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MCSHANE MA, BOYD S, HARDING B, et al: Progressive bulbar paralysis of childhood: A reappraisal of Fazio-Londe disease. Brain 115:1889, 1992. MENDEZ MF, ADAMS NL, LEWANDOWSKI KS: Neurobehavioral changes associated with caudate lesions. Neurology 39:349, 1989. MENDEZ MF, MENDEZ MA, MARTIN R, et al: Complex visual disturbances in Alzheimer s disease. Neurology 40:439, 1990. MESULAM M-M: Slowly progressive aphasia without generalized dementia. Ann Neurol 11:592, 1982. MESULAM MM, GROSSMAN M, HILLIS A, et al: The core and halo of primary progressive aphasia and semantic dementia. Ann Neurol 54 (Suppl 5):S11, 2003. MITSUYAMA Y: Presenile dementia with motor neuron disease in Japan: Clinico-pathological review of 26 cases. J Neurol Neurosurg Psychiatry 47:953, 1984. MOLLARET P: La Maladie de Friedreich. Paris, Legrand, 1929. MORENO MARTINEZ JM, GARCIA DE LA ROCHA ML, MARTIN ARAQUEZ A: Monomelic segmental amyotrophy: A Spanish case involving the leg. Rev Neurol (Paris) 146:443, 1990. MORRIS JC, COLE M, BANKER BQ, WRIGHT D: Hereditary dysphasic dementia and the Pick-Alzheimer spectrum. Ann Neurol 16:458, 1984. MULDER DW, KURLAND LT, OFFORD KP, BEARD CM: Familial adult motor neuron disease: Amyotrophic lateral sclerosis. Neurology 36:511, 1986. MUNSAT TL, SKERRY L, KORF B, et al: Phenotypic heterogeneity of spinal muscular atrophy mapping to chromosome 5q11.2-13.3 (SMA 5q). Neurology 40:1831, 1990. MURATA Y, YAMAGUCHI S, KAWAKAMI H: Characteristic magnetic resonance imaging ndings in Machado-Joseph disease. Arch Neurol 55: 33, 1998. NACHMANOFF DB, SEGAL RA, DAWSON DM, et al: Hereditary ataxia with sensory neuronopathy: Biemond s ataxia. Neurology 48:273, 1997. NAKANO KK, DAWSON DM, SPENCE A: Machado disease: A hereditary ataxia in Portuguese emigrants to Massachusetts. Neurology 22:49, 1972. NEARY D: Non-Alzheimer s disease forms of cerebral atrophy. J Neurol Neurosurg Psychiatry 53:929, 1990. NEARY D, SNOWDEN JS, BOWDEN DM: Neuropsychological syndromes in presenile dementia due to cerebral atrophy. J Neurol Neurosurg Psychiatry 49:163, 1986. NEE LE, ELDRIDGE R, SUNDERLAND T, et al: Dementia of the Alzheimer type: Clinical and family study of 22 twin pairs. Neurology 37:359, 1987. NIELSEN JE, KRABBE K, JENNUM P, et al: Autosomal dominant pure spastic paraplegia: A clinical, paraclinical and genetic study. J Neurol Neurosurg Psychiatry 64:61, 1998. NIELSEN SL: Striatonigral degeneration disputed in familial disorder. Neurology 27:306, 1977. NIKOSKELAINEN E, SAVONTAUS ML, WANNE OP, et al: Leber s hereditary optic neuroretinopathy A maternally inherited disease: A genealogic study in four pedigrees. Arch Ophthalmol 105:665, 1987. NYGAARD TG, DUVOISIN RC: Hereditary dystonia-parkinsonism syndrome of juvenile onset. Neurology 36:1424, 1986. NYGAARD TG, WILHELMSEN KC, RISCH NJ, et al: Linkage mapping of dopa-responsive dystonia (DRD) to chromosome 14q. Nature Genet 5: 386, 1993. OKAZAKI H, LIPKIN LE, ARONSON SM: Diffuse intracytoplasmic ganglionic inclusions (Lewy type) associated with progressive dementia and quadriparesis in exion. J Neuropathol Exp Neurol 20:237, 1961. OPPENHEIM H: Textbook of Nervous Diseases (A. Bruce, transl). Edinburgh, Schulze, 1911, p 512. PAKKENBERG B, MOLLER A, GUNDERSEN HJG, et al: The absolute number of nerve cells in substantia nigra in normal subjects and in patients with Parkinson s disease estimated with an unbiased stereological method. J Neurol Neurosurg Psychiatry 54:30, 1991. PAPP MI, KAHN JE, LANTOS PL: Glial cytoplasmic inclusions in the CNS of patients with multiple system atrophy (striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome). J Neurol Sci 94: 79, 1989.
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We may never know exactly what the common people of ancient times believed about the stars. We can read the translations of the works of the scribes, but what about the shepherds, the nomads, and the people in the ages before writing existed They must have noticed that stars come in a variety of brightnesses and colors. Even though the stars seem to be scattered randomly (unless the observer knows that the Milky Way is a vast congregation of stars), identifiable star groups exist. These star groups do not change within their small regions of the sky, although the vault of the heavens gropes slowly westward night by night, completing a full circle every year. These star groups and the small regions of the sky they occupy are called constellations.
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Some of these, the heavy metals, have already been considered. In addition, a large number of synthetic organic compounds are widely used in industry and are frequent sources of toxicity, and the list is constantly being expanded. The reader is referred to the references at the end of the chapter, particularly to the most current text, edited by Spencer and Schaumburg, for details concerning these compounds. Here we can do little more than enumerate the most important ones: chlorinated diphenyls (e.g., DDT) or chlorinated polycyclic compounds (Kepone), used as insecticides; diethylene dioxide (Dioxane); carbon disul de; the halogenated hydrocarbons (methyl chloride, tetrachloroethane, carbon tetrachloride, trichloroethylene, and methyl bromide); naphthalene (used in moth repellants); benzine (gasoline); benzene and its derivatives [toluene, xylene, nitrobenzene, phenol, and amyl acetate (banana oil)] and the hexacarbon solvents (n-hexane and methyl n-butyl ketone). With a few exceptions, the acute toxic effects of these substances are much the same from one compound to another. In general, the primary effect is on nonneurologic structures. Neural symptoms consist of varying combinations of headache, restlessness, drowsiness, confusion, delirium, coma, and convulsions, which, as a rule, occur late in the illness or preterminally. Some of these industrial toxins [carbon disul de, carbon tetrachloride and tetrachloroethane, acrylamide, n-hexane, and diethylene glycol (Sterno; see Rollins)] may cause polyneuropathy, which becomes evident with recovery from acute toxicity. Extrapyramidal symptoms may result from chronic exposure to carbon disul de. A syndrome of persistent fatigue, lack of stamina, inability to concentrate, poor memory, and irritability has also been attributed to chronic exposure to solvents, but these symptoms are quite nonspeci c, and evidence for such a syndrome is unsupported by convincing experimental or epidemiologic studies. Of the aforementioned industrial toxins, the ones most likely to cause neurologic disease are toluene (methyl benzene) and the hexacarbons. The chronic inhalation of fumes containing toluene (usually in glue, contact cement, or certain brands of spray paint) may lead to severe and irreversible tremor and cerebellar ataxia, affecting movements of the eyes (opsoclonus, ocular dysmetria) and limbs, as well as stance and gait. Cognitive impairment is usually associated; corticospinal tract signs, progressive optic neuropathy, sensorineural hearing loss, and hyposmia occur in some patients. Generalized cerebral atrophy and particularly cerebellar atrophy are evident in CT scans (Fornazzari et al, Hormes et al). Also, it has become apparent that acute toluene intoxication is an important cause of seizures, hallucinations, and coma in children (King et al). The prolonged exposure to high concentrations of n-hexane or methyl-n-butyl ketone may cause a sensorimotor neuropathy, so-called glue-sniffer s neuropathy (page 1132). These solvents are metabolized to 2,5-hexanedione, which is the agent that damages the peripheral nerves. The neuropathy may result from exposure in certain industrial settings (mainly the manufacture of vinyl products) or, more often, from the deliberate inhalation of vapors from solvents, lacquers, glue, or glue thinners containing n-hexane (see also Chap. 46). Impure trichloroethylene, through its breakdown product dichloroacetylene, has a predilection for the trigeminal nerve, which can be damaged selectively. Hydrogen peroxide poisoning, usually by accidental ingestion, causes multiple small cerebral infarcts through a mechanism
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but less in those with AIDS or in individuals who are otherwise immunocompromised. In immunocompetent patients, the addition of intrathecal methotrexate and intravenous cytosine arabinoside increases median survival to more than 3 years (DeAngelis), and apparent cure is not unknown. However, this combined treatment is associated with a high risk of a leukoencephalopathy (see further on and Fig. 31-23) and causes considerable unpleasant systemic side effects. More recent regimens, as outlined by Glass and colleagues, consist of several cycles of intravenous methotrexate (3.5 g/m2) and citrovorum, administered at 2- to 3-week intervals and at times continued inde nitely if tolerated. The side effects of these treatments are modest and there is no need for repeated lumbar punctures or the placement of an Ommaya reservoir. Most of our patients have not developed mucositis or the other of the usual side effects of this type of chemotherapy. Radiation treatment may be used subsequently, but there is then a higher incidence of delayed leukoencephalopathy and dementia. Ocular lymphoma is eradicated only by radiation. Corticosteroids are added at any point as needed to control prominent neurologic symptoms. The median survival time has been in the range of 3.5 years with intravenous methotrexate alone and 4 years or more if radiation is given subsequently. Some patients are alive at 10 years. Metastatic Carcinoma Among secondary intracranial tumors, only metastatic carcinoma occurs with high frequency. Occasionally one encounters a rhabdomyosarcoma, Ewing tumor, carcinoid, etc., but these tumors are so infrequent that their cerebral metastases seldom become a matter of diagnostic concern. The pathophysiology of metastatic carcinoma the complex biologic mechanisms that govern the detachment of tumor cells from the primary growth, their transport to distant tissues, and their implantation on the capillary endothelium of the particular organ in which they will eventually grow has been well reviewed by Rusciano and Burger and by Posner. Autopsy studies disclose intracranial metastases in approximately 25 percent of patients who die of cancer (Posner). About 80 percent of the metastases are in the cerebral hemispheres and 20 percent in posterior fossa structures, corresponding roughly to the relative size and weights of these portions of the brain and their blood ow. Cancers of the pelvis and colon are exceptional in this respect, having a somewhat higher tendency than this to spread to the posterior fossa. Intracranial metastases assume three main patterns those to the skull and dura, those to the brain itself, and those spreading diffusely through the craniospinal meninges (meningeal carcinomatosis). Almost as common as intracranial metastases are those to the spinal bones, which in time cause compression of the spinal cord. This problem is discussed in Chap. 44. Metastatic deposits in the spinal cord itself are infrequent but are seen from time to time; they are more common, for example, than a paraneoplastic necrotic myelopathy (see further on). Metastases to the skull and dura can occur with any tumor that metastasizes to bone, but they are particularly common with carcinoma of the breast and prostate and with multiple myeloma. These secondary deposits usually occur without metastases to the brain itself and reach the skull either via the systemic circulation (as in carcinoma of the breast) or via Batson s vertebral venous plexus a valveless system of veins that runs the length of the vertebral column from the pelvic veins to the large venous sinuses of the skull, bypassing the systemic circulation (the route supposedly taken by carcinoma of the prostate). Metastatic tumors of the
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