No abstract available.
Vasospasm, Intracranial*

No abstract available.
Cerebral Infarction ; Vasospasm, Intracranial

No abstract available.
Intracranial Aneurysm* ; Surgical Instruments* ; Vasospasm, Intracranial*

No abstract available.
Latex* ; Polystyrenes* ; Potassium Channels* ; Potassium* ; Vasospasm, Intracranial*

Numerous approaches to the prevention and treatment of cerebral vasospasm have been made. Its etiology and pathogenesis are still not well understood, and there is no animal model that duplicates all of the key aspects of human cerebral vasospasm. It is therefore not surprising that most of the attempts to prevent or treat this condition have failed. Since 1980, there has been some progress toward the satisfactory management of this detrimental condition, but much remains to be done. In the present article, experimental therapies are examined in detail, followed by a review of promising new treatments presently in clinical trials and generally accepted management in reducing the ischemic complications related to cerebral vasospasm.
Humans ; Models, Animal ; Therapies, Investigational ; Vasospasm, Intracranial

Somatosensory evokd responses(SSERs) and auditory evoked responses(AERs) were studied in 33 patients with cerebral aneurysms and arteriovenous malformations(AVMs) to see if these tests were useful indicators of cerebral vasospasm. 7/21 had abnormal SSER and 5/28 an abnormal AER. The SSER was abnormal in 4/7 patients with severe vasospasm but in only 1/13 without spasm or with mild or moderate spasm. Abnormal SSERs in patients with severe vasospasm indicated a poor prognosis. Abnormalities on the SSER and AER correlated best with the degree of clinical deficit. These tests seemed insufficiently sensitive to reliable detect impending ischemia.
Arteriovenous Malformations* ; Humans ; Intracranial Aneurysm* ; Ischemia ; Prognosis ; Spasm ; Vasospasm, Intracranial

The literature concerning cerebral vasospasm associated with subarachnoid hemorrhage(SAH) due to ruptured intracranial aneurysm contains no definitive study of patients to determine whether there is (1) any clinical picture consistently present coincident with known cerebral vasospoasm, (2) any relationship between mortality and known vasospasm, and (3) any relationship between serious brain damage(morbidity) and known vasospasm. To answer these important questions, experience with 138 consecutive acute SAH patients due to ruptured intracranial aneurysm was studied. The results were (1) The vasospasm was seen in 61 patients(44.2%) and the clinical vasospasm was seen in 41 patients(29.8%);(2) The average interval between last SAH and vasospasm was 8.3 days;(3) The most common neurological deficit was a hemiparesis or a hemiplegia;(4) There is no relationship between mortality and vasospasm.
Brain ; Humans ; Intracranial Aneurysm* ; Mortality ; Paresis ; Vasospasm, Intracranial

The literature concerning cerebral vasospasm associated with subarachnoid hemorrhage(SAH) due to ruptured intracranial aneurysm contains no definitive study of patients to determine whether there is (1) any clinical picture consistently present coincident with known cerebral vasospoasm, (2) any relationship between mortality and known vasospasm, and (3) any relationship between serious brain damage(morbidity) and known vasospasm. To answer these important questions, experience with 138 consecutive acute SAH patients due to ruptured intracranial aneurysm was studied. The results were (1) The vasospasm was seen in 61 patients(44.2%) and the clinical vasospasm was seen in 41 patients(29.8%);(2) The average interval between last SAH and vasospasm was 8.3 days;(3) The most common neurological deficit was a hemiparesis or a hemiplegia;(4) There is no relationship between mortality and vasospasm.
Brain ; Humans ; Intracranial Aneurysm* ; Mortality ; Paresis ; Vasospasm, Intracranial

Cerebral vasospasm leading to delayed ischemic neurological deficits (DINDs) is one of the most serious complications after aneurysmal subarachnoid hemorrhage (SAH). There are many evidence, against which demonstrate the role of angiographically confirmed vasospasm as the sole cause of DINDs. The authors review literatures that support a potential role of thromboembolism as a possible cause of DINDs after aneurysmal SAH. Although there is some controversy regarding the relation between the cerebral vasospasm in large arteries and cerebral ischemia, vasospasm still remains one of the primary causes of DINDs. In addition, thromboembolism intensifies or supplements the effects of vasospasm as a possible alternative.
Aneurysm* ; Arteries ; Brain Ischemia ; Subarachnoid Hemorrhage* ; Thromboembolism* ; Vasospasm, Intracranial

OBJECTIVE: We present an evaluation of the clinical outcome and an investigation of the optimal use of papaverine angioplasty for the treatment of symptomatic vasospasm following subarachnoid hemorrhage. METHODS: The authors retrospectively analyzed 24 cases of symptomatic vasospasm treated by papaverine angioplasty from July 1994 to February 1998. Detailed clinical features and detailed techniques of papaverine angioplasty including sex, age, symptoms, time interval from symptom onset to angioplasty, papaverine dose, concentration and duration of infusion were investigated. RESULTS: After papaverine angioplasty, immediate angiographic vasodilatation was achieved in 23 cases (96%). Fifty eight percent showed clinical improvement within 24 hours but symptomatic vasospasm recurred in 21% of them. Retreatment with papaverine for the recurred cases showed a less response than the initial treatment. Statistical analyses showed that time interval from symptom onset to angioplasty was the factor related to the effects of papaverine angioplasty. CONCLUSION: Our study shows that optimal timing of papaverine angioplasty is very important for clinical improvement.
Angioplasty* ; Papaverine* ; Retreatment ; Retrospective Studies ; Subarachnoid Hemorrhage ; Vasodilation ; Vasospasm, Intracranial*