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Eighteen adult patients presenting with acute transverse myelitis (ATM) were evaluated using magnetic resonance imaging. Only 7 had abnormal scans showing an area of increased signal intensity within the cord solely on T2 weighted images; Tl weighted images were normal. The MRI abnormality did not correlate with the cause of the transverse myelitis, the extent of maximum neurological deficit, or the prognosis. A scan performed more than 5 days after the onset of disease was most likely to be positive. Even though the prognostic value of MRI in ATM may be limited, it remains a valuable technique for ruling out other causes of noncompressive spinal cord lesions, such as hemmorhage, vascular malformation, or tumor.
The nucleus basalis of Meynert has been studied extensively in the recent literature. Interest in this nucleus has resulted from the discovery that it is a major source of cortical cholinergic input and that there is neuronal loss in the nucleus basalis in some dementing illnesses. Consistent and severe involvement of the nucleus basalis of Meynert has been found in Alzheimer's disease and in the dementia accompanying Parkinson's disease. Occasional involvement is present in other dementing illnesses, such as progressive supranuclear palsy, Parkinsonism-Dementia complex of Guam, dementia pugilistica, Pick's disease, Korsakoff's syndrome, Down's Syndrome and Creutzfeldt- Jakob disease. Huntington's disease spares this nucleus. However, the role of the nucleus in cognitive function is as yet undetermined. Even its alteration with normal aging remains controversial. This review details the pathological studies of this region to date, with particular emphasis on the dementias. Its role in the dementias of Alzheimer's disease and Parkinson's disease is specifically addressed.
Extensive recent literature on drugs used to enhance cognitive functioning, reflects the growing social problem of dementia. Many clinical trials have been undertaken with variable success. In most cases the disorder studied has been Alzheimer's disease. The pharmacological approach has been designed to rectify the presumed pathophysiological processes characteristic of the condition. Agents tested include cerebral vasodilators, cerebral metabolic enhancers, nootropics, psychostimulants, neuropeptides and neurotransmitters with a special emphasis on drugs used to enhance cholinergic function. Ethical and practical issues concerning clinical drug trials in dementia will be discussed.
The cognitive profile of early onset Parkinson’s disease (EOPD) has not been clearly defined. Mutations in the parkin gene are the most common genetic risk factor for EOPD and may offer information about the neuropsychological pattern of performance in both symptomatic and asymptomatic mutation carriers. EOPD probands and their first-degree relatives who did not have Parkinson’s disease (PD) were genotyped for mutations in the parkin gene and administered a comprehensive neuropsychological battery. Performance was compared between EOPD probands with (N = 43) and without (N = 52) parkin mutations. The same neuropsychological battery was administered to 217 first-degree relatives to assess neuropsychological function in individuals who carry parkin mutations but do not have PD. No significant differences in neuropsychological test performance were found between parkin carrier and noncarrier probands. Performance also did not differ between EOPD noncarriers and carrier subgroups (i.e., heterozygotes, compound heterozygotes/homozygotes). Similarly, no differences were found among unaffected family members across genotypes. Mean neuropsychological test performance was within normal range in all probands and relatives. Carriers of parkin mutations, whether or not they have PD, do not perform differently on neuropsychological measures as compared to noncarriers. The cognitive functioning of parkin carriers over time warrants further study. (JINS, 2011, 17, 1–10)
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