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Subdural hygroma: diagnosis with computed tomography.
Nine cases are reported that fulfilled the criteria for diagnosis of subdural hygroma. With the availability of serial computed tomographic (CT) scans, it is possible to document non-invasively the appearance of CSF-density subdural fluid where no prior blood accumulation has been present.
Ipsilateral median somatosensory evoked potentials recorded from human somatosensory cortex.
Somatosensory evoked potentials (SEP) to ipsilateral and contralateral median nerve stimulations were recorded from subdural electrode grids over the perirolandic areas in 41 patients with medically refractory focal epilepsies who underwent evaluation for epilepsy surgery. All patients showed clearly defined, high-amplitude contralateral median SEPs. In addition, four patients showed ipsilateral SEPs. Compared with the contralateral SEPs, ipsilateral SEPs were very localized, had a different spatial distribution, were of considerably lower amplitude, had a longer latency (1.2-17.8 ms), did not show an initial negativity, and were markedly attenuated during sleep. Stimulation of the subdural electrodes overlying the sensory hand area was associated with contralateral hand paresthesias, but no ipsilateral hand paresthesias, occurred. It was concluded that subdurally recorded cortical SEPs to ipsilateral stimulation of the median nerve (M) reflect unconscious sensory input from the hand possibly serving fast bimanual hand control. The anatomical pathway of these ipsilateral short-latency MSEPs is not yet known. Transcallosal transmission seems unlikely because of the short delay between the ipsilateral and contralateral responses in selected cases. The infrequent occurrence of ipsilateral subdurally recorded SEPs and their low amplitude and limited distribution suggest that they contribute very little to the short-latency ipsilateral median SEPs recorded on the scalp.
The cortical generators of the contingent negative variation in humans: a study with subdural electrodes.
Contingent negative variations (CNVs) and Bereitschaftspotentials (BPs) were recorded from subdural electrodes implanted in 14 patients with intractable epilepsy. For recording CNVs, a Go/NoGo S2 choice reaction-time paradigm was employed. Two seconds after presentation of a low tone burst (S1), either a medium (S2m) or a high tone burst (S2h) was delivered at random. Patients were instructed to make middle finger extensions after S2m but not after S2h. For recording BPs, patients repeated self-paced middle finger extensions. BPs were recorded from the primary motor area (MI), the primary sensory area (SI) and the supplementary sensorimotor area (SSMA). CNVs showed a patchy distribution in the prefrontal area and SSMA for the early component and in the prefrontal area, MI, SI, temporal area, occipital area and SSMA for the late component. These results suggest that the CNV recorded from the scalp is the summation of multiple cortical potentials which have different origins and different functions. The cortical distribution of the late CNVs was different from that of BPs. Late CNVs are not equivalent to BPs and are not related to motor preparation alone. After S2, 3 kinds of potentials, probably related to decision making, somatosensory feedback and motor execution under specific conditions, respectively, were observed.
Male adolescent with subdural parietal abscess: a probable complication of substance abuse.
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Different generators in human temporal-parasylvian cortex account for subdural laser-evoked potentials, auditory-evoked potentials, and event-related potentials.
In order to localize cortical areas mediating pain we now report subdural cortical potentials evoked by auditory stimulation (auditory-evoked potentials - AEPs) and by cutaneous stimulation with a laser (laser-evoked potentials - LEPs). Stimulation with the laser evokes a pure pain sensation by selective activation of nociceptors. LEPs were maximal over the inferior aspect of the central sulcus and had the same polarity on either side of the sylvian fissure. AEPs were maximal posterior to the LEP maximum and had opposite polarity on opposite sides of the sylvian fissure, consistent with the location of a known generator in the temporal operculum. Auditory P3 (event-related) potentials were maximal over the temporal base. These findings demonstrate that the LEP generator is not in secondary somatosensory cortex on the parietal operculum and is different from the P3 generator.
Bilateral intracranial granulomas as a complication of infected subdural peritoneal shunt.
Intracranial granuloma in childhood is considered to be a very rare disorder. A three-year-old child is described who had bilateral intracranial granulomas originating from the ends of bilateral subdural-peritoneal shunts. Serial computerized tomographic examinations revealed variable and peculiar findings. Since subdural-peritoneal shunt is used in neonate, intracranial granuloma must be considered as a potential complication of unremoved subdural-peritoneal shunt.
Subdural hygroma in association with middle fossa arachnoid cyst: acetazolamide therapy.
Intracranial arachnoid cysts are cerebrospinal fluid-filled collections between arachnoid layers. While many are silent, arachnoid cysts can become symptomatic if there is sudden expansion, haemorrhage or rupture with the development of subdural hygroma or subdural hematoma. Several studies have demonstrated the association of arachnoid cysts with subdural hygroma and subdural hematoma. We describe a 9-year-old girl with a moderate-sized middle-fossa arachnoid cyst and bilateral frontal subdural hygroma presenting with raised intracranial pressure. She was treated with acetazolamide which resulted in resolution of the subdural hygroma and relief of symptomatology.
Usefulness of 3-D reconstructed images of the human cerebral cortex for localization of subdural electrodes in epilepsy surgery.
Three-dimensional (3-D) images of 14 patients, in whom subdural electrodes were implanted for epilepsy surgery evaluation, were produced by fusing computerized tomography (CT) scans and magnetic resonance images (MRI) to determine the exact location of the electrodes. In 25% (198 of 806) of the subdural electrodes an exact location for resection strategy was not evident from the X-rays. The location of these electrodes ('doubtful location', DL) was compared to the 3-D images. Intraoperative inspection served as the gold standard. Concordance score was defined as good for 75-100% concordance, moderate for 50-75%, and poor for less than 50% concordance of the DL electrodes to the intraoperatively determined location. A comparative analysis of the 3-D images and X-ray films showed a highly significant difference (P < 0.0002) in favor of 3-D images. The concordance score for the DL electrodes in the 3-D images was good in 93% of the patients and moderate in 7%. In contrast, the concordance score was good in only 7% of the patients for the two-dimensional (2-D) skull films, moderate in 57%, and poor in 36%. Interobserver reliability was better for 3-D images (93%) than for the 2-D X-rays (43%). These findings suggest that 3-D images aid preoperative planning for resective epilepsy surgery.
[Favorable outcome of a subdural hematoma diagnosed in utero].
UNLABELLED: The subdural hematoma detected in utero is unusual but probably under-diagnosed and has a bad prognostic. CASE REPORT: A newborn had a subdural hematoma detected with a prenatal ultrasonography at 31 weeks' gestation, probably in keeping with the regular treatment of AAS. Diagnosis was possible through antenatal MRI at 34 weeks' gestation. The mother chose to follow her pregnancy. The operation at day 3 had no complications and neurological progress at 12 months was very good. CONCLUSION: A subdural hematoma detected in utero may have a good prognostic. Prenatal MRI is useful for the check-up. However, medical and ethical problems remain in these cases.
The use of subdural grids in the management of focal malformations due to abnormal cortical development.
Because of the spatial limitations of scalp electroencephalographic recordings and the lack of reproducible results using functional MR imaging techniques to map various eloquent areas of the cortex, the accurate mapping of the extent of epileptogenicity and function currently are best accomplished through invasive electrocorticographic recordings and direct cortical stimulation, respectively. The purpose of this article is to give an overview of the presurgical diagnostic tools used in patients with suspected malformations caused by abnormalities of cortical development with special emphasis on subdural electrodes. The indications and the role of invasive subdural electrode evaluation are discussed.
Biphasic response after brain death induction: prominent part of catecholamines release in this phenomenon.
BACKGROUND: The physiopathology of hemodynamic instability that occurs after brain death remains unknown. The aim of this study was to examine the initial response to brain death induction. METHODS: After anesthesia and monitoring, 16 pigs were randomized into a control group (C, n = 8) and a brain death group (BD, n = 8). We inflated a subdural catheter balloon to induce brain death. We analyzed hemodynamic and plasmatic biochemical data for 180 minutes after brain death induction. Energetic compounds were measured. We expressed the results in comparison with the C group. RESULTS: The C group remained stable. One minute after brain death, the Cushing reflex appeared, with a hyperdynamic response to plasma catecholamines levels increasing (norepinephrine and epinephrine, 3.1-fold, p = 0. 02, and 3.8-fold, p = 0.07, respectively). After a return to baseline, we recorded a second hyperdynamic profile 120 minutes later. At this time, a second peak of catecholamines appeared (6. 3-fold, p = 0.04, and 9.1-fold, p = 0.02, concerning norepinephrine and epinephrine). At the same time, we observed brief myocardial lactate production (+175%, p < 0.01), with a rise of troponine I (+64%, p = 0.03). The energetic index was similar in both groups: 0. 85 (+/-0.02) in the C group vs 0.87 (+/-0.02) in the BD group. CONCLUSIONS: In this model, biphasic plasmatic catecholamine release appears to primarily explain the physiopathology of the hemodynamic response to brain death induction.
Role of neural and humoral factors in hyperdynamic reaction and cardiac dysfunction following brain death.
BACKGROUND: Although hemodynamic instability and cardiac dysfunction after brain death are reported in the potential organ donor, the underlying mechanisms, for example, neurohumoral changes, myocardial injury, and altered loading conditions, have not been differentiated in clinical and experimental settings. In the present study, we performed a load-independent analysis of cardiac function, focusing on the influence of brain death-associated neural and humoral factors. METHODS: In a canine in situ cross-circulated heart model, brain death was induced by inflation of a subdural balloon catheter. Preload, afterload, and coronary perfusion pressure were kept identical in all hearts throughout the experiment. In Group H (humoral factors), the hearts of healthy dogs were perfused with blood from brain-dead support dogs (n = 6). In Group N (neural factors), the hearts of brain-dead dogs were perfused with blood from healthy support dogs (n = 6). In Group H + N (humoral and neural factors), the hearts of brain-dead dogs were perfused parabiotically in situ with the animals' own blood (n = 6). Systolic and diastolic pressure-volume relationships and coronary blood flow were measured. RESULTS: Induction of brain death led to a significant hyperdynamic response in all groups, with a maximal reaction in Group H + N followed by Group H and Group N. After the initial hyperdynamic phase, cardiac function returned to baseline within 15 minutes and remained stable in all groups for the 2-hour observation period. CONCLUSIONS: (1) Both neural and humoral factors contribute to the initial hyperdynamic reaction after brain death, and only in combination do they cause a maximal hemodynamic effect. (2) If loading conditions and perfusion pressure are kept constant, no cardiac dysfunction occurs after brain death. This indicates that poor cardiac function in the potential donor may reflect altered loading conditions and impaired coronary perfusion rather than neurohumorally mediated direct myocardial injury.
Lumbar cerebral spinal fluid drainage during long-term electrocorticographic monitoring with subdural strip electrodes: elimination of cerebral spinal fluid leak.
We performed this study to determine the efficacy of continuous lumbar cerebral spinal fluid (CSF) drainage in controlling CSF leak during subdural strip electrode monitoring of epilepsy patients. Subdural strip electrodes were placed in 14 patients. In seven patients, a lumbar sub-arachnoid catheter was placed for continuous CSF drainage. In seven patients, no lumbar drain was placed. The duration of scalp CSF leak during strip electrode monitoring was significantly reduced in patients undergoing lumbar CSF drainage compared to those without lumbar drains (chi 2 = 40.9, P < 0.05). In one patient spinal headache developed which resolved with lumbar drain removal. Lumbar drainage eliminates scalp CSF leakage and can improve patient comfort. This technique should be further studied to determine if it reduces infection risk during long-term invasive monitoring.
Characterization of the mu rhythm during rapid eye movement sleep.
OBJECTIVE: The rolandic mu rhythm, a resting activity of somatosensory cortex, is a striking feature of the waking human electroencephalogram. This study will demonstrate that activity with identical features occurs during rapid eye movement (REM) sleep. METHODS: Eye and chin leads were added during prolonged closed circuit television (video) electroencephalographic (EEG) recording with scalp (12 patients) or subdural electrodes including 64 contract grids over the frontoparietal cortices (5 patients). Sleep staging was performed by reformatting into standard polysomnography montages (using two EEG channels, and eye and chin channels) and applying standard scoring criteria. The recordings were then reviewed using all EEG channels to assess rhythmic EEG activity by a reader blinded to the sleep staging. RESULTS: During scalp recordings, 7-10 Hz central rhythms were seen during wakefulness in 7 patients, with 6 of these also having similar rhythms during REM sleep. Similar activity was seen over somatosensory cortex during wakefulness and REM in all invasively recorded patients. This activity was blocked by contralateral body movement or contralateral somatosensory stimuli, even during REM sleep. It was absent in other sleep stages. CONCLUSIONS: This REM sleep activity recapitulates all the characteristics of the waking rolandic mu rhythm. This demonstrates functional similarity between the states of wakefulness and REM sleep.
Somatosensory evoked high frequency oscillations recorded from subdural electrodes.
OBJECTIVES: To examine high frequency oscillations (HFOs) of somatosensory evoked potentials (SEPs) recorded directly from subdural electrodes to investigate the relationship between the primary somatosensory cortex and HFOs. METHODS: SEPs were recorded directly from subdural electrodes previously implanted in 3 patients for clinical evaluation prior to surgical treatment of intractable epilepsy. RESULTS: The primary sensory cortex (area 3b) was proposed as the source of somatosensory HFOs, because the distribution of HFOs recorded from the subdural electrodes agreed with the distribution of the N20-P20 components of the somatosensory evoked potential. The somatosensory HFOs showed a strictly somatotopic source arrangement. There was a polarity inversion of the prophase component and also the N20-P20 component of HFOs across the central sulcus. However, the phase was synchronized in the latter part of the HFOs. CONCLUSIONS: We propose that the origins of the early and latter parts of HFOs are different, and that there was a clear somatotopy.
Functional mapping in epilepsy patients' information from subdural electrodes.
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Source localization of interictal epileptiform spike potentials estimated with a dipole tracing method using surface and subdural EEG recordings.
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