Otogenic intracranial complications.
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BACKGROUND: Misdiagnosis of spontaneous intracranial hypotension remains a problem, despite increasing recognition. METHODS: Three patients with spontaneous intracranial hypotension presented with typical findings on lumbar puncture, magnetic resonance (MR) imaging, and radioisotope cisternography. All patients showed subdural effusions in the posterior fossa on axial T2-weighted MR imaging. Axial MR images of 112 patients with other conditions were also screened for this finding. RESULTS: One of three patients had typical orthostatic headache, and the other two had continuous headache. The finding of subdural effusions in the posterior fossa on axial T2-weighted MR imaging disappeared after treatment. Similar findings were found in 14 of 112 patients with other conditions. Most of the patients were over 60 years old or had dementia or previous radiation therapy. CONCLUSIONS: Subdural effusions in the posterior fossa can be identified by T2-weighted axial MR imaging, and are useful for the diagnosis of spontaneous intracranial hypotension and for verifying the effectiveness of treatment.
BACKGROUND: Invasive monitoring for the investigation of medically intractable epilepsy may be associated with undesirable morbidity. We performed a review of our recent experience to determine the incidence of major complications. METHODS: We reviewed the clinical records of all patients who underwent invasive EEG monitoring at our institution between 2000 and 2004. RESULTS: One-hundred and sixteen patients (57 males, 59 females) with a mean age of 32 years of age underwent intracranial placement of electrodes for epilepsy surgery investigation. Subdural strips were placed in 115 patients with a mean of eight strips per patient. Subdural grids were inserted in 11 patients and depth electrodes in five. Fourteen of the 15 patients with grids or depth electrodes also had strips. Coverage was unilateral in 37 patients and bilateral in 79 patients. Electrodes were placed over the frontal lobe in 78 cases, temporal in 93, parietal in 24, and occipital in 27 patients. The average duration of investigation was 12.3 days (range 3-29). The evaluation led to the performance of a surgical resection in 85 patients (74%). Complications were seen in four patients with subdural strips (3%), and in two patients with grids (13%), characterized by clinical infection, intracranial hemorrhage, aseptic meningitis, transient neurological deficits, and status epilepticus. Mortality was nil. CONCLUSIONS: In comparison with previously published literature on the topic, the major complication rate in this group of patients appears to be low.
OBJECTIVES: Spinal subdural abscess is rare and only 48 cases have been described to date. In this report, we present an additional spinal subdural tuberculous abscess. METHOD: Tuberculous meningitis was diagnosed with clinical and laboratory findings in a 45-year-old man. A spinal subdural abscess was demonstrated using MRI. Presence of the abscess was revealed by surgical intervention. The diagnosis was confirmed by pathological examination. RESULTS: The patient had been treated for tuberculous meningitis 2 years previously. The disease recurred when anti-tuberculous therapy was prematurely discontinued. During the second treatment, the patient also underwent a ventriculo-peritoneal shunt operation for hydrocephalus. Dizziness and weakness of both legs developed after the postoperative period. Spinal MRI showed a spinal subdural abscess as a iso-intense mass with spinal cord in the T1 and T2 weighted images, ring like enhancement and compression on the spinal cord at T3-T4 level. The patient underwent surgery and the abscess was drained. CONCLUSION: Tuberculosis may cause a spinal subdural abscess and although it is a rare disorder, when encountered MRI is very useful in the diagnosis.
STUDY DESIGN: A new method for prevention of cerebrospinal fluid leakage was studied. OBJECTIVE: To prevent cerebrospinal fluid leakage, we developed a polytetrafluoroethylene fascia patch inlay method. BACKGROUND: One of the major risks of the anterior approach for intra-dural spinal cord lesions is the cerebrospinal fluid leakage. METHODS: A small hemangioblastoma located on the ventral side of the cervical cord was resected with an anterior approach. The dural closure was performed using this polytetrafluoroethylene fascia patch inlay method. RESULTS: The patient had a satisfactory clinical course with no cerebrospinal fluid leakage. CONCLUSION: This polytetrafluoroethylene fascia patch inlay method is very effective. This method may provide both prevention of CSF leakage and future spinal cord adhesion to the dura.
STUDY DESIGN: Case report. OBJECTIVE: To report a rare cause of spinal cord compression. SETTING: University Hospital, Wales, UK. CASE REPORT: A 67-year-old gentleman on oral anticoagulation for atrial fibrillation presented with a 4-h history of progressive loss of sensation and weakness in both legs; there was no history of trauma. On examination, he had a flaccid paraplegia with altered sensation in the L1,2,3 dermatomes and complete anaesthesia in the L4,5 distribution. Knee and ankle jerk reflexes were absent, plantars were equivocal and anal sphincter tone was reduced. The patient's international normalized ratio (INR) was 4.1. An MR scan showed an extensive intradural haematoma compressing the cauda equina. The anticoagulation was reversed and an urgent T12-L2 laminectomy was performed; findings were a circumferential haematoma at L1 extending in the anterior canal between T10 and L3. The patient had an uneventful postoperative course generally, but at 1 week there was no neurological recovery. CONCLUSION: This case highlights that anticoagulation even when well controlled is not without risk. This is particularly of concern as the number of patients receiving long-term anticoagulation therapy has doubled between 1993 and 1998.
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A healthy 22-year-old man received an initial injection of 12 mL of lignocaine/bupivacaine solutions (2 mL test, then 10 mL) into an epidural catheter. This produced a satisfactory regional blockade that seemed to be epidural but, when a supplementary 6 mL injection was given 1 h later, the patient developed impaired motor function as far as the upper cranial nerves, with loss of pinprick sensation to the shoulder. The emergence of fluid dribbling freely from the catheter prompted measurement of the pressure, which was 36 mmHg. The fluid was proved not to be cerebrospinal fluid (CSF) by the absence of glucose (on dextrostix), by the appearance of turbidity with added thiopentone, and later by microscopy. Slow aspiration of 7 mL of the presumed injectate reduced the pressure in the catheter to 8 mmHg, which promptly reversed the additional excessive blockade, allowing surgery to proceed uneventfully. The retrieval of injectate argues strongly that the catheter tip had found its way subdurally, and the promptness of the reversal with aspiration argues for a mechanical rather than a pharmacological cause for the extensive neurological dysfunction after the second injection. Pressure measurement and aspiration may be helpful in other similar cases.
Congenital factor VII deficiency is a rare (1:500,000) autosomally recessive coagulopathy with variable expression and high penetration. In infants the most devastating presentation is that of intracranial haemorrhage. An infant is described with severe factor VII deficiency who developed postnatal intracranial haemorrhage. The baby was treated with factor VII concentrate (ImmunoA.G., Vienna, Austria). Three weeks after the haemorrhage he developed a dural venous sinus thrombosis. Although factor VII-deficient patients may need treatment with factor VII concentrate, this needs to be carefully monitored because of the thrombotic risk.
A 13-year-old female with a past history of lumbar laminectomy developed a subdural block 18 h after the commencement of an epidural infusion of bupivacaine 0.125% and fentanyl 2 micrograms.ml-1. Signs at presentation included bilateral abducens nerve palsies in the absence of headache and a previously unreported unilateral third cranial nerve palsy. An epidurogram displayed subdural placement.
We describe three middle-aged and previously healthy patients in whom idiopathic spontaneous subdural hemorrhage occurred, giving rise to headache with minimal or no neurological signs and resolving with conservative management. Previous reports of this condition describe an associated severe neurological impairment, a poor prognosis, and a necessity for surgical evacuation. Our cases indicate that mild and self-limiting spontaneous subdural hemorrhage may occur and is perhaps underdiagnosed in our patients' age group because it presents non-specifically with headache.
PURPOSE: To study the efficacy of extensive coverage of the brain surface with subdural grids in defining extratemporal cortical areas amenable for resection in patients with refractory extratemporal epilepy (R-ExTE) and normal or nonlocalizing magnetic resonance imaging (MRI) scans. METHODS: Sixteen patients with R-ExTE were studied. Eleven patients had simple partial, eight had complex partial, and three had supplementary motor area seizures. Seizure frequency ranged from three per month to daily episodes. Interictal EEG showed large focal spiking areas in 11 patients, secondary bilateral synchrony in four, and was normal in one patient. Surface ictal recordings were nonlocalizing in six patients, and in 10, they disclosed large ictal focal spiking areas. MRI was normal in 10 patients, and in six patients, focal nonlocalizing potentially epileptogenic lesions were found. All patients were given an extensive coverage of the cortical convexity with subdural electrodes through large unilateral (n = 13) or bilateral (n = 3) craniotomies. Bipolar cortical stimulation was carried out through the implanted electrodes. RESULTS: Interictal invasive recording findings showed widespread spiking areas in 13 patients and secondary bilateral synchrony in three. Ictal invasive recordings showed focal seizure onset in all patients. There were six frontal, two parietal, one temporooccipital, four rolandic, and three posterior quadrant resections. Thirteen patients had been rendered seizure free after surgery, and three had > or =90% of seizure-frequency reduction. Pathologic findings included gliosis (n = 10), cortical dysplasia (n = 5), or no abnormalities (n = 1). Six patients had transient postoperative neurologic morbidity. CONCLUSIONS: Extensive subdural electrodes coverage seems to be an effective way to investigate patients with R-ExTE and normal or nonlocalizing MRI findings.
PURPOSE: To determine the value of scalp epileptiform EEG data and subdural interictal spikes in localizing temporal epileptogenesis among patients requiring invasive recordings. For this delineation, we related such factors to site of subdural seizure origin in 27 consecutive patients. METHODS: Patients with temporal lobe epilepsy whose non-invasive lateralizing data were inconclusive and therefore required subdural electroencephalography were studied. All patients had (a) 24-h scalp telemetered EEGs, (b) adequate bitemporal subdural placements with an inferomesial line extending from a posterior burr hole anteriorly to <2.5 cm from anterior uncus and a lateral line reaching within 2.5 cm of the temporal tip, and (c) > or =2 subdurally recorded seizures. RESULTS: Three hundred one (96%) of 314 subdurally recorded clinical seizures involving all 27 patients arose from a discrete focus; 266 (85%) arose from mesial temporal regions, which was the origin of the majority of seizures in 24 (89%) patients. The majority of subdural seizures arose ipsilateral to the majority of scalp EEG spikes in 22 (81%) of 27, and most subdural seizures of 15 (75%) of 20 arose ipsilateral to scalp seizures. Lateralization of interictal subdural spikes correlated with that of subdural seizures in 74-92% of patients, depending on the method of spike compilation: for example, most subdural seizures arose from the same lobe of most consistent principal temporal spikes in 92% of patients. These indices of epileptogenesis also appeared more commonly on the side of effective (> or =90% improvement) temporal lobectomy than contralaterally in the following proportions: most consistent principal subdural spikes, 86% of patients ipsilateral vs. 9% contralateral; scalp-recorded clinical seizures, 55% vs. 18%; scalp EEG spikes, 45% vs. 9%. CONCLUSIONS: Even among patients whose scalp data are sufficiently complex to require invasive recording for clarification, lateralization of temporal scalp interictal and ictal epileptiform activity and subdural interictal spikes should be included when assessing the side of temporal epileptogenesis.
PURPOSE: To assess the effect of vagus nerve stimulation (VNS) on interictal epileptiform activity in the human hippocampus. Clinical studies have established the efficacy of vagus nerve stimulation in patients with epilepsy (VNS Study Group, 1995), although the electrophysiologic effects of VNS on the human hippocampus and mesial temporal lobe structures remain unknown. METHODS: We report a case study in which a patient with an implanted VNS underwent intracranial electrode recording before temporal lobectomy for intractable complex partial seizures. Epileptiform spikes and sharp waves were recorded from a depth electrode placed in the patient's left hippocampus. Spike frequencies and sharp-wave frequencies before and during VNS were compared using both a 5- and a 30-Hz stimulus. Different stimulation rates were tested on different days, and all analyses were performed using a Student's t test. RESULTS: We found no significant differences in spike frequency between baseline periods and stimulation at 5 and 30 Hz. In contrast, stimulation at 30 Hz produced a significant decrease in the occurrence of epileptiform sharp waves compared with the baseline, whereas stimulation at 5 Hz was associated with a significant increase in the occurrence of epileptiform sharp waves. CONCLUSIONS: VNS produces a measurable electrophysiologic effect on epileptiform activity in the human hippocampus. Although a clinical response to VNS did not occur in our patient before surgery, 30-Hz VNS suppressed interictal epileptiform sharp waves that were similar in appearance to those seen during the patient's actual seizures. In contrast, 5-Hz stimulation appeared to increase the appearance of interictal sharp waves.
PURPOSE: To study propagation properties of focally originating frontal lobe seizures: principally direction and promptness of ictal spread. METHOD: Forty-eight scalp EEG-recorded and 17 subdurally recorded seizures in two separate groups of patients were visually scrutinized. RESULTS: Initial propagation was directed more commonly to contiguous frontal cortex than to the opposite hemisphere in both studies: 58% and 86% for scalp and subdural recordings, respectively. Eighteen (38%) of scalp EEG seizures propagated within 5-10 s of apparent onset, whereas 16 (33%) did so after 11-20 s; no evidence of propagation could be discerned in the remaining 14 (29%). Of subdurally recorded attacks, only four (24%) propagated in the first 4 s; six (35%) did so after a delay of 5-10 s; six (35%) either failed to propagate or did so after > or =20-s latency. Latency to initial propagation was between 5 and 20 s in 41 (63%) of the 65 seizures in both studies. Ictal activity remained within the frontal lobe of origin for > or =10 s in 39 (81%) of scalp-recorded seizures and 11 (65%) of subdural seizures. It remained so confined for > or =15 s in 26 (54%) and nine (53%), respectively. Twenty-four (50%) of scalp-recorded seizures displayed evidence of opposite hemisphere (bisynchronous or other contralateral) involvement, occurring 5-10 s after onset in eight (17%) seizures and 10-20 s after onset in 16 (33%). Similarly, the subdural study documented spread to the opposite hemisphere in 11 (65%) of seizures with a latency ranging from 1 to 45 s. CONCLUSIONS: Frontal lobe seizures in this study propagated less promptly than reputed, and initial spread occurred more commonly to the frontal lobe of origin than to the opposite hemisphere. Such properties underlie the good lateralizing value of clinical semiology of frontal lobe seizures.
PURPOSE: We propose an experimentally and clinically testable hypothesis, concerning the origin of very fast (> approximately 70 Hz) EEG oscillations that sometimes precede the onset of focal seizures. These oscillations are important, as they may play a causal role in the initiation of seizures. METHODS: Subdural EEG recordings were obtained from children with focal cortical dysplasias and intractable seizures. Intra- and extracellular recordings were performed in rat hippocampal slices, with induction of population activity, as follows: (a) bath-applied tetramethylamine (an intracellular alkalinizing agent, that opens gap junctions); (b) bath-applied carbachol, a cholinergic agonist; and (c) focal pressure ejection of hypertonic K+ solution. Detailed network simulations were performed, the better to understand the cellular mechanisms underlying oscillations. A major feature of the simulations was inclusion of axon-axon gap junctions between principal neurons, as supported by recent experimental data. RESULTS: Very fast oscillations were found in children before seizure onset, but also superimposed on bursts during the seizure, and on interictal bursts. In slice experiments, very fast oscillations had previously been seen on interictal-like bursts; we now show such oscillations before, between, and after epileptiform bursts. Very fast oscillations were also seen superimposed on gamma (30-70 Hz) oscillations induced by carbachol or hypertonic K+, and in the latter case, very fast oscillations became continuous when chemical synapses were blocked. Simulations replicate these data, when axonal gap junctions are included. CONCLUSIONS: Electrical coupling between principal neurons, perhaps via axonal gap junctions, could underlie very fast population oscillations, in seizure-prone brain, but possibly also in normal brain. The anticonvulsant potential of gap-junction blockers such as carbenoxolone, now in clinical use for treatment of ulcer disease, should be considered.
PURPOSE: We studied the relation between quantitative interictal subdural EEG data and visually defined ictal subdural EEG findings in children with intractable neocortical epilepsy, and determined whether interictal EEG data are predictive of ictal EEG onset zones. METHODS: Thirteen children (aged 1.2-15.4 years) underwent prolonged intracranial EEG recording, using 48- to 120-channel subdural electrodes. Three distinct 10-min segments of the continuous interictal EEG recording were selected for each patient, and the spike frequency for each channel was determined by using an automatic spike-detection program. Subsequently the average spike frequency of each electrode was compared with ictal assessment (onset, spread, and no early ictal involvement). In addition, 50 distinct interictal spikes were averaged for each patient, and the amplitude and latency after the leading spike (averaged spike showing the earliest peak) were measured for each electrode and analyzed with respect to ictal EEG findings. RESULTS: Reproducibility of the spike-frequency pattern derived from three 10-min segments was high (Kendall's W, 0.85 +/- 0.08). Electrodes showing the highest spike frequency, the highest spike amplitude, and the leading spike were found to be a part of the seizure onset in 13 of 13, 12 of 13, and 10 of 13 cases, respectively. There was significant correlation between ictal assessment and spike frequency as well as spike amplitude. A receiver operating characteristics analysis showed that a cutoff threshold at 14% of the maximal spike frequency resulted in a specificity of 0.90 and a sensitivity of 0.77 for the detection of seizure-onset electrodes. CONCLUSIONS: Quantitative interictal subdural EEG may predict ictal-onset zones in children with intractable neocortical epilepsy.
It is essential to delineate an epileptogenic zone and to define the eloquent cortices at or close to the epileptogenic zone in patients with neocortical epilepsy for epilepsy surgery. Prolonged implantation of the subdural electrode in presurgical evaluation is currently one of the best clinical methods to provide the essential information before epilepsy surgery. Electric cortical stimulation and recording of sensory evoked potentials by means of subdural electrodes are widely used for functional cortical mapping. Bereitschaftspotential (BP) is clinically useful to delineate the primary and nonprimary motor cortices such as supplementary motor area proper (SMA proper) and pre-SMA, because BP occurs for any type of voluntary movements of the body, and because it is not associated with the risk of seizure induction in contrast with high-frequency cortical electric stimulation. Single-pulse electric cortical stimulation to record motor evoked potentials (MEPs) also could complement currently used high-frequency cortical electric stimulation, especially for mapping of the primary motor and premotor cortices with lower risk of seizure induction.