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This condition and pseudohypoparathyroidism (page 834) were mentioned in relation to the hereditary metabolic disorders In the past, the usual cause of hypoparathyroidism was surgical removal of the parathyroid glands during subtotal thyroidectomy, although there were always idiopathic cases as well With the more widespread use of radiation and drug therapy for thyroid disease, the number of surgically created cases has become small in proportion to nonsurgical ones The latter may occur in pure form, presumably as an agenesis of the parathyroid glands, with unmeasurable levels of parathyroid hormone in the blood, or as part of the DiGeorge syndrome of agenesis of the thymus and parathyroid glands, organs that are embryologically derived from the third and fourth branchial clefts Hypoparathyroidism is also part of a familial disorder in which a de ciency of thyroid, ovarian, and adrenal function, pernicious anemia, and other defects are combined, based presumably on a derangement of autoimmune mechanisms Other causes are intestinal malabsorption, pancreatic insuf ciency, and vitamin D de ciency In all instances the low levels of parathormone and normal responses to injected hormone permit the recognition of a primary defect of the parathyroid glands and distinguish it from all other conditions in which there is hypocalcemia and hyperphosphatemia The clinical manifestations, mainly attributable to the effects of hypocalcemia, are tetany, paresthesias, muscle cramps, laryngeal spasm, and convulsions Children with this disease may be irritable and show behavioral changes In adults with chronic hypocalcemia, calcium deposits occur in the basal ganglia, dentate nuclei, and cerebellar cortex In such patients we have observed unilateral tremor, a restless choreoathetotic hand, bilateral rigidity, slowness of movement and exed posture resembling Parkinson disease, and ataxia of the limbs and gait in various combinations Interestingly, the multiple skeletal and developmental abnormalities that characterize both pseudo- and pseudo-pseudohypoparathyroidism (short stature, round face, short neck, stocky body build, shortening of metacarpal and metatarsal bones and phalanges from premature epiphyseal closure) are rarely seen in pure hypoparathyroidism A similar deposition of ferrocalc in the walls of small blood vessels of the lenticular and dentate nuclei and to a lesser extent in other parts of the brain is a common nding in normal older individuals (Fahr disease) It also occurs in animals Occasionally it reaches a degree of severity that destroys striatal or dentate neurons In such cases, lms of the skull and particularly CT scans will reveal the deposits Cases of Fahr disease have been reported for years (Fig 37-9, page 835), but the cause of the deposits is un-
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Effects of Hyperthermia on the Cerebellum
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The damaging effects of hyperthermia, like those of anoxia, involve the brain diffusely In the case of hyperthermia, however, the changes are disproportionately severe in the cerebellum The acute manifestations of profound hyperthermia are coma and convulsions, frequently complicated by shock and renal failure Patients who survive the initial stage of the illness frequently show signs of widespread cerebral affection, such as confusion and pseudobulbar and spastic paralysis These abnormalities tend to resolve gradually, leaving the patient with a more or less pure disorder of cerebellar function The most extensive account of the pathologic effects of hyperthermia is that of Malamud and colleagues These authors studied 125 fatal cases of heat stroke, but their observations are prob-
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ably applicable to hyperthermia of other types In patients who survived less than 24 h, the changes consisted mainly of a loss of some of the Purkinje cells and swelling, pyknosis, and disintegration of those that remained In cases surviving beyond 24 h, there was almost complete degeneration of the Purkinje cells, with gliosis throughout the cerebellar cortex as well as degeneration of the dentate nuclei The changes in the cerebellar cortex were equally pronounced in the hemispheres and vermis The unanswered question is whether high temperature alone is an adequate cause or whether it must be combined with hypoxia and ischemia It is of interest that we have not seen this syndrome in patients with infective fevers, malignant hyperthermia, or the malignant neuroleptic syndrome either the neuropathologic changes or the clinical cerebellar syndrome in survivors
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Cerebellar Syndromes Associated with Celiac Disease (Sprue, Gluten Enteropathy)
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Most often, the neurologic association with this disease has been a peripheral neuropathy as described on page 1142 In addition, a progressive cerebellar ataxia of gait and limbs, sometimes with polymyoclonus in association with a gluten-sensitive enteropathy, has been the subject of several reports The underlying cause is an intestinal allergy to gluten in wheat that produces a villus atrophy of the intestinal mucosa It has been called celiac disease of children and sprue in adults Between 05 and 1 percent of the Caucasian population are affected with the intestinal disorder The classic features are diarrhea and malabsorption but many individuals are asymptomatic (see also page 993) The neurologic disorder may appear several years after onset of the enteropathy and, in addition to ataxia, usually includes signs of peripheral neuropathy and, in some cases, myelopathy and encephalopathy (dementia) or psychiatric symptoms (Hallert et al) A rare spinocerebellar syndrome has been described by Cooke and Smith According to Finelli et al, neurologic abnormalities occur in approximately 10 percent of cases of adult celiac sprue This subject has been reviewed by Bhatia et al and extensively by Hadjivassiliou et al The latter authors emphasize the frequent occurrence of ataxia in patients with gluten sensitivity (indicated by circulating antibodies to gliadin (which is another term for gluten) and more speci cally, antibodies to transglutaminase and endomysium) but, curiously, often without overt signs of bowel disease There is also an association of sprue in more than 90 percent of patients with the HLA DQ2 and DQ8genotype The few cases that have come to autopsy have shown severe cerebellar atrophy, a nding that may also be disclosed by MRI Hadjivassiliou et al observed lymphocytic in ltration and perivascular cuf ng in the cerebellar cortex and peripheral nerves in one autopsied case but not in another, changes that they took to represent immunologic injury to these parts Despite these associations, some authors have been skeptical of a gluten ataxia (see the editorial by Cross and Golumbek and the contrary case for a valid connection by Hadjivassilou and colleagues, 2002) Reports of improvement in the ataxia following the institution of a gluten-free diet have been con icting The situation is further complicated by the nding that antigliadin antibodies (which are not autoantibodies but are directed against gluten, the offending agent), while not speci c for celiac disease, do correspond to the presence of neurologic manifestations (ataxia and neuropathy); however, the more speci c antiendomysium and
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antitransglutaminase autoantibody markers of sprue have little apparent relation to the presence of neurologic disease Even more confusing is the claim that half of these patients will have one or another antibody but no clinical enteropathy, making it necessary to perform a small bowel biopsy to detect villous atrophy A glutenfree diet is necessary, not only to reduce the enteropathy, if present, but also to reduce the chances of the later development of a bowel lymphoma The medical issues relating to celiac disease and the use of antibody tests and bowel biopsy are reviewed by Farrell and Kelly We have sought evidence by antibody testing and bowel biopsy of sprue in numerous patients with an ataxia of obscure origin and have only once found it Nevertheless, the evidence presented in the writings of several authors, particularly Hadjivassiliou, suggest that sprue may underlie some cases of subacute ataxia in adults Always to be considered in the differential diagnosis is paraneoplastic cerebellar degeneration and Creutzfeldt-Jakob disease Vitamin E de ciency may induce a similar syndrome with features of spinocerebellar dysfunction (see page 251) Jejunoileal bypass operations, in addition to causing a chronic arthropathy, neuropathy, and vasculitic skin lesions, may give rise to an episodic confusion and cerebellar ataxia associated with a lactic acidosis and abnormalities of pyruvate metabolism Overfeeding and fasting are provocative factors (Dahlquist et al)
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