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A hamartoma of the hypothalamus (part of von Recklinghausen disease or of polyostotic brous dysplasia) is a leading cause of precocious puberty in both boys and girls; in a number of such cases, so-called gelastic seizures have been conjoined (Breningstall, see page 278) Neurologic study entails computed tomography (CT) and MRI imaging of the hypothalamus, ovaries, and adrenals Adiposogenital Dystrophy (Froehlich Syndrome) Under this title, in 1901, Froehlich rst described the association of obesity and gonadal underdevelopment He related the disorder to a pituitary tumor But a few years later, 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 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, aggression, or antisocial behavior Diabetes insipidus may be added 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 (page 864) Hypothalamic Disorders Associated with Alterations in Weight Precise 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, in overeating and obesity Bray and Gallagher, who analyzed eight cases of the latter type, concluded that the critical lesion was a bilateral destruction of the ventromedial regions of the hypothalamus Most of the reported cases of this type have been due to tumors, particularly craniopharyngioma, and some to trauma, in ammatory 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 persons 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 ability to store fat A rare disorder of infants has been described under the title of diencephalic syndrome Progressive and ultimately fatal emaciation (failure to thrive), despite normal or near-normal food intake, in an otherwise alert and cheerful infant is the main clinical feature The lesion has usually proved to be a low-grade astrocytoma of the anterior hypothalamus or optic nerve (Burr et al) Extrahypothalamic parts of the brain, if diseased, may also be associated with increased food-seeking behavior, food ingestion, and weight gain Examples are involvement of limbic structures, as in the Kluver-Bucy syndrome (page 448) and basal frontal lobe lesions leading to gluttony Anorexia Nervosa and Bulimia The special syndromes called anorexia nervosa and bulimia have been dif cult to classify and are mentioned in this chapter only because they are associated with.

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numerous electrically inexcitable motor nerves and signs of extensive denervation Others, however, have questioned the speci city of this nding since the inability to excite motor nerves may also signify a distal demyelinating block, from which complete recovery is possible (Triggs et al) Nevertheless, most cases of very abrupt and severe denervating paralysis, particularly if postinfectious, are due to this form of GBS (Ropper 1986) Postmortem examinations in these cases have disclosed severe axonal degeneration in nerves and roots, with minimal in ammatory changes and little demyelination, even early in the disease Based on prominent deposits of complement and the presence of macrophages in the periaxonal space, a humoral antibody directed against some component of the axolemma has been postulated by Grif n and associates Visser and colleagues reported similar ndings in a series of acute motor polyneuropathies from Holland The outbreaks of motor neuropathy that occur seasonally in rural China have many of the same characteristics These cases appear to be triggered largely by C jejuni infections Some but not all sporadic instances of acute axonal GBS have been preceded by the same infection It is noteworthy, however, that infection with the same bacteria can induce a typical demyelinating form of GBS A proportion of cases, perhaps one quarter, are associated with circulating antibodies to the GM1 ganglioside of peripheral nerve, and some of these in turn re ect recently preceding infection with C jejuni The acronyms AMAN (acute motor) and AMSAN (acute motor-sensory axonal neuropathy) are equivalents to axonal GBS Another variant of this illness of which we have seen several instances has been an acute multifocal neuropathy with electrophysiologic motor conduction block that leaves the re exes unaltered and is related to anti-GM1 antibody (Capasso et al) A chronic form of this illness, termed multifocal motor neuropathy, is more common and better understood (see further on) Most experience with the generalized axonal form of GBS indicates that recovery is prolonged and complete resolution of weakness is uncommon Intravenous administration of immune globulin (IVIG) and plasma exchange, the usual treatments for GBS as discussed later, have had slight bene cial effect but their use is not associated with the degree of improvement seen in demyelinating cases Whether this acute axonal polyneuropathy is a distinct entity or a variant of GBS cannot be answered with certainty This may prove to be a semantic issue, depending on one s de nition of the clinical, immunologic, and pathologic boundaries of GBS Certainly, there is a degree of axonal damage in all severe cases of GBS, even when the predominant process is demyelinating Currently we prefer to distinguish these cases from typical GBS if only to lower expectations for the response to immune treatments and for the ultimate clinical recovery It should be reemphasized that the presence of electrically inexcitable nerves alone may be due to conduction block and give a misleading impression of axonal damage; the prognosis for cases with conduction block may be quite good The differential diagnosis includes critical illness polyneuropathy and the rarer entities of porphyric neuropathy and tick paralysis Laboratory Findings The most important laboratory aids are the electrodiagnostic studies and the CSF examination The CSF is under normal pressure and is acellular or contains only a few lymphocytes in all but 10 percent of patients; in the latter group, 10 to 50 cells (rarely more) per cubic millimeter, predominantly lymphocytes, may be found The number of cells then decreases rapidly in a matter of 2 to 3 days; persistent pleocytosis suggests an alter-.

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On the secondary market for bonds, as interest rates rise, bond prices fall and inversely as interest rates fall, bond prices rise This is to the result of new issues being auctioned at the new interest rate