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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fasted Wistar rats were subjected to either a mild mechanical injury, 6 min of transient forebrain ischemia, or a mild mechanical injury followed 1 h later by 6 min of forebrain ischemia. EEG and evoked potentials were assessed intermittently and morphological analyses were performed after 7 days postinjury survival. In all groups complete qualitative recovery of electrical activity and general behavior was observed with 7-day survival. However, rats subjected to combined concussion and ischemia displayed EEG spike activity and a delayed return of EEG and evoked potentials during acute recovery not evident in other groups. No overt neuronal cell loss was seen in trauma alone and was minimal or absent in ischemia alone. However, extensive bilateral CA1 and subicular pyramidal cell loss was found in the septal and mid-dorsal hippocampi in the combined trauma and ischemia group. In contrast, no overt axonal injury was found in any group. We conclude that even mild mechanical injury can potentiate selective ischemic hippocampal neuronal necrosis in the absence of overt axonal injury. This potentiation also occurs in conjunction with more generalized electrophysiological disturbances such as EEG evidence of postischemic neuronal hyperactivity suggesting that mild concussion may also decrease the threshold for post-ischemic neuronal excitation. These results suggest the potential of this model for examining common or different injury mechanisms in mechanical and ischemic brain injury.
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PMID:Increased vulnerability of the mildly traumatized rat brain to cerebral ischemia: the use of controlled secondary ischemia as a research tool to identify common or different mechanisms contributing to mechanical and ischemic brain injury. 270 84

We investigated the neuronal distribution of microtubule-associated protein 2 in gerbil brain and monitored the progression of ischemic damage immunohistochemically by using this protein as a dendritic marker. The reaction for microtubule-associated protein 2 in normal gerbil brain clearly visualized neuronal soma and dendrites but other structures such as axonal bundles, glia and endothelial cells exhibited little immunoreactivity. In a reproducible gerbil model of unilateral cerebral ischemia, we could detect the ischemic lesions as early as 3 min after right common carotid occlusion at the subiculum-CA1 region of the ipsilateral hippocampus as faint loss of the reaction in the dendrites. After ischemia for 30 min, the ischemic lesions were clearly detected as loss of the reaction in the nerve cell bodies, dendrites and the neuropil in the hippocampus, cerebral cortex, thalamus and the caudoputamen. Although the mechanism for prompt disappearance of the immunohistochemical reaction for microtubule-associated protein 2 is not clear, the present investigation suggests that dendrites in the vulnerable regions may be quite susceptible to ischemic stress and that the immunohistochemical procedure for microtubule-associated protein 2 may be very useful for demonstration of dendritic damage in various pathophysiological states of the central nervous system.
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PMID:Microtubule-associated protein 2 as a sensitive marker for cerebral ischemic damage--immunohistochemical investigation of dendritic damage. 279 44

Incomplete infarction of the tibial nerve was produced in 37 rats by injecting arachidonic acid into the femoral artery. Sciatic-tibial motor nerve conduction studies were performed 1, 2, 3 and 7 days later. In all animals the evoked motor responses were of low amplitude and morphological examination showed axonal degeneration. In 20 rats the response elicited by proximal stimulation was of lower amplitude than the distal response indicating focal conduction block in a proportion of those axons which had survived the ischemia and were not degenerating distally. The conduction block resolved over several days and in all but one rat had disappeared by 7 days. Morphological examination of semithin sections and single teased myelinated axons revealed no evidence of segmental demyelination. The rapid resolution of conduction block and the lack of significant segmental demyelination suggest that it has a metabolic basis. We suggest that hypoperfusion of the subperineurial region of the proximal tibial nerve, the region surrounding the infarct through which surviving axons pass, may be sufficient to temporarily block impulse transmission in these surviving axons without producing morphological changes.
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PMID:Conduction block without demyelination following acute nerve infarction. 283 41

We describe a patient with chronic multifocal demyelinating neuropathy associated with persistent conduction block. Multifascicular lesions in sural nerve included a complete loss of myelinated fibers, demyelination, remyelination, onion bulb formation, and axonal attenuation. On the basis of these morphometric results we hypothesize that nerve ischemia may be involved in the pathogenesis of chronic multifocal demyelinating neuropathy.
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PMID:Is ischemia implicated in chronic multifocal demyelinating neuropathy? 277 Oct 81

We report a case of a mixed sensorimotor, predominantly axonal mononeuritis multiplex that developed after a severe meningococcal septicemia and disseminated intravascular coagulation (DIC) with associated distal limb necrosis. Ischemia resulting from the DIC-induced multiple vascular occlusions is suggested as the leading cause of this neuropathy.
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PMID:Peripheral neuropathy in meningococcal septicemia. 299 4

Functional activity of the Golgi apparatus in postischemic neurons was evaluated by using thiamine pyrophosphatase (TPPase) activity as an histochemical marker for the trans cisternae. Ischemia was produced in rats by permanent occlusion of vertebral arteries and 30-minute occlusion of the carotid arteries. This insult produces irreversible ischemic injury to neurons in the striatum and CA1 zone of hippocampus but only reversible injury to neurons in the paramedian cortex and CA3 hippocampus. The number of neurons with TPPase activity in controls correlated in part with neuronal size and was found in greater than 90% of neurons in cortex and CA3 hippocampus, 70% in CA1 hippocampus, and 40% in striatum. Ischemia plus recirculation for 30 minutes resulted in a decrease in the number of neurons with TPPase activity by 50% in CA1 hippocampus and by 80% in the three other areas. Resistant neurons in cortex and CA3 hippocampus showed partial recovery of TPPase activity by 2 hours after ischemia although the number of neurons was still less than that in controls (55% and 72%, respectively; p less than 0.01). At 24 and 48 hours, TPPase activity in cortical and CA3 neurons was similar to controls. In contrast, irreversibly injured neurons in striatum and CA1 hippocampus showed a persistent loss of TPPase activity during the entire postischemic period. Furthermore, TPPase activity remained significantly decreased in CA1 hippocampus even though previous studies in our laboratory indicated partial recovery of Golgi cisternae before subsequent cell death at 48 to 72 hours. Since TPPase activity has been correlated with functional activity within the Golgi apparatus these results suggest that glycosylation of glycoproteins and glycolipids may be markedly impaired in neurons after cerebral ischemia. The persistent abnormalities in Golgi function may contribute to the development of irreversible injury by interfering with the normal maintenance of plasma membranes and axonal transport.
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PMID:Postischemic alterations in ultrastructural cytochemistry of neuronal Golgi apparatus. 302 52

Spinal stenosis, which may be congenital/developmental or acquired in origin, is a narrowing of the spinal canal, nerve root canals, or intervertebral foramina. Compression of the spinal cord or nerve roots may lead to structural neuronal damage, neuronal ischemia or edema, and axonal transport block. The most frequent symptom in patients with spinal stenosis is back pain and some have classic neurogenic claudication. We have performed urodynamic evaluations in 2 patients with combined cervical and lumbar spinal stenosis. A girl with achondroplastic dwarfism had urgency incontinence and detrusor hyperreflexia. An adult man with acquired degenerative spinal stenosis had difficulty voiding and findings compatible with the cauda equina syndrome.
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PMID:Urodynamic evaluation of patients with spinal stenosis. 318 19

Experimental spinal cord injury in animals induced by weight drop produces neurological deficit and paralysis. Correlation of the progressive morphological changes in the lesion by both light and electron microscopy with the biochemical alterations revealed ischemia, edema, hemorrhage, tissue necrosis, granular changes in axons, vesicular degeneration of myelin and axonal calcification. The biochemical pathology was that of degradation of axonal (neurofilaments) and myelin proteins (MBP and PLP) with increased activities of proteolytic enzymes and particularly the neutral proteinase. The level of total calcium increased progressively in the lesion to a peak at 8 hrs. and subsequently remained constant thereafter. The capacity of calcium for activating proteinases and lipases and fostering the degradation of axon and myelin proteins as well as the liberation of arachidonic acid required for the synthesis of prostanoids must be relevant. An increased production of prostanoids is indicated by elevation of thromboxane (TxB2), a stable metabolite of TXA2 at 1 hour after injury. The 6-keto-PG1(1)a was also increased but to a lesser extent. We suspect that the activation of arachidonic acid metabolism contributes to post-traumatic vascular injury and the progressive ischemia. These putative roles for calcium in proteolysis and lipolysis, inducing degradation of macromolecules and production of prostanoids which initiate edema, lysolecithin a myelinolytic factor and mitochondrial dysfunction in spinal cord injury are discussed.
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PMID:The multimolecular cascade of spinal cord injury. Studies on prostanoids, calcium, and proteinases. 332 36

A spectacular spongiotic lesion, symmetrical in distribution and restricted to the pars reticulata of the substantia nigra (SNPR) has recently been described in hyperglycemic rats surviving 1-18 h after a brief period of transient ischemia. The purpose of this study was to clarify the pathogenesis of the lesion. In order to study whether the lesion was due to changes occurring during ischemia, local cerebral blood flow (l-CBF) and energy metabolites were measured in the substantia nigra (SN) and in other brain areas. Furthermore, brains were examined by light and electron microscopy immediately after ischemia and in the early recirculation period. Autoradiographic CBF measurements showed ischemia flow levels in the SN of 30-40% of control, similar in normo- and hyperglycemic rats. Thus, although ischemic, this structure had a considerable amount of residual flow. There was also a corresponding partial preservation of the adenylate energy charge. However, lactate levels were high, and in hyperglycemic subjects they rose to values previously described during status epilepticus (about 25 mumol/g). In hyperglycemic animals, neuronal alterations were consistently present in SNPR by the end of the 10-min period of ischemia. They included clumping of nuclear chromatin and subplasmalemmal clearing of the perikaryon. Some mitochondrial swelling was present in neuronal perikarya and in dendrites. The normal alignment of microtubules in the dendrites was disturbed, but there was no or only slight swelling of the dendrites. Aggregation of synaptic vesicles was a conspicuous finding in axonal terminals, which were also slightly swollen. Otherwise, the axons appeared largely spared. Microvessels looked quite intact. Similar cellular changes were observed in the early recovery period. Dendrites, however, started to swell, and their expansion finally caused the spongiotic appearance of the pars reticulata. The appearance of the dendritic lesions is strongly suggestive of transmitter-mediated ("excitotoxic") damage. However, it seems likely that the marked acidosis is injurious as well. We tentatively conclude that both mechanisms interact to give the final lesion. The results, and those previously obtained in epileptic seizures, suggest that mitochondria of SN neurons and neuronal processes are particularly prone to damage.
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PMID:Pathogenesis of substantia nigra lesions following hyperglycemic ischemia: changes in energy metabolites, cerebral blood flow, and morphology of pars reticulata in a rat model of ischemia. 336 99

Current-generation CT scanners enable the visualization in vivo of structures and substructures that were previously unobservable. Certainly the orbit and optic nerve/sheath complex have demonstrated a great number of pathologic and normal anatomic variations. It has been found in patients with elevated intracranial pressure that what was previously thought to be simple papilledema in fact masks a surprisingly large component of optic papilla protrusion. There may be a variable amount of increased intercellular/axonal fluid within the optic disk in patients with increased intracranial pressure; however, a significant factor in the "swollen disk" is the simple transmission of pressure along the optic nerve sheath to the papilla, causing it to bulge. Further investigations with dynamic CT reveal that there is decreased perfusion of the optic disk in the active phase of severe increased intracranial pressure in patients with papilledema and/or protrusion as compared with normal control subjects. This depressed flow pattern seems to originate subacutely and appears to resolve in certain patients after normalization of the elevated pressure. These findings apparently indicate that clinical intervention in cases of intracranial hypertension to restore the hemodynamic status of the optic disk would be timely, and thereby avert irreversible damage. This suggests and supports the theory that increased intracranial pressure may lead to rapid vision loss by the mechanical mechanism of pressure projected directly to the junction of the optic nerve and optic nerve head, leading to decreased perfusion, ischemia, axonal flow stasis, and resultant optic nerve atrophy.
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PMID:"Papilledema": neuroradiologic evaluation of optic disk protrusion with dynamic orbital CT. 349 33


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