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Object The authors conducted a retrospective study to examine data on rates of obliteration of arteriovenous malformations (AVMs) with use of various combinations of treatment modalities based on Gamma Knife surgery (GKS). The authors believe that this study is the first to report on patients treated with embolization followed by staged GKS. Methods The authors identified 150 patients who underwent GKS for treatment of AVMs between 1994 and 2004. In a retrospective study, 4 independent groups emerged based on the various combinations of treatment: 92 patients who underwent unstaged GKS, 28 patients who underwent embolization followed by unstaged GKS, 23 patients who underwent staged GKS, and 7 patients who underwent embolization followed by staged GKS. A minimum of 3 years of follow-up after the last GKS treatment was required for inclusion in the retrospective analysis. Angiograms, MR images, or CT scans at follow-up were required for calculating rates of obliteration of AVMs. Results Fifty-seven of 150 patients (38%) supplied angiograms, and overall obliteration was confirmed in 43 of these 57 patients (75.4%). An additional 37 patients had follow-up MR images or CT scans. The overall obliteration rate, including patients with follow-up angiograms and patients with follow-up MR images or CT scans, was 68 of 94 (72.3%). Patients who underwent unstaged GKS had a follow-up rate of 58.7% (54 of 92) and an obliteration rate of 75.9% (41 of 54). Patients who underwent embolization followed by unstaged GKS had a follow-up rate of 53.5% (15 of 28) and an obliteration rate of 60.0% (9 of 15). Patients who underwent staged GKS had a follow-up rate of 82.6% (19 of 23) and an obliteration rate of 73.7% (14 of 19). Patients who underwent embolization followed by staged GKS had a follow-up rate of 85.7% (6 of 7) and an obliteration rate of 66.7% (4 of 6). Conclusions Gamma Knife surgery is an effective means of treating AVMs. Embolization prior to GKS may reduce AVM obliteration rates. Staged GKS is a promising method for obtaining high obliteration rates when treating larger AVMs in eloquent locations.

The purpose of this study was to explore the relationship between neurologic function, using a quantitative measurement of continuous somatosensory evoked potentials (SSEPs), and intracranial pressure (ICP) following traumatic brain injury. During a 6 year period, severely head-injured patients with a Glascow Coma Scale ≤ 8 who were not moribund were monitored with SSEPs and ICP measurements. SSEPs from each hemisphere and ICP were recorded hourly for each patient. Neurologic outcomes were scored using the Glasgow Outcome Scale at three months post injury. Although initial SSEP amplitude did not correlate well with outcome, final SSEP summed peak to peak amplitude from both hemispheres (p = .0001), the best hemisphere (p = .0004), and the worst hemisphere (p = .0001) correlated well with the Glasgow Outcome Scale groups. Of a total of 72 patients, 40 had deteriorating SSEPs and 32 had stable or improving SSEPs. Peak ICP values were not statistically different in these groups (p = .6). Among patients with deteriorating SSEPs, 52.5% lost the greatest proportion of hemispheric electrical activity prior to ICP elevation. In the remaining patients, the percent reduction of SSEP activity after peak ICP levels was not statistically different from the percent reduction in SSEP activity prior to the peak ICP levels (p = .9). This data suggests that in a select group of patients with severe head injury, ICP does not cause SSEP deterioration, but rather is the consequence of deterioration of brain function.

✓ Evidence from models of traumatic brain injury implicates excitotoxicity as an integral process in the ultimate neuronal damage that follows. Concentrations of the excitatory amino acid glutamate were serially measured in the cerebrospinal fluid (CSF) of patients with traumatic brain injuries and in control patients for comparison. The purpose of the study was to determine whether glutamate concentrations were significantly elevated following traumatic brain injury and, if so, whether they were elevated in a time frame that would allow the use of antagonist therapy. Cerebrospinal fluid was sampled fresh from ventricular drains every 12 hours and analyzed using high-performance liquid chromatography for the excitatory amino acids. The peak concentrations of glutamate in the CSF of the 12 brain-injured patients ranged from 14 to 474 µM and were significantly higher than those in the three control patients, 4.9 to 17 µM (Mann-Whitney U-test, p < 0.02). Glutamate concentrations in five of the eight patients who were still being sampled on Day 3 were beyond the control group range. The implication of this study is that severely head-injured patients are exposed to high concentrations of a neurotoxic amino acid for days following injury and thus may benefit from antagonist intervention.

We have analyzed predictors of mortality following closed head injury in a series of 1,031 consecutive patients with closed head injury admitted to hospital from January 1986 through December 1990. All patients were treated in a uniform manner and surgical intervention was performed as soon as possible in patients with intracranial mass lesions. Logistic analysis was used to identify patient and injury characteristics that were independent predictors of mortality within this patient group. Significant predictors were Glasgow Coma Score at admission (p = 0.0000), age (p = 0.0000), bilaterally unreactive pupils (p = 0.0000), presence of multiple systemic injuries (p = 0.0004), presence of an intracranial mass lesion (p = 0.0006), and presence of unilateral pupillary abnormalities (p = 0.0279). In an attempt to clarify the relationship between the incidence of these characteristics in series of severely head-injured patients reported during the last 2 decades and the mortality reported in those series, regression analysis was carried out comparing the mean age reported in the series, incidence of mass lesions, and reported mortality. Sixty-four percent of the variability in reported mortality rates could be accounted for by differences in mean age of the patients and mass lesion incidence (p = 0.0035). We conclude that apparent improvements in head injury mortality in the last 2 decades may be partly or wholly due to different population characteristics in the reported series. Multiple injuries appear to be important contributors to patient mortality, and in the interest of improved description of head injury populations, the Injury Severity Score should be reported with age, mass lesion incidence, and Glasgow Coma Score.

We present a patient with an intramuscular pelvic arteriovenous malformation that was initially diagnosed as a tumor of the sciatic nerve sheath. Endovascular embolization, attempted as a preoperative maneuver, was complicated by diffuse pulmonary emboli and death. To our knowledge, this is the first such reported case. Its presentation here broadens the differential diagnosis of sciatic nerve sheath tumors, emphasizes the diagnostic and management issues of masses presenting as peripheral nerve tumors, and provides clinicopathological evidence regarding the cause of neurological symptoms.

Secondary neurulation is the morphogenetic process whereby the caudal segments of the neural tube are derived from cells in the embryonic tail bud. Comparative studies have demonstrated similar characteristics in the mechanism of secondary neurulation among tailless species, which are thought to be due to the evolutionary reduction in tail length (Hughes and Freeman, 1974). In order to explore this hypothesis further, light and scanning electron microscopy was used to study early stages of neurulation in the tail buds of hamster embryos. The golden Syrian hamster is a relatively common laboratory rodent with a reduced tail. In this species, secondary neurulation first became apparent in embryos with approximately 17 pairs of somites. This was well before closure of the posterior neuropore which occurred at the 21-somite stage. The lumen of the neural tube appeared to extend into the tail bud in an even and progressive fashion accompanied by reorientation and rearrangement of tail-bud cells. The mechanism appeared to be similar to that reported in long-tailed rodents.