The infratentorial compartment represents the second most common location of arachnoid malformations. Ten arachnoid cysts of the posterior fossa, operated on between 1970 and 1983, are reviewed. These lesions, although congenital and developmental in nature, may present at any age, and males are more frequently affected. A high rate of birth-related trauma (50% in this series) is conceivably due to fetal macrocranium, and the enlarged head and psychomotor retardation prevail in infancy and childhood. In arachnoid cysts occurring during adulthood, symptoms and signs more clearly indicate a dysfunction of the posterior fossa. Besides computerized tomography, pneumoencephalography and metrizamide techniques are recommended to rule out a Dandy-Walker syndrome in doubtful cases, and to obtain information about the cerebrospinal fluid (CSF) circulation. It is particularly important to establish the presence and type of communication of cysts with the CSF pathways. Although infratentorial cysts often communicate, they can be space-occupying masses because of increasing CSF retention, which may be due to a ball-valve mechanism or to inadequate communication. The frequently associated hydrocephalus (seven of the 10 cases in this series had hydrocephalus) seemed to be dependent mainly upon mechanical factors. The authors discuss the indications for intracranial surgery versus shunting procedures and report the results achieved by direct cyst excision.
From January 1, 1990, to April 30, 1994, 412 patients were admitted to our intensive care unit in coma after head injuries. Our study group consisted of 37 patients who were retrospectively identified as harboring lesions or developing new lesions within a 12-hour period from the time of admission. We defined the evolution of a lesion as an increase or decrease in the size of an already present hematoma or as the appearance of a totally new lesion. There were 25 male and 12 female patients (mean age, 34.9 yr), and the cause of trauma was road traffic accidents in 32 patients. Nine patients presented with shock, and six had evidence of abnormal coagulation at admission. Patients were divided into two different groups. In Group 1, 15 patients harbored lesions that evolved toward reabsorption. In Group 2, 22 patients harbored hematomas that evolved toward lesions requiring surgical removal. Fifteen of these patients had initial diagnoses of diffuse injury that evolved in this manner, whereas the remaining seven patients had already been operated upon and had developed second, noncontiguous, surgical lesions. Patients with lesions that required surgical evacuation had their computed tomographic (CT) scans obtained earlier and had a higher incidence of clinical deterioration. There was a significant difference in the evolution of the different lesions (P < 0.001), with subdural hematomas being more prone to reabsorption and intracerebral and extradural hematomas being more likely to increase in size or to appear as new lesions. Second CT scans were obtained because of clinical deterioration in 10 patients and because of increase in intracranial pressure in 5 patients. Scheduled CT scans were obtained in 13 patients, whereas in the remaining 9 patients, the diagnosis emerged from a combination of scheduled CT scans and intracranial pressure monitoring. There was a trend toward a poorer result among the patients with clinical deterioration, which, however, was not significant. A significant proportion of post-traumatic patients, particularly those who are unconscious, harbor early evolving intracranial lesions. When the first CT scan is performed within 3 hours after injury, a CT scan should be repeated within 12 hours.
Nonoperative management for selected cases of acute subdural hematomas is at least as safe as surgical management. GCS scoring at the scene and in the emergency room combined with early and subsequent CT scanning is crucial when making the decision for nonoperative management. This strategy requires that administration of long-lasting sedatives and paralytic medications be avoided before the patient arrives at the neurosurgical center.
The authors report a case of pituitary apoplexy associated with oculomotor defects and focal cerebral signs; the visual pathways were intact. Computed tomography documented a mass of heterogeneous density within an enlarged sella turcica and a right parietal infarct. Angiograms revealed bilateral carotid spasm and occlusion of the right angular artery. Treatment was conservative. Control angiograms showed spontaneous resolution of the vasospasm and recanalization of the cortical artery. The patient made a complete neurological recovery; he needed only treatment with vasopressin due to transient diabetes insipidus. The risk of vasospasm and brain ischemia should be kept in mind when treating pituitary apoplexy. The early occurrence of vasospasm in our case suggests the participation of powerful vasoactive agents liberated from the tumor.
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