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Autism as impairment in the formation and use of meaning: an attempt to integrate a functional and a neurological model.

Neurological approaches and functional approaches to impairments in autism provide different perspectives on the disorder. This study attempted an integration of the two approaches, based specifically on the role of the mesolimbic/neostriatal system in imparting adaptive meaning to percepts and problems that autistic persons have in making adaptive use of meaning.

Autistic Disorder↗

Hand preference in patients with allergy, juvenile cancer, and schizophrenia.

Patients with allergy (n = 50), juvenile cancer (n = 50), and schizophrenia (n = 37), and nonpatient controls (n = 200) were asked to indicate their hand preferences on a 7-point scale (1 = left always, 7 = right always) for the 32-item Waterloo Handedness Questionnaire. Except for patients with schizophrenia, who exhibited a higher incidence of mixed hand preference, groups showed a clear rightward bias. Further analyses suggested that mixed hand preference in schizophrenia was evident more often for unskilled than skilled hand activities.

Adolescent↗

Dementia paralytica (neurosyphilis): a clinical case study.

This study reminds clinicians that syphilis presents in many guises. Wars, migration and sexual promiscuity prepare the ground for its return as an important cause of neurological and psychiatric syndromes. Our patient's diagnosis was not suspected at earlier admission. Stage III spirochaetosis was improved by high dose penicillin.

Alcoholism↗

Motor control.

Explore the source record for details and available documents.

Animals↗

Spasticity: its physiology and management. Part I. Neurophysiology of spasticity: classical concepts.

Spasticity, seen so frequently in clinical situations, presents motor signs resembling those produced experimentally by transecting the brain stem of a cat at the intercollicular level. This paper reviews experimental results which elucidate the roles of different brain regions in the genesis of classical decerebrate rigidity and demonstrate the function of the gamma motor system in the maintenance of the rigidity. Interruption of the gamma-spindle loop of a muscle (i.e. interrupting the monosynaptic reflex arc subserving the stretch reflexes) abolishes rigidity in that muscle. This reflex-mediated gamma support of decrebrate rigidity is also a prominent feature of clinical spasticity, making classical decerebrate rigidity a useful model for studying the neural mechanisms underlying spasticity. Not all rididities, however, are gamma dependent. Those rigidities surviving dorsal root rhizotomy are called alpha rigidity. Alpha rigidity results when a brain lesion disrupts descending systems which normally exert a net inhibitory effect upon alpha motoneurons.

Animals↗

Extrapyramidal motor abnormalities associated with late-life psychosis.

Studies of extrapyramidal motor function in patients with schizophrenia have contributed to our understanding of the phenomenology and therapeutic outcome associated with neuroleptics. An increasing body of literature suggests that extrapyramidal motor abnormalities associated with schizophrenia may be linked to the pathophysiological mechanisms responsible for schizophrenia. Similarly, it has been documented that the extrapyramidal system may be involved in motor abnormalities in patients with Alzheimer's disease (AD). The present study was undertaken to examine motor function in schizophrenia and AD patients with psychosis. Quantitative instrumental procedures were used to examine rigidity, tremor, and bradykinesia in 13 neuroleptic-naive patients with schizophrenia, 13 AD patients with psychosis, and 26 age-comparable controls. Both schizophrenia and AD patients had significantly higher tremor and rigidity scores than did normal subjects. This comparative study of schizophrenia and AD patients with psychosis suggests that the effect of dementia in patients with psychosis is to prolong movement time, whereas abnormal parkinsonian postural tremor tends to be associated with psychosis in the absence of dementia.

Aged↗

Local changes in cerebral glucose utilization during ketamine anesthesia.

Ketamine produces both excitatory and depressant actions in the brain, but there have been conflicting results regarding which structures are affected and the magnitude of the alteration in cerebral metabolism produced. The authors applied the 2-[14C]deoxyglucose method quantitatively to a study of ketamine anesthesia (10 or 30 mg/kg intravenously) in the rat. Ketamine caused both increases and decreases in local cerebral glucose utilization. The areas with altered glucose utilization could be grouped into functional systems. Some structures of the limbic system showed large increases in glucose utilization; indeed the 70 per cent increases in cingulate gyrus and hippocampus were the largest of all regions examined. The extrapyramidal motor system and corpus callosum showed significant but less dramatic (20-40 per cent) increases. On the other hand, decreased metabolism occurred in the somatosensory and auditory systems, with the greatest reduction (40 per cent) in the inferior colliculus. Within some structures, such as the caudate nucleus and visual cortex, a striking redistribution of metabolism which is characterized by a change in the autoradiographic pattern of activity was noted. Reduced glucose utilization in the somatosensory and auditory systems suggests that a selective sensory deprivation occurs during ketamine anesthesia while the increased metabolism in the limbic system is consistent with neurophysiologic studies which have demonstrated seizure activity in this region. Compared with other anesthetics, which tend to produce a generalized decrease in metabolism, the cerebral metabolic effects of ketamine are unique and emphasize that it produces a state of "anesthesia" which is quite different from that of other commonly used drugs.

Anesthesia↗

Supraspinal mediation of dopamine-serotonin interactions in extrapyramidal motor functions in the rat.

The effects of intracerebroventricularly (i.c.v.) or intrathecally (i.t.) administrated 8-OH-DPAT on catalepsy, induced by the specific DA D2 antagonist raclopride (16 mg kg-1 s.c.), were studied in rats. It was found that 8-OH-DPAT (0.5 or 2.0 micrograms kg-1) injected by the i.c.v. route produced a statistically significant of raclopride-induced catalepsy at both doses. In contrast, 8-OH-DPAT (0.2 or 2.0 micrograms kg-1) given by the i.t. route had no statistically significant effect on the raclopride-induced catalepsy. These results suggest that the antagonistic effect of 8-OH-DPAT on catalepsy, induced by DA blocking agents, is primarily mediated at the supraspinal level.

8-Hydroxy-2-(di-n-propylamino)tetralin↗