SummaryA 27-year-old woman developed severe adhesive arachnoiditis after an obstetric spinal anaesthetic with bupivacaine and fentanyl, complicated by back pain and headache. No other precipitating cause could be identified. She presented one week postpartum with communicating hydrocephalus and syringomyelia and underwent ventriculoperitoneal shunting and foramen magnum decompression. Two months later, she developed rapid, progressive paraplegia and sphincter dysfunction. Attempted treatments included exploratory laminectomy, external drainage of the syrinx and intravenous steroids, but these were unsuccessful and the patient remains significantly disabled 21 months later. We discuss the pathophysiology of adhesive arachnoiditis following central neuraxial anaesthesia and possible causative factors, including contamination of the injectate, intrathecal blood and local anaesthetic neurotoxicity, with reference to other published cases. In the absence of more conclusive data, practitioners of central neuraxial anaesthesia can only continue to ensure meticulous, aseptic, atraumatic technique and avoid all potential sources of contamination. It seems appropriate to discuss with patients the possibility of delayed, permanent neurological deficit while taking informed consent. Case reportA 27-year-old woman with no significant medical history and in her first pregnancy underwent spinal anaesthesia for caesarean section for fetal compromise at another hospital at 42 weeks' gestation, after going into spontaneous labour. With the patient sitting, the skin over the L4-5 interspace was cleaned once by a consultant anaesthetist using a SOLU-I.V.Ò MAXI swabstick (Solumed, Laval, Canada) impregnated with 2% chlorhexidine gluconate and 70% isopropyl alcohol. There was no delay between opening the swabstick packaging and its use on the patient's skin. It is not clear whether the swabstick and its packaging were disposed of immediately. The prepared area was allowed to air-dry for 3 min before a 24-G needle (Becton, Dickinson & Company, Franklin Lakes, NJ, USA) was placed at L4-5 on the first attempt by a consultant anaesthetist wearing a sterile surgical gown and gloves, mask and hat, using an aseptic technique. After aspiration of free-flowing, clear cerebrospinal fluid (CSF), 2.5 ml bupivacaine 0.5% with 12.5 lg fentanyl was administered over approximately 15 s. A few seconds after the end of the injection, the patient complained of severe, burning pain in the lower back radiating into the legs bilaterally, worse on the right than the left. The pain began to recede as the block took effect and this was formally assessed 10 min after the

The amygdala complex substantially contributes to the generation and propagation of focal seizures in patients suffering from temporal lobe epilepsy (TLE). A cellular substrate for increased excitability in the human amygdala, however, remains to be identified. Here, we analyzed the three-dimensional morphology of 264 neurons from different subregions of the amygdaloid complex obtained from 17 "en bloc" resected surgical specimens using intracellular Lucifer Yellow (LY) injection and confocal laser scanning microscopy. Autopsy samples from unaffected individuals ( n=3, 20 neurons) served as controls. We have identified spine-laden, spine-sparse and aspinous cells in the lateral, basal, accessory basal and granular nuclei. Semiquantitative analysis points to significant changes in neuronal soma size, number of dendrites and spine densities in specimens from epilepsy patients compared to controls. Neuronal somata in the epilepsy group were smaller compared to controls ( P<0.01), neurons had fewer first-order dendrites ( P<0.01), whereas the maximum density of spines per dendritic segment in these cells was increased in TLE patients ( P<0.01). There were also dendritic alterations such as focal constrictions or spine bifurcations. These changes were consistent between amygdaloid subregions. The dendritic morphology of amygdaloid neurons in TLE patients points to substantial changes in synaptic connectivity and would be compatible with altered neuronal circuitries operating in the epileptic human amygdala. Although the morphological alterations differ from those described in hippocampal subregions of a similar cohort of TLE patients, they appear to reflect a characteristic pathological substrate associated with seizure activity/propagation within the amygdaloid complex.

Forty-five percent of patients achieved a worthwhile improvement after pure MST, if Engel outcome Class III is deemed a worthwhile improvement. The alternative five-tiered classification resulted in 50% with worthwhile improvement (excellent, good, or fair outcome), 45% with poor, and 5% with worse outcome. Lesions that are detectable on MR imaging, and large MST areas are predictive of worse results. Significant intraoperative problems may arise, but this happens infrequently. There is a notable rate of transient morbidity but the rate of permanent morbidity is not significant.

The results of this study link ACVRL1 (HHT Type 2 gene) to the formation of the clinically sporadic variants of vascular malformations of the CNS most commonly seen in patients with HHT, that is, AVMs and DAVFs.

Except for the relatively long history of epilepsy, the presence of AS is not associated with specific clinical or electrocorticographic features of mesial TLE. However, patients without AS are particularly at risk for deterioration of short-term verbal memory following amygdalohippocampectomy.

Although clinical and electrophysiological evidence indicates that the amygdaloid body plays an important role in the pathogenesis of temporal lobe epilepsy, there are very few detailed data on histopathological changes in this nucleus in epilepsy patients. In the present study we have examined the lateral nucleus of the amygdaloid body in 70 surgical specimens from patients with temporal lobe epilepsy and in 10 control specimens with respect to neuronal density and gliosis. The results were compared to the neuronal loss in the hippocampal formation. Our goal was to examine the pathological alterations of the amygdaloid body and their correlation with other morphological changes in temporal lobe epilepsy. In epilepsy patients with Ammon's horn sclerosis or focal lesions of the temporal lobe, the neuronal density of the lateral amygdaloid nucleus was significantly decreased as compared to normal controls (P < 0.001). Overall, the mean volumetric density in epilepsy patients was reduced to 59% of that in normal individuals. There was no correlation between the neuronal density in the lateral amygdaloid nucleus and that in the different segments of the hippocampal formation or to the age at onset or the duration of epilepsy. The neuronal loss of the amygdaloid nucleus correlated well with the presence of fibrillary gliosis. Our findings demonstrate that the amygdaloid body is severely altered in most patients with temporal lobe epilepsy and that these changes are independent of those in the hippocampus. The presence of neuronal loss and gliosis in the amygdaloid nucleus of patients with focal lesions but no Ammon's horn sclerosis is compatible with an involvement of the amygdala in secondary epileptogenesis.

Based on a series of 235 temporal mediobasal tumors, a classification system was designed to aid in decision making about operability, surgical risk, and approach.

Object. The authors conducted a study to determine the results of decompressive surgery without fusion in selected patients who presented with radicular compression syndromes caused by degenerative lumbar spondylolisthesis and in whom there was no evidence of hypermobility on flexion—extension radiographs. Methods. The medical records and radiographs obtained in 49 patients were reviewed retrospectively. Clinical status was quantified by summing self-assessed Prolo Scale scores. All 49 patients (55% female, mean age 68.7 years) presented with leg pain accompanied by lumbalgia in 85.7% of the cases. Preoperatively the median sum of Prolo Scale scores was 4. The mean preoperative degree of forward vertebral displacement was 13.5% and was located at L-4 in 67% of the cases. Osseous decompression alone was performed in 53%, and an additional discectomy at the level of displacement was undertaken in the remaining patients because of herniated discs. Major complications (deep wound infection) occurred in 2%. During a mean follow-up period of 3.73 years, 10.2% of the patients underwent instrumentation-assisted lumbar fusion when decompression alone failed to resolve symptoms. At last follow up the median overall Prolo Scale score was 8. Excellent and good results were demonstrated in 73.5% of the patients. Prolonged back pain (r = 0.381) as well as the preoperative degree of displacement (r = 0.81) and disc space height (r = 0.424) influenced outcome (p ≤ 0.05); additional discectomy for simultaneous disc herniation at the displaced level did not influence outcome (p > 0.05). Conclusions. These results appear to support a less invasive approach in this subgroup of elderly patients with degenerative lumbar spondylolisthesis—induced radicular compression syndromes and without radiographically documented hypermobility. Additional discectomy for simultaneous disc herniation of the spondylolisthetic level did not adversely influence the outcome. Complication rates are minimized and fusion can eventually be performed should decompression alone fail. A prospective controlled study is required to confirm these results.