Early cerebral blood volume after severe traumatic brain injury in patients with early cerebral ischemia.

Recent early cerebral blood flow (CBF) studies on severe head injury have revealed ischemia in a substantial number of patients with a variety of CT diagnoses. However, the underlying derangements causing this early ischemia are unknown, but cerebral blood volume (CBV) measurements might offer some insight into this pathology. Therefore, acute CBF and CBV measurements were performed in 51 adult severely head injured patients within 24 hours after injury. For this purpose the stable Xenon-CT procedure was used for assessment of CBF, and a dynamic CT imaging technique was used for determining CBV. All ischemic patients were found among 35 subjects studied within 4 hours after injury (31%). Based on the occurrence of regional ischemia seven patients with varying anatomical lesions on CT were selected for comparison between CBF and CBV in ischemic and non-ischemic areas. Both CBF (p < 0.02) and CBV (p < 0.02) exhibited significantly lower values in the ischemic zones. Ten patients showing a subdural hematoma (SDH) were studied preceding surgery and seven were ischemic in at least one lobe or brainstem. Ipsilateral CBF was lower than CBF in the contralateral side (p < 0.1). CBV at the ipsilateral side was significantly reduced compared to the contralateral side (p < 0.05). Follow-up studies were performed in three ischemic patients and in one borderline ischemic patient immediately after removal of SDH showing a striking increase in both CBF and CBV. In the remaining 26 subjects follow-up studies were obtained between day 2 and day 8 and all patients showed CBF values within the normal range. These data evidently support the suggestion that compromise of the microvasculature is the cause of early ischemia, rather than vasospasm of the larger conductance vessels. This has implications for acute post-traumatic therapeutical strategies and management of the severely head injured patient and may lead to testing of new drugs that are effective in interfering with processes causing this ischemia.

Regional cerebral blood volume after severe head injury in patients with regional cerebral ischemia.

OBJECTIVE: Recent early cerebral blood flow (CBF) studies in cases of severe head injury have revealed ischemia in a substantial number of patients with a variety of computed tomographically demonstrated diagnoses. The underlying derangements causing this early ischemia are unknown, but cerebral blood volume (CBV) measurements might offer some insight into this pathological abnormality. METHODS: For this purpose, stable xenon-enhanced computed tomography was used for assessment of CBF, and a dynamic computed tomographic imaging technique was used for determining CBV. Based on the occurrence of regional ischemia (CBF < 20 ml/100 g/min), seven patients with varying anatomic lesions revealed by computed tomography were identified for comparison between CBF and CBV in ischemic and nonischemic areas. RESULTS: Both CBF (15+/-4.3 versus 34+/-11 g/min, P < 0.002) and CBV (2.5+/-1.0 versus 4.9+/-1.9 ml/100 g) exhibited significantly lower values in the ischemic zones than in the nonischemic zones (means+/-standard deviations). Among 26 patients with or without ischemia observed during their initial follow-up studies, which were conducted between Days 2 and 8, all patients showed CBF and CBV values within the low-normal range. CONCLUSION: These data evidently support the suggestion that compromise of the microvasculature is the cause of early ischemia, rather than vasospasm of the larger conductance vessels.

Glutamate release and cerebral blood flow after severe human head injury.

Elevations of extracellular glutamate have been found in patients with prolonged brain ischemia and focal cerebral contusions, following severe head injury. About 30% of severely head injured patients develop cerebral ischemia, defined as CBF < 18 ml/100g/min. Patients with both global and regional cerebral ischemia have the worst outcome. However, the relationship between CBF and EAA release is not well understood in head injured humans, and may differ from the findings in normal animals. To study the relationship between EAA release and CBF after severe head injury, we performed cerebral blood flow measurements using stable xenon enhanced computed tomography and correlated these with glutamate release in the extracellular fluid, measured by continuous microdialysis, in 25 severely head injured patients. Sustained cerebral blood flow reductions below the threshold for ischemic neuronal damage was closely related to massive excitatory amino acid release, as in previous animal studies. In patients without secondary ischemia, or focal contusions, delayed post-traumatic glutamate release appeared to be only transient or did not occur at all.

Thresholds for cerebral ischemia after severe head injury: relationship with late CT findings and outcome.

Cerebral ischemic insults in at least 30% of severely head injured patients at a very early stage following trauma and are associated with early death. To date, the threshold for ischemia of 18 mL/100g/min used in human head injury studies has been adopted from animal studies (by temporary occlusion of the middle cerebral artery). Since the traumatized brain becomes more susceptible to irreversible damage if accompanied by ischemia one may question whether the threshold for ischemic vulnerability is higher than 18 mL/100 g/min. Cerebral ischemia can cause atrophy. Therefore, the authors obtained computerized tomography (CT) scans in 33 comatose head-injured patients (Glasgow Coma Score of 8 or less) at least 3 months following injury and compared ventricle sizes (as a reflection of atrophy) with cerebral blood flow (CBF) obtained within 4 h (average 2.3 +/- 0.8 h) after injury. Ventricular measurements were performed in three fashions: the third ventricular size (cm), the bicaudate cerebral ventricular index (BCVI), and the hemispheric ventricular index (HCVI). No significant correlation was found between early CBF and any of the ventricule sizes. Applying a multiple correlation analysis with four independent parameters [CBF, CBF/time postinjury, CBF/(time postinjury)2, age], only age emerged as a significant indicator for predicting ventricle size (p < 0.001). We also compared CBF data, obtained within 4 h after trauma, from survivors at 3 months after injury (mean CBF of 32 mL/100 g/min) with CBF data from non-survivors (CBF 20 mL/100 g/min). The difference in CBF between survivors and nonsurvivors was significant at p < 0.001 (Wilcoxon rank-sum test). The proportion of patients with CBF less than or equal to 20 mL/100 g/min was 56% in the nonsurvivors and only 5% in survivors. The difference in the proportions was significant at p < 0.001 (chi-square test). We conclude that a measure of atrophy does not correlate with ultra-early CBF. However, based on the clear distinction between survivors and nonsurvivors, we suggest the threshold for ischemia after head injury be redefined as a CBF of 20 mL/100 g/min.

Central cementoossifying fibroma of the maxillary sinus: a review of six cases.

We present the radiographic findings of six patients with central cementoossifying fibromas of the maxilla. CT typically demonstrated large, spherical tumors in the maxillary alveolar ridge, filling and expanding the maxillary sinus and extending to involve the ipsilateral hard palate. The central tumors ranged from having soft-tissue density with scattered foci of high density to being heavily calcified.

Epilepsy surgery: removing the thorn from the lion's paw.

In the United States, 10,000 to 20,000 patients have epilepsy uncontrolled by medication. The addition of a second-line drug to the primary regimen has a 2% to 11% chance of controlling the seizures. We present a series of 35 patients with intractable epilepsy who had surgical resection of their seizure focus. Seventy-five percent of the patients with temporal lobe epilepsy were made seizure free, with an additional 14% sustaining a greater than 90% reduction in seizures (decrease in number and frequency). Seventy-one percent of the patients with extratemporal lobe epilepsy (seizures originating outside the temporal lobe) had a worthwhile reduction (> 90%) in their seizures. Two patients sustained permanent clinically significant deficits as a result of their presurgical evaluation or resection. There were no deaths. Epilepsy surgery offers a cure for the "incurable" patient with a morbidity of 5% to 6%.

MR angiography artifact due to metal joint of ventriculoperitoneal shunt mimicking severe carotid stenosis.

An artifact due to the metal joint of a ventriculoperitoneal shunt resulted in a diagnosis of severe internal carotid artery stenosis at magnetic resonance angiography. Conventional x-ray angiography showed the presence of the metal joint and revealed that the artery was not stenotic.

Documented reversal of global ischemia immediately after removal of an acute subdural hematoma. Report of two cases.

The authors report two cases of severe head injury with acute subdural hematoma, in which cerebral blood flow (CBF) and cerebral blood volume (CBV) measurements were obtained prior to evacuation of the subdural hematoma and again immediately after removal. The first patient, a 21-year-old man with a motor response localizing to pain, had a global CBF of 18.2 ml/100 gm/min and a decreased global CBV of 3.7 ml/100 gm at 2.3 hours after injury. Immediately after removal of the subdural hematoma (8.1 hours after injury), CBF and CBV measurements revealed increases to 35.5 ml/100 gm/min and 5.8 ml/100 gm, respectively. The second patient, a 49-year-old woman with a normal flexor motor response to pain, had preoperative global values of 15.8 ml/100 gm/min for CBF and 2.0 ml/100 gm for CBV at 3 hours after injury. Postoperatively (9.3 hours after injury), the CBF and CBV values increased to 41.6 ml/100 gm/min and 4.0 ml/100 gm, respectively. The first patient, with only borderline ischemia and removal of the subdural hematoma within 3 hours, made a good recovery, while the second patient, with prolonged lower levels of CBF, remained in a persistent vegetative state. The low values of preoperative CBV argue for compression of the microcirculation as the cause of ischemia.

Imaging the sphenoid bone and basiocciput: anatomic considerations.

The sphenoid bone is a complex structure with an intricate embryologic origin. It is centrally located within the skull base and articulates with almost every structure in the skull and face. The sphenoid bone contains multiple foramina and fissures accommodating numerous vessels and nerves. This report reviews the embryology of the sphenoid bone and its normal postnatal changes, and describes the normal anatomy of the sphenoid bone and its numerous foramina and fissures. Computed tomography (CT) and magnetic resonance (MR) are used to illustrate developmental changes and normal anatomy.

Imaging the sphenoid bone and basiocciput: pathological considerations.

Many diverse pathologic processes can involve the sphenoid bone because of its complex embryologic origin. In addition to primary neoplasia, the central location of the sphenoid predisposes it to involvement by many intracranial and extracranial lesions. The presence of multiple foramina and fissures offer "paths of least resistance" that allow the spread of pathology across the skull base. Sphenoid sinus disease also accounts for a number of pathologic entities occurring in this vicinity. This article reviews the more common lesions affecting the sphenoid bone as well as their CT and MR appearance.

Intussusception: hydrostatic pressure equivalents for barium and meglumine sodium diatrizoate.

The pressures generated by a barium suspension and various solutions of meglumine sodium diatrizoate in water were measured with a manometer. A pressure of 120 mm Hg was produced by a 3.5-foot (105-cm) column of 60% wt/vol barium and a 5-foot (150-cm) column of either a 1:3 or 1:4 solution of meglumine sodium diatrizoate and water. This is the pressure used to reduce an intussusception with air.