Central Cerebral Atrophy Research Articles

Early brain atrophy in HIV infection: a radiological-stereological study.

Patients with the acquired immunodeficiency syndrome (AIDS) frequently develop neurological abnormalities, and atrophy has been reported in neuropathological studies of brains from patients with AIDS. Our aim was to see whether increased ventricular volume, indicating central cerebral atrophy develops at an early stage of HIV-infection, before patients are severely immunodeficient. We also wished to follow ventricular size over time and to investigate whether enlargement would be more marked in patients, who became clinically demented. We studied 32 HIV-seropositive men who had several CT studies. At the time of the first CT the patients were divided into two groups, an immunocompetent group (IC) with CD4 cell count >400 and an immunodeficient group (ID) with CD4 cell count <400. These were compared with a control group of 44 seronegative men. Subsequent CT studies were used to measure changes in ventricular size with time. Ventricular volume was estimated with an unbiased stereological method previously applied to CT. Mean (geometric) ventricular volume was 15 ml (6-54 ml) in the controls, 23 ml (10-72 ml) in the IC group and 27 ml (8-80 ml) in the ID group. The increase in size in both patient groups was statistically significant compared with controls: P=0.005 (IC) and 9 x 10(-5)(ID). Regression analysis of the follow-up CT studies showed a significant increase in volume in the HIV group (r=0.74, P=0.002), but not in the AIDS group (r=0.41, P<0.1).

Abstract

This review describes the cerebral complications of diabetes mellitus from a neuropsychological, neurophysiological and neuroradiological perspective. In addition, possible pathogenetic mechanisms are discussed. Neuropsychological studies of diabetic patients generally report modest deficits in learning and memory and information processing. Notably, in elderly diabetic patients cognitive deficits may be more prominent. Recent epidemiological studies show that in the elderly diabetes is associated with an increased risk for dementia. Neurophysiological studies show increased latencies of evoked potentials and event-related potentials. Neuroradiological findings are enhanced peripheral and central cerebral atrophy, as well as focal lesions.The pathophysiology of the effects of diabetes on the brain has not been fully elucidated. The putative involvement of cerebral metabolic and microvascular disturbances, similar to those implicated in the pathogenesis of peripheral diabetic neuropathy, is discussed. In addition, the role of repeated hypoglycaemic episodes, cerebrovascular disease and hypertension is addressed. Finally, the potential differential effects of insulin dependent and non-insulin dependent diabetes on the brain are discussed, as well as possible links with brain ageing.

Cerebral complications of diabetes: clinical findings and pathogenetic mechanisms

This review describes the cerebral complications of diabetes mellitus from a neuropsychological, neurophysiological and neuroradiological perspective. In addition, possible pathogenetic mechanisms are discussed. Neuropsychological studies of diabetic patients generally report modest deficits in learning and memory and information processing. Notably, in elderly diabetic patients cognitive deficits may be more prominent. Recent epidemiological studies show that in the elderly diabetes is associated with an increased risk for dementia. Neurophysiological studies show increased latencies of evoked potentials and event-related potentials. Neuroradiological findings are enhanced peripheral and central cerebral atrophy, as well as focal lesions.The pathophysiology of the effects of diabetes on the brain has not been fully elucidated. The putative involvement of cerebral metabolic and microvascular disturbances, similar to those implicated in the pathogenesis of peripheral diabetic neuropathy, is discussed. In addition, the role of repeated hypoglycaemic episodes, cerebrovascular disease and hypertension is addressed. Finally, the potential differential effects of insulin dependent and non-insulin dependent diabetes on the brain are discussed, as well as possible links with brain ageing.

Head and Neck Injuries in Soccer

Head injuries have been shown to account for between 4 and 22% of soccer injuries. Clinical and neuropsychological investigations of patients with minor head trauma have revealed organic brain damage. 69 active football (soccer) players and 37 former players of the Norwegian national team were included in a neurological and electroencephalographic (EEG) study to investigate the incidence of head injuries mainly caused by heading the ball. 3% of the active and 30% of the former players complained of permanent problems such as headache, dizziness, irritability, impaired memory and neck pain. 35% of the active and 32% of former players had from slightly abnormal to abnormal EEG compared with 13 and 11% of matched controls, respectively. There were fewer definitely abnormal EEG changes among typical 'headers' (10%) than among 'nonheaders' (27%). The former players were also subjected to cerebral computed tomography (CT), a neuropsychological examination and a radiological examination of the cervical spine. One-third of the players were found to have central cerebral atrophy and 81% to have from mild to severe (mostly mild to moderate) neuropsychological impairment. The radiological examination of the cervical spine revealed a significantly higher incidence and degree of degenerative changes than in a matched control group.

The significance of age-related enlargement of the cerebral ventricles in healthy men and women measured by quantitative computed X-ray tomography.

(1) To establish the range of cerebral atrophy across the adult age spectrum in optimally healthy, rigorously evaluated individuals. (2) To determine, across the age spectrum, the relation of gender and cerebral atrophy (as measured by ventricular enlargement) to cognitive function. Cross-sectional comparison by age and gender. Ambulatory research unit. Sixty-four healthy men (mean age +/- SD = 49 +/- 18 yr) and 43 healthy women (51 +/- 18 yr) volunteers enrolled in a longitudinal study of healthy aging. The population was selected for optimal health; all were rigorously screened to exclude medical and psychiatric illness. Brain atrophy by CT scan and cognitive function by standardized neuropsychological testing. After correction for inter-subject variability in cranial volume, women had smaller lateral, but not third, ventricles. For both genders, there were significant differences with age in ventricular volume. After an approximately constant 20% increase in ventricular volume per decade in both genders, a precipitous increase in volume was found beginning in the fifth decade in men and in the sixth decade in women. In men and women, there was a significant negative correlation between ventricular volume and the sum of performance scale scores on the Wechsler Adult Intelligence Scale (WPSS) but not in the sum of the verbal scale scores (WVSS). However, after controlling for age, ventricular volume no longer significantly contributed to the relation between age and WPSS. In unequivocally healthy individuals, gender plays an important role in age-associated central cerebral atrophy as measured by progressive ventricular enlargement. Increase in ventricle volume independent of age, does not explain normal age-related declines seen in WPSS scores.

Brain damage in former association football players

Thirty-three former football players from the National Football Team of Norway were examined by cerebral computer tomography (CT). The CT studies, evaluated for brain atrophy, visually and by linear measurements compared two different normal materials. One third of the players were found to have central cerebral atrophy. It is concluded that the atrophy probably was caused by repeated small head injuries during the football play, mainly in connection with heading the ball.

Relation between central cerebral atrophy, memory defects and prolactin secretion

Concentrations of prolactin in cerebrospinal fluid (CSF) and in serum were determined from 26 neurological patients with or without minor central cerebral atrophy. Neuropsychological memory tests also were performed on these patients. Twenty-eight neurological patients with peripheral nervous lesions and without endocrine dysfunctions served as controls for prolactin levels. Patients with central cerebral atrophy had significant loss of recall capacity, though they did not differ significantly from the normal population in their intellectual performances. CSF and serum prolactin levels in the patients with central cerebral atrophy and/or memory defects did not differ from the values obtained in the patients without cerebral atrophy. Thus, prolactin levels do not appear to reflect either central cerebral atrophy or memory dysfunctions, most likely due to the minor degree of neuronal atrophy around the third ventricle that occurs in patients with these findings.

Changes of prolactin secretion and memory functions in central cerebral atrophy : M.T. Hyyppä and M. Tenkku (Turku, Finland)

Over the years, our ideas about estrogen signaling have greatly expanded. In addition to estradiol having direct nuclear actions that mediate transcription and translation, more recent experiments have demonstrated membrane-initiated signaling. Both direct nuclear and estradiol membrane signaling can be mediated by the classical estrogen receptors, ERα and ERβ, which are two of the numerous putative membrane estrogen receptors. Thus far, however, only ERα has been shown to play a prominent role in regulating female reproduction and sexual behavior. Because ERα is a ligand-gated transcription factor and not a typical membrane receptor, trafficking to the cell membrane requires post-translational modifications. Two necessary modifications are palmitoylation and association with caveolins, a family of scaffolding proteins. In addition to their role in trafficking, caveolin proteins also serve to determine ERα interactions with metabotropic glutamate receptors (mGluRs). It is through these complexes that ERα, which cannot by itself activate G proteins, is able to initiate intracellular signaling. Various combinations of ERα–mGluR interactions have been demonstrated throughout the nervous system from hippocampus to striatum to hypothalamus to dorsal root ganglion (DRG) in both neurons and astrocytes. These combinations of ER and mGluR allow estradiol to have both facilitative and inhibitory actions in neurons. In hypothalamic astrocytes, the estradiol-mediated release of intracellular calcium stores regulating neurosteroid synthesis requires ERα–mGluR1a interaction. In terms of estradiol regulation of female sexual receptivity, activation of ERα–mGluR1a signaling complex leads to the release of neurotransmitters and alteration of neuronal morphology. This review will examine estradiol membrane signaling (EMS) activating a limbic-hypothalamic lordosis regulating circuit, which involves ERα trafficking, internalization, and modifications of neuronal morphology in a circuit that underlies female sexual receptivity.

Low cerebrospinal fluid prolactin levels in patients with central cerebral atrophy

Low cerebrospinal fluid prolactin levels in patients with central cerebral atrophy