Localizing components of a complex task: sentence processing and working memory.

Three areas of the left hemisphere play different roles in sentence comprehension. An area of posterior middle and superior temporal gyrus shows activation correlated with the structural complexity of a sentence, suggesting that this area supports processing of sentence structure. The lateral anterior temporal gyrus is more activated bilaterally by all sentence conditions than by word lists; thus the function of the area probably does not directly support processing of structure but rather processing of words specific to a sentence context. Left inferior frontal cortex also shows activation related to sentence complexity but is also more activated in word list processing than in simple sentences; this region may thus support a form of verbal working memory which maintains sentence structural information as well as lexical items.

Operative treatment of meralgia paresthetica: transection versus neurolysis.

The question of the superior operative technique for meralgia paresthetica is unsettled. Operative treatment by either neurolysis or transection of the lateral femoral cutaneous nerve was performed in 21 patients with meralgia paresthetica after complete failure of conservative treatment; neurolysis in 10 patients and transection in 11 patients were performed by five neurosurgeons. The average follow-up period was 74 months (+/- 52 mo). The results were scored as complete relief, partial relief, or failure. Direct comparison of neurolysis and transection confirmed the superiority of transection as a treatment for meralgia paresthetica (Mann-Whitney-U test, P = 0.022; one-sample sign test, P = 0.0020).

Neuronal hypertrophy in the human supraoptic and paraventricular nucleus in aging and Alzheimer's disease.

In the literature, activation of the hypothalamo-neurohypophyseal system (HNS) in normal aging has been demonstrated in rat and human. This activation might be secondary to an age-related decline in vasopressin binding sites in the kidney, or to cell loss in the supraoptic (SON) and paraventricular nuclei (PVN) and/or to an age-related decline in noradrenergic (NA) innervation of the hypothalamus. This study shows neuronal hypertrophy in SON and PVN in normal aging and an additional hypertrophy in Alzheimer's disease. No cell loss could be demonstrated in both conditions.

Cell loss and shrinkage in the nucleus basalis Meynert complex in Alzheimer's disease.

Marked neuron loss in the nucleus basalis of Meynert complex (NBMC) in Alzheimer's disease has repeatedly been reported in the literature. However, most of these studies quantitated only magnocellular, hyperchromatic (putative cholinergic) neurons of just a small part of the NBMC, and counts were expressed as numerical density. Applying a 3-dimensional-sampling design throughout the entire rostrocaudal extent of the NBMC and sampling neurons regardless of their size and staining characteristics, an overall neuron loss of only 15.5% was demonstrated for the whole NBMC. Neuron loss varied from 0% rostrally in the NBMC up to 36% in the most caudal part of the nucleus basalis of Meynert. Moreover, a significant increase in the number of small-sized neurons and a significant decrease in the number of large, putative cholinergic neurons could be detected, suggesting that apart from neuron loss neuron shrinkage appears to be another characteristic neuropathological feature of this degenerating cholinergic NBMC system. Preservation of these magnocellular cholinergic neurons in shrunken form renders it likely that cholinergic dysfunction, characteristic of Alzheimer's disease, may be responsive to neurotrophic influences.

Galanin-like immunoreactivity within Ch2 neurons in the vertical limb of the diagonal band of Broca in aging and Alzheimer's disease.

The neuropeptide galanin is known to inhibit the evoked release of acetylcholine in ventral hippocampus of the rat. Co-localization of this peptide with choline acetyltransferase in neurons of the cholinergic septal nuclei has been demonstrated in the rat and non-human primate. The severe deficiency of the cholinergic hippocampal projection system arising mainly from the vertical limb nucleus of the diagonal band of Broca, also referred to as Ch2 region, is a constant finding in Alzheimer's disease, a disorder which is neuropathologically characterized by the appearance of senile plaques, neurofibrillary tangles and congophilic angiopathy in neo- and archicortical structures. In the present study for the first time galanin immunoreactivity in the human Ch2 region is morphologically investigated and related to the severity of hippocampal plaques and neurofibrillary tangles in Alzheimer's disease. An inverse relationship between decreasing galanin immunoreactivity in the Ch2 region and amounts of senile plaques and neurofibrillary tangles in the hippocampus is indicated. Considering the cholinergic deficiency in Alzheimer's disease as a secondary phenomenon to primary cortical and hippocampal lesions, and realizing the inhibitory effect of galanin upon acetylcholine release in hippocampus, this preliminary study suggests that a decreased galanin immunoreactivity in Ch2 in Alzheimer's disease, reflects a possible negative feedback mechanism to a degenerating cholinergic projection system.