever, malaria, septicemia, WaterhouseFriderichsen syndrome. Subarachnoid hemorrhage from ruptured aneurysm, arteriovenous malformation, occasionally trauma (Chaps. Miscellaneous: cortical vein thrombosis, some forms of viral encephalitis (herpes), focal embolic infarction due to bacterial endocarditis, acute hemorrhagic leukoencephalitis, disseminated (postinfectious) encephalomyelitis, intravascular lymphoma, thrombotic thrombocytopenic purpura, diffuse fat embolism, and others. Using the clinical criteria outlined above, one can usually ascertain whether a given case of coma falls into one of these three categories. Concerning the group without focal or lateralizing or meningeal signs (which includes most of the metabolic encephalopathies, intoxications, concussion, and postseizure states), it must be kept in mind that residua from previous neurologic disease may confuse the clinical picture. Thus, an earlier hemiparesis from vascular disease or trauma may reassert itself in the course of uremic or hepatic coma with hypotension, hypoglycemia, diabetic acidosis, or following a seizure. Occasionally, for no understandable reason, one leg may seem to move less, one plantar reflex may be extensor, or seizures may be predominantly or entirely unilateral in a metabolic coma, particularly in the hyperglycemic-hyperosmolar states. Babinski signs and extensor rigidity, conventionally considered to be indicators of structural disease, do sometimes occur in profound intoxications with a number of agents. The diagnosis of concussion or of postictal coma depends on observation of the precipitating event or indirect evidence thereof. This state, called nonconvulsive status or spike-wave stupor and described in Chap. With respect to the second group in the above classification, the signs of meningeal irritation (head retraction, stiffness of neck on forward bending, Kernig and Brudzinski signs) can usually be elicited in both bacterial meningitis and subarachnoid hemorrhage. In such cases the spinal fluid must be examined in order to establish the diagnosis. In the third group of patients, it is the focality of sensorimotor signs and the abnormal pupillary and ocular reflexes, postural states, and breathing patterns that provide the clues to serious structural lesions in the cerebral hemispheres and their pressure effects upon segmental brainstem functions. As the brainstem features become more prominent, they may obscure earlier signs of cerebral disease. It is worth emphasizing once more that profound hepatic, hypoglycemic, hyperglycemic, and hypoxic states may resemble the coma due to a brainstem lesion in that asymmetrical motor signs, focal seizures, and decerebrate postures arise and deep coma from drug intoxication may obliterate reflex eye movements. Unilateral cerebral infarction due to anterior, middle, or posterior cerebral artery occlusion produces no more than drowsiness, as a rule; however, with massive unilateral infarction due to carotid artery occlusion, coma can occur if extensive brain edema and secondary tissue shift develop. Rapidly evolving hydrocephalus causes smallness of the pupils, rapid respiration, extensor rigidity of the legs, Babinski signs, and sometimes a loss of eye movements. Finally, it should be restated that diagnosis has as its prime purpose the direction of therapy. The treatable causes of coma are drug and alcohol intoxications, shock due to infection, cardiac failure, or systemic bleeding, epidural and subdural hematomas, brain abscess, bacterial and fungal meningitis, diabetic acidosis or hyperosmolar state, hypoglycemia, hypo- or hypernatremia, hepatic coma, uremia, status epilepticus, Hashimoto encephalopathy, and hypertensive encephalopathy.

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The diagnosis of these states is predicated on the assumption that the failure in perception occurs in spite of intact visual acuity and adequate language and mental function breast cancer in lymph nodes buy cheap nolvadex on line. When examined carefully pregnancy after 40 order 10 mg nolvadex amex, agnosic patients usually do not satisfy all these criteria and instead have a number of other derangements that may at least in part explain their perceptual incompetence menstruation yoga sequence buy generic nolvadex 10mg on line. Often there is a unisensory or polysensory disturbance womens health 6 week boot camp buy nolvadex with american express, an inadequacy of memory or of naming, or an impairment of visual oculomotor or visuomanual control. Anatomic studies have established that disturbances of recognition of complex forms, human faces, and spatial arrangements accompany right (nondominant) parieto-occipital lesions more often than left-sided ones. Disturbances of perception of graphic symbols of objects, of color discrimination, and naming- in short, all of the lexical aspects of recognition- are virtually always associated with left parieto-occipital lesions. Variations in the clinical effects of such lesions are dependent not only on their location and size but also on the particular tests used to elicit these effects and whether they involve learning, recognition, and recall. But there have been many critics of the concept of agnosia as a higher-order perceptual disturbance that can be clearly separated from loss of elementary sensation. Such a division is said to perpetuate an archaic view of sensory reception in the brain as consisting of two separable functional attributes: elementary sensation and perception. Bay, for example, claimed that careful testing of patients with visual agnosia always brings to light some degree of diminished vision in combination with general defects such as confusion and mental deterioration. Others (Geschwind; Sperry and colleagues) have emphasized that the visual agnosias depend on disconnections of the visual receptive zones of the brain from the language areas of the left hemisphere, the learning and memory zones of the temporal lobes, the suprasensory zones of the parietal lobes, and the motor regions. The reported cases of visual agnosia emphasize the complexity of the perceptive process and the inadequacy of our knowledge of the physiology of the several receptive zones of the occipital lobes. The fact that in some cases there are impairments of primary sensation that can be elicited by careful testing of visual function- using tachistoscopic stimuli, visual adaptation, perception of pattern, flicker-fusion, etc. However, even when present, such abnormalities would not fully explain the loss of discrimination and the inability to visualize or imagine the form and color of objects, their spatial arrangements, and their names. Failure of a sensation to activate these visual memories must involve a higher-order disturbance of cerebral function in the heteromodal association areas. Here sensory and motor functions are always integrated, the latter being essential for proper scanning and exploring by the sense organs. And to reduce the agnosias to a series of disconnections between the striate and parastriate cortex and other parts of the brain, although an interesting approach, leads to an overly simplified mechanistic view of cerebral activity, which probably will not be sustained as more knowledge of cerebral physiology is acquired. There is still a great need for the study of cases in which sensation and perception have been tested in detail and the anatomy of the lesion, in its stable end stage, has been carefully determined. Contralateral (congruent) homonymous hemianopia, which may be central (splitting the macula) or peripheral; also homonymous hemiachromatopsia B. If deep white matter or splenium of corpus callosum is involved, alexia and color-naming defect C. With more extensive lesions, visual illusions (metamorphopsias) and hallucinations (more frequent with rightsided than left-sided lesions) C. Balint syndrome (parieto-occipital) Disturbances of the Nondominant Cerebral Hemisphere A line of disagreement, as old as neurology itself, pertains to the relationship between the two cerebral hemispheres. Fechner, in 1860, speculated that since the two hemispheres, joined by the corpus callosum, were virtual mirror images of one another and functioned in totality in conscious life, separating them would result in two minds. William McDougall rejected this idea and is said to have offered to have his own brain divided by Charles Sherrington should he have an incurable disease. He died of cancer, but the callosotomy was considered unnecessary, for already there were indications from the work of Sperry and colleagues that when separated, the two hemispheres had different functions, as indicated in the next section, "Disconnection Syndromes. It is in the sphere of visuospatial perception that right hemispheral dominance is most convincing. Lesions of the right posterior cerebral region result in an inability to utilize information about spatial relationships in making perceptual judgments and in responding to objects in a spatial framework. This is manifest in constructing figures (constructional apraxia), in the spatial orientation of the patient in relation to the environment (topographic agnosia), in identifying faces (prosopagnosia), and in relating a scattering of visual stimuli to one another (simultanagnosia). The idea that attention is a function of the right hemisphere derives from the neglect of left visual space and of somatic sensation in the anosognosic syndrome and also from the apathy that characterizes such patients. Certainly the popular notion of the right hemisphere as "emotional" in contrast to the left one as "logical" has no basis in fact and represents a gross oversimplification of brain function and localization. Similar issues arise, of course, in relation to handedness and language dominance in the left hemisphere as discussed in the following chapter. Here we only comment on how intriguing it is that praxis and linguistic skill are aligned on the same side of the brain, suggesting that an essential property of the dominant hemisphere is its ability to comprehend and manipulate symbolic representations of all types. In more recent years, these ideas were resurrected and modernized by Geschwind and greatly extended by Sperry and by Gazzaniga. Geschwind called attention to several clinical syndromes resulting from interruption of the connections between the two cerebral hemispheres in the corpus callosum or between different parts of one hemisphere. When the entire corpus callosum is destroyed by tumor or surgical section, the language and perception areas of the left hemisphere are isolated from the right hemisphere. Patients with such lesions, if blindfolded, are unable to match an object held in one hand with that in the other. Furthermore, if rapid presentation is used to avoid bilateral visual scanning, such patients cannot match an object seen in the right half of the visual field with one in the left half. They are also alexic in the left visual field, since the verbal symbols that are seen there and are projected to regions of the right hemisphere have no access to the language areas of the left hemisphere. If given a verbal command, such patients will execute it correctly with the right hand but not with the left; if asked to write from dictation with the left hand, they will produce only an illegible scrawl. Many remarkable conclusions regarding the nature of behavior and the special roles of each cerebral hemisphere have been drawn from clever observations of patients with callosal section. Extensive discussion of these neuropsychologic abnormalities cannot be undertaken here; suffice it to say that these are not features seen in patients with the usual neurologic diseases, but they are nonetheless of interest to neurologists and are discussed in the writings of Gazzaniga. In most lesions confined to the posterior portion of the corpus callosum (splenium), only the visual part of the disconnection syndrome occurs. Cases of occlusion of the left posterior cerebral artery provide the best examples. Since infarction of the left occipital lobe causes a right homonymous hemianopia, all visual information needed for activating the speech areas of the left hemisphere must thereafter come from the right occipital lobe. The patient with a lesion of the splenium of the corpus callosum or the adjacent white matter cannot read or name colors because the visual information cannot reach the left language areas. There is, however, no difficulty in copying words; presumably the visual information for ac- tivating the left motor area crosses the corpus callosum more anteriorly. This is the syndrome of alexia without agraphia mentioned earlier and discussed further on page 422. A lesion that is limited to the anterior third of the corpus callosum (or a surgical section of this part, as in patients with intractable epilepsy) surprisingly does not result in an apraxia of the left hand. Object naming and matching of colors without naming them are also done without error. However, blinded, the patient cannot name a finger touched on the left hand or use it to touch a designated part of the body. Of interest to the authors is the fact that one sometimes encounters patients with a lesion in all or some part of the corpus callosum without being able to demonstrate any aspect of the aforementioned disconnection syndromes. Notable is the observation that in some patients with a congenital agenesis of the corpus callosum (a not uncommon developmental abnormality), none of the interhemispheral disconnection syndromes can be found. One can only suppose that in such patients information is transferred by another route- perhaps the anterior or posterior commissure- or that dual dominance for language and praxis was established during early development. They are mentioned here only briefly and are considered in more detail in the following chapter. The patient has severely impaired repetition, but fluent and paraphasic speech and writing and relatively intact comprehension of spoken and written language. However, most often the lesion is in the supramarginal gyrus, as discussed in Chap. Although the patient is able to hear and identify nonverbal sounds, there is loss of ability to discriminate speech sounds, i. Special Neuropsychologic Tests In the study of focal cerebral disease, there are two complimentary approaches- the clinical-neurologic and the neuropsychologic.

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