Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment for hypertensive cerebellar hemorrhage still remains controversial as to whether direct surgical procedure is indicated or not. This is so even after the introduction of CT scan which easily demonstrates the location and size of the hematoma and the presence of hydrocephalus. In this paper, we present our experience of 20 patients with cerebellar hemorrhage treated by stereotactic evacuation using Komai's CT-stereotactic apparatus. All the patients had vertigo, cerebellar symptoms, dysfunction of brain stem or consciousness disturbance. The hematomas on CT scan were more than 28 mm in diameter. Acute obstructive hydrocephalus occurred in 90% of the patients with hematoma 40 mm or larger in size. The patients with consciousness disturbance were immediately operated on after the attack, and a drainage tube was placed in the hematoma cavity to drain cerebrospinal fluid and liquefied hematoma for one to eight days. On the other hand, when patients with hematoma around 30 mm in diameter complained vertigo for about two weeks, they also were operated on stereotactically. After the operation, their symptoms improved rapidly. The stereotactic operation could aspirate about 85% of the estimated hematoma volume and improved the hydrocephalus, except in one case in which the patient rapidly deteriorated to coma level with a large cerebellar hemorrhage and brain stem damage. This stereotactic evacuation of cerebellar hematoma using a plasminogen activator is effective for not only the removal of hematoma, but also for the treatment of secondary hydrocephalus following obstruction of the fourth ventricle by cerebellar hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stereotactic evacuation of hypertensive cerebellar hemorrhage using plasminogen activator. 267 56

In the past five years, the authors have performed stereotactic evacuation of hypertensive thalamic hematoma using Komai's CT-stereotactic apparatus in 44 cases. Liquefied hematoma was aspirated through a stereotactic cannula, and solid hematoma difficult to aspirate was dissolved by a plasminogen activator (Urokinase) and drained out through a silastic catheter. The mean ratio of the total volume of evacuated hematoma to the estimated volume by CT image was 83.8%. The recovery from motor paresis and consciousness disturbance was observed during the early postoperative days in most patients. Functional outcome (ADL) at 3 months after operation was as follows: 24 cases (54.5%) recovered to a full or partial (self-cared) social life, 15 (34.1%) required partial care at home and 2 (4.5%) remained bedridden. Although 3 patients died within 1 month after operation, the cause of death in these patients was admitted to have no direct relation to operative procedure or to rebleeding due to the Urokinase injection. Postoperative functional prognosis was not affected by the timing of the operation. The important factors affecting ADL were preoperative neurological grade and CT classification. This stereotactic method apparently exceeded the conventional craniotomy method in the functional outcome.
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PMID:[Stereotactic evacuation of hypertensive thalamic hematomas using plasminogen activator (urokinase)]. 351 66

A 75-year-old right-handed woman was admitted to our hospital because of sudden onset of consciousness disturbance. She had taken angiotensin converting enzyme (ACE) inhibitor for hypertension. A neurological examination showed consciousness disturbance, total aphasia, right central facial palsy and right hemiparesis. Diffusion-weighted imaging revealed hyper-intense lesions in the middle cerebral artery territory, particularly in the insular cortex. Magnetic resonance angiography demonstrated occlusion of the left middle cerebral artery. Electrocardiogram monitoring during hospitalization detected an atrial fibrillation. Therefore, we diagnosed her as cardioembolic stroke. She was treated with intravenous alteplase of 0.6 mg/kg. Sixty minutes after alteplase infusion, she developed orolingual angioedema. Immediately she was treated with methylprednisolone intravenously, and the angioedema improved. Orolingual angioedema should be considered as a complication associated with alteplase in a patient who has taking ACE inhibitor.
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PMID:[Orolingual angioedema as complication after rt-PA in stroke patient treated with ACE inhibitor]. 1845 63

We report the use of intravenous tissue plasminogen activator (t-PA) therapy in a 38-year-old patient who was later diagnosed with unilateral moyamoya syndrome. The patient had a sudden onset of unconsciousness, vomiting, dysarthria, and tetraparesis. A neurologic examination revealed consciousness disturbance, right central facial nerve palsy, dysarthria, and tetraparesis with bilateral exotropia and horizontal gaze palsy. A magnetic resonance imaging scan on admission did not reveal fresh cerebral infarction or hemorrhage, but magnetic resonance angiography revealed severe stenosis at the terminal portion of left internal carotid artery, the anterior cerebral arteries, and the right vertebral artery. We suspected infarction of brain stem. The patient was treated with intravenous t-PA approximately 2.5 hours after onset, and the patient demonstrated a remarkable recovery 1 day after onset and had only a minimal deficit at discharge (12 days after onset). Cerebral angiography 7 days after onset confirmed the diagnosis of moyamoya disease. The present case suggests that therapeutic intravenous t-PA may be applicable for an acute ischemic stroke patient coexisting with moyamoya disease after careful evaluation and discussion with patient and family.
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PMID:Intravenous tissue plasminogen activator therapy for an acute ischemic stroke patient with later diagnosed unilateral moyamoya syndrome. 2283 75

Our objective is to present a case of fatal multiple systemic emboli after intravenous thrombolysis for cardioembolic stroke. A 64-year-old woman with atrial fibrillation was admitted for evaluation of sudden consciousness disturbance, right hemiplegia, and aphasia. Diffusion-weighted imaging showed no early ischemic changes of the brain, and magnetic resonance angiography (MRA) showed occlusion of the left middle cerebral artery (MCA). One hour after initiation of 0.6 mg/kg of intravenous alteplase, the MCA was partially recanalized. Her symptoms disappeared the following day. We began intravenous heparin for secondary prevention of cardioembolic stroke. However, on the third day (52 hours after thrombolysis), she suddenly developed a coma and left hemiplegia. MRA showed acute occlusion of the right internal carotid artery (ICA). She developed acute kidney injury and sudden shock and then died of fatal cardiorespiratory arrest on the fourth day. Autopsy revealed occlusion of the mitral valve orifice by a spherical fresh red thrombus that led from the left atrial appendage. Acute embolic infarcts were identified in the spleen and right kidney, the latter secondary to occlusion of the right renal artery with fresh red thrombus. Intravenous thrombolysis and subsequent anticoagulation therapy may destabilize pre-existing intracardiac thrombus, potentially leading to recurrent stroke, multiple systemic embolisms, and the fatal "hole-in-one" effect.
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PMID:Fatal multiple systemic emboli after intravenous thrombolysis for cardioembolic stroke. 2354 21