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

A series of 17 patients aged from 9 months to 32 years with refractory epilepsy due to hypothalamic hamartoma were treated by total removal (one case) and disconnection (16 cases) between 1997 and 2002. The mean age at seizure onset was 16 months. Sixteen patients had gelastic seizures, 14 had partial seizures and three had generalized tonic-clonic seizures. The mean seizure frequency was 21 per day. Four patients had borderline intelligence quotient and the others were mentally retarded. Five patients presented with precocious puberty, one with acromegaly, and four suffered from obesity. Brain magnetic resonance imaging, performed at least twice in each patient, showed the hamartoma as a stable homogeneous interpeduncular mass implanted either on the mammilary tubercle or on the wall of the third ventricle with variable extension to the bottom. Ictal single photon emission computed tomography, performed in four patients, showed hyperperfusion within the hamartoma in two patients. Twenty-five operations were performed in the 17 patients. The first patient underwent total removal of the hamartoma, whereas the following 16 patients underwent disconnection through open surgery (14 procedures) and/or endoscopy (9 procedures). Eight patients became seizure-free, one patient had only brief gelastic seizures, and eight patients were dramatically improved with a mean follow up of 18.6 months (8 days to 43 months). Surgery was safe in all but two patients: the first patient had transient hemiplegia and the third cranial nerve paresis, and the other developed hemiplegia due to ischemia of the middle cerebral artery territory. The quality of life, and behavior and school performance were greatly improved in most patients. Our series illustrates the feasibility and relative safety of disconnection surgery for hypothalamic hamartomas with seizure relief in 53% of patients and dramatic improvement in the others. Surgical observations led us to propose a new anatomical classification according to the anatomical relationship between the hamartoma and the adjacent hypothalamus and third ventricle. Endoscopic disconnection seems to be a very safe way to treat hamartomas in intraventricular locations.
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PMID:Disconnecting surgical treatment of hypothalamic hamartoma in children and adults with refractory epilepsy and proposal of a new classification. 1262 81

A 63-year-old man presenting remittent fever and multiple arthralgia was diagnosed as adult-onset Still's disease (AOSD), and started with prednisolone treatment. However, he suddenly developed loss of consciousness, paresis of the right upper extremity and aphasia shortly after the treatment. We detected an increased signal of brain tissue lactate at the branch territory of left middle cerebral artery by MR spectroscopy (MRS), but no lesions by diffusion-weighted nor T2-weighted MRI, suggesting acute brain ischemia of embolic mechanism. Most of the symptoms resolved in a couple of hours after the onset, showing spectacular shrinking deficit (SSD). The patient also revealed complication of antiphospholipid antibody syndrome (APS), which may be associated with ischemic event. This is the first case of acute brain ischemia with SSD, which occurred in AOSD with APS. MRS was superior to diffusion MRI in detection of acute brain ischemia.
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PMID:[A case of brain ischemia presenting spectacular shrinking deficit in adult-onset Still's disease associated with antiphospholipid antibody syndrome]. 1266 Nov 9

After atraumatic birth, three neonates presented with muscle hypotonia and weakness. Flaccid paresis of the upper extremities, spasticity of the lower extremities, dissociate sensory loss and autonomic dysfunction developed later. This ruled out the initial, tentative diagnoses of cerebral palsy, spinal muscular atrophy or hereditary neuropathy. Diagnostic imaging revealed marked thinning of the cervical spinal cord in all patients. The possible aetiology of these lesions is considered. In all cases, an antenatal or perinatal infarction is thought to be the most probable cause. Different clinical pictures following intrauterine spinal cord ischemia are discussed. Spinal cord lesion must be considered even after atraumatic birth.
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PMID:Cervical spinal cord atrophy in the atraumatically born neonate: one form of prenatal or perinatal ischaemic insult? 1269 May 68

Recent experiences from several centers indicate that the overall risk of spinal cord ischemia during thoracoabdominal aortic aneurysm repair has decreased to 5-8%. The results from these centers are rather consistent, despite the use of a variety of spinal protection strategies. An alternative to the various distal aortic perfusion techniques is selective spinal cooling by cold saline lavage. The principle advantage of selective hypothermia is the avoidance systemic heparinization and extracorporeal by-passes, while affording comparable spinal protection. The primary method of spinal cooling was pioneered by Cambria et al. at Massachusetts General Hospital. In their experience, paraplegia or paresis occurred in 6.9% of patients (5-year period, 170 cases). An alternative to the Cambria method utilizes readily available perfusion supplies and offers the potential advantages of lower cerebral spinal fluid-systemic blood pressure differences, more expedient cooling, and deeper spinal hypothermia. This report describes this method and the clinical course of a patient treated with it.
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PMID:Selective deep spinal hypothermia with vacuum-assisted cerebral spinal fluid drainage for thoracoabdominal aortic surgery. 1293 25

Early recognition of limb ischemia may allow prompt, effective therapy for peripheral arterial injuries. A review of cases of peripheral arterial trauma at the Toronto General Hospital since 1953 revealed that 50% of the injuries were not immediately recognized. An expanding hematoma, pulsatile hemorrhage or the onset of a bruit and thrill signifies arterial damage in penetrating wounds. Ischemia may be difficult to recognize in patients with soft tissue or skeletal trauma, but the presence of distal pallor, coolness, paresis, cyanosis, anesthesia, poor capillary refill and disproportionate pain indicates significant arterial damage and necessitates surgical exploration. The diagnosis of arterial "spasm" in such instances is untenable and can only be made after direct inspection, or on the return of pulses after reduction of a fracture or release of a tight cast. Restoration of arterial continuity by end-to-end anastomosis is the recommended technique for all arterial injuries, since after ligation of even minor vessels, ischemia may ensue, and amputation may occasionally be necessary.
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PMID:THE RECOGNITION AND MANAGEMENT OF PERIPHERAL ARTERIAL INJURIES. 1428 3

In 1891 Georg Avellis described a so-called "laryngeal hemiplegia" that can be caused by peripheral lesions of the vagal and glossopharyngeal nerves and rarely by infarctions of the medulla oblongata, thus representing a classical brainstem syndrome. In this study we describe two patients with an Avellis' syndrome caused by brainstem ischemia. Contemporary publications about Avellis' syndrome in brainstem lesions seem to be very inhomogenous. They report various diseases with unilateral laryngeal palsy due to nucleus ambiguus lesions with diverse additional neurological symptoms. We conclude that according to Avellis' original description only the combination of ipsilateral palatolaryngeal paresis and contralateral hemiparesis and/or hemihypesthesia should to be interpreted as Avellis' syndrome.
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PMID:[Avellis' syndrome in brainstem infarctions]. 1466 Nov 58

The etiology of benign paroxysmal positioning vertigo (h-BPPV) of the horizontal semicircular is unknown. Insight was obtained from two patients with h-BPPV and associated hearing impairment. Based on the different inner ear lesion patterns in neurolabyrinthitis contrary to ischemic labyrinthine infarction we assessed multiple vestibulo-cochlear functions for the first time in two patients who suffered from h-BPPV with sudden unilateral hearing loss. While in patient no. 1 the lesion pattern (posterior canal paresis in addition to the sudden hearing loss) could possibly be caused by ischemia of the common cochlear artery, the lesion pattern of patient no. 2 (hearing loss and ipsilateral paresis of the posterior and horizontal semicircular canal) exceeds the typical vascular labyrinthine territories and may indicate viral neurolabyrinthitis.
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PMID:Horizontal canal benign paroxysmal positioning vertigo with ipsilateral hearing loss. 1469 85

A 29-yr-old chimpanzee (Pan troglodytes) presented after an acute onset of right facial and forearm paresis that progressed to paralysis within 24 hr, with subsequent development of right leg paresis. Magnetic resonance imaging (MRI) of the head revealed an abnormal region of increased signal intensity in the left frontal, parietal, and temporal cerebral hemispheres, corresponding to the vascular territory of the middle cerebral artery, with resultant compression of the left lateral ventricle. The findings were consistent with a cerebral infarct (stroke). MRI is the most sensitive test for early detection of cerebral changes due to ischemia and was essential in obtaining a diagnosis in this case. The chimpanzee responded well to treatment with long-term anticoagulant aspirin and a short, tapered course of prednisone and regained full gross motor function.
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PMID:Diagnosis and treatment of a cerebral infarct in a chimpanzee (Pan troglodytes). 1530 16

Peripheral nerve pathology related to chronic hyperinsulinemia and hypoglycemia has yet to be fully explored. Here we conducted a systematic quantitative analysis of morphological alterations in peripheral sensory and motor nerve fibers and endoneurial microvasculature in longstanding insulinoma-carrying rats (I-rats; n=12). Age-matched normal rats (n=6) served as controls. Over the 15-month observation period, two of I-rats developed paresis of the hind limbs when their blood glucose level fell below 1.7 mmol/l. These animals showed a massive myelinated fiber loss associated with active degeneration of residual myelinated fibers and multiple endoneurial microvascular occlusions at the sciatic nerve level. The rest of the non-paretic I-rats showed a decreased density of large myelinated fibers with axonal degeneration in the peroneal nerve and an increased density of small myelinated fibers with preserved morphology in the sural nerve. This was associated with endoneurial microangiopathic changes indicative of endoneurial ischemia/hypoxia in the sciatic and peroneal nerves, and an increase in endoneurial microvascular density in the sciatic and sural nerves. In conjunction with previous data, these findings suggest that the observed increase in endoneurial microvascular density may be a compensatory response to endoneurial ischemia/hypoxia induced by chronic hyperinsulinemia in I-rats without paresis. In conclusion, the present study showed characteristic morphological alterations in peripheral sensory and motor nerve fibers associated with microangiopathy indicative of endoneurial ischemia/hypoxia in the sciatic and peroneal nerves, and provides the first evidence for the occurrence of endoneurial necrosis in the sciatic nerve, to which the hind limb paresis can be ascribed in I-rats.
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PMID:Peripheral nerve endoneurial microangiopathy and necrosis in rats with insulinoma. 1536 26

Cerebral ischemia was produced by moderate compression for 30 min of a specific brain area in the sensorimotor cortex of Sprague-Dawley rats. On day 1, that is 24 h after the transient sensorimotor compression, ischemia-exposed animals displayed a marked focal neurological deficit documented as impaired beam walking performance. This functional disturbance was mainly due to contralateral fore- and hind-limb paresis. As assessed by daily beam walking tests it was shown that there was a spontaneous recovery of motor functions over a period of five to seven days after the ischemic event. Using histopathological analysis (Nissl staining) we have previously reported that the present experimental paradigm does not produce pannecrosis (tissue cavitation) despite the highly reproducible focal neurological deficit. We now show how staining with fluorescent markers for neuronal death, that is Fluoro-Jade and TUNEL, respectively, identifies regional patterns of selective neuronal death. These observations add further support to the working hypothesis that the brain damage caused by cortical compression-induced ischemia consists of scattered, degenerating neurons in specific brain regions. Postsurgical administration of the AMPA receptor specific antagonist, LY326325 (30 mg/kg; i.p., 70 min after compression), not only improved beam walking performance on day 1 to 3, respectively but also significantly reduced the number of Fluoro-Jade stained neurons on day 5. These results suggest that enhanced AMPA/glutamate receptor activity is at least partially responsible for the ischemia-produced brain damage detected by the fluorescent marker Fluoro-Jade.
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PMID:Fluoro-Jade and TUNEL staining as useful tools to identify ischemic brain damage following moderate extradural compression of sensorimotor cortex. 1536 48


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