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Kjellberg and colleagues and Chapman impotence used in a sentence order 800 mg viagra vigour amex, using proton beam radiation, in the past treated more than 1,100 pituitary adenomas without a fatality and with few complications (Kliman et al). An endocrine deficit will follow in most instances and must be corrected by hor mone replacement therapy. Several equivalent methods (gamma Knife, Cyberknife) are more accessible and have become widely used. The advantage of these radiothera peutic methods is that tumor recurrence is rare. A disad vantage is that the radiation effect is obtained only after several months. Estrada and colleagues have also reported that external beam-radiation therapy may be employed after unsuccessful transsphenoidal surgery for Cushing disease. There are a few reports, however, of a decline in memory ability after radiation treatment of all types. Large extrasellar extensions of a pituitary growth must be removed by craniotomy, usually with a trans frontal approach, followed by radiation therapy. Visual field defects often remain, but some improvement in vision can be anticipated. Pituitary Apoplexy 1his syndrome, described origi nally by Brougham, Heusner, and Adams, occurs as a result of infarction of an adenoma that has outgrown its blood supply. Pituitary apoplexy may threaten life unless the acute addisonian state is treated by hydrocortisone. If there is no improve ment after 24 to 48 h, or if vision is markedly affected, transsphenoidal decompression of the sella is indicated. Factors that may precipitate the necrosis or hemorrhage of a pituitary tumor are anticoagulation, pituitary func tion testing, radiation, bromocriptine treatment, and head trauma; most cases, however, occur spontaneously. Ischemic necrosis of the pituitary, without the presence of a tumor followed by hypopituitarism, occurs under a variety of circumstances, the most common being in the partum or postpartum period (Sheehan syndrome). Fully 75 percent of such tumors occur in women, and the average age at onset is 50 years. Most prominent among the symptoms are a slowly devel oping unilateral exophthalmos, slight bulging of the bone in the temporal region, and radiologic evidence of thick ening or erosion of the lesser wing of the sphenoid bone. Variants of the clinical syndrome include anosmia; oculo motor palsies; painful ophthalmoplegia (sphenoidal fissure and Tolosa-Hunt syndromes; see Table 47-2); blindness and optic atrophy in one eye, sometimes with papilledema of the other eye (Foster Kennedy syndrome); mental changes; seizures ("uncinate fits"); and increased intracranial pres sure. Sarcomas arising from skull bones, metastatic carcinoma, orbitoethmoidal osteoma, benign giant cell bone cyst, tumors of the optic nerve, and angiomas of the orbit must be considered in the differential diagnosis. The tumor is resectable without further injury to the optic nerve if the bone has not been invaded. The diagnosis depends on the finding of ipsilateral or bilateral anosmia or ipsilateral or bilateral blindness-often with optic atrophy and mental changes. The tumors may reach enormous size before coming to the attention of the physician but as many are small and found incidentally with cerebral imaging. The unilateral visual disturbance may consist of a slowly developing central scotoma. Abulia, confusion, forgetfulness, and inappropriate jocularity (witzelsucht) are the usual psychic disturbances from compression of the inferior frontal lobes (see Chap. The pre senting symptoms were visual failure-a slowly advanc ing bitemporal hemianopia with a sella of normal size. Often the field defects are asymmetrical, indicating a combined chiasmal-optic nerve involvement. If removal is incomplete or the tumor recurs or undergoes malignant changes, radiation therapy of one type or another is indicated. The outlook is then guarded; several of our patients succumbed within a few years. They produce a variable clinical picture depending on their location in the medulla, pons, or midbrain. Most often, this tumor begins in childhood (peak age of onset is 7 years), and 80 percent appear before the twenty-first year. Symptoms have usually been present for 3 to 5 months before com ing to medical notice. In most patients the initial mani festation is a palsy of one or more cranial nerves, usually the sixth and seventh on one side, followed by long tract signs-hemiparesis, unilateral ataxia, ataxia of gait, para paresis, and hemisensory and gaze disorders in addition to pseudobulbar dysarthria and palsy. Patients in the latter group survive longer than those whose illness begins with cranial nerve palsies. The course is slowly progressive over several years unless some part of the tumor becomes more malignant (anaplastic astrocytoma or glioblastoma multiforme) or, as rarely happens, spreads to the menin ges (meningeal gliomatosis), in which instance the illness may terminate fatally within months. The main problem in diagnosis is to differentiate this disease from a pontine form of multiple sclerosis, a vascular malformation of the pons (usually a cavern ous hemangioma), or brainstem encephalitis, and to distinguish the focal from the diffuse type of glioma (see below). A study of 87 patients by Barkovich and coworkers emphasized the importance of distinguishing between diffusely infiltrating and focal nodular tumors. The patient was a 3-year-old male with progressive crania] nerve and long tract deficits. In a few instances of diffuse brainstem glioma, surgical exploration is neces sary to establish the diagnosis (inspection and possibly biopsy). A series of 16 patients treated by Pollack and colleagues emphasizes that the focal and exo phytic brainstem tumors are almost all low-grade astro cytomas; these tumors, in contrast to the more diffuse type, usually respond well to partial resection and permit long-term survival because they recur only slowly and do not undergo malignant transformation. Gangliocytomas or mixed astrogangliocytomas are rare imitators of nodu lar glioma in the brainstem.

The lesion has usu ally proved to be a low-grade astrocytoma of the anterior hypothalamus or optic nerve (Burr et al) impotence in men purchase viagra vigour with a visa. 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. 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. The temperature rises to 41 °C (106°F) or higher and remains at that level until death some hours or days later, or it drops abruptly with recovery. 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. Closely related is the neuroleptic malignant St ndrome, which is the result of an idiosyncratic J reaction to neuroleptic drugs ("Neuroleptic Malignant Syndrome" in Chap. Wolff and colleagues have described a syndrome of periodic hyperthermia, associated with vomiting, hypertension, and weight loss and accom panied by an excessive excretion of glucocorticoids; the symptoms had no apparent explanation, although there was a symptomatic response to chlorpromazine. Spon taneous periodic hypother mia, probably first described by Gowers, has been found in association with a cholesteatoma of the third ventricle (Penfield) and with agenesis of the corpus callosum (Noel et al). Episodically, there are symptoms of autonomic dishlrbance-salivation, nausea and vomiting, vasodila tation, sweating, lacrimation, and bradycardia; the rectal temperahlre may fall to 30°C (86°F), and seizures may occur. Chronic hypothermia is a more familiar state than hyperthermia, being recorded in cases of severe hypo thyroidism, hypoglycemia, and uremia; after prolonged immersion or exposure to cold; and in cases of intoxi cation with barbiturates, phenothiazines, or alcohol. It tends to be more frequent among elderly patients, who are often found to have an inadequate thermoregulatory mechanism. In seek ing causative lesions, as in patients dying with cardiac changes after head injury or subarachnoid hemorrhage, one searches in vain for a lesion in the various hypo thalamic nuclei. A sudden elevation in intracranial pressure is involved in most cases, usually accompanied by a brief bout of extreme systemic hypertension but without obvious left ventricu lar failure-which is one reason the pulmonary edema has been attributed to a "neurogenic" rather than a cardiogenic cause. Also, it has been shown that experi mental lesions in the caudal hypothalamus are capable of producing this type of pulmonary edema, but almost always with the interposed event of brief and extreme systemic hypertension. Both the pulmonary edema and hypertensive response can be prevented by sympathetic blockade at any level, suggesting that the adrenergic discharge and the hypertension it causes are essential for the develop ment of pulmonary edema. The rapid rise in vascular resistance and systemic blood pressure is similar to the pressor reaction obtained by destruction of the nucleus of the tractus solitarius, as described in Chap. At issue is whether the hypothalamus exerts a direct sympathetic influence on the pulmonary vasculature, allowing a leakage of protein-rich edema fluid, or if the edema is the result of sudden and mas sive overloading of the pulmonary circulation by a shift of fluid from the systemic vasculature. The latter theory, essentially one of momentary right-heart failure, is cur rently favored but does not explain all aspects of the syn drome. Likewise, the role of circulating catecholamines and adrenal steroids has not been fully elucidated. These issues have been summarized in the text on neurologic intensive care by Ropper and colleagues. One can be cer tain that permanent coma from small lesions in the cau dal diencephalon (thalamus) may occur in the absence of any changes in the hypothalamus and, conversely, that chronic hypothalamic lesions may be accompanied by no more than drowsiness or confusion or no mental change at all. Most of the same effects can be induced by very high levels of circulating norepineph rine and corticosteroids. Again, the hypothalamus is implicated, but as yet no direct evi dence links this structure to direct cardiac control. When aroused, he was aggressive, like the patient of Reeves and Plum (see earlier). Among the cases of acquired changes in personality and sleep patterns from ventral hypothalamic disease that we have seen, a few have been impressive because of a tendency to a hypomanic, hypervigilant state with insomnia, lasting days on end, and an impulsiveness and disinhibition suggestive of involvement of the frontal connections to the hypothalamus. These and other cognitive disorders with hypo thalamic lesions are difficult to interpret and are usually transient. Often the lesions are acute or postoperative and involve adjacent areas, making it impossible to attribute them to the hypothalamus alone. For days or weeks, the patients, mostly adolescent boys, sleep 18 or more hours a day, waking only long enough to eat and attend to toilet needs. The hypothalamus has been implicated on the basis of these symptoms, but without definite pathologic confirmation. We have had some experience with patients having this disorder; a further discussion can be found in "Kleine-Levin Syndrome" in Chap.

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The fistula in these latter cases is more often traumatic than congenital in origin erectile dysfunction klonopin generic 800 mg viagra vigour amex. The s1te of trauma 1s m the frontal or ethmoid sinuses or the cribriform plate, and S. These cases usually have a good prognosis; mortality is much lower than in ordinary cases of pneumococcal meningitis. Suspicion of its presence is raised by the recent onset of anosmia or by the occurrence of a watery nasal discharge that is salty to the taste and increases in olume. A "dipstick" used for urine testing is sometimes adequate but these are regrettably decresingly available on general hospital wards. A high protein, suf ficient to make a handkerchief stiff on drying, suggests it is of nasal mucosal origin. If the fluid fails to cause a handkerchief to stiffen on drying, a spinal fluid leak is suspected. Overwhelming sepsis itself, or the multiorgan failure that it engenders, may cause an encephalopathy; but if there is meningitis, it is imperative, in deciding on the choice of antibiotics, to identify it early. Although this approach undoubtedly results in many negative spinal fluid exru:ru nations, it is preferable to the consequence of overlooking bacterial meningitis. Viral meningitis (which is far more common than bacterial meningitis), subarachnoid hemor rhage, chemical meningitis (following lumbar puncture, spinal anesthesia, or myelograph), and tube ulous, leptospiral, sarcoid, and fungal enmgoeceph tis, d allergic-immune reactions enter mto the differential diag nosis as well, as discussed in later sections. A number of nonbacterial meningitides must be considered in the differential diagnosis when the men ingitis recurs repeatedly and all cultures are negative. Rarely, a fulminant case of cerebral angiitis or intravascular lymphoma will present with headache, fever, and confusion in conjunction with a meningeal inflammatory reaction. The other intracranial purulent diseases and therr differentiation from bacterial meningitis are considered further on in this chapter. Treatment should begin while awaiting the results of diagnostic tests and may be altered later in accordance with the laboratory findings. Whereas peni cillin formerly sufficed to treat almost all meningitides acquired outside the hospital, the initial choice of anti biotic has become increasingly complicated as resistant strains of meningitic bacteria have emerged. The selec tion of drugs to treat nosocomial infections also presents special difficulties. In recent years, many reports have documented an increasing incidence of pneumococcal isolates that have a relatively high resistance to penicillin, reaching 50 percent in some European countries. Current estimates are that, in some areas of the United States, 15 percent of these isolates are penicillin-resistant to some degree (most have a relatively low level of resistance). Recommendations for the institution of empiric treatment of meningitis have been reviewed by van de Beek and colleagues (2006) and by Tunkel and colleagues, often updated, and are summarized in modified form in Table 32-2. The choice of agents varies every few years based on epidemiology and geographic region, but these ones given here are a good approximation to current practice in developed countries. For severe penicillin allergy, consider vancomycin and chloramphenicol (for menin gococcus) and trimethoprim-sulfamethoxazole (for Listeria). A high failure rate has been reported with chloramphenicol in patients with drug-resis tant pneumococcus. In children and adults, third-generation cephalospo rins such as ceftriaxone, combined with vancomycin is probably the best initial therapy for the three major types of community-acquired meningitides. In areas with low numbers of high-level penicillin-resistant pneumococci, it is possible to avoid adding vancomycin or rifampin. Ampicillin should be added to the regimen in cases of suspected Listeria meningitis, particularly in an imrnu nocompromised patient. When serious allergy to penicillin and cephalosporins precludes their use, chloramphenicol may be a suitable alternative in some regions, but not for Listeria. Throughout the course of treat ment, it is necessary to have access to a laboratory that can carry out rapid and detailed drug-resistance testing. If Pseudomonas is considered possible, such as after neurosurgery; an antipseudomonal cephalosporin such as ceftazidime or cefapime should be added. Once the sensitivity of the organism has been determined, therapy may have to be altered or may be simplified by using vancomycin or nafcillin alone. They also provide recommendations on the use of prophylactic antibiotics after a basilar skull fracture, a controversial problem that is reviewed in Chap. Table 32-3 lists the approximate dosages of the most used antibiotics, and Table 32-4 gives reasonable choices of antibiotic for the treatment of specific bacterial isolates. Duration of Therapy Most cases of bacterial men ingitis should be treated for a period of 10 to 14 days except when there is a persistent parameningeal focus of infection (otitic or sinus origin), in which cases longer treatment may be needed. Antibiotics should be adminis tered in full doses parenterally (preferably intravenously) throughout the period of treatment. Repeated lumbar punctures are not necessary to assess the effects of ther apy as long as there is progressive clinical improvement. Seizmes and coma were reduced in incidence as a result of the administration of corticosteroids, but neu rologic sequelae, such as hearing loss, were not affected. Based on a number of smaller studies, some authorities in the field of bacterial meningitis have endorsed the administration of dexamethasone in the doses mentioned above, but only if they can be started before antibiotics, and only in those with presumed pneumococcal infec tion (see Tunkel and Scheid). Nonetheless, the incidence of deafness was reduced (Nguyen et al; Scarborough et al). It is not always possible to deter mine with certainty at the first presentation those cases that will be cultme positive but one is referred back to the prediction "rules" validated by Nigrovic and colleagues. Newer drugs are available for methicillin-resistant staphyloccocal infec tions but are not well studied for staphylococcal meningitis: linezolid, quinupristin-dalfopristin, and daptomycin.