Expanding cysts of the septum pellucidum, although rare, may be a cause of significant neurological dysfunction. Most become symptomatic as a result of obstruction of the interventricular foramina and produce headaches, papilledema, emesis, and loss of consciousness. Behavioral, autonomic, and sensorimotor symptoms occur when an expanding cyst impinges on the structures of the hypothalamoseptal triangle or impairs the deep cerebral venous drainage. Neuroophthalmological symptoms may develop as a consequence of hydrocephalus or direct compression of visual structures. The authors describe the case of a young boy with an expanding septum pellucidum cyst who presented with a sudden, severe headache and loss of consciousness. In addition, he had a history of hyperactivity and progressively declining school performance. All symptoms resolved following decompression of the cyst. Seventeen cases from the literature are reviewed. The pathophysiological mechanisms underlying the development of symptoms secondary to expanding septum pellucidum cysts are outlined, and the related clinical neuroanatomy is described. A model is proposed for the natural history of expanding septum pellucidum cysts that provides a rational basis for understanding their clinical behavior and response to intervention. In most cases, fenestration or shunting will relieve the obstructive hydrocephalus and mass effect caused by the cyst and will produce rapid symptomatic improvement.
Damaged endothelium is one of the pathological changes of the cerebral vasospastic vessels following subarachnoid hemorrhage. Our recent study shows that oxyhemoglobin (OxyHb) induces apoptosis in vascular endothelial cells. Apoptosis generally requires the action of various classes of proteases, including a family of cysteine proteases, known collectively as the caspases. This study was undertaken to investigate the activation of caspases and the ef®cacy of caspase inhibitors, z-IETD-fmk and z-LEHD-fmk, for oxyhemoglobin-induced apoptosis in vascular endothelial cells. Cultured bovine brain microvascular endothelial cells (passages 5±9) were used for this study. OxyHb (10 mmol/L) was added during the 24±72 h incubation with and without caspase-8 or 2 9 inhibitors (z-IETD-fmk and z-LEHD-fmk). Counting surviving cells, DNA laddering, western blotting of poly(ADP-ribose) polymerase, and measurement of caspase activities were employed to con®rm the cytotoxic effects of OxyHb and the protective effects of the caspase inhibitors. OxyHb produced cell detachment in a time-dependent manner and increased caspase-8 and -9 activities in the cells. z-IETDfmk and z-LEHD-fmk (100 mmol/L) attenuated OxyHbinduced cell loss, DNA laddering, and proteolytic cleavage of PARP, although a lower concentration (10 mmol/L) of caspase inhibitors showed partial effects. OxyHb activates caspase-8 and -9 in cultured vascular endothelial cells, and blocking the action of the caspases with the inhibitors ef®ciently prevents loss of vascular endothelial cells from OxyHb-induced apoptosis in vitro. These results suggest that the caspase cascade participates in OxyHb-induced apoptosis.
Shaken baby syndrome refers to the constellation of nonaccidental injuries occurring in infants and young children as a consequence of violent shaking. The typical victim of shaken baby syndrome is a male infant younger than six months of age who is alone with the perpetrator at the time of injury. Occurrence of the syndrome is unrelated to race, gender, socioeconomic status, or education. The characteristic injuries observed in shaken baby syndrome include subdural hemorrhages, retinal hemorrhages, and fractures of the ribs or long bones. Although each of these injuries may result from violent shaking of the victim, the most severe brain injuries result from the addition of a forceful impact of the infant's or child's head against a firm surface. The unique anatomic features of the infant's head and skeletal system, which account for the type and pattern of injuries observed in shaken baby syndrome, are emphasized in this article.
Endoscopic fenestration of symptomatic septum pellucidum cysts produces immediate relief of the mass effect of the cyst and resolution of associated symptoms. Cannulation of the lateral ventricle before cyst fenestration prevents inadvertent injury to the fornices, thalamus, internal capsule, caudate nucleus, and septal and thalamostriate veins. The endoscopic approach allows the surgeon to ensure communication within the ventricular system, thus avoiding placement of a shunt. Preliminary ultrastructural analysis indicates that the cyst walls derive from the septum pellucidum rather than the choroid plexus or arachnoid. The cellular machinery necessary for fluid secretion was identified in some specimens.
The effect of the dosage and timing of administration of naloxone after spinal cord injury in rats via the ventral compression technique is presented. The rat ventral compression technique allows for a ventral compression of the spinal cord without the requirement of a previous laminectomy. It therefore facilitates the creation of an experimental lesion that is similar to that observed in the human clinicopathological situation. The first part of the two-part study presented herein involved the determination of the optimal dose of naloxone, administered intraperitoneally 45 minutes after the creation of the lesion. Of the groups studied (control group through 10.0 mg/kg group), 2.0 mg/kg of naloxone proved to be superior to both lesser and greater dosages. The second part of the study involved the administration of a 2.0 mg/kg dose of naloxone at varying intervals ranging from 10 minutes before lesioning to 24 hours after lesioning. A multiphasic response was again demonstrated, with an optimal time of administration occurring 45 minutes after the creation of the lesion. A significant effect was offered by a midrange dose of naloxone (2.0 mg/kg), administered at 45 minutes after injury (P less than 0.02 by analysis of variance and Duncan's multiple range test). These findings are discussed with respect to recent evidence regarding the effects of narcotic antagonists on both mu and kappa narcotic receptors. Past and future experiments must account for these responses to multiphasic dosage and timing of administration. Failure to do so may lead to erroneous conclusions.
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