Unlike the cases of sarcoid polyneuropathy we have reported (Zuniga et al), in the series of 11 patients with sarcoid neuropathy studied by Said and colleagues (2002), only 2 were known to have pulmonary granulomas before the onset of neuropathic symptoms; 6 had a focal or multifocal neuropathic syndrome (including 1 with a clinical and electrophysiologic pattern that simulated multifocal conduction block). The remainder had a nonspecific symmetric polyneuropathy, 1 of which had an acute onset. Facial diplegia was common in sarcoid, as is well known. The pathologic changes in nerve and muscle biopsy specimens consisted mainly of epineurial granulomas and endoneurial inflammatory infiltrates, 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 Said’s patients were levels of angiotensin-converting enzyme elevated in the serum.
Lyme Neuropathies (See Also Chap. 31)
The neuropathy that develops in 10 to 15 percent of patients with this disease takes several forms. Cranial nerve involvement is well known, unior bilateral facial palsy being by far the most frequent manifestation. Other cranial nerves may also be affected as may almost any of the spinal roots, mostly in the cervical or lumbar region. Even phrenic nerve palsy has been attributed to Lyme disease in a few cases. A concurrent mild or moderate aseptic meningoradiculitis (10 to 100 mononuclear cells/mm3) is characteristic (although this may also occur in HIV and CMV and other forms of neuritis). The CSF glucose is usually normal but has been slightly depressed in a few cases with multiple radiculopathies. Some of the CSF cells may have immature features suggesting a lymphomatous infiltration. (See further on and Chap. 31 for further details of the laboratory diagnosis.) 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 most characteristic of Lyme disease during its disseminated phase, that is, from 1 to 3 weeks after the tick bite or from the appearance of the typical rash. The disease tends to be seasonal in the period of maximal tick exposure. The special polyradiculitis form of Lyme is discussed further on.
Besides the just 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 footor wrist-drop—a distinctly rare pattern, or a thoracoor lumbar mononeuropathy causing sagging of the innervated body part); (2) lumbar or brachial plexopathy (the latter being well described but rare); (3) a predominantly sensory polyneuropathy in which paresthesias and loss of superficial 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 2 such cases in more than 400 patients with Guillain-Barré but the syndrome appears to be more common in Europe following Borrelia infection).