Remission of HIV-associated Myelopathy After HAART

HIV-associated myelopathy (HM) is the leading cause of spinal cord disease in HIV-infected patients. Typically, it affects individuals with low CD4 T cell counts, presenting with slowly progressive spastic paraparesis associated with dorsal column sensory loss as well as urinary disturbances.

Other etiologies must be first ruled out before establishing the diagnosis. We report here the case of a 37-year-old woman with advanced HIV disease, who developed HIV-associated myelopathy.

The patient showed a gradual improvement after beginning with highly active antiretroviral therapy (HAART) and, finally, she achieved a complete functional recovery. In addition, neuroimaging and neurophysiological tests normalized.

In the pre-HAART era, HM usually developed in the advanced stages of the HIV infection, with a progressive course until the patient's death. Even though pathologic abnormalities of HM were found at autopsy in 22-55% of patients with advanced HIV infection, signs and symptoms of myelopathy had only been recorded in 26-60% of these patients during life.

The pathogenesis of HM remains elusive, with no evidence for a direct effect of HIV on the spinal cord. Diagnosis is largely clinical and it is also based upon the presence of MRI changes, most commonly spinal cord atrophy or intrinsic cord signal abnormalities.

Slowing or absence of waves in the SSEP also supports the diagnosis. Other possible causes of spinal cord disease mimicking this condition must be first ruled out before a diagnosis can be made.

These include infections caused by CMV, HSV-2, HTLV-I and II, toxoplasma, tuberculosis and syphilis, as well as vitamin B12 deficiency, lymphoma, multiple myeloma, ischaemia and spinal cord compression. In the present case, all these conditions were excluded.

So far, four other cases have been published in the literature, reporting a remission of symptoms after initiating HAART, although neurophysiological tests were not carried out in two of them.

Furthermore, in one case report, HM was the first symptom of HIV infection in a patient who preserved his CD4 count but showed high values of viral load. Eyer-Silva et al described a patient with symptomatic recovery after starting on lopinavir.

This patient was previously under HAART, with unsuccessful viral control. SSEP here were only carried out after starting the treatment and recovery was incomplete.

Finally, there is another patient in whom symptomatic recovery could be confirmed after initiating HAART, but in this case slight impairment of central conduction time could be demonstrated.

This patient is the first case showing full recovery after beginning with antiretroviral therapy. This recovery was documented by clinical, neuroimaging and neurophysiological tests. Clinical response correlated well with viral control, while neurophysiological parameters followed a slower recovery.

In conclusion, the authors write, “Although the pathogenesis of HM is unknown, the clinical improvement that seems to parallel the immunological recovery in this patient suggests that HIV is likely to be the cause of this disease, either directly or due to an abnormal secretion of cytokines.”

10/06/04