EFORE recent diagnostic procedures were introduced for the diagnosis of hydrocephalus, one of the most accepted indicators for progressive hydrocephalus in infants was head circumference. However, formulating a diagnosis of arrested hydrocephalus on the basis of this indicator alone would be questionable. Whittle and colleagues 41 used continuous ICP monitoring to as-sess 46 children and adolescents in whom a clinical diagnosis of arrested hydrocephalus had been made. They found that 80% of patients who had previously been treated had a nonfunctioning shunt and that 63% of patients who had received no previous treatment had episodic or persistent increased ICP. When serial psychometric testing demonstrated a fall in cognitive functioning, ICP monitoring revealed abnormal ICPs in 88% of patients. The results of this study may indicate that CSF dynamics change over time, shifting hydrocephalus between active and inactive states; however, the factors affecting such changes remain uncertain.In 1996, we reported on the specific clinical features of infantile hydrocephalus that continues into adulthood, Object. Long-standing overt ventriculomegaly in adults (LOVA) is a unique form of hydrocephalus that develops during childhood and manifests symptoms during adulthood. The aim of the present study was to analyze the specific pathophysiological characteristics of LOVA.Methods. The specific diagnostic criteria for LOVA include severe ventriculomegaly in adults that is associated with macrocephalus measuring more than two standard deviations in head circumference and/or neuroradiological evidence of a significantly expanded or destroyed sella turcica. Twenty patients who fulfilled these criteria, 14 males and six females, were retrospectively studied. These patients' ages at diagnosis ranged from 15 to 61 years (mean 39.4 years). All had symptoms and/or signs indicating that hydrocephalus first occurred at birth or during infancy in the absence of any known underlying disease. The authors performed a pathophysiological study that included specific variations of magnetic resonance (MR) imaging, such as fluid-attenuated inversion recovery and cardiac-gated cine-mode imaging; intracranial pressure (ICP) monitoring; three-dimensional computerized tomography (CT) scanning; and other techniques.Hydrocephalus was caused by aqueductal stenosis in all patients. Severe ventriculomegaly involving the lateral and third ventricles was associated with a marked expansion or destruction of the sella turcica in 17 cases. Cardiac-gated cine-MR imaging did not reveal any significant movements of cerebrospinal fluid in the aqueduct. Three-dimensional CT ventriculography confirmed that the expanded third ventricle protruded into the sella and, sometimes, extended a diverticulum. Fourteen patients revealed symptoms and signs that indicated increased ICP with prominent pressure waves. Dementia or mental retardation was seen in 11 patients, gait disturbance in 12, and urinary incontinence in eight; all three of these symptoms were observed in sev...
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.
Neuroendoscopic surgery was used to treat patients with various forms of hydrocephalus with specific pathophysiology, including long-standing overt ventriculomegaly in adulthood (LOVA), isolated unilateral hydrocephalus (IUH), isolated IV ventricle (IFV), disproportionately large IV ventricle (DLFV), isolated rhombencephalic ventricle (IRV), isolated quarto-ventriculomegaly (IQV), dorsal sac in holoprosencephaly (DS), and loculated ventricle (LV). A total of 26 operative procedures were performed, with neuroendoscopic surgery in 22 patients, 12 with unique forms of noncommunicating hydrocephalus and 10 with various types of postshunt isolated compartment. These procedures included III ventriculostomy, aqueductal plasty by both rostral and caudal approaches, foraminal plasty in the foramen of Monro/foramen of Magendie, septostomy, IV ventriculostomy, fenestration of septation in the loculated ventricle, fenestration of arachnoid cyst or cystic tumor obstructing a ventricle with or without tumor removal, and dorsal sac ventriculostomy. The characteristics of the cerebrospinal fluid (CSF) dynamics in the individual specific pathophysiologies were delineated by cardiac-gated cine-mode magnetic resonance imaging (MRI) before and after the endoscopic procedure. The consequent success rate (success = restoration of communication of the CSF pathway in the individual patients) was 19/22 (86.4%). The progression of ventricular dilatation was stopped in 17 of 19 patients (89.5%) in whom the endoscopic procedure was successful (radiologically arrested hydrocephalus). Improvement in the clinical symptoms and signs (clinically arrested hydrocephalus) was obtained in 15 of the patients (68.2% of all patients: 5 with LOVA, 3 with IQV, 5 with IUH and 2 with LV). Seven patients (2 LOVA, 2 IFV, 1 DS, 1 DFLV and 1 IRV) underwent a shunt procedure after the neuroendoscopic procedure(s). The postoperative changes of ventriculomegaly were complicated, reflecting the differences in the brain parenchymal compliance and postoperatively corrected CSF flow dynamics in the major CSF pathway.
✓ 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.
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