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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Middle cerebral artery ligation in the rat produces decreases in catecholamine concentrations at brain sites uninjured by ischemic damage and a transient increase in spontaneous horizontal activity. Development of this hyperactivity can be blocked by postoperative treatment with the antidepressant, desmethylimipramine, or by preoperative destruction of norepinephrine terminals with 6-hydroxydopamine. These results suggest that ischemic damage to the cerebral cortex which injures some axonal branches of elaborately arborizing catecholamine-containing neurons may alter the biochemical and functional state of the entire system in its intact collateral axons. Thus the concept of stroke as a local injury producing symptoms by local structure-function relationships is conceptually inadequate, and poststroke symptoms must be evaluated with these "whole brain" concepts in mind. We suggest that the poststroke symptoms of apathy and depression may represent emotional changes which result from pathophysiological processes in catecholamine neurons far from the site of the stroke.
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PMID:Pharmacological treatment following experimental cerebral infarction: implications for understanding psychological symptoms of human stroke. 58 47

1. Electrical activity of neurones of the locus coeruleus (LC) was studied in rats anaesthetized with urethane. By stimulating the dorsal pathway (DP) of axons of LC neurones in the mid=brain and observing field responses in the dorsolateral tegmentum of the pons, micro-electrodes were oriented to record unit discharges of LC neurones. They were evoked by DP stimulation mainly during the negative wave of the field response. 2. In the extraceullar records of spike discharges of LC meurones A and B spikes were distinguished. Very often the third component (C spike) was observed to ride on the descending stroke of the B spike. When present in the evoked discharge, it was also seen in the spontaneous discharge. 3. The DP-elicited unit discharges of LC neurones were classified into three types. The type 1 response had a fixed latency and a distinct A-B step. In the type 2 response the A spike occurred with a fixed latency, but the B spike followed it with variable delays, sometimes exceeding 5 msec. Being supported by the data of the collision test with spontaneous discharges, the type 1 and 2 responses were assumed to be due to antidromic excitation. The type 3 response whose characteristic was a wide variation of the latency from stimulation to stimulation was categorized as orthodromic excitation. Among seventy-four responses, forty-four were type 1, eight type 2 and twenty-two type 3. The conduction velocities of axons of LC neurones, determined from the latencies of the A spike of the type 1 and 2 responses, ranged from 0-3 to 1-4 m/sec with a mean of 0-69 m/sec. 4. Delay of the B spike in antidromic excitation was observed as a unique property of LC neurones. It was seen in the response to a single shock of DP (type 2 response) or in the response to the second shock of DP following the first one shortly (type 1 response). Since delay of the B spike in the type 2 response could not be ascribed to refractoriness, it was suggested that DP stimulation produced an inhibitory effect upon LC neurones. 5. LC neurones were invaded antidromically from the frontal or visual cortex, hippocampus, cerebellum or from varied combinations of them. About 70% of LC neurones were activated antidromically from the frontal cortex. The antidromic latencies ranged from 15 to 90 msec. 6. Some LC neurones were activated trans-synaptically by stimulation of those forebrain sites which received axonal projections from LC. All LC neurones examined were excited trans-synaptically by eletrical stimulation of the skin and the optic nerve. The sensory inputs arising from a vast area of the skin or those from the skin and the optic nerve were proved to converge on to the same LC neurones.
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PMID:Some electrophysiological properties of neurones of rat locus coeruleus. 87 73

Fifteen patients admitted to Philadelphia General Hospital with acute strokes had repeated measurements of cerebral blood flow measured by the 133Xenon inhalation method. A progressive decline in cerebral blood flow in both hemispheres was observed during the first week after infarction in twelve of these patients. This decline could be partially explained by loss of autoregulation, but could not be correlated with level of consciousness, clinical status of PCO2. This progressive decline in flow in the non-ischemic hemisphere indicates a process more complex than a simple destruction of axonal afferants to neurons as implied by the term diaschisis. The flow changes in the non-ischemic hemisphere are likely caused by a combination of the immediate effects of decreased neuronal stimulation modified by loss of autoregulation, release of vasoactive substances, cerebral edema, and other factors.
Stroke
PMID:Diaschisis with cerebral infarction. 92 57

Maximal motor conduction velocity of ulnar nerve was measured in 7 patients 80-93 years old, who suffered from cerebro-vascular stroke. In 2 cases motor conduction velocity was significantly decreased. Specimens for histopathological study were taken from the spinal cord at the C8 and Th1 segments and from the ulnar nerve at the elbow level on the side opposite to the hemiparesis. In 100 sections of each senile case and in 3 control cases of younger individuals the motoneurons of the retro-postero-lateral nucleus with visible nucleoli were counted. In the ulnar nerve qualitative and quantitative examinations were performed. The study showed a significant loss of motoneurons in the nucleus and a loss of myelinated fibers especially the thickest ones in the ulnar nerve in elderly cases. In teased preparations axonal degeneration and segmental demyelination of some fibers were seen. Morphological changes in some cases, resulted in a slowed down motor conduction velocity.
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PMID:Histological and electrophysiological changes of the lower motor neurone with aging. 99 62

Peripheral neuropathy has attracted relatively little attention in mitochondrial myopathy. However, mitochondrial myopathies are clinically heterogeneous disorders that can affect multiple systems including peripheral nerves other than the skeletal muscle. In addition to the survey of the literature, we studied 6 cases of mitochondrial myopathy with peripheral neuropathy; 3 cases of oligo-systemic involvement confined mainly to skeletal muscles and peripheral nerves, and 3 cases of multi-systemic involvement diagnosed as myoclonus epilepsy with ragged-red fibers (MERRF) or mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). This study suggests that peripheral neuropathy may be relatively common and has similar clinical and laboratory features in a broad spectrum of mitochondrial myopathies. The clinical manifestation is usually of mild sensorimotor neuropathy with frequent subclinical involvement. Sensory disturbances are more evident than manifestations of motor neuropathy which is usually subclinical. It is also noteworthy that there exist some cases of oligo-systemic involvement, which present with peripheral neuropathy as main clinical manifestations. Electrophysiological findings include decreased nerve conduction velocities and neuropathic electromyograms. Peripheral nerves show loss of myelinated fibers, particularly of large ones, and the remaining fibers have disproportionately thin myelin sheaths with or without onion-bulb formation. Thus the pathological process is axonal degeneration with demyelination resulting from involvement of both neurons (axons) and Schwann cells.
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PMID:Peripheral neuropathy of mitochondrial myopathies. 166 Jan 82

Using immunohistochemistry, we studied the origins and pathways of parasympathetic and sensory nerve fibers to the pial arteries in four squirrel monkeys. Following its application to the surface of the middle cerebral artery, the retrograde axonal tracer True Blue accumulated in parasympathetic neurons of the sphenopalatine ganglion and the internal carotid ganglion. The latter is strategically located where the internal carotid artery enters the cranium. Fibers from the sphenopalatine ganglion reach the internal carotid artery in the cavernous sinus region after running as rami orbitales. Before reaching the internal carotid artery, the fibers bypass aberrant sphenopalatine ganglia, with the most distant, the cavernous ganglion, being located in the cavernous sinus region. True Blue also accumulated in sensory neurons of the ophthalmic and maxillary divisions of the trigeminal ganglion and in sensory neurons of the internal carotid ganglion. Fibers from the ophthalmic division of the trigeminal ganglion reach the internal carotid artery as a branch through the cavernous sinus, bypassing the cavernous ganglion. Fibers from the maxillary division also bypass the cavernous ganglion after reaching it via a recurrent branch of the orbitociliary nerve. Thus, the cavernous ganglion forms a confluence zone for parasympathetic and sensory fibers in the region. In addition, parasympathetic and sensory fibers leave the confluence zone to follow the abducent and trochlear nerves backward to the basilar artery and tentorium cerebelli, respectively. Clinical implications are discussed.
Stroke 1991 Mar
PMID:Pathways of parasympathetic and sensory cerebrovascular nerves in monkeys. 170 17

Magnetic stimulation of the motor cortex is of value in the diagnosis and management of several neurological disorders. Marked latency prolongation is suggestive of demyelination of central motor pathways, whereas low-amplitude responses with little delay are more typical of disorders causing neuronal loss or axonal degeneration. Subclinical abnormalities may be demonstrated, and the technique has a potential role for quantification and monitoring of disease progress. The pattern of early electrophysiological abnormality is of prognostic value in stroke patients.
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PMID:Magnetic stimulation of cortex: clinical applications. 185 Apr 31

Axonal injury and behavioral changes were evaluated 3-7 days after traumatic brain injury. Previous research from this laboratory demonstrated that clinical central nervous pathology is produced by dynamic brain compression using a stroke-constrained impactor. We wanted to determine if the technique also would produce diffuse axonal injury after recovery from the procedure. The experiments were performed at Wayne State University School of Medicine using aseptic techniques while assuring analgesic care. Impacts were performed at 4.3 m/sec or 8.0 m/sec, with congruent to 10% compression (2.5 mm). Extensive axonal injury was observed at 3 and 7 days postinjury using both velocity-compression combinations. Regions displaying axonal injury were the subcortical white matter, internal capsule, thalamic relay nuclei, midbrain, pons, and medulla. Axonal injury also was evident in the white matter of the cerebellar folia and the region of the deep cerebellar nuclei. Behavioral assessment showed functional coma lasting up to 36 h following 8.0 m/sec impacts, with impaired movement and control of the extremities over the duration of the postinjury monitoring time. These experiments confirm that the cortical impact model of traumatic brain injury mimics all aspects of traumatic brain injury in humans and can be used to investigate mechanisms of axonal damage and prolonged behavioral suppression.
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PMID:Characterization of axonal injury produced by controlled cortical impact. 237 65

We studied functional disturbances following left middle cerebral artery occlusion in rats. Neuronal function was evaluated by [14C]2-deoxyglucose autoradiography 1 day after occlusion. We analyzed the mechanisms of change in glucose utilization outside the infarct using Fink-Heimer silver impregnation, axonal transport of wheat germ agglutinin-conjugated-horseradish peroxidase, and succinate dehydrogenase histochemistry. One day after occlusion, glucose utilization was remarkably reduced in the areas surrounding the infarct. There were many silver grains indicating degeneration of the synaptic terminals in the cortical areas surrounding the infarct and the ipsilateral cingulate cortex. Moreover, in the left thalamus where the left middle cerebral artery supplied no blood, glucose utilization significantly decreased compared with sham-operated rats. In the left thalamus, massive silver staining of degenerated synaptic terminals and decreases in succinate dehydrogenase activity were observed 4 and 5 days after occlusion. The absence of succinate dehydrogenase staining may reflect early changes in retrograde degeneration of thalamic neurons after ischemic injury of the thalamocortical pathway. Terminal degeneration even affected areas remote from the infarct: there were silver grains in the contralateral hemisphere transcallosally connected to the infarct and in the ipsilateral substantia nigra. Axonal transport study showed disruption of the corticospinal tract by subcortical ischemia; the transcallosal pathways in the cortex surrounding the infarct were preserved. The relation between neural function and the neuronal network in the area surrounding the focal cerebral infarct is discussed with regard to ischemic penumbra and diaschisis.
Stroke 1989 Sep
PMID:Neuronal network disturbance after focal ischemia in rats. 247 23

We studied histopathologic changes in cerebral cortex of 20 rats after middle cerebral artery occlusion by using the Fink-Heimer suppressive silver impregnation method and conventional stains. At 6 hours after occlusion, Fink-Heimer-stained sections revealed abundant coarsely granular, intensely argyrophilic neurons in the ischemic cortex. These distinctive argyrophilic neurons could be clearly differentiated from neurons that suffered postmortem changes; argyrophilic neurons were present in all layers of the lateral parietal cortex but in only the superficial cortical layers II and III in the parasagittal area of the frontoparietal cortex and the temporo-occipital area. At 24 hours after occlusion as the ischemic region progressed to pannecrosis, argyrophilic neurons were still evident in peri-infarct regions, with more prominent neuritic silver deposits but no changes in number or spatial distribution. Over 2-7 days, the argyrophilic neurons gradually disappeared while many fine silver-impregnated degenerating terminals appeared in the peri-infarct regions. At 3-6 weeks after occlusion, no more argyrophilic neurons were seen in the cortex although degenerating axons were still present in the deep white matter. Our results indicate selective neuronal damage in the superficial cortical layers and massive axonal degeneration in the cerebrum surrounding infarcts. The neuronal damage does not appear to progress beyond 6 hours after middle cerebral artery occlusion. The Fink-Heimer method has many advantages over existing conventional stains for documenting selective neuronal damage in focal cerebral ischemia.
Stroke 1989 Nov
PMID:Selective cortical neuronal damage after middle cerebral artery occlusion in rats. 247 27


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