Cerebral cortical atrophy

Cerebral cortical atrophy (alcohol-associated dementia)... 

Other neurological syndromes (e.g., cerebral cortical atrophy, myopathy, cerebellar degeneration) are also associated with alcoholism, but their pathogenesis is less certain than that of nutritional deficiency disorders. Abstinence from alcohol plus vitamin replacement and physical therapy comprise the standard treatment approach for these conditions. 

Effects on the nervous system tremor, peripheral neuropathy (motor and sensory), paresthesia, ataxia, pyramidal signs, cerebral cortical atrophy, hydrocephalus, convulsions, parkinsonian syndrome, degenerative changes in the nerve cells, personality changes, permanent brain damage. 

Special laboratory MRI/CT n or cerebral/ cortical atrophy n or cerebral/ cortical atrophy... 

Rouser, G., G. Feldman, and C. Galli Fatty acid compositions of liuman brain lecithin and sphingomyelin in normal individuals, senile cerebral cortical atrophy, Alzheimer s disease, metachromatic leucodystrophy, Tay-Sachs, Niemann-Pick diseases. J. Amer. Oil Chem. Soc.42,411 (1965 a). 

Similar findings were reported by Haberland et al. (1971) in another severely impaired patient, untreated until diagnosis at age 13, who died of pneumonia at age 25. This patient had severe mental retardation, extrapyramidal motor symptoms, and epilepsy. Microcephaly, cerebral cortical neuronal degeneration, cerebral white matter atrophy and sclerosis, and cerebellar findings similar to Crome s case were described. In addition, these anthors reported abnormal levels of glycoproteins and glycolipids. 

In cases of severe non-fatal episodes of lead encephalopathy, the neurological sequelae that occur are qualitatively similar to those often seen after traumatic or infectious cerebral injury, with permanent sequelae being more common in children than in adults. The most severe paediatric sequelae are cortical atrophy, hydrocephalus, convulsive seizures, and severe mental retardation (Mellins and Jenkins, 1955 Perlstein and Attala, 1966 Chisolm, 1968). Children who recover from acute lead encephalopathy but are re-exposed to lead almost invariably show evidence of permanent CNS damage (Chisolm and Harrison, 1956). Even if further lead exposure is minimized, 25 to 50% show severe permanent sequelae, such as seizure disorders, blindness, and hemiparesis (Chisolm and Barltrop, 1979). 

Generally, but not invariably, postmortem macroscopic examination of the brain reveals cerebral atrophy with narrowed convolutions, widened sulci, and enlarged lateral and third ventricles. On microscopic examination brain specimens from patients with a clinical diagnosis of Alzheimer s disease are characterized by widely spread cortical senile plaques, neurofibrillary tangles, and granulovascular degeneration. 

Currently, there is a commonly expressed view that decreased cortical volume in schizophrenia is the result of a reduction of cortical neuropil, presumably due to an atrophy of neural dendrites and axons (e.g., (Selemon and Goldman-Rakic, 1999)). A direct prediction of this model is that neuron density should be increased in proportion to the decrease in cortical volume. While there is some evidence for increased density in the prefrontal cortex (Selemon et al., 1995, 2003), there are also a number of negative findings (Akbarian et al., 1995 Cotter et al., 2002 Cullen et al., 2006 Thune et al., 2001). In auditory areas, the available studies have not shown an altered neuron density, even with hemispheric comparisons (Beasley et al., 2005 Cotter et al., 2004 Smiley et al., 2002). An alternative hypothesis is that reduced cortical volume is accompanied by a loss of neuron number, but this issue remains to be addressed in the auditory cortex. In other brain areas, there is some evidence for decreased neuron number, although the differences are often subtle and statistically nonsignificant (Benes et al., 1986 Dorph-Petersen et al., 2007 Stark et al., 2004 Thune et al., 2001). Changes in total cell number in the cerebral cortex have been difficult to determine, because these measurements require a clearly identified reference volume. 

AD is characterized by marked atrophy of the cerebral cortex and loss of cortical and subcortical neurons. The pathological hallmarks of AD are senile plaques, which are spherical accumulations of the protein -amyloid accompanied by degenerating neuronal processes, and abundant neurofibrillary tangles, composed of paired helical filaments and other proteins. In advanced AD, senile plaques and neurofibrillary tangles are most abundant in the hippocampus and associative regions of the cortex, whereas areas such as the visual and motor cortices are relatively spared. This corresponds to the clinical features of marked impairment of memory and abstract reasoning, with preservation of vision and movement. 

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