[Experimental studies of the effect of cerebral cortex decortication on the healing process of traumatic injuries].
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The effect of excitatory amino acid antagonists on antagonist on neuropeptide Y (NPY) and cholinergic neurons in the striatum of the rat was studied by means of NPY immunocytochemistry, DFP histochemistry for acetylcholinesterase (AChE), and biochemical determinations of choline acetyltransferase (ChAT). Intrastriatal infusion of drugs revealed that striatal neurons containing NPY are more sensitive than cholinergic neurons to the neurotoxic actions of kainic acid (KA), quinolinic acid (QA) and L-glutamic acid (GA); all 3 compounds produced a marked loss of NPY neurons, but only a moderate decrease in the number of AChE neurons or ChAT activity. Co-injection experiments showed that the neurotoxicity of QA and GA, but not that of KA, can be antagonized by the specific N-methyl-D-aspartate (NMDA) receptor antagonist 3-((+/-)-2-(carboxypiperazine-4-yl))-propyl-1-phosphonic acid (CPP). Destruction of the glutamatergic corticostriatal projection by cerebral decortication protected striatal NPY and cholinergic neurons against KA neurotoxicity. These results indicate that striatal NPY and cholinergic neurons receive prominent cortical amino acid afferents, and that the neurotoxic effect of QA and GA on these neurons is mediated through NMDA receptors.
A behavioral quantal theory of brain function is formulated on the basis of a newly discovered step-wise relationship invariably present among the findings of three experiments by Tsai, et al. on the effects of (1) cerebral decortication, (2) cranial x-radiation, as well as (3) insulin, metrazol, and electroconvulsive shocks upon white rats' adaptive behavior during their learning of successive habit reversals and one-trial reversal problems. Confirmatory results from earlier investigators who studied effects of various current strengths of ECS upon learning and retention of various maze habits are also cited in support of the behavioral quantal theory of brain function which is proposed here as a close-up, more refined alternative to Lashley's continuity theory of mass action.
A man with cerebral palsy had his right cerebral cortex removed at the age of 18 years because of intractable epilepsy. The operation cured the epilepsy, but at the age of 45 years and after a number of unipolar depressions, he experienced rapid-cycling bipolar illness. Mood swings that were highly stereotypical and regular occurred. The mood disorder responded poorly to lithium carbonate alone, but responded well when carbamazepine was added to the regimen.
Motor cortical inputs and proprioreceptive muscle afferents largely target the same spinal cord region. This study explored the idea that during development the two inputs interact via an activity-dependent mechanism to produce mature patterns of innervation. In rats, the forelimb motor cortex was ablated unilaterally at either postnatal day 7 (P7), the beginning of corticospinal synaptogenesis in the cervical cord, or at P50. Comparisons were made with sham-operated animals. At P70, muscle afferents from the extensor digitorum communis muscle, contralateral to the lesion, were transganglionically labeled with cholera toxin B-subunit. Lower cervical spinal cord sections were immunostained for cholera toxin B, parvalbumin, and cJun. Our small lesions had no obvious effects upon forelimb function. However, developmental lesions, but not adult lesions, were shown to significantly increase the number of muscle afferent boutons present in the contralateral ventral horn, compared with sham-operated controls. Also, the ratio of parvalbumin-positive neurons contralateral/ipsilateral to the developmental lesion (but not adult lesions) was decreased and the ratio of cJun-positive motoneurons increased. Thus, an early motor cortex lesion resulted in retention of a proportion of muscle afferent synapses to the ventral horn that are known to be lost during normal development. Parvalbumin and cJun are markers of neuronal activity suggesting that spinal circuitry develops permanently altered activity patterns in response to an early cortical lesion, although this plasticity is lost in the mature animal.
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A number of surgical procedures are available for patients with epilepsy associated with diffuse hemispheric disorders. In this report, 16 pediatric patients had hemispherectomy: 5 underwent hemidecortication and 11 had peri-insular hemispherotomy. The clinical records were retrospectively reviewed, and the results and complications of the procedures were documented. The procedure was feasible in very young children and in the absence of ventriculomegaly.
The purpose of this study is three-fold: First, to determine the levels of gross and fine motor functions in children before and after hemidecortication, using standardized measurement tools; second, to investigate if predictors of these outcomes can be characterized; and third, to explore if both clinical measures and functional magnetic resonance imaging (MRI) potentially can identify optimal timing of surgery. The Gross Motor Function Measure and the Quality of Upper Extremity Skills Test are shown to be comprehensive, standardized outcome measures of movement performance in affected children. Age at surgery and interval between age at seizure onset and age at surgery could be the most reliable predictors of clinical outcomes. Functional MRI studies are valuable in exploring the potential of the cortical reorganization that sustains residual sensorimotor function. The combination of clinical measures with functional MRI is a promising method of inquiry into developmental and plasticity processes.
We present a 61-year-old male patient with progressive dementia. A brain SPECT with Tc-99m-bicisate was performed for confirmation of clinically suspected Alzheimer-dementia. At the time of the SPECT-investigation marked apraxia and aphasia besides severe dementia were present. Electrophysiological as well as anatomical neuroimaging findings showed non-diagnostic alterations. SPECT revealed distinct perfusion defects, which made Alzheimer Dementia unlikely. The further course of the patient was determined by rapidly progressive deterioration with development of akinetic mutism. Thereafter, increased levels of neuron-specific enolase as well as 14-3-3 proteins were found in the cerebro-spinal fluid (CSF). The patient finally died with signs of cerebral decortication. Due to the clinical course and the CSF-findings the patient's final diagnosis was Creutzfeldt-Jakob-disease, nevertheless no autopsy was performed. The presented case report underscores the clinical utility of perfusion brain SPECT in the differential diagnosis of dementias.
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The authors report 5 cases of avoiding phenomenon of the hand from parietal lesions. Four of these patients were operated for intractable epilepsy, from a parietal cortectomy that implicated a certain amount of white matter. The avoiding phenomena observed are analyzed as elementary motor perturbations rather than a disturbance of motor comportment. The authors distinguish two types of avoiding phenomena: 1--Avoiding phenomenon of dystonic type occurs during any motor activity and persists during all its development. It is probably related to the removal of the cortex of the post-central gyrus and of the anterior part of the superior parietal lobule; 2--The initial avoiding phenomenon is brief and occurs only at the beginning of the movements which implicate solely the upper limb; it seems related to the removal of the internal part of the superior parietal lobule that corresponds approximately to areas 5 and 7 from Brodmann. Some hypotheses are discussed concerning the possible physio-pathological mechanisms of these disturbances.
A method for the extraction and quantification of Dopamine from small areas of rat brain has been developed. The extraction with solvents eliminates the column cromatography separations and allows the simultaneous processing of a good number of samples. Sample retrieval is quite high (70%) and very reproducible. The evaluation was made from areas with a minimal weight of 0.225 g. The quantification of Dopamine was obtained using spectrofluorometric techniques, reading the fluorescence of the trihydroxy indol derivate. The linear relation between the instrument readings and the concentration of Dopamine is from 0 to 0.5 microng/ml. The maximal concentration of Dopamine was found in the decorticated cerebral hemispheres (1.485 microng/g), the next highest values in the diencephalon (1.046 microng/), and the minimal concentration in the cerebellum (0.283 microng/g). The concentration of the whole brain was 0.701 microng/g.
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