Behavioral effects of pubertal anabolic androgenic steroid exposure in male rats with low serotonin

The goal of this study was to assess the interactive effects of chronic anabolic androgenic steroid (AAS) exposure and brain serotonin (5-hydroxytryptamine, 5-HT) depletion on behavior of pubertal male rats. Serotonin was depleted beginning on postnatal day 26 with parachlorophenylalanine (PCPA 100 mg/kg, every other day); controls received saline. At puberty (P40), half the PCPA-treated rats and half the saline-treated rats began treatment with testosterone (T, 5 mg/kg, 5 days/week). Behavioral measures included locomotion, irritability, copulation, partner preference, and aggression. Animals were tested for aggression in their home cage, both with and without physical provocation (mild tail pinch). Brain levels of 5-HT and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were determined using HPLC. PCPA significantly and substantially depleted 5-HT and 5-HIAA in all brain regions examined. Chronic T treatment significantly decreased 5-HT and 5-HIAA in certain brain areas, but to a much lesser extent than PCPA. Chronic exposure to PCPA alone significantly decreased locomotor activity and increased irritability but had no effect on sexual behavior, partner preference, or aggression. T alone had no effect on locomotion, irritability, or sexual behavior but increased partner preference and aggression. The most striking effect of combining T+PCPA was a significant increase in attack frequency as well as a significant decrease in the latency to attack, particularly following physical provocation. Based on these data, it can be speculated that pubertal AAS users with low central 5-HT may be especially prone to exhibit aggressive behavior.     

Association of C-reactive protein with mild cognitive impairment

BackgroundInflammation is proposed to play a role in the development of Alzheimer's disease, and may also be involved in the pathogenesis of mild cognitive impairment (MCI). This study examined the association of inflammatory markers in serum or plasma with prevalent MCI and MCI subtypes in a population-based sample.MethodsOlmsted County, MN, residents aged 70–89 years on October 1, 2004, were evaluated using the Clinical Dementia Rating Scale, a neurological evaluation, and neuropsychological testing. Information ascertained for each participant was reviewed by an expert panel of neuropsychologists, physicians, and nurses, and a diagnosis of normal cognition, MCI, or dementia was made by consensus. C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis alpha (TNFα), and adiponectin were measured at baseline.ResultsAmong 313 subjects with MCI and 1570 cognitively normal subjects, a CRP level in the upper quartile (>3.3 mg/L) was significantly associated with MCI (odds ratio [OR], 1.42; 95% confidence interval [CI], 1.00–2.01) and with nonamnestic MCI (OR, 2.05; 95% CI, 1.12–3.78) after adjusting for age, sex, and years of education. However, there was no association with amnestic MCI (OR, 1.21; 95% CI, 0.81–1.82). No association was observed with the other inflammatory markers.ConclusionsPlasma CRP is associated with prevalent MCI and with nonamnestic MCI in elderly, nondemented persons in a population-based setting. These findings suggest the involvement of inflammation in the pathogenesis of MCI.     

Disorders of tumoral calcification of the spine: illustrative case study and review of the literature

Tumoral calcium pyrophosphate dihydrate crystal deposition disease and tumoral calcinosis (TC) are rare non-neoplastic conditions which may cause symptoms of spinal cord compression when they manifest in the perispinal tissues. There is little information available to compare these conditions with each other. We report a case of a patient with such a calcified mass impinging on the spinal cord. A 39-year-old woman on hemodialysis presents with progressive quadriparesis and monoplegia and is found to have a large calcified mass impinging on the spinal cord at the level of C3-4. The mass is excised by an anterior approach with corpectomy and fusion. Pathology was tumoral calcium pyrophosphate dihydrate crystal deposition disease versus TC. Both conditions are very rare in the perispinal tissues with 21 reported cases of tumoral calcium pyrophosphate dihydrate deposition disease and 39 cases of TC. Both cause compressive symptoms depending on the site of occurrence. Tumoral calcium pyrophosphate deposition disease is characterized by smaller, round, masses typically in ligamentous structures which may erode into adjacent bone. Tumoral calcinosis displays larger, lobulated, irregular lesions which do not erode into bone. Either lesion may contain calcium pyrophosphate dihydrate or hydroxyapatite. Treatment is surgical decompression, though lesions may recur.     

Identification of hemodynamic compromise by cerebrovascular reserve and oxygen extraction fraction in occlusive vascular disease.

Cerebrovascular reserve (CVR) and oxygen extraction fraction (OEF) are used to identify hemodynamic compromise in symptomatic patients with carotid occlusive vascular disease, but evidence suggests that they are not equivalent. The authors studied the relationship between CVR and OEF to evaluate their equivalence and stages of hemodynamic compromise. Symptomatic patients (N = 12) with carotid occlusion were studied by stable xenon-computed tomography CBF after intravenous acetazolamide administration for CVR, followed within 24 hours by positron emission tomography (PET) for OEF. Middle cerebral artery territories were analyzed by hemisphere and level. Hemispheric subcortical white matter infarctions were graded with magnetic resonance imaging. Both hemispheric and level analysis of CVR and OEF showed a significant (P = 0.001), negative linear relationship [CVR (%) = -1.5 (OEF) + 83.4, (r = -0.57, P = 0.001, n = 24]. However, 37.5% of the hemispheres showed compromised CVR but normal OEF and were associated (P = 0.019) with subcortical white matter infarction. CMRO2 was elevated in stage II hemodynamic compromise (CVR < 10%, OEF > 50%). CVR and OEF showed a significant negative linear relationship in stage II hemodynamic compromise but revealed hemispheres in hemodynamic compromise by CVR but normal OEF that were associated with subcortical white matter infarction.     

The role of xenon CT measurements of cerebral blood flow in the clinical determination of brain death

The demonstration of absent blood flow to the brain is often used as a confirmatory test of brain death. Traditionally, cerebral angiography and dynamic radionuclide brain scanning have been used for this purpose. Recently, xenon CT cerebral blood flow techniques have been developed and applied to a wide variety of clinical problems, including the confirmation of brain death. We report our experience with xenon CT studies performed over a 7-year period (1983-1989) in 30 patients with brain injuries. These patients met clinical criteria for brain death within 24 hr of the study. Twenty patients had average global flow values of less than 5 ml/100 ml/min. Seven patients demonstrated mixed flow patterns, whereby large areas of brain showed flow values of less than 5 ml/100 ml/min and residual pockets of flow greater than 5 ml/100/ml/min. Globally symmetric normal to hyperemic flows were seen in three patients. Our study suggests that the demonstration of average global flows of less than 5/ml/100 ml/min is confirmatory of brain death. Demonstration of persistent flow to the entire brain or regions of the brain is not diagnostic of brain death but also does not exclude such an outcome in patients with severe brain injuries. Xenon-derived flow information may be clinically useful in determining the patient's prognosis and in counseling the patient's family.