[Subdural fluid collection in infancy and childhood--with special reference to subdural fluid pressure (author's transl)].
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Fifty-one cases with subdural hygroma experienced in the past 20 years were retrospectively reviewed. Eight patients showed definite ventricular dilation differing from simple restoration of the ventricles following disappearance of the cavity. The mean age was 72.4 years. Six patients presented with mental change as the initial symptom. On the initial computed tomography (CT), 75% of the cases had bilateral lesions, all were low density, and 88% were crescent shaped. Trepanation performed on six patients yielded watery clear or xanthochromic fluid. Nine to 61 days (mean 4 weeks) after admission, definite ventricular dilation was observed. Cisternography performed in four patients was all abnormal, although cerebrospinal fluid (CSF) pressure was within normal range. Cerebral blood flow images using 123I-iodoamphetamine and single photon emission CT in four patients revealed periventricular low uptake which was disproportionately large compared with the ventricular span on CT. A ventriculoperitoneal shunt was placed in four patients. The final outcome, however, was poor irrespective of treatment. These findings indicate that an impairment of the CSF circulation was not the sole cause of the ventricular dilation. Low CSF pressure and the disproportionately large periventricular low perfusion, compared with the ventricular span on CT scan, suggest a pre-existing periventricular parenchymal damage, which had been subsequently compromised by the presence of subdural mass lesion. Therefore, attention should be paid in aged patients with bilateral low dense, crescent-shaped subdural hygroma, presenting with mental change, for the risk of subsequent ventricular dilation which may affect the functional outcome.
A 70-year-old male presented with rapid neurological deterioration and fever 3 months after suffering a closed head trauma. He underwent craniotomy for possible subdural empyema based on computed tomography and clinical findings. Dural incision revealed an outer membrane typical of chronic subdural hematoma which covered a clear, yellowish fluid containing Campylobacter fetus. Histological examination confirmed the capsule of the hematoma, with a necrotic focus infiltrated by neutrophils. Administration of intravenous imipenem and topical tobramycin and cefalothin achieved total resolution of his neurological deficits. Development of the infected subdural effusion was probably secondary to bacterial infection in the pre-existing chronic subdural hematoma in the resolving stage. The presence of the hematoma capsule always carries the risk of development of an infectious focus.
Hyperostosis of the sphenoid ridge or convexity of the skull associated with meningioma en plaque (MEP) is often confused with other hyperostosing conditions, such as fibrous dysplasia or osteoma. The authors present nine cases, six of them proven, of hyperostosing MEP with specific attention to the CT features. All nine cases had one or more CT features that were characteristic or suggestive of MEP. These included periosteal pattern of hyperostosis, inward bulging of the vault lesion, surface irregularity of the hyperostotic bone, and intracranial changes. The role of CT in evaluating MEP is compared with other neuroradiologic techniques. The results indicate that high-resolution CT is the neuroimaging method of choice in evaluating MEP.
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Nineteen patients with traumatic subdural hygroma (TSH) who were admitted between 1988 and 1992, were reviewed. Diagnosis of TSH was made by serial computerized tomography (CT) after initial head injury, and patients were followed for up to 19 months after head injury. The patients ranged in age from 53 to 91 years (mean 75.6 yrs). Fifteen patients were treated conservatively, and 4 patients underwent surgery. Patients had disturbance of consciousness (transient in 5 cases, persisting in 3 cases), headache (10 cases), vomiting (6 cases), and vertigo (2 cases). TSH began to develop within 24 hs in 10 patients after initial head injury, and in 13 (68%) of 19 patients, TSH was demonstrated within 72 hs after the initial head injury. Chronic subdural hematoma (CSH) developed in 5 (26%) of 19 patients and 2 patients underwent surgery. In 15 patients, who were treated conservatively, TSH disappeared in 10 patients, and decreased in 4 patients, but remained unchanged in 1 patient. Clinically, 11 patients improved. Three patients remained unchanged. One patient, who had cerebral contusion, died of pneumonia. In 4 patients, who underwent surgery, including 2 patients with CSH, TSH disappeared in all patients. Two patients improved, and 1 patient was unchanged. Another patient, who had cerebral contusion and normal pressure hydrocephalus, died. In general, clinical outcome was satisfactory, except for the patients who had accompanying parenchymal lesions before or after head injury. Surgical treatment was limited to the patients who had rapidly enlarging TSH and neurological deterioration.
A case is reported of subdural bone formation in a patient with histologically verified glioblastoma multiforme. No history of trauma or chronic neurologic problems were obtainable.
Follow-up results for 13 cases of acute subdural haematoma, which were identified by CT scan within two days of head injury and treated conservatively, were classified into two groups: In the first group of seven cases the acute subdural haematoma disappeared spontaneously within two weeks; in the second group the other six cases revealed clinical signs and CT scan findings which were identical to chronic subdural haematoma and underwent surgery within three weeks after the head injury. This group showed low ICP signs, such as the chronic stage of cerebral thrombosis, atrophic brain or subdural fluid collection with acute subdural haematoma at the initial CT scan, and most of these cases had only minor head injury. Common features of the operative findings in this second group, in which chronic subdural haematoma developed, included the identification of an external haematoma capsule based on the fibrin layer and granulation tissue beneath the dura. Also, fluid type haematoma was present under these structures, but no inner membrane of the haematoma could be identified other than the non-transparent white arachnoid membrane. Our results indicate the importance of a low ICP in determining whether or not acute subdural haematoma progresses to chronic subdural haematoma.
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Subarachnoid-pleural fistula is a rare type of cerebrospinal fluid (CSF) fistula, and there are only several cases reported in the literature. The authors describe a 65-year-old male patient in whom a diagnosis of T7-8 disc herniation had been made. He underwent surgery via a right lateral extracavitary approach. Postoperatively he developed progressive respiratory distress and headache. A chest x-ray film revealed a pleural effusion, and computerized tomography (CT) myelography demonstrated a subarachnoidal-pleural fistula at the level at which the herniated disc had been removed. The patient had been managed via a CSF drainage system and a chest tube. He was discharged after relief of symptoms was attained. Subarachnoid-pleural fistulas can be secondary to traumatic injury and surgery, or they can be spontaneous. Patients present with rapidly filling pleural effusion and headache. A diagnosis can be established using CT myelography or myeloscintigraphy. Treatment is conservative, with the placement of a chest tube and insertion of a CSF drainage catheter, and surgical repair should be considered only if the conservative therapy fails.
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