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

The authors report the observation of a 61-year-old female patient who, following a right frontal-temporal ischemia, presented disorientation with respect to her surroundings. She was convinced during her hospital stay that her house had been transformed into a hospital. There was no evidence of intellectual confusion or deterioration, and the neuropsychological examination revealed visuo-spatial disturbances only. A low basal cerebral blood flow was found in the right anterior hemisphere which further decreased when the patient was asked where he was. It is hypothesized that confabulatory responses corresponded to a disinhibition of the left hemisphere from the control of the hemisphere dominant in dealing with visuo-spatial data.
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PMID:[The delusion of place: contribution of the measurement of cerebral deficit]. 326 38

The clinical syndrome of border-zone ischemia is described in eight patients. Cerebral damage in four occurred during or after cardiac surgery and the other four patients had each experienced a period of severe hypotension. Cerebral blindness and visual disorientation are the most regular features and are produced by ischemic lesions in the parieto-occipital region, the common border-zone territory between all three arterial territories. Some patients show bibrachial sensorimotor impairment and a disturbance of volitional saccadic eye movement caused by more anteriorly placed ischemia in the anterior-middle artery border zone. Some show a temporary dyslexia/dysgraphia and memory defect related to bilateral parietotemporal lesions in the middle-posterior border zone.
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PMID:Clinical features of ischemia in cerebral arterial border zones after periods of reduced cerebral blood flow. 361 13

Fifteen right-handed patients with Multi-Infarct Dementia underwent cognitive testing by the Jacobs Mini-Mental Scale (MMQ), and xenon contrast CT scanning. Local cerebral blood flow (LCBF) and local partition coefficient (L lambda) values were measured by stable xenon contrast CT scanning and potential methodological errors were discussed. Reduced values were graded: 0 = normal, 1 = mild, 2 = moderate, 3 = severe. Graded values were pooled and plotted on composite brain maps to display locations of abnormal L lambda and LCBF values. Topographic brain maps, showing most frequent locations of reduced L lambda values, confirmed the common anatomical locations of multiple cerebral infarcts to be distributed in both thalami, temporal lobes, basal ganglia, left internal capsule and right cingulate cortex. Gray matter flow values were reduced in similar cortical and subcortical regions. There were no correlations between MMQ scores and reduced LCBF values for caudate and lenticular nuclei. Direct and statistically significant correlations were found between reduced MMQ scores and mean LCBF values for left or right frontal cortex, left or right temporal cortex and left or right thalamus. Subgrouping MMQ tests according to functions assessed, indicated that left mid-temporal ischemia correlated with dyscalculia and memory disturbances while ischemia of both frontal lobes correlated with disorientation to time and place.
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PMID:CT-CBF correlations of cognitive deficits in multi-infarct dementia. 650 9

Cortical blindness is defined as a loss of vision due to bilateral retrogeniculate lesions (geniculocalcarine blindness). Gerstmann's syndrome is a combination of disorientation for left and right, finger agnosia, and profound agraphia, alexia, and acalculia. It is due to a lesion in the left angular gyrus, situated at the confluence of the temporal, parietal, and occipital lobes. We report on a patient who suffered from severe underdiagnosed eclampsia and who developed bilateral extensive medial temporal, parietal, and calcarine ischemic infarctions during an eclamptic fit. In addition, ischemia destroyed the left angular gyrus. The combination of these lesions led to Gerstmann's syndrome with additional cortical agnosia and cortical diplopia. For the first few months following the ischemic insult, the patient had been cortically blind. Thereafter, the patient slowly regained a visual acuity of 0.1 in both eyes. She then experienced monocular and binocular diplopia. Her ocular motility was normal; there was no phoria or tropia. Monocular and binocular diplopia slowly became less severe over the following year. Now, 2 years after the incident, the patient has a visual acuity of 0.2 in both eyes and no double vision. However, the handicapping symptoms of Gerstmann's syndrome, which make leading a normal life impossible, have persisted--the patient still cannot cope alone, mainly due to the severe disorientation for left and right. The picture of cortical agnosia, cortical diplopia, and Gerstmann's syndrome is a very rare combination. Visual recovery and rehabilitation in cortical blindness are severely affected and made difficult by the symptoms of Gerstmann's syndrome. In our case the reason for such a dramatic clinical picture was eclampsia, whose prodomes had not been diagnosed in time.
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PMID:Eclamptogenic Gerstmann's syndrome in combination with cortical agnosia and cortical diplopia. 749 36

Extracranial-intracranial (EC-IC) bypass grafting procedures were specially designed for treatment of bilateral internal carotid artery occlusion. When performed in an expeditious manner, EC-IC bypass procedures have produced effective and durable results, despite the recent disfavor given to this procedure. This communication reports a 68-year-old white man who developed generalized cerebral ischemia manifested as confusion, incoherence, disorientation, ataxia, and numerous episodes of syncope daily. A cerebral angiogram revealed bilateral external carotid arteries and left solitary vertebral artery critical stenosis. Transcranial Doppler study demonstrated reduction of cerebral and vertebral-basilar perfusion. However, the patient's EC-IC bypass graft had remained patent since 1985. The patient's recurrent symptoms of global ischemia and syncope resolved after carotid endarterectomy, vein patch external carotid artery, and vertebral-to-common carotid artery transposition. This report reiterates the value of the EC-IC bypass procedure and presents the surgical management of symptomatic external carotid and vertebral artery stenosis in patients after EC-IC bypass procedures.
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PMID:Revascularization of cerebral ischemia after previous bilateral extracranial-intracranial bypass procedures. 947 4

The authors report a rare case in which a large cerebral arteriovenous malformation (AVM) located in the left parietooccipital region presented with venous ischemia in the contralateral hemisphere. A 74-year-old man was admitted to the hospital because he was experiencing a loss of appetite, disorientation, and left hemiparesis. Computerized tomography scans revealed a low-density area in the right temporal lobe. Angiography demonstrated a large AVM in the left parietooccipital lobe and dilation, stagnation, and meanders of cortical veins in the contralateral hemisphere. The authors speculated that the elevated sinus pressure caused by a huge venous return of blood from the AVM produced venous ischemia in the contralateral hemisphere.
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PMID:Large cerebral arteriovenous malformation presenting with venous ischemia in the contralateral hemisphere. Case report. 1240 94

A 56-year-old man presented with fever, disorientation, and testicular pain. He was receiving azathioprine immunosuppression for autoimmune hepatitis. Orchiectomy identified occlusion of spermatic cord vessels by intravascular large B-cell lymphoma (IVLBL) and ischemic changes in the testis. Tumor cells were positive for CD 10, CD 20, CD 30, and Epstein-Barr virus (EBV) latent membrane protein 1 (LMP-1) and early region RNA (EBER). He was treated with the cessation of azathioprine, chemotherapy, anti-CD 20 immunotherapy, and radiotherapy. Twenty months after diagnosis, he is alive with no evidence of lymphoma or hepatitis. This is the first report of IVLBL presenting with testicular ischemia. It highlights the importance of prompt diagnosis and intervention to achieve durable response. That this lymphoma arose in the setting of immunosuppressive therapy introduces additional complexity relating to pathogenesis, clinical behavior, and treatment.
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PMID:Testicular ischemia due to intravascular large B-cell lymphoma: a novel presentation in an immunosuppressed individual. 1461 32

We are presenting the case of a 63 year-old man with a dural arteriovenous malformation of the transverse sigmoid sinus who developed focal deficits followed by less localized symptoms such a disorientation, lethargy and eventually comatose status. Initial cerebral angiography showed retrograde filling of the cortical and deep cerebral venous system with marked delay in venous empting. Following embolization clinical symptoms completely cleared at the time that control angiography showed retrograde venous flow turning anterograde. Patient's symptoms recurred four months later when there was a relapse of retrograde cerebral venous drainage at the time he developed thrombosis of the superior longitudinal and right transverse sinuses. Sinus thrombosis and thrombosis of the central retinal artery were coincidental with hypercoagulability related to hyperhomocysteinemia. Since control angiography still showed persistence of the AV shunting radical excision of the involved dural sinuses was performed. The final outcome was excellent. The physiopathological mechanism responsible for neurological deficits in our patient most likely was ischemia of venous origin secondary to venous hypertension resulting from retrograde cerebral venous drainage. The clinical and angiographic presentation in few similar cases reported in the literature is reviewed.
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PMID:Unruptured dural arteriovenous malformation of the transverse-sigmoid sinus presenting with focal symptoms and coma. 1555 3

Dendrites and spines undergo dynamic changes in physiological conditions, such as learning and memory, and in pathological conditions, such as Alzheimer's disease and epilepsy. Long-term dendritic plasticity has also been reported after ischemia/hypoxia, which might be compensatory effects of surviving neurons for the functional recovery after the insults. However, the dendritic changes shortly after ischemia, which might be associated with the pathogenesis of ischemic cell death, remain largely unknown. To reveal the morphological changes of ischemia-vulnerable neurons after ischemia, the present study investigated the alteration of dendritic arborization of CA1 pyramidal neurons in rats after transient cerebral ischemia using intracellular staining technique in vivo. The general appearance of dendritic arborization of CA1 neurons within 48 h after ischemia was similar to that of control neurons. However, a dramatic increase of dendritic disorientation was observed after ischemia with many basal dendrites coursed into the territory of apical dendrites and apical dendrites branched into the region of basal dendrites. In addition, a significant increase of apical dendritic length was found 24 h after ischemia. The increase of dendritic length after ischemia was mainly due to the dendritic sprouting rather than the extension of individual dendrites, which mainly occurred in the middle segment of the apical dendrites. These results reveal a plasticity change in dendritic arborization of CA1 neurons shortly after cerebral ischemia.
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PMID:Dendritic plasticity of CA1 pyramidal neurons after transient global ischemia. 1652 77

This is the case report of a 44-year-old woman presented with an acute stroke immediately after electroconvulsive therapy (ECT). The patient had no significant medical history other than chronic depression. She was taking sertraline, and she had had multiple previous ECT treatments without any complications. While being monitored in the recovery room within 10 minutes after the last ECT session, she was found to have sudden onset of left-sided flaccid hemiplegia and numbness along with slurred speech. On arrival to our hospital, she was found to have flaccid hemiplegia on the left side involving the face, arm, and leg (face and arm more than the leg involvement), severe dysarthria, and mild neglect syndrome (National Health Institute Stroke Scale of 14). Noncontrast computed tomography (CT) of the head showed no signs of early ischemia, and iodine contrast CT angiography revealed right middle cerebral artery (MCA) (distal M1 segment) clot. Patient received intravenous recombinant tissue plasminogen (rt-PA) at 2.5 hours after the onset of symptoms, and then a total of 3.0 mg of intra-arterial (IA) rt-PA. Angiography at the end of the procedure showed successful recanalization of the M1 segment and normal vessel caliber with adequate distal flow. After the procedure, the patient made rapid improvements in all of her initial symptoms during the first 24 hours. An extensive stroke workup failed to reveal any cause of the stroke, including usual stroke and hypercoagulable risk factors. This was an acute embolic stroke immediately following an ECT, and without the aggressive thrombolytic therapy, the patient's outcome would have been poor because there was an M1 segment clot with a major MCA syndrome with relatively high National Institute of Health Stroke Scale. The neurological side effect profile of ECT is reported to be minimal with most common symptoms being headache, disorientation, and memory complaints. There is no clear cause-and-effect relationship in this case, and the stroke after ECT is extremely rare. In such rare event of stroke while receiving ECT, there is an effective treatment available using both intravenous and IA thrombolysis as reported in this case.
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PMID:Acute embolic stroke after electroconvulsive therapy. 1663 11


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