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Moreover, if damage to the cell had attained only the stage of central chromatolysis, complete morphologic recovery could be expected- a process that took a month or longer. After this time, the degrees of paralysis and atrophy were closely correlated with the number of motor nerve cells that had been destroyed; where limbs remain atrophic and paralyzed, less than 10 percent of neurons survived in corresponding cord segments. Lesions in the motor nuclei of the brainstem are associated with paralysis in corresponding muscles, but only if severe in degree. The disturbances of swallowing, respiration, and vasomotor control are related to neuronal lesions in the medullary reticular formation, centered in the region of the nucleus ambiguus. Atrophic, areflexic paralysis of muscles of the trunk and limbs relates, of course, to destruction of neurons in the anterior and intermediate horns of the corresponding segments of the spinal cord gray matter. Stiffness and pain in the neck and back, attributed to "meningeal irritation," are probably related to the mild inflammatory exudate in the meninges and to the generally mild lesions in the dorsal root ganglia and dorsal horns. Probably these lesions also account for the muscle pain and paresthesias in parts that later become paralyzed. Abnormalities of autonomic function are attributable to lesions of autonomic pathways in the reticular substance of the brainstem and in the lateral horn cells in the spinal cord. Treatment Patients in whom acute poliomyelitis is suspected require careful observation of swallowing function, vital capacity, pulse, and blood pressure in anticipation of respiratory and circulatory complications. With paralysis of limb muscles, foot boards, hand and arm splints, and knee and trochanter rolls prevent foot drop and other deformities. Respiratory failure, due to paralysis of the intercostal and diaphragmatic muscles or to depression of the respiratory centers in the brainstem, calls for the use of a positive-pressure respirator and, in most patients, for a tracheostomy as well. The authors know of no systematic study of the potency of antiviral agents in this disease. Prevention Prevention, of course, has proved to be the most significant aspect and one of the outstanding accomplishments of modern medicine. The cultivation of poliovirus in cultures of human embryonic tissues and monkey kidney cells- the achievement of Enders and associates- made possible the development of effective vaccines. The first of these was the injectable Salk vaccine, containing formalin-inactivated virulent strains of the three viral serotypes. This was followed by the Sabin vaccine, which consists of attenuated live virus, administered orally in two doses 8 weeks apart; boosters are required at 1 year of age and again before starting school. Since 1965, the reported annual incidence rate of poliomyelitis in the United States has been less than 0. The only obstacle to complete prevention of the disease is inadequate utilization of the vaccine. Conceivably, with an increasing lack of immunity in underdeveloped nations, outbreaks of poliomyelitis could occur once again. Prognosis Mortality from acute paralytic poliomyelitis is between 5 and 10 percent- higher in the elderly and very young. If the patient survives the acute stage, paralysis of respiration and deglutition usually recovers completely; in only a small fraction of such patients is chronic respirator care necessary. Many patients also recover completely from muscular weakness, and the most severely paralyzed improve to some extent. Branching of axons of intact motor cells with collateral reinnervation of muscle fibers of denervated motor units may also play a part. Slow recovery of slight degree may then continue for a year or more, the result of hypertrophy of undamaged muscle. The tendency of West Nile virus to cause a poliomyelitis has already been mentioned. Fifty-two cases were recorded by the Centers for Disease Control and Prevention over a 4-year period. Most of these have been due to one of the echoviruses and a lesser number to Coxsackie enteroviruses, particularly strains 70 and 71.

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The most chronic lesion takes the form of a centrally placed gray cleft or cavity, with collapse of the surrounding tissue and reduction in thickness of the corpus callosum. Microscopically, corresponding to the gross lesions, one observes clearly demarcated zones of demyelination, with variable involvement of the axis cylinders and an abundance of fatty macrophages with gliosis at the margins. Infrequently, lesions of a similar nature are found in the central portions of the anterior and posterior commissures and the brachia pontis. These zones of myelin destruction are always surrounded by a rim of intact white matter. The predilection of this disease process for commissural fiber systems has been stressed, but it is certainly not confined to these fibers. Symmetrically placed lesions have been observed in the columns of Goll, superior cerebellar peduncles, and cerebral hemispheres, involving the centrum semiovale and extending, in some cases, into the adjacent convolutional white matter. As a rule, the internal capsule and corona radiata, subcortical arcuate fibers, and cerebellum are spared. In several cases, the lesions of deficiency amblyopia (see above) have been added; in others, the lesions of Wernicke disease. Many of the reported cases, as first pointed out by Jequier and Wildi, have involved cortical lesions of a special type: the neurons in the third layer of the frontal and temporal lobe cortices had disappeared and were replaced by a fibrous gliosis. Morel, who first described this cortical laminar sclerosis, did not observe its association with Marchiafava-Bignami disease. However, when Jequier and Adams reviewed his original cases (unpublished), all had Marchiafava-Bignami disease. In a subsequent report by Delay and colleagues comprising 14 cases of cortical laminar sclerosis, the cortical lesion was also consistently associated with a corpus callosum lesion. We believe the cortical lesions are best explained as secondary to the callosal degeneration. The clinical features of the illness are otherwise quite variable, and a clear-cut syndrome of uniform type has not emerged. Many patients have presented in a state of terminal stupor or coma, precluding a detailed neurologic assessment. In others, the clinical picture was dominated by the manifestations of chronic inebriation and alcohol withdrawal- tremor, seizures, hallucinosis, and delirium tremens. In some of these patients, following the subsidence of the withdrawal symptoms, no signs of neurologic disease could be elicited, even in the end stage of the disease, which lasted for several days to weeks. In yet another group, a progressive dementia has been described, evolving slowly over a 3- to 6-year period before death. Emotional disorders leading to acts of violence, marked apathy, moral perversions, and sexual misdemeanors have been noted in these patients; dysarthria, slowing and unsteadiness of movement, transient sphincteric incontinence, hemiparesis, and apractic or aphasic disorders were superimposed in others. The last stage of the disease is characterized by physical decline, seizures, stupor, and coma. An impressive feature of these varied neurologic deficits in some patients has been their tendency toward remission when nutrition was restored. In two cases that have come to our attention, the clinical manifestations were essentially those of bilateral frontal lobe disease: motor and mental slowness, apathy, prominent grasping and sucking reflexes, gegenhalten, incontinence, and a slow, hesitant, widebased gait. In both of these cases, the neurologic abnormalities evolved over a period of about 2 months, and both patients recovered from these symptoms within a few weeks of hospitalization. Death occurred several years later as a result of liver disease and subdural hematoma, respectively. In each case, autopsy disclosed an old lesion typical of Marchiafava-Bignami disease confined to the central portion of the most anterior parts of the corpus callosum, but one had to look closely to see the gray line of gliosis. In view of the great variability of the clinical picture and the obscuration in many patients of subtle mental and neurologic abnormalities by the effects of chronic inebriation and other alcoholic neurologic disorders, the diagnosis of Marchiafava-Bignami disease is understandably difficult. In rare cases these findings have reversed over time after vitamin therapy, leaving residual callosal atrophy (Gambini). The occurrence, in a chronic alcoholic, of a frontal lobe syndrome or a symptom complex that points to a diagnosis of frontal or corpus callosum tumor but in whom the symptoms remit should suggest the diagnosis of Marchiafava-Bignami disease. The image appearance may be mistaken for multiple sclerosis or gliomatosis cerebri. Pathogenesis and Etiology Originally, Marchiafava-Bignami disease was attributed to the toxic effects of alcohol, but this is an unlikely explanation in view of the prevalence of alcoholism and the rarity of corpus callosum degeneration. Further, the distinctive callosal lesions have not been observed with other neurotoxins. Very rarely, undoubted examples of Marchiafava-Bignami disease have occurred in abstainers, so that alcohol cannot be an indispensable factor.

When they are associated with vomiting, transient blindness, leg weakness with "drop attacks," and loss of consciousness, there is a high likelihood of brain tumor. With respect to its onset, this headache resembles that of subarachnoid hemorrhage, but the latter is far longer-lasting. In its entirety, this paroxysmal headache is most typical of the aforementioned colloid cyst of the third ventricle, but it can occur with other tumors as well, including craniopharyngiomas, pinealomas, and cerebellar masses. This technique has not yet been incorporated into the routine evaluation because its sensitivity has not been established; our own experience suggests that it may miss a proportion of cases. Treatment the administration of prednisone, 45 to 60 mg/day in single or divided doses over a period of several weeks, is indicated in all cases, with gradual reduction to 10 to 20 mg/day and maintenance at this dosage for several months or years, if necessary, to prevent relapse. The headache can be expected to improve within a day or two of beginning treatment; failure to do so brings the diagnosis into question. When the sedimentation rate or Creactive protein are elevated, their return to normal is a reliable index of therapeutic response. Headaches of Temporal Arteritis (Giant-Cell Arteritis, Cranial Arteritis) (See also Chap. All of our patients have been more than 55 years of age, most of them above age 65. From a state of normal health, the patient develops an increasingly intense throbbing or nonthrobbing headache, often with superimposed sharp, stabbing pains. The pain is usually unilateral, sometimes bilateral, and often localized to the site of the affected arteries in the scalp. The pain persists to some degree throughout the day and is particularly severe at night. The superficial temporal and other scalp arteries are frequently thickened and tender and without pulsation. Jaw claudication and ischemic nodules on the scalp, with ulceration of the overlying skin, have been described in severe cases. Many of the patients feel generally unwell and have lost weight; some have a low-grade fever and anemia. Usually the sedimentation rate is greatly elevated ( 50 mm/h and usually over 75 mm/h), and a few patients have a neutrophilic leukocytosis. As many as 50 percent of patients have generalized aching of proximal limb muscles, reflecting the presence of polymyalgia rheumatica (see page 189). The importance of early diagnosis relates to the threat of blindness from thrombosis of the ophthalmic or posterior ciliary arteries. This may be preceded by several episodes of amaurosis fugax (transient monocular blindness, page 692). Ophthalmoplegia may also occur but is less frequent, and its cause, whether neural or muscular, is not settled. For this reason the earliest suspicion of cranial arteritis should lead to biopsy of the appropriate scalp artery and the immediate administration of corticosteroids. Microscopic examination discloses an intense granulomatous or "giant-cell" arteritis. If biopsy on one side fails to clarify the situation and there are sound clinical reasons for suspecting the diagnosis, the other side should be sampled. Arteriography of the external carotid artery branches is probably the most sensitive test but is seldom used; ultrasound examination has recently been introduced to display a dark halo and irregularly thick- Headaches of Pseudotumor Cerebri (Benign, or Idiopathic Intracranial Hypertension) the headache of pseudotumor cerebri assumes a variety of forms. Typical is a feeling of occipital pressure that is greatly worsened by lying down, but many patients have- in addition or only- headaches of migraine or tension type. Indeed, some of them respond to medications such as propranolol or ergot compounds. None of the proposed mechanisms for pain in pseudotumor cerebri seems to be adequate as an explanation, particularly the idea that cerebral vessels are displaced or compressed, since neither has been demonstrated. It is worth noting that facial pain may also be a feature of the illness, albeit rare. A more complete description of the clinical features, pathophysiology, and treatment can be found in Chap. Assuming the supine position almost immediately relieves the cranial pain and eliminates vomiting, but a blood-patch procedure may be required in persistent cases.

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Diagram of probable cellular events in acute inflammatory polyneuropathy Hartung and colleagues have found high levels of (Guillain-Barre syndrome). This change appears to be mediated by the mononuclear exudate, but the these cells. The lesion is more intense, polymorphonuclear leukocytes being to be a necessary factor in the initial attack on mypresent as well as lymphocytes. If the axonal damage is distal, the nerve cell body will survive, and sensitized to myelin is strong evidence of their role regeneration and clinical recovery is likely. Indeed, the very earliest change that could be detected by Hafer-Macko and colleagues was the deposition of complement on the inner layer of myelin. All attempts to isolate a virus or microbial agent from nerves or to demonstrate one by electron microscopy have failed, and it is more likely that a variety of agents- viral, bacterial (particularly C. Whether the aforementioned antibodies against various gangliosides of peripheral nerve are pathogenically active is also uncertain. Any polyneuropathy that brings the patient to the brink of death or to respiratory failure within a few days will usually be of this variety. There may be particular difficulty in the case of an acute lesion of the cord in which tendon reflexes are initially lost (spinal shock), or with necrotizing myelopathy, where a permanent loss of tendon reflexes follows extensive destruction of spinal gray matter (pages 781 and 1064). In all these infectious cases the illness is marked by fever, meningoencephalitic symptoms, early pleocytosis in the spinal fluid, and purely motor and usually asymmetrical areflexic paralysis. An irregular distribution of weakness between proximal and distal parts, the absence of facial weakness and the appearance of symptoms in one limb after another are always suggestive of this type of neoplastic infiltration of nerve roots. These include a polyneuropathy of critical illness (see further on); an accelerated neuropathy of renal failure that is seen mainly in diabetic patients receiving peritoneal dialysis (both discussed further on); acute hypophosphatemia induced by hyperalimentation; polymyopathy produced by the administration of highdose corticosteroids (page 1237); and the prolonged effects of neuromuscular blocking drugs, resulting in the accumulation of their metabolites in patients under conditions of renal failure and acidosis. Treatment General medical aspects In severe cases, respiratory assistance and careful nursing are paramount, since the disease remits naturally and the outlook for recovery is favorable in the majority. About one quarter of our patients in the recent era of treatment have required mechanical ventilation. The comments that follow are applicable to most other forms of acute and subacute neuromuscular respiratory failure such as myasthenia gravis. Measurement of maximal inspiratory force and expiratory vital capacity suffices for the bedside estimation of the adequacy of diaphragmatic strength and respiratory function. The trend of these measurements are a guide to the likelihood of respiratory failure. As in poliomyelitis, the strength of the neck muscles and trapezii, which share the same segmental innervation as the diaphragm, tends to parallel diaphragmatic strength. A rough estimate of breathing capacity may be obtained by having the patient count quickly on one deep breath. The ability to reach 20 generally corresponds to a vital capacity of greater than 1. If a downward trend in these measurements is recognized and the vital capacity diminishes to below about 10 mL/kg, endotracheal intubation and mechanical ventilation are considered. It should be noted that a fairly severe degree of impaired ventilation may occur before the first sign of dyspnea appears and even before there is any elevation of arterial carbon dioxide content. If respiratory failure arises gradually, over days or longer, there is slight tachycardia, diaphoresis, restlessness, and tachypnea. Attempts to forestall the use of a positive-pressure ventilator by negative-pressure cuirass-type devices have been unsatisfactory in our experience. Patients with oropharyngeal weakness require intubation even earlier in order to prevent aspiration, but mechanical ventilation is not always necessary at the same time. These treatments are so demanding that the patient should be admitted to an intensive care unit staffed by personnel skilled in maintaining ventilation and airway patency. The other major aspects of the treatment in severely affected patients involve the management of cardiovascular autonomic instability and the prevention of the many general medical problems that attend any immobilizing critical illness. Hypotension from dysautonomia, which occurs in about 10 percent of severely affected patients, is treated by intravenous volume infusion and by the use of vasopressor agents for brief periods. Extremes of hypertension are managed by short-acting and titratable antihypertensive medications, such as intravenous labetalol. The choice and dosing of an antihypertensive drug is important, since these episodes may be rapidly succeeded by precipitous declines in pressure. It is not clear if severe autonomic changes can be anticipated but various provocative maneuvers such as ocular pressure to elicit heart block are used in some units; we generally omit them. Prevention of electrolyte imbalance, gastrointestinal hemorrhage, and particularly pulmonary embolism in patients who are bedbound (by the use of subcutaneous heparin or pneumatic compression boots), all require careful attention.