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Within several months to a year or two, the more generalized aspects of mental deterioration become apparent, and the aphasic-agnosicapraxic aspects of the syndrome become increasingly prominent If one of the foregoing restricted de cits remains uncomplicated over a period of years, one is justi ed in suspecting some cause other than Alzheimer disease, such as Binswanger disease, hydrocephalus, frontotemporal dementia (see further on), or embolic infarction of one part of the temporal or parietal lobe Also, as stated earlier, a hemianopic visual eld defect, cortical sensory loss, or hemiparesis is seldom if ever due to Alzheimer disease However, more complex disturbances of visual perception taking the form of impaired recognition of objects (object agnosia) or faces ( prosopagnosia), visual scanning, color identi cation, stereoacuity, separation of gures from background, and hand-eye coordination are frequent in the more advanced stages (Mendez et al).

Rarely there is a partial or even a complete Balint syndrome While it is true that most patients with Alzheimer disease walk normally until relatively late in their illness, infrequently a shortstepped gait and imbalance draw attention to the disease and worsen slowly for several years before cognitive manifestations become evident The general decrepitude in appearance that accom-.

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Neural Development in the Fetus The human fetus is capable of a complex series of re ex activities, some of which appear as early as 5 weeks of postconceptional age. Cutaneous and proprioceptive stimuli evoke slow, generalized, patterned movements of the head, trunk, and extremities. More discrete movements appear to differentiate from these generalized activities. Re exes subserving blinking, sucking, grasping, and visceral functions, as well as tendon and plantar re exes, are all elicitable in late fetal life. They seem to develop along with the myelination of peripheral nerves, spinal roots, spinal cord, and brainstem. By the 24th week of gestation, the neural apparatus is functioning suf ciently well to give the fetus some chance of survival should birth occur at this time. However, most infants fail to survive birth at this age, usually ow-

release of histamine into the skin as the result of a scratch It can be elicited in sensitive individuals by scratching the skin (dermatographia) The wheal and the deeply colored red areola are caused by the direct action of histamine on blood vessels, while the are depends upon the integrity of the axon re ex, in which antidromic stimulation of small sensory C bers results in the release by the same bers of vasoactive substances such as histamine In familial dysautonomia, the are response to histamine and to scratch is absent It may also be absent in peripheral neuropathies that involve sympathetic nerves (eg, diabetes, alcoholic-nutritional disease, Guillain-Barre disease, amyloidosis, porphyria, etc) The quanti tative sudomotor response to topical acetylcholine, described above, is preferred for its sensitivity and accuracy but requires special equipment.

childhood or adolescence and progressing steadily is usually indicative of hereditary spinocerebellar degeneration (Friedreich ataxia) or one of its variants (see Chap. 39). In early adult life, MS is the most frequent cause and AIDS myelopathy is being increasingly recognized; syphilitic meningomyelitis, formerly of great importance, is now quite uncommon. In middle and late adult life, cervical spondylosis, subacute combined degeneration of the cord (vitamin B12 de ciency), combined system degeneration of the nonpernicious anemia type, radiation myelopathy, tropical spastic paraplegia, spinal arachnoiditis, and thoracic spinal tumor, particularly meningioma, are the other important diagnostic considerations for a slowly progressive syndrome. In most forms of subacute and chronic spinal cord disease, spastic paraparesis is more prominent than posterior column ataxia, Friedreich ataxia and myelopathy due to vitamin B12 de ciency being notable exceptions.

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MAIR WGP, FOLKERTS JF: Necrosis of spinal cord due to thrombophlebitis (subacute necrotic myelitis) Brain 76:563, 1953 MALAMUD N, BOLDREY EB, WELCH WK, FADELL EJ: Necrosis of brain and spinal cord following x-ray therapy J Neurosurg 11:353, 1954 MANCALL EL, ROSALES RK: Necrotizing myelopathy associated with visceral carcinoma Brain 87:639, 1964 MARSHALL J: Observations on re ex changes in the lower limbs in spastic paraplegia in man Brain 77:290, 1954 MARTIN J, DAVIS L: Studies upon spinal cord injuries: Altered re ex activity Surg Gynecol Obstet 86:535, 1948 MESSARD L, CARMODY A, MANNARINO E, RUGE D: Survival after spinal cord trauma: A life table analysis Arch Neurol 35:78, 1978 MIXTER WJ, BARR JS: Rupture of the intervertebral disc with involvement of the spinal canal N Engl J Med 211:210, 1934 MORRISON RE, BROWN J, GOODING RS: Spinal cord abscess caused by Listeria monocytogenes Arch Neurol 37:243, 1980.

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