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Traumatic brain injury in animals and humans is well known to cause axonal damage diffusely scattered throughout the brain without evidence of other brain parenchymal change. This observation has prompted some to posit that such damaged axons are well positioned to mount a regenerative attempt. The present study uses an immunocytochemical marker specific for regenerating neurites to explore this issue. Further, in an attempt to expedite and enhance any potential regenerative effort, this study evaluates the efficacy of intrathecally applied nerve growth factor. Three sets of experiments were performed in adult cats. One group of animals was subjected to moderate fluid percussion brain injury and followed for 7 or 14 days post injury, with the continuous intraventricular infusion of nerve growth factor delivered by implanted osmotic pumps. These animals were compared to a second group of time-matched, sham-operated animals receiving artificial cerebrospinal fluid infusion. To assess axonal damage immunohistochemical staining for the low molecular weight neurofilament subunit (NF-L) was carried out using an NR4 monoclonal antibody. To localize axons exhibiting a regenerative response immunohistochemical staining for the growth associated protein GAP43 was employed. In sham controls, at the light microscopic level NF-L-immunoreactive axonal swellings were numerous at 7 days, but by 14 days post injury their frequency declined markedly. In contrast, GAP43-immunoreactive, disconnected reactive axonal swellings were rarely observed at 7 days but were numerous at 14 days. Ultrastructural analysis at 14 days post injury of carefully matched sections revealed reactive axons demonstrating sprouting consistent with a regenerative effort. Analysis of tissue from animals of 14 days of survival indicated that supplementation with nerve growth factor did not appear to enhance the capacity of damaged brain axons to mount a regenerative attempt. Rather, it appears that regenerative efforts seen reflect a spontaneous response. A third group of adult cats, subjected to the same injury but not subjected to osmotic pump implantation, was allowed to survive for 22-28 days. Animals in this group also demonstrated GAP43 immunoreactivity in reactive axonal swellings in the brain stem. This study demonstrates that diffusely injured axons can mount a sustained regenerative attempt that is associated with a reorganization of their cytoskeleton and accompanied by an up-regulation of growth-associated proteins.

Background: The effect on CSF pressures and symptoms of weight loss induced by gastric surgery was studied in morbidly obese patients with idiopathic intracranial hypertension (IIH)., Methods: Gastric weight reduction surgery was performed in eight morbidly obese women (49 +/- 3 kg/m2 body mass index) who had IIH and elevated CSF pressures. Each had been treated medically for IIH. Two had ventriculoperitoneal shunts, with occlusion in both and hemorrhage and hemiparesis in one. Post--weight-reduction measurement of CSF pressures, signs and symptoms of IIH, and obesity co-morbidity were evaluated., Results: CSF pressures decreased in all eight patients, from a mean of 353 +/- 35 to a mean of 168 +/- 12 mm H2O (p < 0.001), following mean weight loss of 57 +/- 5 kg (p < 0.001) when measured at 34 +/- 8 months after surgery. At follow-up no patient had papilledema, all eight patients had resolution or marked reduction of headache, and resolution of tinnitus occurred in all six patients with this symptom. Neuroimaging was unchanged at 27 +/- 6 months after surgery in six patients. There was also resolution or clinical improvement of additional obesity-related co-morbidity, including diabetes, hypertension, sleep apnea, obesity hypoventilation, joint pains, stress urinary incontinence, and gastroesophageal reflux., Conclusions: Although several complications occurred following obesity surgery over the 11 years of this study, the current low morbidity and mortality with gastric bypass make this a primary option in the severely obese patient with IIH.

A traumatic cerebral contusion causes a zone of perifocal neuronal necrosis, the cause of which is not known; the surgical management of these lesions remains controversial. To determine the pathophysiological mechanisms responsible for brain damage after contusions, the authors performed cerebral blood flow (CBF) mapping studies and related these to change in local cerebral blood volume (CBV) and ultrastructure. In 11 severely head injured patients with contusion, CBF and CBV were measured in pericontusional areas using stable xenon-computerized tomography (CT). These studies demonstrated a profound reduction in perilesional CBF (mean 17.5 +/- 4 ml/100 g/min), which was always accompanied by a zone of edema defined by CT density measurements. Mean CBV in these regions was 2.3 +/- 0.4 ml/100 g, a reduction to approximately one-half the value of 4.8 ml/100 g found in the nonedematous regions, and to approximately 35% of the value of 6.0 ml/100 g found in normal volunteers. Ultrastructural analysis of the pericontusional tissue, taken at surgery in four patients with high intracranial pressure showed glial swelling with narrowing of the microvascular lumina due to massive podocytic process swelling. Additionally, some suggestion of vascular occlusion due to erythrocyte and leukocyte stasis was seen. These data support the conclusion that microvascular compromise by compression and/or occlusion is a major event associated with profound perilesional hypoperfusion, which is a uniform finding within edematous pericontusional tissue.

Sacral schwannoma is a rare lesion (23 reported cases) with a tendency to reach large proportions. Symptoms are back and leg pain, leg weakness, hypoesthesias, paresthesias, constipation, and incontinence. The peak incidence is between ages 30 and 50. Radiographs of the sacrum are abnormal in nearly all cases. Computed tomography and magnetic resonance imaging may reveal large lesions with bony erosion and involvement of the soft tissues. The treatment of this lesion is complete removal, which is curative.