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David W. Rowed, Edward E. Kassel and Anthony J. Lewis

months, he developed diplopia with impaired adduction, abduction, and elevation of the right eye, and impaired supraorbital cutaneous sensation. His pain persisted. Visual acuity remained at 20/25 in both eyes. Initial skull x-ray films and head CT scans appeared consistent with his previous cranial surgery but revealed no additional abnormality. A chest x-ray film was unremarkable. General physical examination, including examination of the nasopharynx, was not helpful. Complete blood count, erythrocyte sedimentation rate, and 2-hour blood glucose determination were

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Keith B. Quattrocchi, Phillip Kissel, William G. Ellis and Edmund H. Frank

these rare and potentially curable lesions is examined. Case Report This 63-year-old man presented with a 2-year history of vague frontal headaches. Examination Evaluation by a neurologist revealed no abnormalities save a mild dementia. A head CT scan at that time demonstrated a 2-cm hyperdense lesion located within the right posterior fossa; the mass enhanced minimally after intravenous injection of a contrast agent. A T 1 -weighted MR image demonstrated a low-signal lesion which was well circumscribed and contiguous with the tentorium cerebelli, and a T

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Julio Cruz, Michael E. Miner, Steven J. Allen, Wayne M. Alves and Thomas A. Gennarelli

, 15 we found an excellent inverse relationship between the global cerebral O 2 extraction and CBF averaged from 16 brain regions. Moreover, in hyperventilated patients with predominantly diffuse head CT findings (as is the case in the present work), we found rCBF changes to be far more global than regional (unpublished observations), further supporting the validity of the global arteriojugular measurements under these circumstances. Intracranial Hypertension The 41 observations were made at a time when ICP had risen to over 20 mm Hg (in spite of profound

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Ehud Arbit, Jatin Shah, Robert Bedford and Graziano Carlon

drain removal. The diagnosis is made based on clinical signs and symptoms, the presence of a large amount of intracranial air on the skull radiograph, and a characteristic appearance on the head CT scan. 8, 12, 14 A prerequisite for the formation of an expanding aerocele is an intracranial pressure gradient that is favorable for the ingress of air. Usually this is created either by a persistent cerebrospinal fluid (CSF) leak or as a result of a patent intracranial shunt system. 10, 18 If CSF escapes and air can enter the intracranial cavity to compensate for the

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Joseph L. Voelker, Robert L. Campbell and Jans Muller

. Cerebral angiography was abnormal in 32 of the 39 patients in which it was performed. An avascular mass effect with elevation of the A 1 segments of the anterior cerebral arteries was generally seen, although Byrd, et al., 13 described a “thin rim-like staining over the posterior aspect of the cyst.” A head CT scan was obtained in 89 patients. In the majority, the cyst was manifest as a round or lobulated, intra- and suprasellar mass with a density similar to that of cerebrospinal fluid (CSF). The cyst was isodense to the brain in four patients, hyperdense in eight

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Laligam N. Sekhar, Shlomo Pomeranz, Ivo P. Janecka, Barry Hirsch and Sai Ramasastry

requires the demonstration of adequate swallowing without aspiration by a modified barium swallow. Recovery to a Grade III facial nerve function according to the classification of House 17 usually occurs 12 to 18 months following the nerve graft reconstruction. Head CT is usually obtained on the day following surgery and before discharge. Angiographic studies are carried out if the ICA was repaired or grafted or there is a suspicion of possible intraoperative damage to the vessel. Following discharge, clinical follow-up examinations are accompanied with CT and/or MR

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Wouter I. Schievink, David G. Piepgras and Fremont P. Wirth

admission he was semicomatose. A head CT scan showed a large left temporal intracerebral hemorrhage with a massive amount of blood in the subarachnoid space. Angiography revealed no change in the size or configuration of the three aneurysms ( Fig. 2 ). The patient underwent a craniotomy with evacuation of the hematoma. At the base of the hematoma, the left 4-mm MCA aneurysm was identified as the clear source of the hemorrhage. Clot extended from the aneurysm into the hematoma. The aneurysm was clipped. The 10-mm left ICA aneurysm was found to be calcified and was also

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Gerrit J. Bouma, J. Paul Muizelaar, Warren A. Stringer, Sung C. Choi, Panos Fatouros and Harold F. Young

that in all patients the Xe-CT was the initial diagnostic study. This study provided information on both CBF and anatomy, as mass lesions requiring immediate surgical intervention can easily be identified on the unenhanced baseline scans. If no mass lesions were present, a complete unenhanced multi-level head CT scan was performed following the Xe-CT CBF study. In this way we were able to perform preoperative CBF studies in a total of 10 patients with acute intracranial hematomas, all of whom have been included in the present series. The protocol was approved by the

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Pedro Lylyk, Fernando Viñuela, Jacques E. Dion, Gary Duckwiler, Guido Guglielmi, Warwick Peacock and Neil Martin

alleviate intracranial massive arteriovenous shunting and concomitant biventricular congestive heart failure. 1, 5, 6, 8 Head CT and MR imaging demonstrate abnormal dilatation of the midline venous structure and the presence of thrombus or calcification in its walls or lumen, compression of the diencephalon, hydrocephalus and brain atrophy, and calcification or hemorrhage. 1 Color Doppler ultrasonography shows hemodynamic changes associated with the malformation as well as intraluminal thrombosis related to therapy. 14 Four-vessel cerebral angiography identifies the

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E. Clarke Haley Jr., Neal F. Kassell, James C. Torner and Participants

clinical criteria: 1) the classic symptoms which include: onset between Days 5 and 12 after SAH; worsening of headache, stiff neck, and/or low-grade fever; insidious onset of confusion, disorientation, and/or decline in level of consciousness; and focal deficit, which may fluctuate in severity; 2) a head CT scan excluding other causes of neurological worsening, such as rebleeding or hydrocephalus; 3) no other identifiable cause of neurological worsening, such as electrolyte disturbance, hypoxia, or seizure; and 4) confirmation of vasospasm by angiography or transcranial