Computed tomography(CT) has enabled early recognition and treatment of focal injuries in patients with head trauma. However, CT has been less beneficial in identifying diffuse brain injury(DBI). The authors have analyzed retrospectively, a series of 132 patients with OBI observed for 2 years from Aug. 1986 to Jul. 1988 to evaluate the significance of the factors affecting outcome. Eighty-three patients were selected as being compatible with moderate and severe diffuse axonal injury(DAI) classified by Gennarelli, defined by coma without a CT lesion that is an obvious cause and coma greater than 24 hr with or without decerebration. The results are summarized as follows: 1) The 38(45.7%) out of 83 patients were found below age of 20, but there was no statistical significance between age distribution and outcome. 2) In case of initial Glasgow coma scale(GCS) of 7 or 8, 32(86.5%) out of 37 patients revealed good outcome, but 18(90%) of 20 patients with a score of 3 or 4 revealed poor outcome(p<0.01). 3) With regard to brain swelling in CT, there was significant statistical difference to outcome(p<0.05). 4) Small hemorrhages on corpus callosum, basal ganglia, basal cistern, peritentorial, lateral ventricle that is characteristic CT findings for DAI were showed 58(70%) out of all cases. It might be concluded that initial GCS, brain swelling and small hemorrhages in CT were significant factors affecting outcome in DAI.
Age Distribution ; Axons ; Basal Ganglia ; Brain ; Brain Edema ; Brain Injuries* ; Coma ; Corpus Callosum ; Craniocerebral Trauma ; Diffuse Axonal Injury ; Hemorrhage ; Humans ; Lateral Ventricles ; Retrospective Studies ; Tomography, X-Ray Computed

OBJECTIVE: Traditionally, the main indications for surgery in vascular-related lesion were based upon reduction or control of seizures, reversal of symptoms of deficits related to mass effect, and prevention of hemorrhage or recurrent hemorrhage. However, the results of surgical treatment for seizure control are disappointing in some reports. Here we describe surgical strategies and our experience in treating patients with intractable seizures associated with vascular-related lesions according to sophisticated presurgical and intraoperative evaluation. METHODS: Twelve(4.5%) patients were selected for this study out of total 264 patients with resective epilepsy surgery at our epilepsy center during four years since 1992. All were treated with anticonvulsant agents but became refractory. These patients operated on under local or general anesthesia for resection surgery, underwent presurgical and intraoperative evaluation for identification of adjacent, beyond or remote epileptogenic area and the eloquent area. RESULTS: Of these 12 patients, vascular malformations(AVM, cavernous angioma) were 7, overt hemorrhage due to vascular lesion were 2 and intractable ongoing seizure after vascular surgery were 3. Other vascular lesion including occlusive disease, moyamoya disease or previous hemorrhage were excluded in this study. The location of the lesion was mainly temporal and peri-Rolandic areas, and dual pathology was verified in 2 cases of 6 temporal lesion. The surgical outcome(class I;7, II;3, III;1, IV;1) was excellent by Engel's classification. CONCLUSION: Control of seizures related to vascular lesions remains strong indication for surgical resection. For this reason, careful presurgical evaluations are essential to evaluate the remote epileptogenic area, especially in temporal lesion. Intraoperative acute recording(ECoG) and functional mapping by electrical stimulation or SSEP are important for maximal resection of epileptogenic area with minimal sequellae.
Anesthesia, General ; Classification ; Electric Stimulation ; Epilepsy* ; Hemangioma, Cavernous ; Hemorrhage ; Humans ; Moyamoya Disease ; Pathology ; Seizures

No abstract available.
Hematoma*

Cortical dysplasia(CD) is recently known as a cause of intractable partial epilepsies that are amenable to surgical treatment. The development of new neuroimaging has facilitated the recognition of these neuronal migration disorders. Here we examine some clinical features that permit early suspicion of focal cortical dysplasia and better surgical results. From a consecutive surgical series of 239 patients with intractable epilepsy since 1992, pathologically verified 31 CD including 6 CD with dysembryoplastic neuroepithelial tumor(DNT) were selected for this study. The location and extent of resection were determined by both epileptogenic zones and the structural lesion, according to presurgical evaluation(neuroimaging, EEG, intracranial recording), intraoperative electrocorticography(ECoG) and functional brain mapping. The series consisted of 21 men and 10 women with ages at seizure onset ranging from 1 to 26 years(mean 11.1year). The duration of the epilepsy prior to surgery ranged from 3 to 30 years(mean 14.3). The CD was verified in 17(11.1%) of 153 cases with temporal lobe epilepsy and 8(16.6%) of 48 cases with extratemporal epilepsy, mainly peri-Rolandic area. The lesion location of CD with DNT were temporal(4 cases) and extratemporal(2 cases). The histology of the surgical specimens showed cortical dyslamination in 26 patients, additional dysplastic neurons in 2 patients, and additional balloon cells in 3 patients. Excellent and good clinical results were achieved in 29 cases. CD should be suspected when intractable partial epilepsy occur in children. Careful investigation of neuroimaging techniques with high resolution MRI and sophisticated presurgical and intraoperative tailoring is essential for better outcome with identification of CD.
Brain Mapping ; Child ; Electroencephalography ; Epilepsies, Partial ; Epilepsy* ; Epilepsy, Temporal Lobe ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Malformations of Cortical Development* ; Neuroimaging ; Neuronal Migration Disorders ; Neurons ; Seizures

In terms of seizure control for the patients with medically intractable temporal lobe epilepsy(TLE), extensive medial resection, especially of the hippocampus, has been advocated in anterior temporal lobectomy. The relationship between the outcome of anterior temporal lobectomy for epilepsy and the size of the hippocampectomy tailored to intraoperative electrocorticographic findings was evaluated in 100 patients, with at least 12 months of follow-up. In 28 patients with small hippocampal resection( Anterior Temporal Lobectomy* ; Classification ; Epilepsy ; Epilepsy, Temporal Lobe* ; Follow-Up Studies ; Hippocampus ; Humans ; Seizures ; Temporal Lobe*

The main pathophysiology of cerebral ischemia caused by occlusive cerebrovascular disease(CVD) are hemodynamic low perfusion and embolic mechanism. The main objects of surgical method for occlusive CVD are improvement of low perfusion and elimination of embolic source with surgical procedure. The causes of occlusive CVD can be devided as a atheromatous and non-atheromatous occlusion. The frequent sites of occlusion in atheromatous origin are carotid bifurcation, carotid siphon and middle cerebral artery(MCA), proximal subclavian and vertebral artery origin, vertebral artery proximal to origin of posterior inferior cerebellar artery(PICA), vertebral artery distal to origin of PICA and mid-basilar artery. The lesions of non-atheromatous occlusive disease are extracranial internal carotid artery(ICA) aneurysm, traumatic dissection with or without false aneurysm of ICA, loops and kinds of ICA, osteophytic or traumatic vertebral artery compression, traumatic dissection with or without false aneurysm of vertebral artery and Moya Moya disease. Depend on occlusion site and disease, the surgical procedures are different. The main surgical procedures for occlusive CVD are carotid endarterectomy, extracranial-intracranial(EC-IC) bypass surgery, vertebral artery endarterectomy, vertebral artery to common carotid artery transposition, resection and end-to-end or interposition vein graft of ICA, indirect revascularization for Moya Moya disease and unroof the transverse foramen of cervical vertebra. The author reviews the surgical indication and procedure of occlusive CVD briefly.
Aneurysm ; Aneurysm, False ; Arteries ; Brain Ischemia ; Carotid Artery, Common ; Endarterectomy ; Endarterectomy, Carotid ; Hemodynamics ; Moyamoya Disease ; Perfusion ; Pica ; Spine ; Transplants ; Veins ; Vertebral Artery

The main pathophysiology of cerebral ischemia caused by occlusive cerebrovascular disease(CVD) are hemodynamic low perfusion and embolic mechanism. The main objects of surgical method for occlusive CVD are improvement of low perfusion and elimination of embolic source with surgical procedure. The causes of occlusive CVD can be devided as a atheromatous and non-atheromatous occlusion. The frequent sites of occlusion in atheromatous origin are carotid bifurcation, carotid siphon and middle cerebral artery(MCA), proximal subclavian and vertebral artery origin, vertebral artery proximal to origin of posterior inferior cerebellar artery(PICA), vertebral artery distal to origin of PICA and mid-basilar artery. The lesions of non-atheromatous occlusive disease are extracranial internal carotid artery(ICA) aneurysm, traumatic dissection with or without false aneurysm of ICA, loops and kinds of ICA, osteophytic or traumatic vertebral artery compression, traumatic dissection with or without false aneurysm of vertebral artery and Moya Moya disease. Depend on occlusion site and disease, the surgical procedures are different. The main surgical procedures for occlusive CVD are carotid endarterectomy, extracranial-intracranial(EC-IC) bypass surgery, vertebral artery endarterectomy, vertebral artery to common carotid artery transposition, resection and end-to-end or interposition vein graft of ICA, indirect revascularization for Moya Moya disease and unroof the transverse foramen of cervical vertebra. The author reviews the surgical indication and procedure of occlusive CVD briefly.
Aneurysm ; Aneurysm, False ; Arteries ; Brain Ischemia ; Carotid Artery, Common ; Endarterectomy ; Endarterectomy, Carotid ; Hemodynamics ; Moyamoya Disease ; Perfusion ; Pica ; Spine ; Transplants ; Veins ; Vertebral Artery

Temporal lobe epilepsy is characterized by complex partial seizures with either primary intracranial neoplasms or other non-neoplastic lesions. We reviewed 64 cases of surgically resected temporal lobes and amygdalo-hippocampal regions for temporal lobe epilepsy ansed by non-neoplastic lesions to elucidate the incidence and histologic features of each histologic group for a period of 2 years. The patient's age ranged from 12 to 49 years and the ratio of male to female was 42:22. There were 37 cases(57.8%) with single pathology and an additional 20 cases(31.3%) with dual pathology. The emaining 7 cases(10.9%) had no structural alternations. The most common temporal lobe pathology was hippocampal sclerosis in 41 cases(64.1%), diagnosed alone in 21 cases and as dual lesions in 20 cases. The hippocampal neuron loss was most pro,omemt in CA1, followed by CA4, CA3, and CA2. Amygdaloid sclerosis was present in 28 cases(43.8%), lases had 13 dual lesions, 25 cases also had hippocampal sclerosis. The 20 dual lesions showed that 6 cortical dysplasia, 10 microdysgenesis, 1 chronic non-specific inflammatory lesion, and 3 cysticercosis were associated with the various degree of mesial temporal sclerosis. Neuronoglial malformative lesions were identified in 21 cases(32.8%) including 16 dual lesion cases, which composed of 15 microdysgenesis and 6 cortical dysplasia. Neurofilament immunostain for cortical dysplasia revealed abnormally beaded disarray of axons in dysplastic pyramidal cells. The remaining pathologic lesions observed were 1 cysticercosis, 1 chronic non-specific inflammatory lesion, 3 arteriovenous malformation, 2 fibrous nodule, and 1 fibrous adhesions of the arachnoid.
Female ; Male ; Humans ; Incidence

Kindling development is a good animal model of epilepsy and neural plasticity. It is induced by repeated subconvulsive electrical or chemical stimulations. This leads to progressive and permanent amplification of seizure activity resulting in permanent brain changes. Immediate early genes(IEGs) are proposed as the master switch for turning on molecular events in long term neural plasticity. The role of c-myc, an IEG, in the development of kindling is not known. This study was conducted to investigate the role of c-myc in the neural plastic changes underlying kinding. Among 115 adult male Spargue-Dawley rats, 51 were kindled by repeated administrations of subconvulsive doses(15-25mg/kg) of pentylenetetrazol(PTZ). Twenty-eight rats experienced various degree of convulsions induced by a single injection of convulsive dose(30-60mg/kg) of PTZ. Eighteen rats experienced mild or severe convulsions induced by a single injection of convulsive dose(30-60mg/kg) of PTZ. Eighteen rats experienced mild or severe convulsion by a single electroconvulsive shock(ECS). Eighteen rats received normal saline as a control group. Animals were sacrificed in 30 minutes, 1 hour and 48 hours after convulsion. C-myc mRNA levels in the hippocampus were quantified using slot-blot hybridization analysis. In the experiment of PTZ kindling, c-myc mRNA expression 30 minutes after convulsion was elevated about 3-8 times compared with controls. C-myc mRNA expression 1 hour after convulsion was elevated about 4 times at stage I, II, and V, ut was not elevated at stage III and IV. C-myc mRNA expression 48 hours after convulsion was elevated about 2-3 times compared with controls. In the experiment of PTZ-induced seizures, c-myc mRNA expression 30 minutes after convulsion was elevated 5-6 times compared with controls. C-myc mRNA expression 1 hour after convulsion was elevated 4-6 times. C-myc mRNA expression 48 hours after convulsion was elevated approximately 2 times. In the experiment of ECS-induced seizures, c-myc mRNA expression was elevated 4 times at 30 minutes and 1 hour after mild convulsion, but decreased at 30 minutes and 1 hour after severe convulsion compared with control. C-myc mRNA expression 48 hours after convulsion was elevated approximately 2 times. These results suggest that the enhanced expression of c-myc mRNA is a non-specific consequence in the development of PTZ kindling. In addition, c-myc does not seem to play an important role in turning on a molecular program underlying kindling.
Adult ; Animals ; Brain ; Epilepsy ; Hippocampus* ; Humans ; Male ; Models, Animal ; Pentylenetetrazole* ; Plastics ; Rats* ; RNA, Messenger* ; Seizures ; Stimulation, Chemical

The treatment for epilepsy has been studied throughout the course of human history. However, radical treatment of epilepsy has only been discovered recently with introduction of surgical treatment until now, palliative drug administration was common practice. During the anesthetic procedure for epilepsy surgery it is necessary for the patient to be alert and to cooperate with the surgeon while mapping and subcutaneous EEG test are carried out during the surgery. For this type of procedure, a new I.V. anesthetic, propofol is considered to be an ideal anesthetic agent because propofol is a short-acting and clear headed I.V. anesthetic agent for induction as the well as the maintenance of genenral anesthesia. In this study, only propofol was administered intravenously in 20 randomiied patients scheduled for brain surgery for epilepsy treatment. The mean infusion rate was 100 mcg/kg/min to maintain a satisfactory anesthesia. For the induction of anesthesia, slightly higher doses were required. The cardiovascular effects of propofol infusion was associated with slightly decrease of systolic, diastolic and mean arterial pressures. Arterial blood gases were analyzed for the evaluation of ventilatory function. PaCO2 were 41+/-4.23 mmHg preoperatively, 44+/-5.28 mmHg 30 min. following sedation, 42+/-6.35 mmHg 30 min. following awakening, 46+/-6.37 mmHg 30 min. following resedation, 44+/-4.79 mmHg at 2 hours and 44+/-6.51 mmHg at 4 hours after resedation and 36+/-3.98 mmHg 30 min. following recovery. PaO2 were 101+/-31.3 mmHg preoperatively, 190+/-47.13 mmHg 30 min. following sedation, 195+/-32 mmHg 30 min. following awakening, 209+/-29.23 mmHg 30 min. and 210+/-34.55 mmHg at 2 hours and 190+/-37.36 mmHg 4 hours following resedation, and 10.2+/-31.36 mmHg 30 min. following. PH were 7.38 preoperatively, 7.34+/-0.04 following sedation, 7.34+/-0.03 30 min. following awakening, 7.34+/-0.03 at 30 min. following resedation, 7.35+/-0.03 at 2 hours and 7.36+/-0.03 at 4 hours following resedation, and 7.38+/-3.98 at 30 min. after recovery. The duration of anesthesia was 8.5-12 hours. The duration of propofol anesthesia ranged from 8 to 9 hours. The awakening time from the cessation of propofol infusion ranged from 3 to 17 minutes. As the result of this study, we came to the conclusion that propofol is an ideal intravenous anesthetic for brain surgery for epilepsy treatment.
Anesthesia* ; Arterial Pressure ; Brain* ; Electroencephalography ; Epilepsy* ; Gases ; Head ; Humans ; Hydrogen-Ion Concentration ; Propofol*