CNS involvement in HIV/AIDS patients is a result of a wide range of processes and depends on different factors such as antiretroviral therapy and patient’s degree of immunosuppression.
Since the administration of HAART therapy in Western countries there has been a decline in the incidence of opportunistic infections and increase in cognitive dysfunction and peripheral neuropathies.
It is also important to note that AIDS patients with CD4 counts less than 200 cells/L are more vulnerable.
Four mechanisms result in CNS manifestations in HIV/AIDS :
Opportunistic infections:
Toxoplasmosis: Is considered the most common opportunistic infection of the CNS,
results in necrotizing encephalitis and is the most common cause of cerebral abscess in these patients.
The causative agent is toxoplasma gondii and patients with CD4 counts < 100 cells/μL are more susceptible to this infection.
CMV: Usually occurs when CD4 counts < 50 cells/μL.
TB: It may be the first clinical evidence of AIDS and is either a consequence of reactivation of previous TB infection or a result of a primary infection.
In most cases a positive chest radiography is evident.
Fungal: cryptococcus neoformans,
aspergillus fumigatus (angioinvasive infection),
candida albicans.
Appear when CD4 counts < 100 cells/μL.
Neurosyphilis: Sexually transmitted disease which is a result of infection with Treponema pallidum.
CNS manifestations may present at any stage of syphilitic infection.
Patients may appear asymptomatic while symptomatic cases include four types taking into account their clinical findings: meningeal,
vascular,
general paresis and tabes dorsalis.
A positive VDRL is highly specific for syphilis.
PML: Is a progressive demyelinating disorder resulting from infection with JC virus.
Patients with CD4 counts ranging from 50 to 100 cells/μL are more prone to developing PML and typically present with cognitive impairment,
altered mental state,
personality and motor-sensory changes,
as well as seizures.
Without treatment the prognosis is poor leading to death within 1 year in the majority of patients.
Bacterial: staphylococcus,
streptococcus,
etc.
Directly from HIV itself:
HIV associated neurocognitive disorders (HANDs) - AIDS Dementia Complex: Takes place during the later stages of AIDS.
Moreover there is evidence of reduction in brain volume for the patient’s age and white matter changes due to demyelination and gliosis.
Patients with a longer period of HIV infection,
CD4 counts < 200 cells/μL and older age at seroconversion are at higher risk for developing this entity.
Clinical findings include cognitive and psychomotor dysfunction with reduced concentration,
apathy,
motor slowing and ataxia.
HIV vascular myelopathy: Also observed in the late stages AIDS.
Clinically they present with paresthesia in the hands and feet,
distal weakness,
especially in the legs and gait ataxia.
CNS Tumors:
Primary CNS Lymphoma: Likely related to EBV.
After toxoplasmosis it is the second most common cerebral mass lesion in AIDS patients.
Almost always of B-cell,
Non-Hodgkins type.
Presenting symptoms: seizure,
neurological deficits,
encephalopathy.
IRIS – Immune reconstitution inflammatory syndrome Develops weeks or months after HAART administration and consists of a paradoxical deterioration of a pre-existing disease in patients with an increase of CD4 counts and therefore improved immune function with a lower viral load.