HIV or human immunodeficiency virus causes AIDS or acquired immunodeficiency syndrome. The HIV virus affects every level of the neural axis, by that I mean that the virus affects the brain, the spinal cord, the nerves as well as the muscles. I shall discuss the neurological manifestations associated with HIV infection in this section starting with the brain.
HIV manifestations in the brain: the brain may be affected soon after the patient gets infected with the HIV virus. Research has shown that soon after entering the human body, HIV virus can be found in the brain. Its first manifestation may be in the form of an aseptic meningitis. The patient has characteristic signs and symptoms of a viral meningitis with headache, neck stiffness, photophobia, body aches and myalgias but when the spinal fluid is analysed no organisms are seen, though the cell count in the spinal fluid may be elevated. This attack of aseptic meningitis subsides on its own (no antibiotics are required). All that is needed is bed rest and some hydration. The HIV virus then enters a dormant state in the brain, remaining silent, causing no overt manifestations.
In the later stages of HIV infection (when the virus has multiplied extensively in the body and the patient’s viral load is high and CD4 counts are low) the virus again manifests in the brain clinically. Viral load refers to the amount of virus in the body usually expressed as the number of viral copies in the blood. CD4 count refers to the number of CD4 cells present in the blood. The CD4 cells are a group of immune cells, the HIV virus selectively destroys CD4 cells and thus makes a patient immunodeficient and prone to opportunistic infections. Opportunistic infections refers to infections which normally do not occur in a person with an intact immune system, in people who have immunodeficiency these infections are a major cause of morbidity and mortality. A number of these infections have been associated with late stage infection with HIV. These include:
1) CNS toxoplasmosis
2) Cryptococcal meningitis
3) Progressive multifocal leukoencephalopathy (PML)
4) Cytomegalovirus infections (CMV infections)
5) Tubercular infections of the brain–tubercular meningitis and tuberculoma
6) Various fungal meningitis
HIV affects other levels of the neural axis. It involves the spinal cord causing a vacuolar myelopathy causing stiffness and weakness of the legs and bladder/ bowel problems.
It affects the peripheral nerves and can cause painful neuropathies. The neuropathy associated with HIV infection is usually distal, painful and symmetrical. The drugs used to treat HIV infections are quite strong and some of them too have been implicated in causing neuropathies. HIV can also cause a Gullian Barre Syndrome like presentation. This is an acute peripheral inflammatory demyelinating polyneuropathy (AIDP) which at times can prove fatal due to involvement of the respiratory muscles.
HIV can also involve the muscles causing diffuse proximal muscle weakness (HIV myopathy). Some of the antiretroviral drugs have again been implicated in causing a toxic myopathy.
HIV infection can also involve the brain diffusely (by that I mean no focal or mass lesions are found). This diffuse involvement of the brain causes AIDS dementia complex or what is also referred to as HIV encephalopathy. The virus involves the subcortical parts of the brain and causes psychomotor slowing, cognitive deficits and memory problems.
Let us now discuss the above one by one.
1) CNS toxoplasmosis: CNS toxoplasmosis is one of the most common opportunistic infections seen with HIV/AIDS. It is caused by Toxoplasma gondii and usually presents with intracranial space occupying lesions. By that I mean, it causes lesions in the brain that occupy space much like any other mass such as tumor (cancer). The lesions due to Toxoplasma may either be single or multiple in number and clinically may present with a seizure (as they irritate the brain) or if they lie near the motor strip they may present with weakness or numbness on one side of the body. If they are multiple in the brain they may cause encephalopathy (patient is obtunded and poorly responsive). How is the diagnosis secured? The diagnosis of CNS toxoplasmosis is usually quite easy as the lesions are readily seen on either a CT scan of the brain or an MRI. Your doctor may order the test with contrast to see the surrounding edema and to differentiate them from other similar appearing lesions.
As I stated earlier the diagnosis is relatively easy if there are multiple lesions. The problem arises when there is only one lesion. Then CNS toxoplasmosis has to be differentiated from other disease processes which too may present with a solitary intracranial lesion, especially primary CNS lymphoma. It is important that the correct diagnosis be made as the treatments for the two differ widely. So in cases like these, we neurologists may order other tests such as a Thallium SPECT (single photon emission computed tomography) which is a special type of scan able to differentiate between infection (toxoplasmosis) and tumor (CNS lymphoma) or a biopsy of the lesion may be attempted. Biopsy of course is an invasive procedure and hence we try hard to avoid it.
At times we emprically treat the patient for CNS toxoplasmosis (as treatment is relatively simple and free from side-effects). The CT scan is repeated after 2 weeks of therapy, if the size of the lesion has regressed then it implies that we are dealing with CNS toxoplasmosis. If the lesion has not regressed in size after treatment for 2 weeks or has increased in size, then the possibility of it representing a solitary CNS lymphoma increases.
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