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Headache During HIV Infection
Updated June, 2011
Claire Creutzfeldt, M.D., Kiran Thakur, M.D., Joseph R. Zunt, M.D., MPH
INTRODUCTION Headache is common during all stages of infection with the Human Immunodeficiency Virus (HIV), from seroconversion to the development of an AIDS related illness. Similar to the general population, the majority of headaches in HIV seropositive persons are due to primary headache syndromes, such as migraine and tension type headaches. However, in the HIV population, a headache can also portend life-threatening illness such as an opportunistic infection (OI) or neoplasm arising in the setting of impaired cellular immunity. This chapter will review the epidemiology of headache, the clinical presentations of CNS infections and neoplasms that may cause headache, the evaluation of headache in an HIV seropositive patient, treatment of HIV-associated headache and the changes in frequency and etiology of headache since the introduction of highly active antiretroviral therapy (HAART), including headache in the setting of immune reconstitution syndrome (IRIS).
EPIDEMIOLOGY Headache in the General Population Headache is common. In studies of the general population, the lifetime prevalence for any type of headache ranges from 69 to 99% (Table 1). Central nervous system disease is uncommon in people presenting to an emergency room or medical clinic for evaluation of headache (Table 2). In one prospective study of patients with brain tumor, only 8% of patients reported headache as the first clinical manifestation of disease (92). In retrospective studies, 48 to 71% of people with brain tumor reported headache at some time during illness (37, 91). Predicting which headache is due to a pathological condition is difficult. Although headaches in people with CNS neoplasms have traditionally been associated with early morning occurrence, a positional or unilateral nature, or nausea and vomiting, none of these attributes, in and of itself, is specific for underlying CNS disease. Headache in HIV Seropositive Persons Headache is the most common form of pain in HIV seropositive persons, more common than painful peripheral neuropathy, and has been reported in 22.7% of people newly diagnosed with AIDS (41) and in up to 55% of HIV seropositive patients (50). Both primary headache, such as migraine or tension-type headache, and secondary headache, such as those caused by opportunistic infections or neoplasms, affect HIV seropositive people. Brew and Miller proposed “HIV headache” as a new term to describe a headache that develops during HIV infection and is similar to HIV aseptic meningitis except without CSF pleocytosis (15). In their retrospective study, they found that 18 of 312 (5.8%) HIV positive patients (mean CD4 count 58.9 cells/mm3) but only 2 of 971 (0.2%) HIV negative patients had unexplained headache. The prevalence rates of headache during HIV infection vary from 3.8% to 47.4% depending on the design of the study, the criteria for headache, the subgroup of patients enrolled and the stage of the disease (11, 51). Headache is common during asymptomatic HIV infection and may be more prevalent following the development of acquired immunodeficiency syndrome (AIDS). In a prospective two-year study, asymptomatic HIV seropositive men reported twice as many new headaches as HIV seronegative men (4.4% vs 2.1%, p = 0.001) (51). People with symptomatic HIV infection or AIDS report headache more often than people with asymptomatic HIV infection (48). In one prospective study, people with AIDS reported more than three times as many headaches as HIV seropositive people without AIDS (39% vs. 11%, p = 0.0001), and progression from asymptomatic to symptomatic HIV infection was associated with an increased incidence of headache (86). In the Women’s Interagency HIV study, the prevalence of self-reported headache was lower in HIV-seronegative women (21.8%) than in seropositive women. Among seropositive women, headache prevalence did not differ significantly between women receiving HAART (26.2%) and women not receiving HAART (29.1%) (85). Primary headache in HIV seropositive people was evaluated in one study that found a prevalence of migraine of 16% and tension type headache of 45.8%. The same study suggested a decrease in the frequency of migraines during progression of the disease (95). The proportion of headache due to opportunistic infection or neoplasm varies with sociodemographics, risk factors for HIV infection and stage of illness. In a study by Lipton and colleagues, 82% of HIV seropositive people presenting to an AIDS clinic or emergency room for evaluation of new onset headache had a CNS mass lesion or meningitis (56). This was from a cohort of 49 patients, 59% of which were intravenous drug users (IVDU), 8% were Caucasian, 33% African American and 55% Hispanic. 84% had AIDS. Another study of HIV seropositive patients presenting to an outpatient clinic with headache found a “focal brain lesion” or meningitis in only 6/93 (6.5%) (38). In this group, 34% were IVDU, 69% were Caucasian, 16% African American, 10% Hispanic and 62% had no previous AIDS opportunistic infection. With the dramatic change in therapeutic options for HIV treatment and prophylaxis of OI, the epidemiology of headache in HIV seropositive persons has also changed. Since the introduction of HAART, the incidence of opportunistic infections has significantly decreased. AZT was licensed in 1987, ddI in 1991. In San Francisco, the proportion of individuals living with AIDS who received HAART increased from 5% in 1995 to 76% in 2003. The incidence of CNS infections among these individuals was 6% per year in 1995 and less than 1% per year in 2003 (30).
RISK FACTORS CD4 count A low absolute CD4 count is the most important risk factor for development of an opportunistic CNS infection or neoplasm. Graham and colleagues reviewed 204 CT scans in 178 HIV seropositive patients presenting with headache but without altered mental status, meningeal signs, neurological findings or symptoms of subarachnoid hemorrhage (44). They found that all mass lesions or white matter lesions occurred in patients with CD4 counts of <200cells/mm3. Cryptococcal meningitis, TE, progressive multifocal leukoencephalopathy (PML), primary CNS lymphoma, AIDS dementia complex, and cytomegalovirus encephalitis are all uncommon when the CD4 count is greater than 200 cells/mm3. The incidence of each of these infections increases as the CD4 count drops from 200 cells/mm3 to 100 cells/mm3 or less (8, 76). However, as new treatments are developed, prophylaxis and life expectancy are changing; one study found a dramatic decrease in the incidence of HIV dementia, cryptococcal meningitis, and lymphoma after the introduction of HAART, but also noted an increased proportion of new cases of HIV dementia in people with a CD4 count in a higher range, i.e. 201-350 (83). Approximately 10% of AIDS patients with cerebral toxoplasmosis or PML have CD4 cell counts >200 cells/mm3 (12). The CD4 count may be misleading during the immune reconstitution inflammatory syndrome (IRIS), whereby a subgroup of patients will exhibit a paradoxical deterioration in their clinical status despite increase in their CD4 count, shortly after initiating HAART. It is thought to result from an exaggerated inflammatory response towards latent opportunistic pathogens. Opportunistic infections (OI) Most opportunistic CNS infections and neoplasms are due to reactivation of previously acquired infections. In the United States, 10% to 40% of people with AIDS are latently infected with Toxoplasma gondii, as determined by presence of anti-Toxo immunoglobulin G (IgG) antibodies in serum. In France, the seroprevalence of anti-Toxo IgG in people with AIDS is 80%. At least one-third of people with anti-Toxo IgG antibodies will develop Toxoplasma encephalitis (TE) (60).Up to 22% of people with biopsy proven TE will not have serum IgG antibodies against Toxoplasma gondii (22, 74). IgM antibodies to Toxoplasma gondii are rarely present in patients with TE. The incidence of TE is reduced in people who take TMP/SMX or dapsone/pyrimethamine as prophylaxis against Pneumocystis carinii pneumonia (16, 18). Cryptococcus neoformans is a ubiquitous yeast that causes meningitis in 7% of people with AIDS (22). In people with cryptococcal meningitis, Cryptococcal polysaccharide capsular antigen (CrAg) is detectable in 99% of serum and 91% of cerebrospinal fluid (CSF) samples (75). Thus, in a patient with negative serum CrAg, the diagnosis of cryptococcal meningitis is virtually excluded. Reactivation of latent viral infection is also associated with CNS disease. Epstein-Barr virus (EBV) is present in the CSF up to 100% of patients with primary CNS lymphoma (24). JC virus is present in the CSF of 92% of people with PML (64). The majority of people in the United States have serum antibodies against EBV and JC (20, 33). Presence of EBV or JC antibodies in the serum is not associated with increased incidence of either primary CNS lymphoma or PML. CMV infection fell precipitously after the introduction of HAART (from 20.9 per 100 person years to 3.5 after introduction of HAART) and occurs primarily in people with CD4 count below 50 cells/mm3,(9). Immune Reconstitution Syndrome (IRIS) Some HIV-infected patients develop an inflammatory response shortly after starting HAART, despite an increase in CD4 lymphocyte count and decreasing viral load (47-49). This clinical phenomenon has been called immune reconstitution syndrome, immune reconstitution disease, and immune reconstitution inflammatory syndrome (IRIS). IRIS can produce two distinct clinical syndromes: unmasking and paradoxical (50-53). Unmasking IRIS is an occult infection unmasked by immune system recovery after HAART initiation in patients who had no signs or symptoms of the infection previously. Paradoxical IRIS is the symptomatic recurrence of a successfully treated infection driven by antigen-specific immune activation in the setting of few or no viable organisms; cultures are usually negative due to previous effective treatment. IRIS has been most frequently described in adults. Retrospective studies report 17-32% of adults initiating HAART develop IRIS (49, 51, 54, 55). The wide variation in prevalence can be partially explained by different IRIS definitions used, pathogens included, degree of immunosuppression and prevalence of opportunistic infections (OIs) in the cohorts studied. The first prospective study of IRIS in South African adults with AIDS reported a 10% incidence of IRIS during the first 6 months of HAART, with most IRIS events associated with a low morbidity (56). A variety of pathogens have been associated with IRIS, including varicella zoster virus, Mycobacterium spp., Cryptococcus neoformans, Molluscum contagiosum, cytomegalovirus, and others. Risk factors associated with IRIS include patients who are antiretroviral naive, lower baseline CD4 cell count, genetic susceptibility factors, and speed of immune reconstitution (2). The majority of IRIS cases occur within 4 to 8 weeks after initiation of or change in ART. Headache is a common feature of CNS-IRIS, although the incidence is unknown for IRIS-associated responses to specific infections. In a study of paradoxical tuberculosis-associated IRIS, the most frequent neurologic symptom was headache (3). Headache can be a presenting clinical feature with any of the common etiologies of CNS-IRIS including CNS Mycobacterial infection, cryptococcal meningitis, and progressive multifocal leukoencephalopathy. In a patient who has been recently started on HAART and presents with acute or subacute headache, CNS-IRIS should be considered in the differential diagnosis. Headache and Sinusitis Sinusitis is a common cause of headache. The prevalence of sinusitis in HIV-infected persons ranges from 10 to 35%, and may be more common in persons with AIDS (73, 82, 88). Streptococcus pneumoniae, Haemophilus influenzae or Moraxella catarrhalis are the most common causative agents of acute bacterial sinusitis, but sinusitis caused by atypical bacteria such as Pseudomonas aeruginosa and Listeria monocytogenes, or fungal species such as Alternaria, Aspergillus, Candida, Cryptococcus, Pseudoallescheria and Rhizopus have been reported in HIV-infected people (65, 66). Non-infectious, or allergic, sinusitis is also common. HIV Therapy Although headache is listed as a potential side effect of almost every HIV medication, there have been few studies directly addressing the relationship of antiretrovirals with headache. Three new antiretroviral agents have been approved by the Food and Drug Administration (FDA) for treatment of HIV-1 infection. Two of these agents, maraviroc (Selzentry) and raltegravir (Isentress), are CCR5 co-receptor antagonists and integrase inhibitors, respectively. The third agent, etravirine (Intelence), is an NNRTI. Similar to other antiretroviral medications, these newer agents have been noted to cause headache as a side effect but the percentage of individuals who discontinue any of these medications due to headache has not been defined. Studies investigating the reason for discontinuing HAART therapy found adverse reactions were reported in 22% to 46.1% of people, but headache was not usually the major adverse reaction (4, 59, 68). In one study, 16% of persons taking zidovudine (AZT) developed headache (86). Amprenavir has also been associated with headache (3). When AZT was used as a single agent and doses were higher, headache was reported more often. In a study of primary headache in HIV seropositive patients, Mirsattari and colleagues found that neither use nor discontinuation of HAART affected development or progression of migraine, tension type headaches or cluster headaches (67). In the Women’s interagency HIV study, headache was not significantly different in seropositive women taking or not taking HAART (26.2% vs 29.1%, respectively) (85). Trimethoprim/sulfamethoxazole (TMP/SMX), used as prophylaxis against Toxoplasma encephalitis (TE) and Pneumocystis carinii pneumonia, has been associated with both headache and aseptic meningitis (47). Licit and Illicit Medications Some medications can exacerbate old headache or induce new headache (Table 5). Chronic usage of medication and other substances, such as caffeine, can induce a "rebound" headache. Illicit drugs most often associated with headache include heroin and cocaine (31, 32, 58). Detoxification from heroin, cocaine or marijuana, as well as from licit medications, is also associated with headache (28). Primary Headaches The International Headache Society classifies headaches according to their characteristics, such as migraine, tension type and chronic daily headaches (Table 6) (1). Primary headaches are the most common headache type in HIV-infected patients. In a study of 115 HIV positive patients, 44 (35%) of whom had headaches, 29 were due to primary headaches (22 migraine, 4 tension type, 3 cluster) and the remaining 15 had a “secondary cause” (67). HIV infection may predispose to the development or exacerbation of primary headaches, and these often do not respond to conventional management (67). Common comorbidities such as depression, anxiety, substance abuse or withdrawal, polypharmacy and insomnia, frequently contribute to the development of headaches and may, in turn, be aggravated by them.
DIFFERENTIAL DIAGNOSIS There are many potential etiologies of headache in an HIV seropositive person. Headache has been associated with primary HIV infection, opportunistic CNS infection, neoplasm, HIV pharmacotherapy, as well as substance abuse, systemic infection and migraine (Table 3). When evaluating an HIV seropositive person with headache, opportunistic infection or neoplasm should be included in the differential diagnosis. The clinical signs associated with these etiologies include: focal neurological signs; new seizure; depressed or altered mental status; headache that varies in quality or severity from prior headaches and headache lasting longer than three days (80, 38). Differential diagnosis is primarily determined by the CD4 count, as most opportunistic infections develop when CD4 count drops below 200 cells/mm3. Despite the significant decrease in the incidence of OI since the introduction of HAART, the median CD4 cell count of patients diagnosed with opportunistic infections has remained the same (72). The one caveat is IRIS-related CNS events that can occur despite CD4 count above 200 cells/mm3; when evaluating patients with headache who present with new headache within the first few months of starting HAART, the nadir CD4 count should be considered when determining risk for OI and the appropriate diagnostic algorithm followed.
CLINICAL MANIFESTATIONS Not all patients with CNS opportunistic infection or neoplasm will report headache (Table 4). Headaches that accompany an opportunistic CNS infection or neoplasm are often associated with systemic symptoms or focal neurologic deficit (Table 7). Recognition of “red flags” that suggest a secondary headache should be recognized as heralding an underlying CNS process in people with and without HIV infection. For example, sudden onset headache or development of great intensity of pain over a short period of time should alert the medical care provider to the possibility of an intracranial abnormality such as an intracranial hemorrhage or a mass lesion. When headache is associated with signs of systemic illness such as fever, neck stiffness or a rash, an infection should be suspected, and further work-up should include blood tests and a lumbar puncture. Table 8 lists the clinical and radiologic features of disorders that may cause headache.
DIAGNOSIS The approach to evaluation of headache should be guided by the following factors: CD4 count at the time of evaluation, presence or absence of fever, serologic status for T. gondii and C. neoformans, findings on neurologic examination, and medication list. Figure 1 suggests an approach to the evaluation of headache in an HIV seropositive person. A detailed history and careful neurological exam can guide further diagnostic evaluation. A convincing history of migraine as defined by IHS criteria, even after transformation to chronic daily headaches, may not require immediate neuroradiologic or CSF evaluations if no focal neurological deficits are present (67). Although an abnormal neurological examination is suggestive of intracranial pathology, headache characteristics are often not helpful; absence of fever, neck stiffness, and altered mental status are not as reliable in the HIV seropositive person (12). A clinical prediction rule has been tested for evaluating HIV seropositive people with headache to identify those in immediate need of imaging (38). Low risk was defined as having neither focal neurological findings, change in mental status or history of seizure and with a CD4 count greater than 200 cells/mm3. Of the 35 subjects in this low risk group, none had abnormal findings on head CT. However, the CD4 count needs to be interpreted with caution, especially if HAART therapy was recently initiated. If immune reconstitution inflammatory syndrome (see above) is suspected, the patient should be evaluated in the same way as someone with a CD4 count less than 200 cells/mm3. The evaluation of headache in people with CD4 counts greater than 200 cells/mm3 should be similar to that for people without HIV infection. If fever is present, lumbar puncture should be considered to evaluate for viral or bacterial meningitis. People with an absolute CD4 count less than 200 cells/mm3 are at risk for developing toxoplasma encephalitis (TE), cryptococcal meningitis, or other opportunistic infection or neoplasm. If serum antigen to Cryptococcus neoformans (CrAg) is absent, cryptococcal meningitis is unlikely. A person without a focal neurologic deficit on neurologic examination is unlikely to have a CNS space-occupying lesion. If a focal deficit is present, the evaluation should include either a computerized tomography (CT) or magnetic resonance imaging (MRI) with and without administration of an intravenous contrast agent. Lesion location and contrast enhancement pattern can determine which infection or neoplasm is most likely (Table 8). If a solitary ring-enhancing mass lesion is present, lumbar puncture may be useful to differentiate between TE and primary CNS lymphoma (see Invasive Diagnostic Tests). Neurosyphilis can occur at any stage of HIV infection and can cause headache. HIV seropositive people with new headache and a reactive rapid plasma reagin (RPR) or venereal diseases research laboratory (VDRL) test should undergo lumbar puncture to confirm or exclude the diagnosis of neurosyphilis. The medical care provider should inquire about licit, illicit and over-the-counter medication usage (Table 5). The provider should also inquire about recent start, discontinuation or taper of medication.
INVASIVE DIAGNOSTIC TESTS Lumbar Puncture: A lumbar puncture should be considered in any person presenting with new-onset headache in the setting of fever. Bacterial or viral meningitis may occur at any stage of HIV infection, and typically occurs in the setting of fever. If neurologic examination reveals a focal deficit, or the patient is obtunded or comatose, CT or MRI of the brain should be performed prior to lumbar puncture. If a space-occupying CNS lesion causes midline shift or is present in the posterior fossa, lumbar puncture should not be performed as it could result in CNS herniation. Cerebrospinal fluid tests should include cell count with differential, glucose, protein, bacterial culture and VDRL. Other tests that should be considered include: fungal cultures and antigen test for C. neoformans. If primary CNS lymphoma, PML, CMV or HSV encephalitis is suspected, polymerase chain reaction (PCR) assays for associated viral pathogens should be included. The sensitivity and specificity of most PCR assays are high (Table 9). Brain Biopsy: Brain biopsy may be considered during the evaluation of solitary ring-enhancing CNS lesion. Although primary CNS lymphoma or TE are the most likely etiologies of such a lesion, the differential diagnosis also includes fungal or atypical bacterial abscess, cryptococcoma, syphilitic gumma, tuberculoma, and neoplasm other than primary CNS lymphoma (39). Several algorithms for the evaluation and treatment of CNS mass lesions in people with AIDS have been published (2, 5, 63). Brain biopsy typically involves a CT or MR guided stereotactic approach rather than open biopsy. Complications of brain biopsy vary from 0 to 7% and include hemorrhage, neurologic deficit, seizures, and rarely, infection or death (13, 54, 61, 93). Stereotactic brain biopsy performed on people with HIV infection provides a diagnosis in 88 to 98% of procedures and has a complication rate similar to the rate in people without HIV infection (19, 34, 39, 52).
MANAGEMENT Treatment of HIV-related headache should begin with evaluation of the patient. If a CNS lesion is not suspected or has been ruled out, therapy should be directed toward relieving discomfort. Many medications for treatment of headache are available. Table 10 lists some non-narcotic medications frequently used for treatment of headache. As the initial trial of a medication for reducing pain is often ineffective, several trials of different medications may be necessary to obtain relief. Maximum analgesic efficacy may not occur for several weeks after achieving the target dose, so each medication should be continued for at least two weeks at target dose prior to determining a medication is ineffective. Choice of medication should be dictated by medication side effect profile and patient's past medical history and prior medication use. Most headache experts recommend a trial of at least two medications from each class of medication. Potential side effects of each medication should be discussed with the patient. Some aspects of primary headache management may be different for HIV seropositive persons. For example, the threshold to treat chronic tension type headache with tricyclic antidepressants should be lower than in people without HIV infection. Frequently, analgesics will interact with antiretrovirals. Indomethacin, Tylenol and ASA can increase the toxicity of AZT (95). Patients with thrombocytopenia or coagulopathy should not be given ASA. The anticonvulsants carbamazepine and gabapentin interact with plasma levels of antiretroviral medications. In the same way, antiretroviral drugs may influence levels of pain medications, so serum drug levels need to be monitored closely. Acute HIV infection often goes undiagnosed but early recognition is becoming more and more important because of the potential clinical benefit of early initiation of antiretroviral therapy. Symptoms usually present within days to weeks after initial exposure and include headache in 32-70% (53). Identification of subjects during this period requires a high index of clinical suspicion. Non-pharmacologic treatments for headache may also provide relief of headache discomfort. Such treatments include: neuroaugmentative techniques, such as transcutaneous electrical nerve stimulation (TENS); anesthetic techniques, such as nerve blocks; and complementary and alternative techniques, such as biofeedback, acupuncture and herbal remedies (46, 57, 69, 90). Patients who do not obtain relief from the treatments noted above, or patients with CNS mass lesions, may be candidates for narcotic analgesics. Although short-acting narcotics do provide relief of headache, prolonged use may cause rebound headache and addiction. If prolonged use of narcotics is anticipated, the medical provider should consider prescribing a long-acting narcotic, such as sustained release morphine or methadone, and refer the patient to a pain clinic.
CONCLUSION Headache is common in HIV-infected people. Evaluation of an HIV seropositive person should be guided by the CD4 count and findings on neurologic examination. If an evaluation does not reveal an intracranial abnormality, pain should be managed with medications and other alternate therapies.
TABLES AND FIGURES Figure 1. Approach to the HIV seropositive patient with headache Figure 2. Approach to Focal CNS Lesions on Imaging Table 2. Prevalence of Selected CNS Diseases in People with Headache. Table 3. Common HIV and Non-HIV Related Causes of Headache in HIV Seropositive People. Table 4. Prevalence of Headache with Various Opportunistic CNS Infections Table 5. Medications frequently associated with headache. Table 6. International classification of Headache Disorders, 2nd edition Table 7. Distinguishing Features of Disorders That May Cause Headache Table 8. Characteristic Findings of Certain CNS Infections and Neoplasms with CT or MR Imaging. Table 10. Non-Narcotic Medications for Treatment of Headache.
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