Neurologic Abnormalities in Human Immunodeficiency Virus Infection

, Department of Psychiatry and Neurology, Tulane University School of Medicine, New Orleans, La 

South Med J. 2001;94(3) 

In This Article

Peripheral Nervous System Manifestations

Even in the early stages of HIV infection, distal sensorimotor polyneuropathy (DSP) may occur. It is characterized by pain (burning, aching, tingling), which is usually worse at night, along with numbness in the extremities.[16,59,60,61] Beginning in the longest nerves, with symptomatic involvement of the soles of the feet, DSP then spreads to the dorsum of the foot. The symptoms generally are symmetrical, and the pain may be so intense that the patient prefers not to walk or have sheets or garments touching the feet. Neurologic examination shows prominent sensory signs (reduced vibration sensibility, loss of pain and temperature in feet, reduced ankle reflexes), usually with preserved strength.

As immunosuppression worsens, the incidence and severity of DSP increases, correlating with increased viral load and reduced CD4 count. Nerve conduction velocities and electromyography (NCV-EMG) show axonal neuropathy affecting both large and small fibers. Distal sensorimotor polyneuropathy also may result from toxic neuropathies caused by alcoholism, vitamin (B12, pyridoxine, thiamine) deficiency, systemic medical conditions (diabetes mellitus), or a toxic effect of drugs used to treat HIV infection (didanosine, stavudine, zalcitabine, or dideoxycytidine) or associated disease (isoniazid, vincristine, dapsone). Use of AZT is more likely to cause myopathy than neuropathy. It is important to differentiate HIV-related neuropathy from neuropathy due to antiretroviral medication. The time frame of the DSP may assist in this (viral-induced DSP develops slowly while DSP from drug toxicity develops more rapidly), and drug withdrawal would be expected to reverse symptoms of drug-related DSP. Symptomatic treatment of neuropathy includes analgesics (including opiates) for aching pain and tricyclic antidepressants and gabapentin for burning pain. Nerve growth factor may also be effective.[62]

If weakness begins distally in the legs, consider spinal cord dysfunction (myelopathy), which may be due to cord compression or polyradiculopathy.[63] Spinal cord dysfunction begins with leg and foot weakness and sensory impairment, invariably with autonomic dysfunction. With spinal cord disease, sensory loss on the soles of the feet then spread to the saddle (buttock) region supplied by sacral roots (S2 to S4). Polyradiculopathy usually causes asymmetrical motor and sensory findings, whereas spinal cord disease is symmetrical and plantar extensor responses are present. Human immunodeficiency virus-related polyradiculopathy is usually due to CMV. Cerebrospinal fluid is found to have polymorphonuclear pleocytosis, with markedly elevated protein and reduced glucose values.

Proximal leg weakness without sensory disturbance suggests muscle disease (myopathy).[64] Myalgias are common in myopathy, and examination shows proximal hip and shoulder girdle weakness. Creatine kinase usually is elevated in myopathy, and NCV-EMG may confirm the presence of a myopathic process.[65] Muscle biopsy is necessary in patients with a presumptive diagnosis of myopathy to determine pathologic changes and thus direct subsequent therapy.[66] If a patient is using AZT, mitochondrial changes may occur as an adverse drug effect. Patients with HIV-associated myopathy and biopsy findings consistent with inflammation sometimes respond to corticosteroid medication.[67,68,69,70]


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