Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A rare aneurysm in the horizontal segment (A1) of the right anterior cerebral artery was found in a 58-year-old male presenting with subarachnoid hemorrhage. No obvious bleeding source was observed on the day of onset, but 7 days later, a definite diagnosis was made based on the discovery of cerebral vasospasm by a repeat angiogram. The aneurysm was clipped via the right frontotemporal approach 15 days after onset. He suddenly developed neurological symptoms such as consciousness disturbance, right hemiplegia, and aphasia on the 4th postoperative day, when remission of the cerebral vasospasm was confirmed by transcranial Doppler ultrasound examinations and cerebral angiography. The ischemic symptoms were probably due to cerebral embolus caused by intraluminal thrombi, which had formed during the maximum phase of vasospasm and became detached during the remission phase.
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PMID:Aneurysm in the horizontal segment of the anterior cerebral artery confirmed by cerebral vasospasm--case report. 171 62

Operative findings of degenerative changes in pituitary adenomas are not uncommon; however, clinical apoplexy is rare. We report the case of a 43-year-old man who presents a sudden right hemiplegia with aphasia and right ophthalmoplegia, in relation with an ischemic pituitary apoplexy and cerebral vasospasm. A few cases of arterial obstruction or vasospasm associated with pituitary apoplexy have been reported in the literature. Cerebral arterial spasm has also been observed after pituitary surgery. Inclusion of blood or necrotic material in the subarachnoid space seems not to be the only mechanism of vasospasm. The role of hypothalamic dysfunction is considered.
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PMID:[Ischemic pituitary apoplexy and cerebrovascular accident]. 666 2

A 24-year-old woman developed subarachnoid hemorrhage from an aneurysm at the bifurcation of the right internal carotid artery. Following successful clipping of the aneurysm she developed a left hemiplegia associated with focal cerebral vasospasm, which markedly improved when systemic blood pressure was raised with intravenous dopamine infusion. Regional cerebral blood flow and oxygen utilization were significantly depressed in both cerebral hemispheres, while blood volume was significantly elevated only on the side with vasospasm. Oxygen extraction was significantly elevated in both hemispheres, indicating a generalized impairment in oxygen delivery to the brain.
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PMID:Cerebral hemodynamics and metabolism in postoperative cerebral vasospasm and treatment with hypertensive therapy. 727 Dec 44

A patient with cerebral vasospasm following subarachnoid hemorrhage (SAH) was investigated by serial measurement of cerebral blood flow (CBF) using the xenon-133 emission tomography method. The CBF was measured before and after acetazolamide injection. On Day 2 after SAH, there was early local hyperperfusion in the middle cerebral artery (MCA) territory, ipsilateral to the left posterior communicating artery aneurysm. The regional CBF of this arterial territory decreased slightly after acetazolamide injection, probably because of vasoplegia and the "steal" phenomenon, and thus surgery was delayed. A right hemiplegia with aphasia and disturbed consciousness occurred 4 days later (on Day 6 after SAH) due to arterial vasospasm, despite treatment with a calcium-channel blocker. The initial hyperemia of the left MCA territory was followed by ischemia. The vasodilation induced by acetazolamide administration was significantly subnormal until Day 13, at which time CBF and vasoreactivity amplitude returned to normal and the patient's clinical condition improved. Surgery on Day 14 and outcome were without complication. It is concluded that serial CBF measurements plus acetazolamide injection are useful for monitoring the development of cerebral vasospasm to determine the most appropriate time for aneurysm surgery.
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PMID:Abnormal cerebral vasodilation in aneurysmal subarachnoid hemorrhage: use of serial 133Xe cerebral blood flow measurement plus acetazolamide to assess cerebral vasospasm. 841 Feb 15

Reports of intraarterial papaverine infusion as treatment for cerebral vasospasm are few and documented complications are uncommon. The authors report the case of a patient with paradoxical aggravation of cerebral arterial narrowing during selective intraarterial papaverine infusion intended to treat vasospasm following aneurysmal subarachnoid hemorrhage (SAH). A 48-year-old man presented to the authors' service with symptomatic vasospasm 10 days after experiencing an SAH. The ruptured anterior communicating artery aneurysm was surgically obliterated the following day, and thereafter maximum hypervolemic and hypertensive therapies were used. However, the patient remained lethargic, and a stable xenon-computerized tomography (CT) cerebral blood flow (CBF) study revealed CBF to be 15 cc/100 g/minute in the left anterior cerebral artery (ACA) and 25 cc/100 g/minute in the right ACA territories. Cerebral arteriography demonstrated diffuse severe left ACA and mild left middle cerebral artery (MCA) vasospasm. In response intraarterial papaverine was infused into the internal carotid artery just proximal to the ophthalmic artery. During the infusion the patient became aphasic and exhibited right hemiplegia. Arteriography performed immediately after the intraarterial papaverine infusion revealed diffuse exacerbation of vasospasm in the distal ACA and MCA territories. A repeat xenon-CT CBF study showed that CBF in the left ACA and the MCA had drastically decreased (2 cc/100 g/minute and 10 cc/100 g/minute, respectively). Despite aggressive management, infarction ultimately developed. This is the first clinical case to illustrate a paradoxical effect of intraarterial papaverine treatment for vasospasm following aneurysmal SAH. The possible mechanisms of this paradoxical response and potential therapeutic reactions are reviewed.
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PMID:Paradoxical aggravation of vasospasm with papaverine infusion following aneurysmal subarachnoid hemorrhage. Case report. 861 66

This study investigated nonspecific behaviors as early indications of vasospasm following subarachnoid hemorrhage. Although symptoms of vasospasm (e.g., lowered level of consciousness, focal deficits such as hemiplegia or aphasia), are well recognized, the significance of early appearance of nonspecific symptoms such as restlessness, unusual behaviors, and impulsive behavior has not been investigated in detail. The study design included descriptive quantitative elements and a small qualitative component. Nonspecific behaviors were recorded, and the prevalence of those behaviors in individuals developing vasospasm was noted. Of 60 participants, 31 developed vasospasm; 24 of the 31 initially presented with nonspecific behaviors (p < .0001). Early detection of cerebral vasospasm allows prompt intervention and treatment, with the goal of preventing further ischemia or infarction.
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PMID:Nonspecific behaviors as early indications of cerebral vasospasm. 1723 10

Aim to investigate the changes of cerebral microcirculation after subarachnoid hemorrhage (SAH) and its association with cerebral vasospasm (CVS) after SAH. CTP was performed in 85 patients with SAH and 35 controls. Cerebral blood flow (CBF), cerebral blood volume (CBV) and mean transit time (MTT) were recorded for final analysis. CTP parameters were compared between (1) SAH group and control group, (2) CVS group and non-CVS group (nCVS), (3) symptomatic CVS (sCVS) group and asymptomatic CVS (asCVS) group. Compared to control group, there were significant differences in CBF and MTT of SAH patients (P<0.05). Among SAH patients, the CBF and MTT (a decreased CBF and a prolonged MTT) of CVS patients were significantly different from those of non-CVS patients (P<0.05). In 46 CVS patients, sCVS group presented significantly lower CBF and more prolonged MTT than asCVS patients (P<0.05). Seven cases with MTT between 6.31 and 12.72 s showed delayed ischemic neurological deficit (DIND), two of whom had hemiplegia, and one died. Our findings suggest that CTP examination contributes to uncover the changes of cerebral microcirculation after SAH, and the changes of cerebral microcirculation are associated with CVS post SAH.
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PMID:Clinical study of changes of cerebral microcirculation in cerebral vasospasm after SAH. 2111 44

Spinal subarachnoid hemorrhages (SAH) can extend into the intracranial subarachnoid space, but, severe cerebral vasospasm is rare complication of the extension of intracranial SAH from a spinal subarachnoid hematoma. A 67-year-old woman started anticoagulant therapy for unstable angina. The next day, she developed severe back pain and paraplegia. MRI showed intradural and extramedullar low signal intensity at the T2-3, consistent with intradural hematoma. High signal intensity was also noted in the spinal cord from C5 to T4. We removed subarachnoid hematoma compressing the spinal cord. The following day, the patient complained of severe headache. Brain CT revealed SAH around both parietal lobes. Three days later, her consciousness decreased and left hemiplegia also developed. Brain MRI demonstrated multiple cerebral infarctions, mainly in the right posterior cerebral artery territory, left parietal lobe and right watershed area. Conventional cerebral angiography confirmed diffuse severe vasospasm of the cerebral arteries. After intensive care for a month, the patient was transferred to the rehabilitation department. After 6 months, neurologic deterioration improved partially. We speculate that surgeons should anticipate possible delayed neurological complications due to cerebral vasospasm if intracranial SAH is detected after spinal subarachnoid hematoma.
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PMID:Intracranial extension of spinal subarachnoid hematoma causing severe cerebral vasospasm. 2562 17

We report on 2 patients who developed widespread cerebral vasospasm and arterial ischemic strokes (AIS) after application of intrathecal (IT) cytarabine. In a 3-year-old child with acute lymphoblastic leukemia (ALL), left leg weakness, hyperreflexia, and clonus were noted 4 days after her first dose of IT cytarabine during the induction phase of her chemotherapy. Cerebral MRI revealed multiple acute cerebral ischemic infarcts and widespread cerebral vasospasm. A 5-year-old girl complained of right arm and leg pain and began limping 11 days after IT cytarabine. Symptoms progressed to right dense hemiplegia, left gaze deviation, headache, and speech arrest. MRI revealed 2 large cortical areas of diffusion restriction in the right frontal and left parietal lobes. Cerebral magnetic resonance angiography (MRA) showed irregular narrowing affecting much of the intracranial arterial circulation. Although the first child fully recovered from her neurologic symptoms, the second patient had persistent hemiplegia on follow-up. Including this report, there are now 4 pediatric ALL cases of severe cerebral vasospasm and AIS in the context of IT cytarabine administration, strongly suggesting a true association. Differential diagnosis and management issues are discussed. Along with the more widespread use of MRI and MRA, the true frequency of this severe adverse effect will become clearer in future. For any child with neurologic symptoms within hours or days of receiving IT cytarabine, a low threshold for cerebral imaging with MRI and MRA is recommended.
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PMID:Severe Cerebral Vasospasm and Childhood Arterial Ischemic Stroke After Intrathecal Cytarabine. 2678 46

Subarachnoid hemorrhage (SAH) results in significant nerve dysfunction, such as hemiplegia, mood disorders, cognitive and memory impairment. Currently, no clear measures can reduce brain nerve damage. The study of brain nerve protection after SAH is of great significance. We aim to evaluate the protective effects and the possible mechanism of methazolamide in C57BL/6J SAH animal model in vivo and in blood-induced primary cortical neuron (PCNs) cellular model of SAH in vitro. We demonstrate that methazolamide accelerates the recovery of neurological damage, effectively relieves cerebral edema, and improves cognitive function in SAH mice as well as offers neuroprotection in blood- or hemoglobin-treated PCNs and partially restores normal neuronal morphology. In addition, western blot analyses show obviously decreased expression of active caspase-3 in methazolamide-treated SAH mice comparing with vehicle-treated SAH animals. Furthermore, methazolamide effectively inhibits ROS production in PCNs induced by blood exposure or hemoglobin insult. However, methazolamide has no protective effects in morality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice. Given methazolamide, a potent carbonic anhydrase inhibitor, can penetrate the blood-brain barrier and has been used in clinic in the treatment of ocular conditions, it provides potential as a novel therapy for SAH.
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PMID:Methazolamide improves neurological behavior by inhibition of neuron apoptosis in subarachnoid hemorrhage mice. 2773 52


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