Clinical Manifestations

The extent and spectrum of neurologic complications of HIV infection, to a significant degree, is linked to the depth of AIDS-induced immunosuppression and the underlying mechanism(s) of that particular neurologic complication. Certain opportunistic infections or neoplasms of the nervous system usually develop only when the number of infected T lymphocytes drops below a certain threshold. For

C. Cajavilca, MD • D. Davis, MD • O.Y. Chernyshev, MD, PhD • A. Minagar, MD (*) Department of Neurology, LSU Health Sciences Center,

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© Springer International Publishing AG 2017

A. Minagar, J.S. Alexander (eds.), Inflammatory Disorders of the Nervous System, Current Clinical Neurology, DOI 10.1007/978-3-319-51220-4_3

example, significant AIDS-associated neurological manifestations usually begin when the CD4+ T lymphocyte count drops to a number lower than 200 CD4+ T lym- phocytes/mm3.

Various mechanisms responsible for the neurologic complications of HIV include neurotoxicity, possible autoimmunity, opportunistic infections, cerebrovascular complications, neoplasms, side effects of antiretroviral therapy (ART), and malnutrition. The early cases of the 1980s were associated with opportunistic infection and neoplasms; however, after the advent of antiretroviral therapies, a myriad of different syndromes such as dementia, myelopathy, and neuropathy have emerged. A list of neurologic complications of HIV and AIDS is presented in Table 3.1.

HIV patients manifest a wide range of neurologic manifestations related to HIV, which demands further diagnostic workup to search for and exclude other possible etiologies. It is important to have a meticulous plan for the state of systemic HIV infection and tendency for opportunistic infections. Diagnostic tests such as serial measurements of peripheral CD4+ lymphocyte count as well as history of exposure to infectious agents should be performed. For example, a demyelinating neuropathy may develop at early stages of infection with a CD4+ count >500/mm3, while a CD4+ lymphocyte count between 200 and 500/mm3 may set the stage for tuberculous meningitis and onset of cognitive impairment. A CD4+ lymphocyte count less than 200/mm3 places the patient at risk for HIV dementia, vacuolar myelopathy, polyneuropathy, toxoplasmosis, encephalitis, progressive multifocal leukoencepha- lopathy (PML), cryptococcal meningitis, and primary CNS lymphoma. The relative correlation between common neurologic manifestations of AIDS and the serum

Table 3.1 Neurologic manifestations of HIV infection of human nervous system

HIV-associated dementia and encephalopathy

HIV-associated neurocognitive disorders

Demyelinating syndrome (at early stages of infection which imitates multiple sclerosis)

Parkinsonian syndrome and other movement disorders

Sleep abnormalities

Various opportunistic infections of the central nervous system which includes:

Toxoplasmosis, neurosyphilis, progressive multifocal leukoencephalopathy

Cytomegalovirus and varicella zoster encephalitis

Fungal and bacterial infections

Primary nervous system neoplastic processes such as central nervous system lymphoma

Aseptic meningitis and lymphomatous meningitis

Vacuolar myelopathy

Viral and bacterial polyradiculitis

Distal symmetric neuropathy

Mononeuritis multiplex

Acute and chronic inflammatory demyelinating polyneuropathy

Cytomegalovirus mononeuritis multiplex

Neurologic side effect medications used for treatment of AIDS and its complications such as didanosine, zalcitabine, stavudine, dapsone, isoniazid, and pyridoxine

Inflammatory myopathy

CD4+ lymphocyte count is of utmost significance when the neurologist treats AIDS patients. It is significant to bear in mind that the HIV latent period may range from 2 to 10 years. During this time, the CD4+ lymphocyte count declines, while viral load increases, and the patient may remain symptom-free.

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