Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within the past several years a number of substances have been identified in the mammalian brain that are capable of (1) preventing the death of injured neurons and (2) promoting the regeneration of severed neuronal processes. The goal of this review article is to update the clinical neurologist in this area by presenting a brief, general overview of this subject, including a glimpse at potential clinical implications. Recent advances in neuronal transplantation and molecular techniques underlying nerve growth are discussed. Possible therapeutic approaches are presented for many neurologic disorders, ranging from stroke to Alzheimer's disease to acquired immunodeficiency syndrome, based on regrowing or saving injured neurons. The clinical neurologist will become important in practical applications and research into prolonging neuronal survival and fostering axonal regeneration. Over the coming years, with further research, it is anticipated that patients will be treated with these or similar modulatory agents.
 ...
PMID:Growth factors for neuronal survival and process regeneration. Implications in the mammalian central nervous system. 257 31

Marked hyperemia may develop in brain following temporary cessation of blood flow and is associated with the morbidity following cardiac arrest, stroke, and head injury. Regional cerebral blood flow was measured using radiolabeled microspheres and compared in 10 symmetrical regions after chronic unilateral trigeminal ganglionectomy (n = 8), trigeminal rhizotomy (n = 4), or sham operation (n = 4) following 10 min of combined brachiocephalic-left subclavian occlusion and hypotension (mean arterial blood pressure less than 50 mmHg) in cats. Blood flow was symmetrical at rest in the three groups and was undetectable during the ischemic period. Within 30 min after re-establishing flow, values in cortical gray matter increased symmetrically to approximately 250 ml.100 g-1.min-1 in the rhizotomy and the sham groups. Increases of similar magnitude were measured on the intact side following trigeminal ganglionectomy but flow was attenuated by greater than 50% ipsilateral to the ganglionectomy. Marked hyperemia developed during reperfusion in thalamus, caudate, deep cortical white matter, midbrain, and pons, but no asymmetries were present in the three groups. These data suggest that cortical hyperemia is mediated by trigeminal neurogenic mechanisms via axonal reflexlike mechanisms and suggest the importance of therapeutic strategies based on blockade of this nerve or its constituent neuropeptides.
 ...
PMID:Postocclusive cerebral hyperemia is markedly attenuated by chronic trigeminal ganglionectomy. 258 25

The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. Forty-three patients with wallerian degeneration seen on MR images after cerebral infarction were studied. When possible, patients with acute stroke were examined with MR imaging prospectively at the onset of symptoms and then at weekly intervals for several months. Focal infarction without distal axonal degeneration is demonstrated for the 1st month following onset of clinical symptoms. At 4 weeks, a well-defined band of hypointense signal appears on T2-weighted images in the topographic distribution of the corticospinal tract. After 10-14 weeks, the signal becomes permanently hyperintense. Over several years, accompanying ipsilateral brain stem shrinkage occurs. The dark signal intensity observed on T2-weighted images between 4 and 14 weeks is believed to result primarily from transitory increased lipid-protein ratio.
 ...
PMID:Wallerian degeneration after cerebral infarction: evaluation with sequential MR imaging. 274 May 1

We used the Fink-Heimer method to study degenerating corticofugal axons after unilateral middle cerebral artery occlusion in 14 adult male Long-Evans hooded rats. Axonal degeneration in the pyramidal tracts was prominent at 1-3 weeks, manifesting in well-defined silver-impregnated axonal bundles coursing from the internal capsule to the pyramids and crossing completely to the contralateral spinal cord. In half of eight rats examined at 1-3 weeks, the cortical infarct included the forelimb region of the sensorimotor cortex, and degenerating corticospinal axons could be traced to the lower cervical segments; in rats with involvement of the hindlimb cortical area as well, axonal degeneration extended to the lumbosacral segments. Terminal degeneration products were present in the forebrain, midbrain, and brainstem within 2 days after arterial occlusion; the number of degenerating terminals peaked at 7 days and decreased gradually thereafter up to 6 weeks. Dense terminal degeneration was observed in the trigeminal nuclear complex of all seven rats studied at 2 and 7 days. In these seven rats, five had small cortical infarcts, and silver-impregnated terminals were observed in the lateral reticular formation; in two rats with large cortical lesions, terminal degeneration was prominent in the medial reticular formation as well. We conclude that infarcts produced by middle cerebral artery occlusion cause axonal degeneration in the brainstem and spinal cord. The Fink-Heimer method may be useful for evaluating the rat middle cerebral artery occlusion model.
Stroke 1989 Oct
PMID:Corticofugal axonal degeneration in rats after middle cerebral artery occlusion. 279 71

"Energy metabolism" is deranged in a wide variety of disorders of the nervous system. This term refers rather loosely to the pathways responsible for the utilization of the major substrates of brain. Primary disorders of energy metabolism are those in which the primary insult affects the cellular machinery required for energy metabolism. A typical example would be a defect in a gene coding for a mitochondrial protein. Biochemically, defects which appear to be hereditary and which lead to disease of the central nervous system have been described in each of the pathways of energy metabolism: glycogenolysis (the break-down of glycogen to glucose); glycolysis (the break down of glucose to pyruvate and lactate); the pyruvate dehydrogenase complex (which oxidizes pyruvate to enter the Krebs tricarboxylic acid cycle); the tricarboxylic acid cycle itself (which completes the oxidation of carbohydrates and other substrates to carbon dioxide); electron transport (which carries out their oxidation to water); the pentose phosphate pathway (an alternate pathway for glucose oxidation); and several "minor" mitochondrial pathways. Clinically, the spectrum of syndromes associated with primary disorders of energy metabolism is wide. Common manifestations include psychomotor retardation, with associated lactic acidosis and/or hypoglycemia. The laboratory abnormalities may be intermittent. Syndromes which have been culled out include congenital lactic acidosis, Leigh disease, intermittent ataxia, Kearns-Sayre-Shy syndrome (KSS), myoclonus epilepsy with ragged red fibers (MERRF), and mitochondrial myopathy-encephalopathy-lactic acidosis-stroke (MELAS). As with other families of inborn errors, both clinical and biochemical heterogeneity occur. Patients with apparently similar clinical syndromes can turn out to have different inborn errors, and patients with abnormalities of the same gene product can have clinically distinguishable syndromes. Secondary disorders are those in which the derangements of energy metabolism are presumably secondary to some other insult but may still be important for the cellular pathophysiology. These include the metabolic encephalopathies and probably a number of well-known neurodegenerative disorders. In the hereditary ataxias, abnormalities of mitochondrial markers are common but do not correlate consistently with the disorders as conventionally classified; a new classification into axonal ataxias, multiple system degenerations, and ataxic encephalopathies may be easier to relate to the pathophysiology.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Energy metabolism in disorders of the nervous system. 297 43

A new experimental model of mechanical brain injury was produced in the laboratory ferret (Mustela putorius furo) using a stroke-constrained pneumatic impactor. Cortical impacts were made on vertex to the intact dura mater overlying the cerebral cortex with contact velocities ranging from 2.0 to 4.0 m/sec and with deformations of 2.0 to 5.0 mm. The dwell time of the impact and the stability of the skull during impact were verified with high speed (1000 to 3000 frames/sec) cineradiography. Systemic arterial blood pressure, heart rate, and respiration were monitored, and postinjury changes were recorded. Anatomic brain injury, including subdural hematoma, subarachnoid hemorrhage, tears or rents of the dura mater, and contusions of the cortex, brainstem, cervical spinal cord, and cerebellum was observed. Injury responses ranged from no apparent anatomic injury or alterations in the systemic physiology at low severity impact (2.0 m/sec, 2.0 mm) to immediate fatality in the highest severity impact groups (4.0 m/sec, 4.0 mm). The range of changes in systemic physiology and of pathology in the brain, brainstem, and spinal cord was a function of both contact velocity and the amount of brain deformation. In two cases where postinjury time was 8-10 h, diffuse axonal injury, indicated by beaded axons and retraction balls, was present in subcortical regions underlying the site of impact. The spectrum of anatomic injury and systemic physiologic responses closely resembled aspects of closed head injury seen clinically. This procedure complements and improves on existing techniques by allowing independent control of contact velocity and level of deformation of the brain to facilitate biomechanical and analytic modeling of brain trauma. Graded cortical contusions and subcortical injury are produced by precisely controlled brain deformations, thereby allowing questions to be addressed regarding the influence of contact velocity and level of deformation on the anatomic and functional severity of brain injury.
 ...
PMID:Controlled cortical impact: a new experimental brain injury model. 319 61

Corticomotor evoked potentials have recently been used in experimental animals and patients as a measure of neurologic function after stroke. However, little is known about the fundamental electrophysiologic properties contributing to the formation of these potentials. To define some of these properties, corticomotor evoked potentials were recorded from the contralateral hindlimb in response to transcortical stimulation in cats anesthetized with halothane. These potentials were obtained hourly for 6 hours after middle cerebral artery occlusion. Four major identifiable components were recorded in control responses. Immediately after infarction, all component amplitudes were significantly attenuated. However, after approximately 5 hours, the early latency components exceeded control values; late latency components were also increased. Corresponding somatosensory evoked potentials were abolished and did not return throughout the recording session. Based on classic neurophysiologic studies, the amplitude increment can be explained as combined activation of low-threshold brainstem facilitatory centers and/or direct activation of subcortical axonal pathways. With further study, corticomotor evoked potentials may be a valuable adjunct to current electrophysiologic monitoring techniques, particularly with regard to defining the extent and location of an infarct, as well as to assessing functional recovery.
Stroke
PMID:Early component changes in corticomotor evoked potentials following experimental stroke. 368 90

The location of the postganglionic parasympathetic cell bodies projecting to cerebral arteries is unknown. Using axonal tracing techniques, we examined whether the sphenopalatine ganglia (associated with the seventh cranial nerve) and otic ganglia (associated with ninth cranial nerve) contain perikarya which send axons to the feline middle cerebral artery (MCA). The tracers horseradish peroxidase (HRP: 3 cats) or wheat germ agglutinin (WGA: 6 cats) were applied to the MCA in a slow release polymeric system. Three days later the SPG, otic ganglia, and rete mirabile were harvested bilaterally and processed for tracer by the TMB method (HRP) or immunohistochemistry (WGA). In a given animal, approximately equal numbers of cells containing axonal tracer were found in both SPG. Labeled fibers occasionally could be seen extending into the vidian nerve. Positive cells were also found in the otic ganglia and in the walls of the internal rete mirabile. These results provide the first identification of parasympathetic cell bodies projecting to cerebral blood vessels.
Stroke
PMID:Cerebrovascular projections from the sphenopalatine and otic ganglia to the middle cerebral artery of the cat. 371 48

Previous experimental studies found that acute intoxication may alter the long-term outcome of standardized spinal cord injury resulting in increased spinal cord necrosis and impaired functional recovery. We examined the effects of acute intoxication (blood alcohol concentration of 100 mg/dl) on hemorrhage and axonal conduction three hours after moderate severity spinal cord contusion induced by a constrained stroke pneumatic impactor. The hemorrhagic spinal cord lesion resulting from standardized injury was significantly increased by acute intoxication. Both local hemorrhage at the injury site and rostro-caudal and total extent of hemorrhage were increased. Also, the ability of nerve axons to recover function during the first three hours post-contusion was impaired by intoxication. These findings confirm that increased post-contusion hemorrhage results when spinal cord contusion injury occurs in the presence of acute intoxication, and suggest that increased intramedullary hemorrhage may contribute to previously observed increases in anatomic damage and impaired functional recovery with alcohol intoxication.
 ...
PMID:Effects of acute alcohol intoxication on spinal cord vascular injury. 380 21

In kittens ranging in age from the eighth postnatal day to twentieth week, 288 striate cortex cells were identified as projecting to the dorsal lateral geniculate nucleus (LGN) on the basis of antidromic activation from LGN and of histological localization of cortical layer VI. These cells (C-G cells) were classified as complex, simple, or visually unresponsive, as in the adult. During the second-third postnatal weeks, most of the C-G cells were visually unresponsive. They often showed a marked step in the negative stroke of spikes evoked by single shock stimulation. When paired shocks with short intervals were applied, the second spike fractionated at the step to reveal the A and B components. This tendency was not observed at 8-9 weeks or later. At the second week, all the visually responsive cells were complex, while simple cells were recorded at 3 weeks or later. Until the fourth week, LGN-latencies of complex cells were very long (11-35 ms), although they were the shortest group at each age. Adult-like latencies were first observed at the fifth week in complex cells and at the eighth-ninth weeks in simple cells. The axonal conduction velocities of complex cells attained to the values suggesting myelination at the fifth week, while those of simple cells much later. These results suggest that complex C-G cells may mature prior to simple cells. By comparison with previous results it is also suggested that myelination of the retino-geniculo-cortico-geniculate projections may occur in a retinofugal order.
 ...
PMID:Postnatal development of the corticofugal projection from striate cortex to lateral geniculate nucleus in kittens. 617 79


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>