ABSTRACT
A patient with a Spetzler-Martin-grade-III AVM, initially embolized and then stereotactically irradiated, who - with a latency of several months - showed progressive neurological deterioration, is reported. Magnetic resonance imaging revealed enormous ipsilateral brain oedema, which did not respond to dexamethasone. Upon further neurological deterioration the former AVM nidus plus an adjacent rim of brain tissue were removed and the patient recovered considerably. It is concluded that embolization in conjunction with irradiation may impair the blood-brain-barrier with resulting long-term oedema in the surrounding brain, and that surgical treatment should be considered in selected cases.
Subject(s)
Arteriovenous Malformations/surgery , Blood-Brain Barrier/injuries , Brain Edema/etiology , Embolization, Therapeutic/adverse effects , Postoperative Complications/etiology , Radiosurgery/adverse effects , Adult , Arteriovenous Malformations/diagnosis , Blood-Brain Barrier/physiopathology , Blood-Brain Barrier/radiation effects , Brain/pathology , Brain/physiopathology , Brain/surgery , Brain Edema/physiopathology , Brain Edema/surgery , Cerebral Angiography , Cerebral Arteries/diagnostic imaging , Cerebral Arteries/pathology , Cerebral Arteries/surgery , Dexamethasone/therapeutic use , Disease Progression , Hemianopsia/etiology , Humans , Magnetic Resonance Imaging , Male , Microsurgery/methods , Neurosurgical Procedures/methods , Postoperative Complications/physiopathology , Reoperation , Time Factors , Treatment Outcome , Vascular Surgical Procedures/methodsABSTRACT
OBJECTIVE: To determine long term functional outcome and length of survival of patients undergoing decompressive craniectomy for space occupying infarction of the middle cerebral artery (MCA), and to identify risk factors associated with death and unfavourable outcomes METHODS: Databases of patients undergoing decompressive craniectomy for space occupying MCA infarction compiled at eight neurosurgical departments (1996-2001) were merged, and 188 patients were evaluated. Mortality was calculated by the Kaplan-Meier method. Clinical outcome was rated using the Glasgow outcome scale (GOS). The prognostic impact of patient related covariates on length of survival and the GOS was analysed multivariately. RESULTS: The unadjusted 3, 6, and 12 month mortality rates were 7.9%, 37.6%, and 43.8%, respectively (median follow up, 26 weeks). In the "best" multivariate model, age >50 years (p<0.02) and the involvement of two or more additional vascular territories (p<0.01) had an unfavourable impact on length of survival. The adjusted six month mortality was as low as 20.0% (no risk factor) and as high as 59.7% (two risk factors). A GOS score of
Subject(s)
Brain/blood supply , Brain/surgery , Functional Laterality , Infarction, Middle Cerebral Artery/surgery , Neurosurgical Procedures/methods , Adolescent , Adult , Aged , Decompression, Surgical , Female , Glasgow Outcome Scale , Hemodynamics/physiology , Humans , Infarction, Middle Cerebral Artery/physiopathology , Male , Middle Aged , Preoperative Care , Prognosis , Prospective Studies , Risk FactorsABSTRACT
The role of TNF-alpha in the course of Wallerian degeneration of the sciatic nerve was studied in control and TNF-alpha deficient mice. In control animals, the characteristic phenomena of Wallerian degeneration such as axon and myelin degeneration as well as macrophage recruitment with subsequent myelin removal were observed. In TNF-alpha deficient mice, in contrast, macrophage recruitment into the degenerating nerves was impaired resulting in a delayed myelin removal. However, the myelin phagocytic capacity of macrophages was not affected as it could be demonstrated by a similar myelin load of control and TNF-alpha deficient macrophages. These data indicate that the main function of TNF-alpha during Wallerian degeneration is the induction of macrophage recruitment from the periphery without affecting myelin damage or phagocytosis.
Subject(s)
Macrophages/immunology , Phagocytosis , Sciatic Nerve/pathology , Tumor Necrosis Factor-alpha/physiology , Wallerian Degeneration/immunology , Wallerian Degeneration/pathology , Animals , Leukocyte Count , Macrophage Activation , Macrophages/metabolism , Mice , Mice, Inbred C57BL , Mice, Knockout , Microscopy, Electron , Myelin Sheath/metabolism , Sciatic Nerve/immunology , Sciatic Nerve/metabolism , Sciatic Nerve/surgery , Tumor Necrosis Factor-alpha/deficiency , Tumor Necrosis Factor-alpha/genetics , Wallerian Degeneration/metabolismABSTRACT
The effects of pentoxifylline (POX) on macrophage migration and myelin uptake were studied in an in vitro model of myelin phagocytosis. The POX is a phosphodiesterase inhibitor which inhibits TNF-alpha (tumor necrosis factor alpha) production and reduces ICAM-1 (intercellular adhesion molecule-1) expression by macrophages. Both of these molecules have earlier been shown to be involved in the process of myelin recognition and degradation. In the present series of experiments, cocultured peripheral nerves and macrophages were treated with different concentrations of POX. Untreated controls were massively invaded by macrophages which ingested the degenerating myelin sheaths. High concentrations of POX (100 microg ml(-1)) inhibited macrophage invasion of the nerves. Lower POX concentrations (50 microg ml(-1)), in contrast, lead to an increased myelin uptake by phagocytic cells without affecting macrophage migration. These data indicate that POX may regulate different effector functions of macrophages such as migration and myelin phagocytosis during Wallerian degeneration. This is important for inflammatory demyelinating conditions in the central or peripheral nervous system (PNS) in which macrophages are also important effector cells. Since POX is used as an immunomodulatory drug in demyelinating diseases, its effects on the described macrophage functions may be of high relevance. An increased myelin uptake during Wallerian degeneration may also support a more efficient axonal regeneration by removing axonal outgrowth inhibitors.
