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AIDS-Related Neurologic Complications at CD4+ Lymphocyte

As it was previously explained, with more annihilation of the immune system and progressive drop in the number of CD4+ T lymphocytes, more neurologic complications appear. Once the peripheral CD4+ lymphocyte count drops to below 200/mL myelopathy, HIV-associated dementia (HAD) and painful distal sensory polyneuropathy present.

The commonality of HAD among untreated HIV patients may vary between 5 and 20%. Its annual incidence in patients with a CD4+ lymphocyte level 100/mm3 or less is 7.3%. As a significantly subcortical dementia, HAD manifests with cognitive decline, behavioral abnormalities (such as apathy, mania, lack of emotional stability, forgetfulness, mental dullness and slowing, and impaired comprehension), and motor dysfunction such as gait difficulty and loss of fine motor skills. HAD uncommonly presents with psychosis and some of these patients may be at risk for suicidal and homicidal ideation. The progression of dementia may be rapid in untreated patients; however, with the use of HAART, patients with HAD may survive 3-5 years [12].

Vacuolar myelopathy is the most prevalent form of chronic AIDS-associated myelopathy in AIDS patients, with a prevalence of 20-50% in various case series [13, 14]. Clinically, HIV myelopathy presents with progressive spastic paraparesis, hyperreflexia with extensor plantar responses, abnormal gait with tendency to fall, urinary retention or incontinence, ataxia, and sensory loss. Neuropathologically, AIDS myelopathy is recognized by the presence of separate or coalescent intramyelin and peri-axonal vacuolation with loss of spinal cord white matter and presence of lipid-laden macrophages [13]. Vacuolar myelopathy of AIDS should be differentiated from HTLV-1-associated myelopathy.

Peripheral neuropathy is one of the most prominent peripheral neurologic complications of HIV infection, which affects up to 15% of patients. Of the various AIDS-related peripheral nervous system complications of AIDS, distal symmetric polyneuropathy (DSP) is the most common. Patients with DSP complain of numbness, pain, paresthesias, gait instability, and autonomic dysfunction. DSP may occur during latent phases but it affects 30% of people with AIDS. Toxic peripheral neuropathies have increased especially in patients treated with HAART.

Uncommonly, cases of motor neuron disease occur in HIV patients who have CD4+ T lymphocyte count less than 200 cells/mm3 and may imitate amyotrophic lateral sclerosis (ALS). However, they differ from ALS because of younger age of onset, rapid progression and deterioration, and clinical improvement when treated with ART [15]. In 2001, Moulignier et al. reported six patients with HIV-related motor neuron disease and proposed certain underlying mechanisms such as neuronal infection, reaction to toxic viral products, cytokine effect, and autoimmunity [15].

With a significant drop of the CD4+ T lymphocytes, the risk of opportunistic infections such as toxoplasmosis, cryptococcal meningitis, and mycobacterial infection such as disseminated mycobacterium avium complex and progressive multifocal leukoencephalopathy (PML) rises. In addition, primary CNS lymphoma is a neoplastic process linked to Epstein-Barr virus with poor prognosis in advanced stages of AIDS.

 
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