Neurosurg Focus
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Comparative Study
Mechanisms underlying the formation and enlargement of noncommunicating syringomyelia: experimental studies.
The pathogenesis of noncommunicating syringomyelia is unknown, and none of the existing theories adequately explains the production of cysts that occur in association with conditions other than Chiari malformation. The authors' hypothesis is that an arterial pulsation-driven perivascular flow of cerebrospinal fluid (CSF) is responsible for syrinx formation and enlargement. They investigated normal CSF flow patterns in 20 rats and five sheep by using the tracer horseradish peroxidase; the effect of reducing arterial pulse pressure was examined in four sheep by partially ligating the brachiocephalic trunk; CSF flow was examined in 78 rats with the intraparenchymal kaolin model of noncommunicating syringomyelia; and extracanalicular cysts were examined using the excitotoxic model in 38 rats. ⋯ In animals with noncommunicating syringomyelia, there was rapid CSF flow into isolated and enlarged segments of central canal, even when these cysts were causing pressure damage to the surrounding spinal cord. Exitotoxic injury of the spinal cord caused the formation of extracanalicular cysts, and larger cysts were produced when this injury was combined with arachnoiditis, which impaired subarachnoid CSF flow. The results of these experiments support the hypothesis that arterial pulsation-driven perivascular fluid flow is responsible for syrinx formation and enlargement.
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In this retrospective study, the authors evaluated confounding risk factors, which are allegedly influential in causing unprovoked posttraumatic epilepsy, in 489 patients from the frontlines of the Iran-Iraq War. Four hundred eighty-nine patients were followed for 6 to154 months (mean 39.4 months, median 23 months), and important factors precipitating posttraumatic epilepsy were evaluated using uni- and multivariate regression analysis. One hundred fifty-seven (32%) of 489 patients became epileptic during the study period. ⋯ The results of multivariate analysis, on the other hand, indicated that the GOS score and motor deficit were of greater statistical importance (X2 = 35.24, p < 0.0001; and X2 = 7.1, p < 0.07, respectively). Factors that did have much statistically significant bearing on posttraumatic epilepsy were the projectile type, site of injury on the skull, patient age, number of affected lobes, related hemorrhagic complications, and retained metallic or bone fragments. Glasgow Outcome Scale score and focal motor neurological deficit are of particular importance in predicting posttraumatic epilepsy after missile head injury.
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The indications for cranioplasty after decompressive craniectomy are cosmetic repair and, mainly, restoration of cerebral protection. Although neurological improvement after cranioplasty is repeatedly noted, the reasons for this still remain unclear. Few observations concerning the impact of CSF hydrodynamic and/or atmospheric pressure were published during the last decades. ⋯ Metabolic deficits, which were observed in the injured as compared with the noninjured hemisphere, were found to improve after reimplantation of the skull bone flap. Cranioplasty appears to affect postural blood flow regulation, CVR capacity, and cerebral glucose metabolism markedly. Thus, early cranioplasty is warranted to facilitate rehabilitation in patients after decompressive craniectomy.