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Biomedical subjects

O Busse

Publications and source records attributed to O Busse.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Zoster neuralgia].

Explore the source record for details and available documents.

Diagnosis, Differential↗
PubMed1995

[Granulomatous vasculitis of the CNS as a complication of herpes zoster ophthalmicus].

A 61-year old man with a history of arterial hypertension suffered a left HZO, and was treated with acyclovir. Three weeks later he suddenly developed moderate left hemiparesis particularly of the leg, severe paresis of the right leg, aphasia and somnolence. Treated with IV acyclovir and high-dose corticosteroids deterioration of the right hemiparesis was apparent. Serological and CSF-studies showed acute varicella-zoster virus infection with intrathecal antibody synthesis (antibody specificity index 2.7). On the third day CT scan revealed infarctions in the territory of both anterior cerebral arteries, at the fifth day additionally left striatocapsular infarction. Selective carotid arteriogram showed bilateral occlusions of anterior cerebral arteries in their proximal segment. With a mean delay of seven weeks granulomatous vasculitis is a rare complication of HZO, leading commonly to ischemic infarctions in the region of the middle cerebral artery. Trigeminovascular connections are the probable pathway of virus-transmission from the trigeminal nerve to ipsilateral branches of the circle of Willis. Because of the presumed pathogenesis immediate therapy with high-dose corticosteroids and acyclovir is justified.

Acyclovir↗
PubMed1995

[Strategies for early admission of stroke patients].

From March to August 1993 we performed a comprehensive educational campaign about stroke and acute stroke therapies to shorten admission delay and to recruit more patients for the ECASS trial [8]. We compared the presentation data of all stroke patients admitted in a six month preeducational period with data of a six month posteducational period. The median admission delay was significantly reduced from eight hours in the preeducational to five hours in the posteducational period. The number of patients undergoing thrombolytic treatment increased. The following factors shortened admission delay: age > 70 years, living in cities, stroke onset during daytime, admission by ambulance, stroke in anterior circulation, cardiogenic embolic stroke, severe symptoms.

Aged↗
PubMed1994

Space-occupying cerebellar infarction. Clinical course and prognosis.

BACKGROUND AND PURPOSE: Because the timing and strategy of surgical intervention in massive cerebellar infarction remains controversial, we report our experience with the management of 52 such patients. METHODS: Case records, computed tomographic scans, surgical reports, and angiograms of 52 patients with space-occupying cerebellar infarction defined by computed tomographic criteria were reevaluated with regard to clinical course, etiology, therapeutic management, mortality, and functional outcome. RESULTS: In most cases clinical deterioration started on the third day after stroke, and a comatose state was reached within 24 hours. Sixteen patients were treated medically, and 30 by suboccipital craniectomy (22 plus ventriculostomy, 12 plus tonsillectomy). Ten patients primarily had ventriculostomy, which in 4 patients was supplemented by craniotomy because of continuing deterioration. Twenty-nine patients made a good recovery, 15 remained disabled, and 8 died. Even comatose patients had a 38% chance of a good recovery with decompressive surgery. Age older than 60 years (P = .0043) and probably initial brain stem signs (P = .0816) and a late clinical stage (P = .0893) were linked with a fatal or disabling outcome. CONCLUSIONS: Decompressive surgery should be the treatment of choice for massive cerebellar infarction causing progressive brain stem signs or impairment of consciousness.

Adult↗
PubMed1992

Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke.

An open angiography-based, dose rate escalation study on the effect of intravenous infusion of recombinant tissue plasminogen activator (rt-PA) on cerebral arterial recanalization in patients with acute focal cerebral ischemia was performed at 16 centers. Arterial occlusions consistent with acute ischemia in the carotid or vertebrobasilar territory in the absence of detectable intracerebral hemorrhage were prerequisites for treatment. After the 60-minute rt-PA infusion, arterial perfusion was assessed by repeat angiography and computed tomography scans were performed at 24 hours to assess hemorrhagic transformation. Of 139 patients with symptoms of focal ischemia, 80.6% (112) had complete occlusion of the primary vessel at a mean of 5.4 +/- 1.7 hours after symptom onset. No dose rate response of cerebral arterial recanalization was observed in 93 patients who completed the rt-PA infusion. Middle cerebral artery division (M2) and branch (M3) occlusions were more likely to undergo recanalization by 60 minutes than were internal carotid artery occlusions. Hemorrhagic infarction occurred in 20.2% and parenchymatous hematoma in 10.6% of patients over all dose rates, while neurological worsening accompanied hemorrhagic transformation (hemorrhagic infarction and parenchymatous hematoma) in 9.6% of patients. All findings were within prospective safety guidelines. No dose rate correlation with hemorrhagic infarction, parenchymatous hematoma, or both was seen. Hemorrhagic transformation occurred significantly more frequently in patients receiving treatment at least 6 hours after symptom onset. No relationship between hemorrhagic transformation and recanalization was observed. This study indicates that site of occlusion, time to recanalization, and time to treatment are important variables in acute stroke intervention with this agent.

Acute Disease↗
PubMed1992

German-Austrian Space Occupying Cerebellar Infarction Study (GASCIS): study design, methods, patient characteristics. The Steering and Protocol Commission.

An open prospective multicentric therapeutic trial to determine the timing and type of therapeutic intervention in patients presenting with secondary deterioration following cerebellar stroke is described. According to the results of retrospective studies a controlled approach comparing different therapies is ethically not feasible. Participants use the same scores and protocol for patient data collection but many choose different therapeutic procedures.

Austria↗
PubMed1991

[Heparin therapy in embolic cerebral infarct. A retrospective study].

Heparin therapy in acute stroke is a controversial issue. It is uncertain, whether heparin has a therapeutic or preventive effect in the early phase of the stroke. From 1984-1989, 1095 patients with acute ischemic stroke were treated, 141 (12.9%) of whom received heparin within 3 days of stroke onset. The mean duration of heparin anticoagulation was 10 days. In 28 cases (20%), heparin was used as antithrombotic agent (25/28 patients suffered a basilar artery occlusion, of whom 22 died). In 113 cases (80%), heparin was used in embolic stroke to prevent recurrence (24% cardioembolic stroke, 54% arterio-arterial embolism, and 22% embolism of unknown etiology). The rate of recurrent stroke in the early phase was 13% with a persistent deficit in 5.3%. The results are comparable with those of other trials reported in the literature. Only 2 patients had an anticoagulation-related haemorrhage with clinical deterioration. Heparin anticoagulation in acute stroke is a low-risk therapy, but its preventive value has not yet been demonstrated.

Adult↗
PubMed1986

CSF cyclic AMP and CSF adenylate kinase in cerebral ischaemic infarction.

The severity of neurological deficits, size of hypodense zone on CT, concentration of cAMP and activity of adenylate kinase in cerebrospinal fluid (CSF) were evaluated at predefined intervals in the acute stage of supratentorial cerebral ischaemic infarction in 52 patients. Patients with cerebral infarction had raised activities of adenylate kinase CSF as compared with normal persons. Patients with marked neurological deficits, only slight improvement of neurological signs and large infarction zones on CT had higher average activities of adenylate kinase and lower concentration of cAMP in CSF. Alterations of CSF adenylate kinase and CSF cAMP values were most distinct on the 3rd day after the stroke. Reasons for the changes may be metabolic disorders following brain ischaemia.

Adenylyl Cyclases↗