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Subdural hematoma has rarely been implicated as a cause of chorea. We describe a case of chorea occurring several months after evacuation of a traumatic subdural hematoma. No other causes of chorea were found. In this case and one previously reported case, signs of tentorial herniation were present prior to surgery. Herniation may damage the basal ganglia, with resultant chorea.
A 48-year-old man with traumatic false aneurysm, arteriovenous fistula of the middle meningeal artery, ipsilateral chronic subdural hematoma, contralateral subdural hydroma, and nontraumatic vertebrooccipital anastomosis was reported with a review of the literature. Traumatic false aneurysm of the middle meningeal artery of 32 cases was already reported in the world, and traumatic arteriovenous fistula of the middle meningeal artery was found in 47 cases, but combination of the both is very rare and only 6 including ours have been found in the literature. In a case that a fracture line crosses over the middle meningeal artery, meningeal false aneurysm or arteriovenous fistula as well as epidural or subdural hematoma is supposed. Therefore common carotid angiography or selective carotid external angiography should be examined thinking of these above mentioned lesions. Comment was made from the anatomic, angiographic, and therapeutic point of view. In our case, the false aneurysms were removed while necessary ipsilateral craniotomy was performed for the chronic subdural hematoma. And operative and histological findings suggest the false aneurysms were on the way to spontaneous disappearance.
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Interhemispheric subdural hematomas are rare. Bilateral interhemispheric subdural hematomas in a patient with a ventriculoperitoneal shunt for hydrocephalus were diagnosed by computerized tomographic (CT) scan after mild head trauma. The value of CT scanning, the clinical presentation and treatment, and a review of the literature are presented.
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Isodense subdural hematomas, particularly bilateral ones, may be difficult to diagnose with CT. Forty-three cases of subdural hematomas were studied by CT, 7 of which were isodense collections. Obliteration or displacement of the cortical sulci in the zone of the extracerebral collection was present in all 7 cases. Infusion scans demonstrated displacement of a cortical vein away from the inner table of the skull in 3 of the 7 cases. This findins is helpful in accurately predicting the size of the extracerebral collection.
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Subdural hematomas, whose absorption values approximate those of adjacent brain, are not visualized in routine computed tomography. Two clues indicating the presence of such "isodense" subdural hematomas are: (1) unilateral effacement of cerebral sulci on the convexities, and (2) midline shift or mass effect on the ventricles in the absence of abnormal areas of diminished or increased density in the brain. Nine cases were detected on pre- and postcontrast studies in 2,500 CT scans of the brain over a 10 month period. Delayed CT scanning 4-6 hr after intravenous contrast injection showed enhancement of the subdural hematoma in three of seven cases.
Subdural hematomas in infants are associated with a high risk of recurrence. In an effort to combat this risk, a surgical procedure consisting of excision of the subdural membranes, a reduction of the craniocerebral disproportion and a restoration of the normal angle of junction of the cerebral bridging veins and the superior sagittal sinus is proposed.
Posterior fossa subdural hematomas in the newborn infant are rare but potentially treatable. The infants are normal after birth, but within days, hydrocephalus hypotonia, and irregular respirations develop. Seizures and third nerve pareses are unusual. We report a neonate in whom this process was identified by computerized tomographic brain scan. We also discuss potential misinterpretations of the computerized tomographic brain scan in neonates.
Eight cases of isodense subdural hematomas were evaluated by computed tomography (CT). CT demonstrated varying degrees of compression of a lateral ventricle, shift of the midline structures and, in some cases, obliteration of the subarachnoid sulci on the side of the lesion. Contrast enhancement was helpful in one case and demonstrated medial displacement of enhanced cortical margins away from the inner table of the skull. Two of the eight patients had no clear history of trauma.
CT findings in 51 patients with subdural hematomas are studied. Direct signs (hyperdensity, hypodensity) and indirect signs (any form of mass lesion) are distinguished. CT is limited with regard to determining correlations between time and the attenuation values. The factors which influence density of the hematoma are discussed. For a rational approach with subdural hematomas, which present diagnostic problems and reveal the limitations of CT diagnosis, a diagnostic scheme is proposed.
The authors present 149 patients suffering from acute (112) and subacute (37) subdural hematomas admitted during the 10-year period 1965 to 1974, with a follow-up period of 2 to 12 years. During the time of observation, 104 patients died and 45 survived; 73% of the patients with acute and 27% with subacute subdural hematomas died. Of the patients with an acute subdural hematoma, 11% went back to work, as against 32% of those with subacute subdural hematomas. The 5-year survival rate was 28% in patients with acute and 76% in patients with subacute subdural hematomas.
The authors report a series of 22 cases of subdural hematomas in patients submitted to anticoagulant therapy. A review of the literature finds 150 cases. Subdural hematomas occurs in about one third of the patients presenting hemorrhage of central nervous system related to anticoagulant therapy. Among subdural hematomas of any cause, the possible role of a previous anticoagulant therapy is stressed in 4,8 to 14% of cases. In most cases, long term anticoagulants were indicated for arterial or heart (ischemic) lesions (16/22 cases). In 6 cases, anticoagulants were indicated for prevention or treatment of pulmonary embolies. In 18 cases, anticoagulant drug is from the group of dicoumarol or phenylindanedione. In 3 cases, the only anticoagulant given to patient was heparin. Pathogenic study suggests that hypocoagulability might not always be the only factor of bleeding: high blood pressure, other drugs and head trauma (10 cases) are often associated. Clinical features, in our series, are similar to those encountered in cases of subdural hematoma of any cause. According to the existence of a cranial injury and to the chronology of anticoagulant therapy, the authors divide their 22 patients into 3 groups. The use of protamin sulfate or human plasma fraction PPSB provides in few minutes a normal coagulability. Neurosurgical treatment in all our cases evacuated in 11 patients a chronic subdural hematoma, in 2 cases an acute, and in 9 cases a subacute hematoma. Results were fair in 19 patients with no sequelae. 3 patients died during the immediate post-operative period. The authors conclude by stressing several preventive measures.
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CT scans of 87 patients with subdural hematoma were compared to those of 393 patients with midline shift caused by other intracranial lesions with regard to attenuation changes in the lesion and the character of the ventricular deformity. Isoattenuating was exhibited by 25% of the subdural hematomas and 5% of the other lesions. In 70 to 80% of the isoattenuating hematomas, the diagnosis could be made on the basis of the characteristic ventricular deformity. Other diagnostic procedures are not necessary in these cases.
Complete spontaneous resolution of bilateral subdural hematoma overa period of 17 months was documented by both radioisotopic brain scan and cerebral angiogram. It is suggested that the favorable response to the medical treatment in some cases should be interpreted with caution.
CT findings of 46 patients with operatively confirmed chronic subdural hematomas are reviewed. The analysis of the EMI scans resulted in three different types of CT findings. Type 1 is characterized by decreased attenuation of the hematoma contents compared to brain tissue. The hematoma is visualized as a lens-shaped low density area between the skull and the surface of the brain. Type 2 apart from low density areas contains zones of increased attenuation due to recent bleeding into a watery chronic subdural hematoma. In many cases sedimentation causes a well-defined horizontal borderline between the thin fluid parts in the anterior portion and the blood debris in the posterior portion of the hematoma sac. Type 3 shows the same average absorption values as normal brain tissue, a direct visualization is not possible. However , the presence of a midline displacement in combination with ventricular compression and absence of a circumscript lesion even after contrast enhancement, allows the diagnosis of a unilateral chronic subdural hematoma in these cases too. Bilateral chronic subdural hematomas may cause considerable diagnostic difficulties if only one or none of the hematomas is visualized. A relatively small midline displacement points to a second bleeding on the opposite side. Most frequent were hematomas of type 1 (37%), type 2 and 3 could be observed in 30,5% resp. 32,5% of cases respectively.