OBJECTIVE:. Long-term data on the natural history of traditionally treated cranial base meningiomas are necessary to judge the benefit of modern cranial

Peripheral hypersensitivity (hyperalgesia and allodynia) are common phenomena both in inflammatory and in neuropathic pain conditions. Several rat models of mononeuropathy (Bennett, Seltzer and Gazelius models) display such symptoms following partial injury to the sciatic nerve. Using immunohistochemistry and behavioral tests, we investigated inflammatory cell and cytokine responses in the sciatic nerve 14 days after injury created in these different models as well as after axotomy. Tactile hypersensitivity ('allodynia') was present in all Gazelius model rats whereas only 38 and 29% of the Bennett and Seltzer models, respectively, displayed this sign of neuropathy. The inflammatory reactions in rats with and without tactile allodynia were compared. Monocytes/macrophages (ED-1), natural killer cells, T lymphocytes, and the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), were significantly upregulated in all nerve injured rats in comparison to sham-operated controls. Interestingly, ED-1-, TNF-alpha- and IL-6-positive cells increased more markedly in allodynic Bennett and Seltzer rats than in non-allodynic ones. The magnitude of the inflammatory response does not seem to relate to the extent of damage to the nerve fibers because axotomized rats displayed much lower upregulation. Our findings indicate that the considerable increase in monocytes/macrophages induced by a nerve injury results in a very high release of IL-6 and TNF-alpha. This may relate to the generation of tactile allodynia/hyperalgesia, since there was a clear correlation between the number of ED-1 and IL-6-positive cells and the degree of allodynia. It is possible that measures to reduce monocyte/macrophage recruitment and the release of pro-inflammatory interleukins after nerve damage could influence the development of neuropathic pain.

OBJECTIVE:. This study was undertaken to analyze the inflammatory components in contused human brain tissue to compare the findings with previous experi

Object. The proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor—α (TNFα) are produced intracerebrally in brain disorders such as trauma, ischemia, meningitis, and multiple sclerosis. This investigation was undertaken to analyze the effect of intracerebral administration of IL-1β and TNFα on inflammatory response, cell death, and edema development.Methods. Intracerebral microinjections of these cytokines were administered to rats. The animals were killed 24 or 72 hours after the injections, and their brains were analyzed by using deoxynucleotidyl transferase—mediated deoxyuridine triphosphate nick-end labeling (TUNEL) with digoxigenin-labeled deoxyuridine triphosphate, immunohistochemical studies, and brain-specific gravity measurement. The IL-1β induced a transient inflammatory response (p < 0.001) and TUNEL staining (p < 0.001), indicating cell death, in intrinsic central nervous system (CNS) cells and infiltrating inflammatory cells. In 73.8 ± 6.77% of the TUNEL-positive cells, small, fragmented nuclei were found. All TUNEL-positive cells expressed the proapoptotic gene Bax, and 69.6 ± 4.6% of the TUNEL-positive cells expressed the antiapoptotic gene Bcl-2; the Bax expression was stronger than the Bcl-2 expression. Taken together, the data indicate that cell death occurred via the apoptotic pathway. The TNFα did not induce inflammation or DNA fragmentation within the analyzed time period. Both IL-1β (p < 0.001) and TNFα (p < 0.01) caused vasogenic edema, as measured by specific gravity and albumin staining. The edematous effect of TNFα persisted 72 hours after injection (p < 0.01), whereas the IL-1β—treated animals had normalized by that time.Conclusions. Intracerebral inflammation, death of intrinsic CNS cells, and vasogenic edema can be mediated by IL-1β, and TNFα can cause vasogenic edema. Suppression of these cytokines in the clinical setting may improve outcome.

Object. The goal of this study was to provide epidemiological and clinical data on the management of cavernomas of the basal ganglia and brainstem from a long-term series at one institution. Methods. All 68 patients who were referred to the authors' department between 1992 and 2000 for deep cavernomas were evaluated by clinic examinations, review of neuroimaging examinations, and review of charts and operative notes. Twenty-nine patients underwent microsurgical procedures, which carried a 69% risk of transitory neurological deterioration. Radical excision was achieved in 25 of these patients, as determined by a review of neuroimages; the remaining four patients all experienced new hemorrhages that led to increased morbidity or even to mortality. Surgical results were better if surgery was performed early, within 1 month posthemorrhage, than if operations were postponed. In selected patients, deep lesions not reaching a pial surface could be safely removed from the thalamus, basal ganglia, or medulla oblongata. Of five patients who underwent gamma knife surgery, two experienced hemorrhages, one at 2 and the other at 5 years following treatment. Patients who did not undergo surgery had a yearly incidence of hemorrhage that was 2% in cases of incidental cavernomas and 7% in symptomatic ones. Conclusions. Over the long term, outcomes were worse following conservative treatment or shunt insertion surgery than after microsurgery of symptomatic cavernomas. Incidental cavernomas carried a low risk of neurological deterioration. Surgery should follow generally accepted indications, but only with the confidence that total removal can be safely achieved. Surgery that is performed within 10 to 30 days following ictus may be preferable to delayed surgery.