These modifications of the standard transsphenoidal approach are useful for lesions within the boundaries noted above, they offer excellent alternatives to transcranial approaches for these lesions, and they avoid prolonged exposure time and brain retraction. Technical details are discussed and illustrative cases presented.

In our experience, the prior practice of delayed cranioplasty (3-6 months postdecompressive craniectomy), requiring repeat hospital admission, does not seem to lower postcranioplasty infection rates nor the need for cerebrospinal fluid diversion procedures. Our current practice emphasizes cranioplasty during the initial hospital admission, as soon as there is resolution on computed tomography scan of brain swelling outside of the cranial vault with concurrent clinical examination. This occurs as early as 2 weeks postcraniectomy and should lower the overall cost of care by eliminating the need for additional hospital admissions.

Blast wave-induced traumatic injury from terrorist explosive devices can occur at any time in either military or civilian environments. To date, little work has focused on the central nervous system response to a non-penetrating blast injury. We have evaluated the effect of a single 80-psi blast-overpressure wave in a rat model. Histological and immunochemical studies showed an early inflammatory response, tissue damage and the initiation of apoptosis. With regard to inflammation, polymorphonuclear leukocytes and lymphocytes infiltrated brain parenchyma within 1 h post-blast. Glial-fibrillary protein, cyclo-oxygenase-2ir, interleukin-1β and tumor necrosis factor were present by 1 h and remained detectable at three weeks post-injury. High mobility group box-1 protein was detectable at three weeks. With regard to tissue damage, S100β and 4-hydroxynonenal were present at 1 h and remained detectable at three weeks. Amyloid precursor protein was detectable at three weeks. As for apoptosis, Cleaved Caspase-3 was detectable at three weeks. Morris water maze assessment of cognitive function showed that blast injured animals required significantly more time to reach the platform on day 1 of training and traveled a greater distance to get to the platform on days 1 and 2. Blast-injured animals showed a significant increase in swimming speed (p<0.001), increased total distance traveled (p<0.001) and increased number of entries into the previous quadrant that had contained the escape platform (p<0.05). Magnetic resonance imaging showed hyperintense regions in the somatosensory area within 1 h. T2 relaxation times and apparent diffusion coefficients show increasing trends in both somatosensory and cortical regions. These data indicate an early and lasting response of brain tissue to non-penetrating blast over-pressure injury. This early inflammatory response is indicative of a mild traumatic brain injury. There is evidence of early hippocampal dysfunction.

A retrospective review of patients presenting to our institution with aneurysmal subarachnoid hemorrhage between 1980-1990 was accomplished. Eleven variables were examined as to their relationship to clinical vasospasm: age, sex, clinical grade, amount of subarachnoid blood on CT, aneurysm location, incidence of vasospasm, incidence of complications, use of calcium channel blockers, time to surgery, length of stay, and outcome. Data were analyzed with univariate and multivariate logistical regression methodology. By univariate analysis, age under 20, amount of subarachnoid hemorrhage, and clinical grade were associated with a higher risk of vasospasm. Using multivariate logistic regression, these factors, along with age under 35, were correlated as being predictive of clinical vasospasm. When all patients are grouped into either good or bad outcome, and a similar analysis is performed, only in the poor outcome group is the amount of subarachnoid hemorrhage and clinical grade correlated with vasospasm. This suggests that there is a group of patients with a predisposition to vasospasm that is independent of subarachnoid hemorrhage and clinical grade, and that these patients may have a more favorable outcome.

The use of the beta-agonist dobutamine in combination with hypervolemic preload enhancement of cardiac performance was analyzed in 23 patients who failed to respond to traditional preload enhancement following aneurysmal subarachnoid hemorrhage. The patients ranged in age from 13 to 82 years, and three had a history of cardiac disease. Each patient underwent placement of a flow-directed balloon-tipped catheter and the following measurements were obtained during hyperdynamic therapy: pulmonary artery wedge pressure, central venous pressure, cardiac index, stroke volume index, total peripheral resistance, and left ventricular stroke work index (LVSWI). Mean baseline cardiac function was found to be within normal limits (LVSWI = 47.6 +/- 4.2 gm/min/sq m and cardiac index = 3.30 +/- 0.22 liter/min/sq m). After baseline measurements were recorded, 5% albumin was infused at 300 cc/hr and dobutamine was initiated at a rate of 5 to 10 micrograms/kg/hr. This hyperdynamic therapy with dobutamine in the presence of volume loading resulted in a 52% increase in cardiac index, a 15% increase in LVSWI, and a 21% decrease in total peripheral resistance. The clinical reversal of ischemic symptoms due to subarachnoid hemorrhage was evident in 18 (78%) of the 23 patients.

We conclude the following: (a) anterior discectomy and fusion with a static (constrained) plating system is appropriate treatment for this type of injury, (b) in the absence of significant neurologic deficit with residual canal or foraminal stenosis, preoperative closed reduction is not necessary, (c) a small percentage of these patients will have vertebral artery injury, thus warranting screening with 16-slice computed tomographic angiography.

Traumatic brain injury is characterized by neuroinflammatory pathological sequelae which contribute to brain edema and delayed neuronal cell death. Until present, no specific pharmacological compound has been found, which attenuates these pathophysiological events and improves the outcome after head injury. Recent experimental studies suggest that targeting peroxisome proliferator-activated receptors (PPARs) may represent a new anti-inflammatory therapeutic concept for traumatic brain injury. PPARs are “key” transcription factors which inhibit NFκB activity and downstream transcription products, such as proinflammatory and proapoptotic cytokines. The present review outlines our current understanding of PPAR-mediated neuroprotective mechanisms in the injured brain and discusses potential future anti-inflammatory strategies for head-injured patients, with an emphasis on the putative beneficial combination therapy of synthetic cannabinoids (e.g., dexanabinol) with PPARα agonists (e.g., fenofibrate).

Cerebral mucormycosis (without associated involvement of and invasion from the nasal sinuses and turbinates) is an extremely rare opportunistic infection of the central nervous system. We report the case of an intravenous drug abuser (who was negative for the human immunodeficiency virus) who presented with hemiparesis on the right side, slurred speech, altered mental status, and an unsteady gait. Imaging studies revealed a large left-side basal ganglia lesion. A stereotactic biopsy obtained a tissue sample that revealed wide, nonseptated hyphal fragments with granulomatous inflammation. The patient was treated with 3 gm of amphotericin B during a 5-month period. The patient had no residual neurological dysfunction after treatment. Open surgical resection was not employed. This case suggests that stereotactic biopsy followed by long-term amphotericin B therapy, in lieu of open surgical resection, represents a viable treatment option for this rare disorder.