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complain of slowly progressive (over years) painful burning and numbness of the feet, ascending to the ankles or midcalves There are few ndings on examination; often only a mild or moderate loss of pinprick and thermal sensation, and ankle re exes that may or may not be reduced Again, there is little or no progression over the years Most of these cases are idiopathic but there is a broad differential diagnosis including the diseases mentioned earlier, as outlined by Mendell and Sahenk (Table 46-5 is adapted from their discussion) Identi able causes for painful sensory neuropathy in elderly include mainly diabetes, alcoholic-nutritional de ciency states, connective tissue disease, amyloidosis, and vasculitis Electrophysiologic tests are likewise normal or virtually so; a few show diminished sural nerve potentials and minor changes of motor amplitudes When these changes cannot be ascribed to diabetes, malnutrition, medications, or the other causes listed in the table, a substantial group of patients is left and are in need of symptomatic relief Some have been helped by gabapentin or by antidepressants (amitriptyline, desipramine, or sertraline) and analgesic cream applied nightly to the soles and toes Surprisingly, a few of the more severe cases have apparently responded to gamma globulin infusions but these observations require corroboration (Gorson and Ropper, 1995) In a number of cases of burning feet, the intradermal sensory nerves in skin biopsy specimens are said to be depleted of bers but the meaning of this nding is not certain (Periquet et al) Multiple Symmetrical Lipomas with Sensorimotor Polyneuropathy Whereas the usual cutaneous lipomas have no neurologic accompaniments, this clinical curiosity, known as LannoisBensaude disease, consists of symmetrical lipomas of the neck and shoulders that are associated with polyneuropathy and sometimes deafness A mitochondrial disorder is suspected Details can be found in the review by Neumann

Multiple sclerosis, called MS by most physicians, is referred to by the British as disseminated sclerosis and by the French as scle rose en plaques It is among the most venerable of neurologic diseases and one of the most important by virtue of its frequency, chronicity, and tendency to attack young adults It is a chronic condition characterized clinically by episodes of focal disorders of the optic nerves, spinal cord, and brain, which remit to a varying extent and recur over a period of many years The neurologic manifestations are protean, being determined by the varied location and extent of the demyelinative foci; nevertheless, the lesions have a predilection for certain parts of the CNS, resulting in complexes of symptoms and signs and radiologic appearances that can often be recognized as characteristic of MS

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Classic features include motor weakness, paraparesis, paresthesias, loss of sight, diplopia, nystagmus, dysarthria, intention tremor, ataxia, impairment of deep sensation, and bladder dysfunction The diagnosis may be uncertain at the onset and in the early years of the disease, when symptoms and signs point to a lesion in only one locus of the nervous system Later, as the disease recurs and disseminates throughout the cerebrospinal axis, diagnostic accuracy approaches 100 percent A long period of latency (1 to 10 years or longer) between a minor initial symptom, which may not even come to medical attention, and the subsequent development of more characteristic symptoms and signs may delay the diagnosis In most cases there is a relapsing-remitting pattern, ie, the initial manifestations improve partially or completely, to be followed after a variable interval by the recurrence of the same abnormalities or the appearance of new ones in other parts of the nervous system However, in fewer than half of patients, the disease takes the form of an intermittently progressive illness (relapsingremitting, the typical type of MS), and sometimes of a steadily progressive one, especially in patients more than 40 years of age at the time of onset (primary progressive MS) Or, as happens more often, an initially relapsing pro le later becomes steadily progressive (secondary progressive MS) Some data are accumulating to suggest that the pathogenesis of the chronic progressive, nonremitting clinical types may be different from that of the relapsingremitting cases, but in the authors opinion this is still questionable A rule that has guided clinicians for many years is that the diagnosis of MS is not secure unless there is a history of remission and relapse and evidence on examination of more than one discrete lesion of the CNS The advent of certain ancillary procedures notably magnetic resonance imaging (MRI) and evoked potentials and their capacity to identify clinically inevident lesions has obviated the exclusive dependence on clinical criteria for the diagnosis.

Before being sectioned, the brain generally shows no evidence of disease, but the surface of the spinal cord may appear and feel uneven Sectioning of the brain and cord discloses numerous scattered patches where the tissue is slightly depressed below the cut surface and stands out from the surrounding white matter by virtue of its pink-gray color (due to loss of myelin) The lesions may vary in diameter from less than a millimeter to several centimeters; they affect principally the white matter of the brain and spinal cord and do not extend beyond the root entry zones of the cranial and spinal nerves It is because of their sharp delineation that they were called plaques by French pathologists The topography of the lesions is noteworthy A periventricular localization is characteristic, but only where subependymal veins line the ventricles (mainly adjacent to the bodies and atria of the lateral ventricles) Other favored structures are the optic nerves and chiasm (but rarely the optic tracts) and the spinal cord, where pial veins lie next to or within the white matter (Fig 36-1; see also MRI in MS, page 783) The lesions are distributed randomly throughout the brainstem, spinal cord, and cerebellar peduncles without reference to particular systems of bers but always con ned predominantly to the white matter In the cerebral cortex and central nuclear and spinal structures, the acute lesions destroy myelin sheaths but leave the nerve cells essentially intact Severe and more chronic lesions, however, may destroy axons and neurons in the affected region, but the essential lesion is still demyelinative

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