11 women with a clinical diagnosis of Premenstrual Syndrome (PMS) and 10 control women with no such diagnosis were compared on pain threshold and pain-tolerance measures in the intermenstrual and premenstrual phases of their menstrual cycles. No significant differences were found between the groups for behavioral measures of pain sensitivity. Ratings of pain intensity, however, were higher in both phases for the PMS group.

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The case of a patient who repeatedly injected himself intravenously with elementary mercury in suicide attempts is presented and the toxicological effects of this chemical form and route of exposure of mercury are examined. A review of the literature reveals that elemental mercury, when injected as opposed to inhaled, causes few of the effects typical of mercurialism; pleuritic chest pain was frequently reported, whereas renal and central nervous system involvement were less common. Evidence of premorbid psychiatric disturbances was found in ten of fourteen non-cardiac catheterization exposures to intravenous elemental mercury. Findings in our patient were consistent with these observations. One additional and noteworthy finding in our case was that documented deposits of elemental mercury in the right parietal lobe of the brain did not correlate with any specific deficits on neuropsychological testing. Consultation-liaison psychiatry plays an important role in the treatment and care of these complex patients.

Single-photon emission computerized tomography demonstrates temporal-parietal (TP) hypoperfusion in many patients with Alzheimer''s disease (AD). However, the specificity of these changes has not yet been determined. We have found TP hypoperfusion in five groups of patients including 1 patient with normal aging, 6 with sleep apnea, 1 with posthypoxic dementia, 5 with multi-infarct dementia and 2 with ''pseudo'' TP hypoperfusion with frontal seizures. These findings suggest that the TP cortex may be particularly sensitive to hypoxia and/or hypotension and that hypoperfusion to TP Cortex is not specific to AD.

Cocaine causes serious neurologic and neuropsychiatric complications. Cocaine-induced seizures are common and appear to be due to the local anaesthetic actions of this compound. Cocaine induced stroke has varied mechanisms. With ischemic stroke there is severe vasospasm induced by rises in brain catecholamines. These changes can persist for many weeks and can be demonstrated using single-photon emission computerized tomography (SPECT). In many patients with psychiatric symptoms such as psychosis or mania, SPECT demonstrates similar changes in cerebral blood flow. In fact, some of the psychiatric symptoms induced by cocaine may be due to decreases in cerebral blood flow. In cocaine abuse, treatment strategies based on decreasing cerebral vasospasm need to be developed.

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