Analysis of the data confirmed the occurrence of asymptomatic infarcts due to vasospasm. These infarcts often developed in noneloquent areas representing perforator territory. MRI investigation of vasospastic lesions referable to intraparenchymal vessels such as perforators complements the study of extraparenchymal major vessel vasospasm in patients with SAH by computed tomographic angiography.

✓ In this retrospective study, the authors analyzed surgical outcomes in patients who suffered an intracerebral hemorrhage (ICH) as a result of a ruptured middle cerebral artery aneurysm. They studied 47 patients who underwent early aneurysm surgery and hematoma evacuation within 24 hours after onset of ICH. The types of ICH were classified into three groups according to their appearance on computerized tomography scanning: 1) temporal ICH; 2) intrasylvian hematoma; and 3) ICH with diffuse subarachnoid hemorrhage (SAH). Overall, 25 patients (53%) achieved a favorable outcome and 18 (38%) died. Factors that could be used to predict a favorable outcome included age less than 60 years, temporal ICH, World Federation of Neurological Surgeons Grade II or III, absence of a surgical complication, and a hematoma volume less than 25 ml. In the patients with temporal ICH, eight of nine patients achieved a good recovery and no patient developed a surgical complication or delayed ischemic deficit. The significant prognostic factor in patients with an intrasylvian hematoma was surgery within 6 hours after onset of symptoms. In patients with temporal ICH or intrasylvian hematoma, the results of the initial neurological examination did not accurately predict outcome. On the other hand, in patients with ICH and diffuse SAH, those patients who developed an ICH with a volume greater than 25 ml had a poor prognosis. These results indicate that aggressive surgical treatment should be performed in patients with a temporal ICH or an intrasylvian hematoma, regardless of the neurological findings on admission; in patients with ICH and diffuse SAH, a careful review of surgical indications is required.

This investigation has revealed the frequency of various intracranial complications that may result from hypervolemic therapy for a delayed ischemic deficit following subarachnoid hemorrhage (SAH). Among 323 patients with SAH, 112 patients developed a delayed ischemic deficit, 94 of whom underwent hypervolemic therapy. Infarction due to vasospasm was found ultimately in 43 of these 94 patients. Twenty-six patients (28%) developed an intracranial complication during hypervolemic therapy: cerebral edema was aggravated in 18, and a hemorrhagic infarction developed in eight. In 13 of 18 patients with aggravation of edema, delayed ischemic deficit developed within 6 days after the SAH; at that time, a massive new infarction was found in four and edema in 10 patients. After hypervolemic therapy, the 18 patients with aggravation of edema deteriorated rapidly, and 14 of them died. In every case in which hemorrhagic infarction followed hypervolemic therapy, a new infarct was found on computerized tomography (CT) when the delayed ischemic deficit became apparent. Hemorrhagic infarction developed as the delayed ischemic deficit resolved, with one exception. In patients who sustained no complication from hypervolemia, the incidence of both massive new infarction and edema at the time when the delayed ischemic deficit was manifested was only 1%. In 44 of 68 patients who sustained no complication from hypervolemia, the delayed ischemic deficit was manifested on or after the 7th day following the SAH. This study suggests that hypervolemic therapy is contraindicated in a patient who is found to have a massive abnormality on CT at the time when a delayed ischemic deficit is manifested, especially when it occurs within 6 days after the SAH. To avoid hemorrhagic infarction, it is important to discontinue hypervolemic therapy as soon as the delayed ischemic deficit resolves.

Introduction We previously reported centripetal propagation of vasoconstriction at the time of thunderclap headache remission in patients with reversible cerebral vasoconstriction syndrome. Here we examine the clinical significance of centripetal propagation of vasoconstriction. Methods Participants comprised 48 patients who underwent magnetic resonance angiography within 72 h of reversible cerebral vasoconstriction syndrome onset and within 48 h of thunderclap headache remission. Results In 24 of the 48 patients (50%), centripetal propagation of vasoconstriction occurred on magnetic resonance angiography at the time of thunderclap headache remission. The interval from first to last thunderclap headache in patients with centripetal propagation of vasoconstriction (14 ± 10 days) was significantly longer than that of patients without centripetal propagation of vasoconstriction (4 ± 2 days). In the patients with centripetal propagation of vasoconstriction at the time of thunderclap headache remission, the incidence of another cerebral lesion (38%, 9 of 24 cases) was significantly higher than in patients without centripetal propagation of vasoconstriction (0%). From findings of sequential magnetic resonance angiography before and after thunderclap headache remission, we observed tendencies in which centripetal propagation of vasoconstriction gradually progressed after the onset of reversible cerebral vasoconstriction syndrome and peaked at the time of thunderclap headache remission. The progress of centripetal propagation of vasoconstriction concluded with thunderclap headache remission. Conclusions Centripetal propagation of vasoconstriction has clinical significance as an indicator of the severity of reversible cerebral vasoconstriction syndrome. The presence of centripetal propagation of vasoconstriction is associated with an increased risk of brain lesions and a longer interval from first to last thunderclap headache. Moreover, repeat magnetic resonance angiography to assess centripetal propagation of vasoconstriction during the time from onset to thunderclap headache remission can help diagnose reversible cerebral vasoconstriction syndrome.

This study found evidence of centripetal propagation of vasoconstriction on MRA obtained at the time of thunderclap headache remission, compared with MRA obtained at the time of reversible cerebral vasoconstriction syndrome onset. If clinicians remain unsure of the diagnosis during early-stage reversible cerebral vasoconstriction syndrome, this time point represents the best opportunity to diagnose reversible cerebral vasoconstriction syndrome with confidence.