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M M Mesulam

Publications and source records attributed to M M Mesulam.

At least 127 records · Page 7Linked to original sources

Neural inputs into the temporopolar cortex of the rhesus monkey.

Temporopolar cortex (TP) can be subdivided into agranular, dysgranular, and granular components. The telencephalic input into the temporopolar cortex arises from the orbitofrontal and medial frontal regions, modality-specific visual and auditory association areas, paralimbic regions, the piriform olfactory cortex, the hippocampus, the amygdala, the claustrum, and the basal forebrain. Afferents from limbic and paralimbic regions are directed mostly to the agranular and dysgranular sectors of the temporal pole, whereas afferents from isocortical association areas are distributed predominantly within the granular sector. The temporopolar cortex provides a site for the potential convergence of sensory and limbic inputs. Auditory inputs predominate in the dorsolateral part of the temporopolar cortex whereas visual inputs become prominent only in the ventral portions of this region. Olfactory inputs are directed mostly to the medial parts of the temporal pole. These medial parts also receive more extensive projections from the amygdaloid nuclei.

Amino Acids↗

Right cerebral dominance in spatial attention. Further evidence based on ipsilateral neglect.

Tasks based on visuomotor scanning and tactile exploration were used to quantitate neglect behavior in patients with unilateral brain damage and in normal control subjects. The results confirm previous observations that contralateral neglect is markedly more severe following right-hemisphere injury and that it is independent of the modality of sensory input or motor output. In addition, patients with right-hemisphere injury also showed multimodal neglect for targets in the hemisphere ipsilateral to the brain lesion. The emergence of both contralateral and ipsilateral neglect in these patients strongly supports a model of right-hemispheric dominance for the distribution of attention within the extrapersonal space.

Aged↗

Behavioral manifestations of central pontine myelinolysis.

A young woman with a clinical history and magnetic resonance imaging scan consistent with central pontine myelinolysis came to medical attention because of prominent behavioral symptoms. Marked clinical recovery occurred despite persistent radiologic abnormalities. Rapid correction of hyponatremia was probably related to the development of the central pontine myelinolysis. A normal computed tomographic scan and the absence of brain-stem signs delayed accurate diagnosis.

Adult↗

Age-related shrinkage of cortically projecting cholinergic neurons: a selective effect.

The number and size of basal forebrain neurons that provide the cholinergic innervation for the cerebral cortex, amygdala, and hippocampus were studied in young and aged mice. The results showed that these neurons became substantially smaller with increasing age. This effect was relatively selective, since the immediately adjacent cholinergic neurons in the striatum did not show a change of similar magnitude. The shrinkage of these basal forebrain neurons may account for the decline of cholinergic innervation that occurs with age. In the material that we examined, aging did not influence the number of cholinergic neurons in the basal forebrain, only their size. It seems, therefore, that the age-related changes in cholinergic function (and their putative behavioral consequences) are not associated with a substantial component of irreversible cell death.

Aging↗

Cholinesterases within neurofibrillary tangles related to age and Alzheimer's disease.

Enzyme histochemistry showed that a substantial number of cortical neurofibrillary tangles contain acetylcholinesterase and butyrylcholinesterase activities in patients with Alzheimer's disease and in nondemented aged individuals. In some areas of the brain, tangles containing each of these two enzymes were differentially distributed. In other areas, there was a very close overlap between the two types of cholinesterase.

Aged↗

Anatomy of cholinesterase inhibition in Alzheimer's disease: effect of physostigmine and tetrahydroaminoacridine on plaques and tangles.

The histochemical distribution of cholinesterases in the cerebral cortex and their response to cholinesterase inhibitors such as physostigmine and tetrahydroaminoacridine (THA) were investigated in brains from patients with Alzheimer's disease and control subjects. In the temporal neocortex of the control subjects, most of the cholinesterase activity was located within axons and cell bodies belonging to cholinergic pathways. In keeping with their well-known cholinomimetic effects, physostigmine and THA effectively inhibited this cholinesterase activity. Cholinesterase-containing normal axons (and in some cases cells) were severely depleted in the cerebral cortex of patients with Alzheimer's disease. Although the cerebral cortex of these patients continued to display abundant cholinesterase activity, the location of this enzyme was largely shifted to the neuritic plaques and neurofibrillary tangles. In fact, the majority of these pathological structures demonstrated intense acetylcholinesterase and butyrylcholinesterase activities. Physostigmine and THA were potent inhibitors of these plaque- and tangle-bound cholinesterases as well. In patients with Alzheimer's disease, cholinesterase inhibitors would therefore appear to have a major and widespread effect directly upon the enzymatic activity of plaques and tangles. Consequently, the clinical effects of anticholinesterases in Alzheimer's disease may be based on mechanisms that are different from those that apply to the normal brain.

Acetylcholinesterase↗

Clinical comparison of Tourette's disorder and obsessive-compulsive disorder.

The authors report on 16 outpatients with Tourette's disorder, 16 outpatients with obsessive-compulsive disorder, and 16 normal control subjects who underwent structured interviews and psychological testing. Previous findings of a high incidence of obsessive-compulsive disorder in patients with Tourette's disorder were confirmed. There was a significantly greater incidence of tics in the patients with obsessive-compulsive disorder and their relatives. Both patient groups had high rates of unipolar depressive and generalized anxiety disorders. Panic and phobic disorders were frequent in the patients with obsessive-compulsive disorder but not in the patients with Tourette's disorder. The patients with obsessive-compulsive disorder showed less coprolalia, echo phenomena, self-destructive behavior, and childhood attention deficit.

Adult↗

Treatment of Gilles de la Tourette's syndrome: eight-year, practice-based experience in a predominantly adult population.

Over 86% of 58 patients with Gilles de la Tourette's syndrome achieved effective pharmacologic control of the symptoms for 3 months or longer. Differences in response patterns were common among patients and required individualized tailoring of management. Dopamine-blocking neuroleptics were the mainstay of therapy. However, frequent mid-course alterations were required as previously successful drugs stopped working or as their side effects became intolerable. While haloperidol and now pimozide are most frequently used, trifluoperazine and thiothixene can provide superior relief in individual patients. A combination of neuroleptics or even a rotation from one to another may occasionally become necessary. No tardive dyskinesia was encountered in this population. Clonidine proved inferior to neuroleptics in the treatment of the motor and vocal tics, but may have a role in some patients with prominent obsessive-compulsive symptomatology.

Adolescent↗

Cholinergic projections from the parabigeminal nucleus (Ch8) to the superior colliculus in the mouse: a combined analysis of horseradish peroxidase transport and choline acetyltransferase immunohistochemistry.

Choline acetyltransferase (ChAT) immunocytochemistry, acetylcholinesterase histochemistry and muscarinic receptor autoradiography demonstrated a cholinergic innervation within the superior colliculus. A method for the concurrent visualization of ChAT and transported horseradish peroxidase showed that a major extrinsic source for this cholinergic input is in the parabigeminal nucleus. We have designated these cholinergic neurons as the Ch8 cell group.

Acetylcholinesterase↗

Three-dimensional representation and cortical projection topography of the nucleus basalis (Ch4) in the macaque: concurrent demonstration of choline acetyltransferase and retrograde transport with a stabilized tetramethylbenzidine method for horseradish peroxidase.

Ninety-six percent of the nucleus basalis neurons that project to the neocortex contain choline acetyltransferase. These projections from the cholinergic component of the nucleus basalis (Ch4) are topographically organized so that each cortical area receives most of its cholinergic input from a different Ch4 sector. The three-dimensional reconstruction of these sectors reveals the presence of a complex structure. A stabilization procedure that was used in these experiments maintains all the advantages of the tetramethylbenzidine method for horseradish peroxidase while eliminating the vulnerability of the reaction-product to high pH and dehydrating agents.

Animals↗

Slowly progressive aphasia without generalized dementia: studies with positron emission tomography.

Slowly progressive aphasia without generalized dementia is a degenerative syndrome selectively affecting dominant hemisphere language areas. We report changes in regional glucose metabolism measured by positron emission tomography in two patients with this condition. Striking abnormalities of glucose utilization in the left cerebral cortex were demonstrated in both patients. The findings of other neurodiagnostic studies were relatively unremarkable. The first patient had a 3-year history of progressive anomia and impaired auditory verbal recall. An electroencephalogram was normal, and computed tomography showed mild left perisylvian atrophy. Positron emission tomography revealed profound hypometabolism in the left temporal regions. The second patient also had a 3-year history of progressive anomia. Electroencephalography, computed tomography, and magnetic resonance imaging scans were normal. Positron emission tomography showed a major reduction in left parietal glucose utilization, with a lesser decrement in left temporal metabolism. Neither patient demonstrated significant contralateral or global abnormalities such as those reported in positron emission tomographic studies of Alzheimer's disease with or without focal clinical features. These observations support the concept of adult-onset progressive aphasia without dementia as a clinical syndrome distinct from Alzheimer's disease.

Aphasia↗

Systematic regional differences in the cholinergic innervation of the primate cerebral cortex: distribution of enzyme activities and some behavioral implications.

Choline acetyltransferase and acetylcholinesterase enzymatic activities were measured in 33 cytoarchitectonic subregions of the cerebral cortex in two rhesus monkeys. As expected, the hippocampus and amygdala were rich in these enzymes. In addition, the paralimbic (mesocortical) regions of the brain (e.g., parahippocampal, insular, caudal orbitofrontal, and temporopolar areas) also contained high levels of both enzymes. In contrast, the concentration of these cholinergic markers was the lowest within all frontal and temporoparietal association areas. As a group, the primary sensory and motor regions contained an intermediate level of choline acetyltransferase activity. Both cholinergic markers also showed a gradual increase from the isocortical toward the more primitive periallocortical subsectors of paralimbic areas. These anatomical patterns have potential implications for the role of cholinergic pathways in the memory process and in the pathogenesis of Alzheimer's disease.

Acetylcholinesterase↗