Individuals infected with the human immunodeficiency virus-Type 1 (HIV-1), are at increased risk for neurobehavioral impairment, particularly in later stages of the disease. Even patients in the medically asymptomatic or minimally symptomatic stages of infection may show mild deficits on comprehensive neuropsychological (NP) test batteries, although the clinical significance of such deficits remains uncertain. The present study used vocational difficulties as markers of clinical significance of NP impairment. In a sample of 289 HIV-infected, nondemented men, those who evidenced NP impairment had a higher unemployment rate (p < .001) than did their unimpaired counterparts. In HIV-positive subjects who remained employed, NP impairment was strongly associated with subjective decreases in job-related abilities. Neither depression nor medical symptoms could explain the relationship between the NP impairment and employment problems. These results are consistent with previous studies investigating other neuropsychiatric disorders, which suggest that even mild NP impairment can interfere with employment status. From this standpoint, such impairment in HIV-infected persons may be described as "clinically significant."

Stress IRT is a sensitive and specific indicator of CRPS-I.

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As part of a longitudinal study, 265 cerebrospinal fluid (CSF) specimens from 204 human immunodeficiency virus type 1 (HIV-1)-seropositive subjects and 43 seronegative controls were evaluated. Of the 204 seropositive persons, 78 (38%) had > or = 1 CSF culture positive for HIV-1; the probability of being culture positive increased as the number of CSF samples obtained increased (P = .0018). Significantly correlated with culture positivity were elevations in CSF protein level (P = .014) and CSF white blood cell count (P = .001). Virus was more readily cultured from clarified CSF (89%, 42/47) than from the cellular fraction (30%, 14/47; P < .00001). Amplification of HIV-1 DNA by polymerase chain reaction (PCR) from 25 seropositive persons was positive in 9 (82%) of 11 culture-positive and in 4 (29%) of 14 culture-negative specimens, while amplification of viral RNA detected all 11 culture-positive and 9 (64%) of the 14 culture-negative CSF specimens. These data support the hypothesis that the development of HIV-1-associated neurocognitive disorders are not dependent solely on the presence of HIV-1 within the central nervous system.

One hundred-nine controls and 386 HIV-infected volunteers enrolled in the HIV Neurobehavioral Research Center (HNRC) longitudinal study. The majority, without acquired immune deficiency syndrome (AIDS), were screened for alcohol/substance abuse; previous diagnosis of HIV-associated dementia; and HIV-unrelated developmental, neurological, medical, and neurobehavioral conditions which potentially impair cognition; and underwent a structured neurological interview and examination, standardized NP testing, and psychiatric interview as part of a more extensive battery. A large subset (N = 377) underwent lumbar puncture for cerebrospinal fluid (CFS) examination. We examined the relationship of sixteen select but independent variables, using stepwise multiple regressions, from demographic/staging, immunological, NP, and psychiatric domains to neurological symptoms in an effort to identify possible predictors of subclinical nervous systems involvement. Results. All categories of neurological symptoms were significantly more prevalent among medically asymptomatic (CDC stage A) subjects than controls, with a further rise in prevalence in those with more advanced stages of infection. The most marked rise was seen in cognitive and sensorimotor complaints. In contrast, significant findings on neurological examination were evident in only the sicker (stage C) subjects. Stage of illness, serum β2-microglobulin, psychiatric indices of depressed mood or anxiety, and NP "motor" performance were the most significant independent variables associated with the presence of neurological symptoms. CSF pleocytosis was seen early (CDC stage A), and may reflect the presence of HIV in the central nervous system (CNS) at the least stages of infection. We also confirmed the value of CSF β2m and neopterin as important markers of advancing disease stage. Whether they predict subclinical CNS involvement is to be determined by longitudinal observations. Conclusion. Neurological complains are common in medically asymptomatic HIV subjects whereas signs are not. The symptoms correlate with commonly determined independent measures of depression, anxiety, NP tests of fine motor speed and strength, as well as indices of disease worsening (CDC stage, serum β2m).

The International Headache Society applies the term exertional headache to head pain precipitated by exertion. The Society recognizes cough headache and sexual headache as distinct diagnoses. All three types of headache share characteristics and mechanisms, and together may be considered as headache provoked by exertional factors ( Table 1). In distinction to more typical headaches, such as tension-type headaches or migraine, HAPEF is brief, lasting seconds to minutes, and begins immediately following the precipitating exertion. Headache provoked by exertional factors may occur by itself, or in association with headaches that are not exertional. Secondary (or symptomatic) HAPEF arises as a result of an underlying disorder; primary (or benign) HAPEF has no underlying cause. Clinicians must consider HAPEF potentially serious until appropriate investigations are undertaken. Fortunately, disorders that underlie secondary headaches usually become apparent with examination or laboratory testing. Clinical features of the headaches may also offer a clue (Table 2). Several theories have been put forth to explain the underlying mechanism of exertional, cough, and sexual headache. The leading explanation regarding all three involves exertional factors leading to a sudden increase in intracranial pressure or an inappropriate reaction in the cerebral vasculature. Because exertion may also be a migraine trigger, neural hypersensitivity, similar to migraine, may also play a role in HAPEF. The literature contains only several small case studies that deal with treatment of exertional headache, and just one double blind, placebo-controlled study. The consensus to date is that secondary HAPEF resolves if the underlying illness can be treated; primary HAPEF responds well to prophylactic treatment. Treatment strategy varies little among headaches precipitated by cough, sex, or other forms of exertion. Avoidance strategies, sometimes combined with medication (particularly indomethacin), can effectively treat headaches produced by exertional factors in most cases.

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