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Traumatic brain stem hemorrhage is often associated with severe head injury and has a high mortality rate. When these patients survive, the midbrain syndromes are usually complicated. The authors report an unusual case with isolated oculomotor nerve palsy caused by acute traumatic midbrain hemorrhage. A 50-year-old woman was brought to Kobe City General Hospital because she had fallen off a bicycle and hit the face severely on the ground. On admission, she was drowsy. Neurological examination revealed normal muscle tone in all extremities without motor or sensory disturbance. Deep-tendon reflexes were symmetrical and there were no Babinski signs present. The left eye lid dropped and the left pupil was 5.5 mm in diameter without responses to light. The eye ball was slightly deviated to the left side on neutral position. There were no extraocular movements except for abduction to the left side. The right pupil measured 3 mm in diameter and was reactive to light promptly. Plane skull films failed to show fractures. Computed tomography (CT) scan 30 minutes after the accident suggested the existence of a hemorrhage in the anterior tegmentum of the left midbrain. Four hours later, a midbrain hemorrhage was diagnosed by consecutive CT scans. She was alert on the next day, although the third nerve palsy remained. The left blephaloptosis disappeared gradually during the next month. At 6 months after the accident, the left pupil was still dilated and did not react to light, either directly or indirectly. Medial gaze recovered almost fully, while both upward and downward movements were still limited. The mechanism of the isolated oculomotor nerve palsy in this case was discussed with a review of the related literature.

Computed tomography (CT) findings of chronic subdural hematomas are usually diagnostic, unless hematomas are isodense and bilateral. The authors report two cases of bilateral chronic subdural hematomas, in which CT scans on admission were both misdiagnosed as delayed subarachnoid hemorrhage (SAH). The first case was a 43-year-old woman who suffered from a sudden onset of headache and nausea. She had no past history of head injury. CT scans on admission did not clearly reveal the Sylvian fissures and the mesencephalic cistern, without any mass effects. A lumbar puncture demonstrated xanthochromic cerebrospinal fluid (CSF), which was considered to be responsible for her headache. Cerebral angiography performed on day 4 failed to demonstrate any cerebral vascular disorders. Follow-up CT scans on day 7 demonstrated a high density lesion in the left subdural space. Magnetic resonance images (MRIs) confirmed a diagnosis of bilateral chronic subdural hematomas. Removal of the hematomas cleared all signs and symptoms smoothly. The second case was a 44-year-old man who was referred from another hospital because of xanthochromic CSF found by lumbar puncture. He began to suffer headache and be subject to vomiting 6 weeks earlier and these symptoms were still present on the day of admission. CT scans did not clearly show the cerebral cisterns without mass effects. Because the second lumbar puncture showed xanthochromic CSF again, SAH from aneurysm was suspected. However, emergency cerebral angiography failed to demonstrate cerebral aneurysms. MRI performed two days later demonstrated bilateral chronic subdural hematomas. Following surgery, the patient improved immediately and was discharged from hospital without any complications. In both cases, a retrospective study of the angiograms revealed the evidence of bilateral avascular areas over the convexities in the venous phase. The reason why these subdural hematomas were missed at the time of angiography was due to too much attention being paid to the arterial phase in an effort aimed only at identifying cerebral aneurysms. There are no reports of chronic subdural hematoma which demonstrated sudden onset of headache associated with xanthochromic CSF.

The authors report a case of benign intracranial hypertension (BIH) treated with a ventriculoperitoneal shunt. A 62-year-old man was referred to the Kobe City General Hospital with several episodes of transient visual obscuration. Neurological examination on admission revealed bilateral papilledema and a right lower quadrantic homonymous hemianopsia. Computed tomography (CT) showed normalized ventricles and a low-density area in the left occipital lobe without mass effects. From the findings of magnetic resonance images (MRIs) the occipital lesion was diagnosed as a chronic intracerebral hematoma. Because the hematoma did not show mass effects. BIH was suspected to be responsible for the papilledema. In spite of intravenous administration of dexamethasone and glycerol for a week, a lumbar puncture showed an opening pressure of 360mm H2O. Several subsequent lumbar punctures failed to improve intracranial hypertension. The mean opening pressure of the last 6 punctures was 392mm H2O. The mean terminal pressure dropped to 32mm H2O after removal of 10m/ of cerebrospinal fluid (CSF). A spinal subarachnoid drainage was inserted at the level of L4-L5 interspace for continuous CSF pressure monitoring. The mean CSF pressure ranged from 20 to 40mmHg. The continuous recording showed typical B waves frequently and plateau waves (A waves) occasionally. Removal of only 8m/ of CSF caused significant pressure reduction immediately. Then, pressure returned to the predrainage level about 35 minutes later. These findings supported the diagnosis of BIH. A ventriculoperitoneal shunt was inserted, which resulted in rapid and complete resolution of the papilledema. Postoperative CSF monitoring returned to normal pressure and waves. This case emphasizes the usefulness of continuous CSF pressure recording for the diagnosis and subsequent therapy of BIH.

A rare subcutaneous leiomyosarcoma metastatizing to the sphenoid bone and presenting exophthalmos is reported. A 56-year-old female presented with protrusion of the right eye and a slowly growing lump on the right temporal region. Six years previously, she had undergone removal of a subcutaneous mass in the back, which was histologically diagnosed in another hospital as leiomyosarcoma. She had undergone four other operations, including removal of local recurrences and a right renal metastasis. On admission, physical examination showed no neurological deficits. Craniogram revealed an osteolytic lesion without marginal sclerosis in the right sphenoid bone. CT showed an inhomogeneously enhanced mass with irregular expansion of the diploic space, which was partly invading the right orbit. MRI demonstrated an extradural mass in the right sphenoid region, which was slightly low-intense in T1-weighted image, high-intense in T2-weighted image, and inhomogeneously enhanced by Gd-DTPA. Right external carotid angiogram showed a highly vascular stain fed by meningeal arteries. Radionuclide bone scintigram showed multiple high-uptake areas in the left femoral head, the ribs, and the sphenoid bone. Preoperative embolization of the tumor vessels fed by the external carotid artery was performed. Following this procedure, the tumor stain disappeared completely. The tumor was totally excised with minimal bleeding through an orbitozygomatic approach. The tumor was loosely adherent to the dura and periorbit. The bone defect was covered with a methylmethacrylate resin plate. the histological examination demonstrated fascicular arrangement of the spindle shaped cells with mitotic figures. Immunohistochemical studies showed that most tumor cells were positive for actin and myosin, but negative for desmin.(ABSTRACT TRUNCATED AT 250 WORDS)

Ten cases of primary oculomotor nerve palsy due to head injury are presented. All ten patients had a dilated, non reactive pupil. Seven had complete oculomotor palsy. Two had partial extraocular palsy or blepharoptosis and one had neither extraocular palsy nor blepharoptosis. The initial ophthalmoplegia was recognized immediately after trauma. Nine patients had severely impaired consciousness on admission, but eight patients recovered fully within two months after the traumatic event, while one patient remained disoriented. Emergency CT scan on admission showed mass lesions in no patients except one who had a hematoma measuring 3 cm in the frontal lobe, but had no herniation sign. Patients with complete oculomotor palsy had a high incidence of traumatic SAH (71%) or skull fracture (57%). Recovery from third nerve palsy was not so good. The follow-up period extended from 3 months to 18 months. Of the 10 patients, none recovered completely from third nerve palsy. The prognoses of blepharoptosis, external ophthalmoplegia and internal ophthalmoplegia were analyzed separately. The recovery rates were 78%, 44% and 20%, respectively, the internal ophthalmoplegia showing poorest recovery. We discuss the mechanism of direct injury to the oculomotor nerve.

A rare case of deep sylvian meningioma is presented. A 62-year-old woman was admitted to our hospital because of one year history of temporal lobe epilepsy. She had no neurological deficit except for EEG abnormality. CT scans showed a small calcified mass in the left temporal lobe adjacent to the sylvian fissure with no enhancement by contrast medium. The mass was low-intense in both T1- and T2-weighted MR images. The T1-weighted image after the infusion of gadolinium revealed enhancement of the middle cerebral artery adjacent to the mass, similar to dural tail sign. Left external carotid angiography did not show any tumor stain nor the dilatation of the middle meningeal artery. Left internal carotid angiography disclosed enlarged middle cerebral artery without tumor stain. A left frontotemporal craniotomy was performed and the mass was totally removed. The tumor was located deep in sylvian fissure without any connection to the dura or ventricular system, which was firmly adherent to the middle cerebral artery. The histological examination of the surgical specimen revealed a psammomatous meningioma. Meningiomas are believed to originate from the arachnoid cap cells and can arise from various intracranial locations where arachnoid cap cells exist. The majority of them are attached to the dura, choroid plexus, or the tela choroidea. Only eleven cases of deep sylvian meningiomas have been presented in the literature. We have reviewed the clinical and radiological findings in such meningiomas. MR findings in deep sylvian meningioma have not been described.(ABSTRACT TRUNCATED AT 250 WORDS)

We report an unusual case of non-traumatic cerebrospinal fluid rhinorrhea associated with aqueductal stenosis and hydrocephalus. The patient was a 10-year-old girl who suddenly developed massive CSF rhinorrhea following severe edema of the left side of her face. CT scan showed marked dilatation of the lateral and third ventricles and enlarged sphenoid sinus of water density, extending to the lateral wall of the left orbit and to the left pterygoid fossa. Immediately after the onset of CSF rhinorrhea, ventricular drainage was performed, but the rhinorrhea persisted. Ventriculography revealed predominant flow of the contrast medium into the left temporal horn and abnormal collection in the sphenoid sinus. Coronal CT scan did not show any focal bony defect, but a thin layer was seen in the base of the left middle fossa. Exploration of the skull base in the left middle fossa was performed through a left frontotemporal craniotomy. An irregular bony defect measuring 7 x 12mm was then found in the anterolateral floor of the middle fossa and the dura was also perforated there. Brain tissue including the temporal horn protruded through the bony defect into the sphenoid sinus. After excision of the herniated brain tissue, repair was accomplished by packing muscle into the bony defect and covering the dural defect with fat reinforced by coating with fibrin glue. Postoperatively, the CSF rhinorrhea has stopped and the edema of her face has disappeared. We discuss the etiology of this unusual spontaneous CSF leakage through the middle fossa and the abnormally enlarged sphenoid sinus.

We report the case of a 29-year-old woman in whom a saccular aneurysm of the distal anterior cerebral artery developed following head trauma due to a car accident. She was semicomatose on admission but had no lateralizing motor signs. Reflexes were symmetrical, with bilateral extensor toe sign. X-ray of the skull showed no fracture but CT scans demonstrated a large frontal hematoma and interhemispheric bleeding. Initial cerebral angiography performed within 12 hours of trauma showed a small protrusion on the pericallosal portion of the left pericallosal artery with no branching point nearby. Angiography was repeated on the 9th day after admission and confirmed the presence of a saccular aneurysm of the pericallosal artery, which had been visible as a small protrusion on the initial angiogram. Traumatic aneurysm was suspected and successful neck clipping of the aneurysm was performed on the 14th day. Preoperative CT and angiographic findings could not rule out a congenital aneurysm but the histological study of the specimen confirmed that it was a traumatic false aneurysm. We discussed the diagnosis and the etiology of posttraumatic aneurysm.