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12 patients with a critically ischemic leg, there was a neuropathy with a pronounced distal predominance sensory loss in the feet was worse than the symptoms might suggest and there was only mild weakness of the toes and depression or loss of the ankle re ex (Weinberg et al) Although paresthesias, numbness, and deep aching pain were characteristic, the patients were more limited by symptoms of their vascular claudication than the neuropathic ones Restoration of circulation to the limb by surgical or other means resulted in some improvement of the regional neuropathy Reviews of the literature on this subject are to be found in the writings of Chalk et al and Eames and Lange A poorly understood but presumably localized ischemic neuropathy occurs in the region of arteriovenous shunts that have been placed for the purpose of dialysis Complaints of transient diffuse tingling of the hand are not uncommon soon after creation of the shunt, but only a few patients develop persistent forearm weakness and numbness and burning in the ngers, re ecting variable degrees of ulnar, radial, and median nerve and possibly also muscle ischemia The possible role of an underlying uremic polyneuropathy in facilitating this neuropathy has not been studied A progressive, symmetrical polyneuropathy due to systemic cholesterol embolism has been described by Bendixen and colleagues An in ammatory and necrotizing arteritis surrounds embolic cholesterol material within small vessels and appears to account for the progression of symptoms This neuropathic process is probably more often discovered at autopsy than it is in the clinic, being eclipsed during life by the cerebral manifestations of cholesterol embolism The entire illness simulates the generalized polyneuropathy of a small-vessel polyarteritis Sarcoidosis Sarcoidosis infrequently produces subacute or chronic polyneuropathy, polyradiculopathy, or mononeuropathies A painful, small- ber sensory neuropathy has also been described by Hoitsma and colleagues Either type of neuropathy may be associated with granulomatous lesions in muscles (polymyositis) or with signs of CNS involvement, most often of the stalk of the pituitary with diabetes insipidus or a myelopathy Involvement of a single nerve with sarcoid most often implicates the facial nerve (facial palsy), but sometimes multiple cranial nerves are affected in succession (see page 1183) Or, there may be weakness and re ex and sensory loss in the distribution of one or more spinal nerves or roots The occurrence of large, irregular zones of sensory loss over the trunk is said to distinguish the neuropathy of sarcoidosis from other forms of mononeuropathy multiplex This type of sensory loss, particularly when accompanied by pain, resembles diabetic radiculopathy (see earlier) Unlike the cases we have reported (Zuniga et al), in the series of 11 patients with sarcoid neuropathy studied by Said and colleagues, only 2 were known to have pulmonary sarcoidosis before the onset of neuropathic symptoms Six had a focal or multifocal syndrome (including one with a clinical and electrophysiologic pattern that simulated multifocal conduction block) The remainder had a more nondescript symmetric polyneuropathy, one of acute onset Facial diplegia was common, as is well known The pathologic changes in nerve and muscle biopsy specimens consisted mainly of epineurial granulomas and endoneurial in ammatory in ltrates, but there were indications of necrotizing vasculitis in 7 cases Among the cases we studied, 6 of 10 had a subacute or chronic sensorimotor polyneuropathy It is notable that in only 2 of their patients were levels of angiotensin-converting enzyme elevated in the serum
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Lyme Disease (See also page 618) The neuropathy that develops in 10 to 15 percent of patients with this disease takes several forms Cranial nerve involvement is well known, uni- or bilateral facial palsy being by far the most frequent manifestation (page 1182) Other cranial nerves are from time to time also affected and the disease may affect almost any of the somatic roots, most evident in the cervical or lumbar ones Even phrenic nerve palsy has been attributed to Lyme disease in a few cases An aseptic meningoradiculitis giving rise to a pleocytosis is particularly characteristic (although this may also occur in HIV and CMV and other forms of neuritis) Some of the CSF cells at times have immature features suggesting a lymphomatous in ltration There may be radicular pain not unlike that of cervical or lumbar disc or plexus disease The triad of cranial nerve palsies, radiculitis, and aseptic meningitis is characteristic of Lyme disease during its disseminated phase, ie, from 1 to 3 weeks after the tick bite or the appearance of the typical rash The disease tends to be seasonal in the period of maximal tick exposure As to peripheral neuropathy with Lyme disease, the clinical situation is more complex Several patterns of neuropathy have been recognized and they tend to appear some months after the Lyme infection and may last for years hence observing no seasonal pattern Besides the previously described cranial neuropathies, the following are the main neuropathic syndromes of Lyme disease: (1) multiple mononeuropathies (involvement of a single major nerve in the limbs, resulting in an isolated foot or wrist drop, is, however, distinctly rare); (2) a lumbar or brachial plexopathy (the latter being well described but rare); (3) a predominantly sensory polyneuropathy in which paresthesias and loss of super cial sensation in the feet and legs are coupled with loss of ankle jerks; (4) a generalized axonal polyneuropathy (Loggigian et al), mainly sensory and sometimes accompanied by a mild encephalopathy; and (5) acute GBS (we have encountered only two such cases in over 400 patients with Guillain-Barre) Electrophysiologic testing indicates that the various peripheral nerve syndromes frequently overlap All of the preceding processes excepting the one that resembles GBS usually occur as subacute or late complications of Lyme disease, several months or rarely years after the initial infection (in untreated cases) These later neuropathic syndromes respond less favorably to treatment than do the acute ones (see further on) There are few adequate pathologic studies of the peripheral nerves in Lyme disease, since the disease is not fatal No one has demonstrated the infective agent in the nerves, although this has been one of the suggested targets of disease Bannwarth Syndrome Special mention is made of an intensely painful lumbosacral polyradiculitis that has long been known in Europe under by the term Bannwarth syndrome (in France it is known as Garin-Bujadoux syndrome) The pathogen is probably a spirochete slightly different from the one that causes Lyme disease in North America In the Bannwarth syndrome, and in occasional cases of otherwise typical Lyme disease, there is an intense in ammatory reaction in the cauda equina giving rise to sciatic and buttock pain and bladder disorder Less frequently a cervical polyradiculopathy occurs with shoulder and arm pain that we have been unable to distinguish on clinical grounds from brachial neuritis The EMG, however, shows a preservation of sensory potentials, which marks the process as radicular rather than plexal (see further on) Headache and a brisk pleocytosis in the spinal uid may accompany the pain and usually precedes radiculopathies by days It should be commented that a similar syndrome of lumbar polyradiculitis may also be caused by the herpes and Epstein-Barr viruses
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