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Headache in HIV Patients

Primary and secondary headache in patients with HIV are very common, seen in 38-61% of HIV-positive individuals [24]. It remains the most common type of pain, even as the natural course of HIV has changed dramatically with widespread use of cART. Early studies conducted prior to about 2005 yielded different headache profiles than recent publications. Before cART was commonly used, secondary headaches were much more prevalent. Since then Kirkland et al. [24] found that whereas 53.5% of a population of 200 HIV patients endorsed problematic headaches, only 2.8% were associated with opportunistic encephalitic infection. The current International Classification of Headache Disorders (ICHD-3-beta) [25] requires certain diagnostic criteria for diagnosis of headache attributed to HIV infection be met (Table 3.3).

Early publications reported that HIV-associated headaches were tension-type in nature [26] or more likely to worsen primary tension-type headache [27]. The headaches were more common with higher viral loads. The clinical features of primary headache in HIV patients in recent years are more similar to migraine, with the exception that nausea is not as prominent [24]. Photophobia and phonophobia (79%) and aggravation by activity (83%) were, in contrast, quite frequently seen. These headaches were frequent (more than 50% of days or 17 days per month), bilateral, and of severe intensity (7.8/10). Half of patients reported the pain as throbbing in nature. Headache severity, frequency, and disability were inversely tightly correlated with lower CD4 counts, but not with duration of HIV. Another

Table 3.3 Headaches attributed to HIV infection: diagnostic criteria

A. Both of the following:

1. Systemic HIV infection has been demonstrated

2. Other ongoing systemic and/or intracranial infection has been excluded

B. Evidence of causation demonstrated by at least two of the following:

1. Headache has developed in temporal relation to the onset of HIV infection

2. Headache has developed or significantly worsened in temporal relation to worsening of HIV infection as indicated by CD4 cell count and/or viral load

3. Headache has significantly improved in parallel with improvement in HIV infection as indicated by CD4 cell count and/or viral load

In most cases, headache is dull and bilateral or has the features of a primary headache disorder (migraine or tension-type headache)

observation was that the overall CD4 counts in these patients with headache were higher (due to cART treatment) than in the early reports, underscoring that this migraine-like headache more likely represented the direct effect of HIV on the nervous system as opposed to secondary causes [24].

The pathophysiology behind direct HIV-associated headache has been discussed by Joshi and Cho [28]. There is an underlying CNS inflammatory response to the HIV-1 virus resulting in release of cytokines which may be associated with pain. HIV aseptic meningitis (from HIV or an unidentified virus) with an absence of CSF pleocytosis may underlie headaches in those in whom another secondary cause is not found. There is a lack of agreement between those who have found an association of headache with increased CSF viral load and those who point out that some asymptomatic patients also have HIV cultured from their CSF. There are some similarities of the CNS between HIV and migraine patients. For instance, in migraine, alterations of plasma membranes with ionic gradients result in cortical neuronal depolarization. This leads to cortical spreading depression, further resulting in glutamate release. This situation is similar to early HIV infection-related activity of viral proteins Tat and gp120 in neurons. Also, N-methyl-d-aspartate (NMDA) receptors are stimulated by Tat, sensitizing the nerves to glutamate and causing excitotox- icity. Gp120, implicated in neuronal injury, may have synergism with glutamate, and its effect can be blocked by an NMDA antagonist. NMDA also plays a role in pain. These authors also mention that the metabolism of tryptophan and serotonin are altered in HIV infection, possibly interrupting endogenous pain modifying mechanisms. Viral-mediated cell death in HIV causes mast cell release of histamine. Mast cells also contain high concentrations of CGRP, a key player in the migraine cascade. It has also been suggested that HIV may affect the trigeminovascular system which triggers the neurovascular response leading to the migraine attack [28].

In the HIV-positive population, new headaches can herald the development of secondary disease and should be regarded as a red flag especially if the CD4 count is below 200, as discussed earlier. Other clues to the need for further testing include any focal neurologic findings, changes in cognition or consciousness, “thunderclap” (ultrafast) onset, worst headache of life, increased headache with strain or cough, papilledema, and constitutional symptoms. Of the secondary CNS lesions associated with headache in HIV, the most common include cryptococcus meningitis, CMV encephalitis, toxoplasmosis, primary CNS lymphoma, PML, CNS tuberculosis, and neurosyphilis. HIV aseptic meningitis may cause headache with or without CSF pleocytosis. Primary angiitis of the nervous system early in the course of HIV infection can occur. In addition, headache can be associated with initiation of cART treatment (especially zidovudine) and with IRIS [29].

 
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