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A variety of neuropathies occur in HIV-infected patients (see 31) Patients with AIDS may develop a chronic symmetric sensorimotor axonal polyneuropathy associated usually with no abnormal cerebrospinal fluid findings Treatment is symptomatic AIDS patients may also develop progressive polyradiculopathy or radiculomyelopathy that leads to leg weakness and urinary retention; sensory loss is less conspicuous than in polyneuropathy The cerebrospinal fluid may show mononuclear pleocytosis and increased protein and low glucose concentrations Cytomegalovirus is responsible in at least some cases The prognosis is generally poor, but some patients respond to intravenous ganciclovir (25 mg/kg every 8 hours for 10 days, then 75 mg/kg daily 5 days per week) An inflammatory demyelinating polyradiculoneuropathy sometimes occurs in HIV-seropositive patients without AIDS and may follow an acute, subacute, or chronic course Weakness is usually more conspicuous distally than proximally and tends to overshadow sensory symptoms Tendon reflexes are depressed or absent The cerebrospinal fluid shows an increased cell count and protein concentration Treatment with plasmapheresis has helped some patients Spontaneous improvement may also occur Seropositive patients without AIDS may also develop a mononeuropathy multiplex that sometimes responds to treatment with plasmapheresis

Axonal polyneuropathy may follow exposure to industrial agents or pesticides such as acrylamide, organophosphorus compounds, hexacarbon solvents, methyl bromide, and carbon disulfide; metals such as arsenic, thallium, mercury, and lead; and drugs such as phenytoin, perhexiline, isoniazid, nitrofurantoin, vincristine, and pyridoxine in high doses Detailed occupational, environmental, and medical histories and recognition of clusters of cases are important in suggesting the diagnosis Treatment is by preventing further exposure to the causal agent Isoniazid neuropathy is prevented by pyridoxine supplementation Diphtheritic neuropathy results from a neurotoxin released by the causative organism and is common in many areas Palatal weakness may develop 2 4 weeks after infection of the throat, and infection of the skin may similarly be followed by focal weakness of neighboring muscles Disturbances of accommodation may occur about 4 5 weeks after infection and distal sensorimotor demyelinating polyneuropathy after 1 3 months

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The neurologic manifestations of Lyme disease include meningitis, meningoencephalitis, polyradiculoneuropathy, mononeuropathy multiplex, and cranial neuropathy Serologic tests establish the underlying disorder Treatment is described in 34

Both a sensorimotor and a purely sensory polyneuropathy may occur as a nonmetastatic complication of malignant diseases (see Table 39 13), and have been associated with circulating anti-MAG or anti-Hu antibodies that can be detected by a paraneoplastic antibody panel that is available commercially The sensorimotor polyneuropathy may be mild and occur in the course of known malignant disease, or it may have an acute or subacute onset, lead to severe disability, and occur before there is any clinical evidence of the cancer, occasionally following a remitting course An autonomic neuropathy may also occur as a paraneoplastic disorder related to the presence of anti-Hu antibodies or to an antibody against ganglionic acetylcholine receptors (anti-nAChR)

Cranial nerve palsies (especially facial palsy), multiple mononeuropathy and, less commonly, symmetric polyneuropathy may all occur, the latter sometimes preferentially affecting either motor or sensory fibers Improvement may occur with use of corticosteroids

7:

Involvement of the vasa nervorum by the vasculitic process may result in infarction of the nerve Clinically, one encounters an asymmetric sensorimotor polyneuropathy (mononeuritis multiplex) that pursues a waxing and waning course Corticosteroids and cytotoxic agents especially cyclophosphamide may be of benefit in severe cases

7 Acute Idiopathic Polyneuropathy (Guillain-Barr Syndrome)

Compressive or entrapment neuropathies, ischemic neuropathies, mild distal sensory polyneuropathy, and severe progressive sensorimotor polyneuropathy can occur in rheumatoid arthritis

formed within the first few days of illness and is best reserved for clinically severe or rapidly progressive cases or those with ventilatory impairment IVIG (400 mg/kg/d for 5 days) is equally helpful and imposes less stress on the cardiovascular system than plasmapheresis Patients should be admitted to intensive care units if their forced vital capacity is declining, and intubation is considered if the forced vital capacity reaches 15 mL/kg, dyspnea becomes evident, or the oxygen saturation declines Respiratory toilet and chest physical therapy help prevent atelectasis Marked hypotension may respond to volume replacement or pressor agents Low-dose heparin to prevent pulmonary embolism should be considered Approximately 3% of patients with acute idiopathic polyneuropathy have one or more clinically similar relapses, sometimes several years after the initial illness Plasma exchange therapy may produce improvement in chronic and relapsing inflammatory polyneuropathy

Malaria, typhoid fever, acute HIV infection, rickettsial illness, visceral leishmaniasis, trypanosomiasis, and dengue are possible etiologies

Identify patients with acute, potentially life-threatening and treatable diseases, or those with transmissible diseases that require isolation The incubation period may be helpful in diagnosis Less than 3 weeks following exposure may suggest dengue, leptospirosis and yellow fever; greater than 3 weeks suggest typhoid fever, malaria, and tuberculosis

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