Lesions in the central tegmental tract in autopsy cases of developmental brain disorders

We retrospectively analyzed central tegmental tract (CTT) lesions in 120 consecutive autopsy cases of developmental brain disorders to investigate the significance of symmetrical CTT lesions. Magnetic resonance imaging (MRI) findings of CTT lesions have been sporadically reported in various cases of child neurological diseases. In this study, symmetrical CTT lesions were observed in 25 (20.8%) among 120 cases of developmental brain disorders. These 25 cases were classified into three groups (groups I-III) in decreasing order of the severity of the lesion. Compared to five cases of group I in which CTT lesions were accompanied by diffuse tegmental damage, 20 cases of groups II or III developed relatively selective CTT lesions in which the medial longitudinal fasciculus and/or medial or lateral lemniscus were preserved. The causes of brain disorders in all three groups seemed to be different, and lysosomal disorders and congenital brain anomalies were frequently seen in cases in groups II and III, respectively. The dentato-rubro-olivary system is known to be involved in palatal myoclonus, and five out of 13 cases in group II showed myoclonic epilepsy. Compared with 95 cases without the CTT lesion, the changes in the pontine reticular formation were more closely associated with the CTT lesion than those in the inferior olivary nucleus. In conclusion, in cases of developmental brain disorders, the neuropathology of the symmetrical CTT lesion should be investigated.     

Beneficial effect of mild hypothermia and detrimental effect of deep hypothermia after cardiac arrest in dogs.

BACKGROUND AND PURPOSE: Mild cerebral hypothermia (34 degrees C) induced immediately after cardiac arrest improves outcome. Deep postarrest hypothermia (15 degrees C) has not been studied. METHODS: We used our dog model of normothermic ventricular fibrillation (no blood flow) of 12.5 minutes, reperfusion by brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 72 hours. Head surface cooling and bypass cooling were performed from start of reperfusion to 1 hour. Five groups of six dogs each were compared: group I, normothermic controls; group II, deep hypothermia (15 degrees C); group III, moderate hypothermia (30 degrees C); group IV, mild hypothermia (34 degrees C); and group V, mild hypothermia with head surface cooling begun during no flow. RESULTS: In control group I, five dogs remained comatose (overall performance category [OPC] 4) and one severely disabled (OPC 3). In group II, four dogs achieved OPC 4 and two dogs OPC 3 (NS versus group I). Compared with group I, OPCs were better in group III (p less than 0.05), group IV (p less than 0.05), and group V (p less than 0.05). Neurological deficit scores were also better in groups III, IV, and V than in groups I or II (p less than 0.05). Total brain histological damage scores were better in group III (p = 0.02), group IV (p = 0.06), and group V (p less than 0.05) than in group I. In group II, OPC and neurological deficit scores were the same and histological damage scores numerically worse than in group I and all were worse than in groups III, IV, and V (p less than 0.05). Cardiovascular complications and myocardial morphological damage in groups II and III were worse than in groups I, IV, and V (p less than 0.05). CONCLUSIONS: Mild or moderate cerebral hypothermia induced immediately after cardiac arrest improves cerebral outcome, more likely when initiated during arrest, whereas deep postarrest hypothermia can worsen cerebral and cardiac outcome.     

EEG findings in depressive pseudodementia and dementia with secondary depression

We report EEG findings in 33 elderly patients with mixed symptoms of depression and dementia, followed longitudinally to confirm diagnosis. Two groups of patients, dementia with depressive features (mixed-DEM, group I, n = 23) and patients with depressive pseudodementia (mixed-DEP, group II, n = 10), were defined. In addition, we also included, for comparison purposes, 35 patients with probable AD without depressive features (group III), 23 patients with major depression without cognitive impairment (group IV), and 61 healthy elderly controls (group V). We found significant group differences on waking EEGs between those mixed patients who did well after treatment for depression (depressive pseudodementia) compared to patients having dementia with secondary depression. The differences paralleled those between the 'pure' groups of demented and depressed patients. In patients with either depression or depressive pseudodementia, the EEG was usually normal or showed only mild abnormalities. In contrast, the majority of patients with either dementia or dementia with secondary depression had abnormal EEGs, with approximately one-third having moderate (or severe) abnormalities. Although the EEG was usually normal or only mildly abnormal in patients with pseudodementia or depression, these groups (II and IV) did show a significant slowing of the dominant posterior rhythm compared to controls. They also had a higher percentage of generalized abnormal EEGs than controls and this difference was significant between group IV (depression) and controls.     

Combined EEG and MEG analysis of early somatosensory evoked activity in children and adolescents with focal epilepsies.

OBJECTIVE: The study aimed to evaluate differences between EEG and MEG analysis of early somatosensory evoked activity in patients with focal epilepsies in localizing eloquent areas of the somatosensory cortex. METHODS: Twenty-five patients (12 male, 13 female; age 4-25 years, mean 11.7 years) were included. Syndromes were classified as symptomatic in 17, idiopathic in 2 and cryptogenic in 6 cases. 10 patients presented with malformations of cortical development (MCD). 122 channel MEG and simultaneous 33-channel EEG were recorded during tactile stimulation of the thumb (sampling rate 769 Hz, band-pass 0.3-260 Hz). Forty-four hemispheres were analyzed. Hemispheres were classified as type I: normal (15), II: central structural lesion (16), III: no lesion, but central epileptic discharges (ED, 8), IV: lesion or ED outside the central region (5). Analysis of both sides including one normal and one type II or III hemisphere was possible in 15 patients. Recordings were repeated in 18 hemispheres overall. Averaged data segments were filtered (10-250 Hz) and analyzed off-line with BESA. Latencies and amplitudes of N20 and P30 were analyzed. A regional source was fitted for localizing S1 by MRI co-registration. Orientation of EEG N20 was calculated from a single dipole model. RESULTS: EEG and MEG lead to comparable good results in all normal hemispheres. Only EEG detected N20/P30 in 3 hemispheres of types II/III while MEG showed no signal. N20 dipoles had a more radial orientation in these cases. MEG added information in one hemisphere, when EEG source analysis of a clear N20 was not possible because of a low signal-to-noise ratio. Overall N20 dipoles had a more radial orientation in type II when compared to type I hemispheres (p=0.01). Further N20/P30 parameters (amplitudes, latencies, localization related to central sulcus) showed no significant differences between affected and normal hemispheres. Early somatosensory evoked activity was preserved within the visible lesion in 5 of the 10 patients with MCD. CONCLUSIONS: MEG should be combined with EEG when analyzing tactile evoked activities in hemispheres with a central structural lesion or ED focus. SIGNIFICANCE: At time, MEG analysis is frequently applied without simultaneous EEG. Our results clearly show that EEG may be superior under specific circumstances and combination is necessary when analyzing activity from anatomically altered cortex.     

Degenerative changes in the cerebellum in adult non-lymphoblastic leukemia

Neuropathological investigations have been performed on 61 patients of both sexes, aged 17-60 years, deceased owing to nonlymphoblastic leukemias. The cerebellar degenerative changes appeared in 51 percent of cases mainly in the grey matter. Distinct rarefaction or atrophy of the cerebellar granular layer and the dentate nuclei were frequent phenomena. The following classification of the cerebellar granular layer damage was used: I degrees - focal rarefaction, II degrees - diffuse distinct rarefaction, III degrees - focal atrophy, IV degrees - diffuse atrophy. The investigations suggest that polychemotherapy is one of the causes of cerebellar degenerative changes, especially atrophy of the granular layer and dentate nuclei, as well as demyelination. In leukemias of short duration more frequently than in the remaining cases lymphocytic perivenous infiltrations appeared in the white matter. It seems to be a consequence of immunopathological reactions between the neoplasm and the nervous tissue in cases with more dynamic course of the disease.     

Investigation to sequelae of acute encephalopathy

We investigated 22 children with sequelae of acute encephalopathy. The patients were divided into 4 groups; group I with almost complete recovery (2 cases), group II with mild mental deterioration (4 cases), group III with severe mental deterioration (8 cases) and group IV with severe mental deterioration and severe physical disabilities (8 cases). There was no difference between 4 groups with regard to the past history, and status at the onset. The period of rehabilitation in hospital was different, being 0.4 month in group I, 2.6 months in group II, 3.0 months in group III and 3.6 months in group IV. The rehabilitation approach consisted mainly of medical therapy and range of motion exercise in the early stage followed trainings for walking and cognition. Family support was essential during the entire course. Evaluation with the functional independence measure was very useful for the rehabilitation.     

Reversibility of the chronic post-stroke state.

Forty patients with cerebral infarction associated with occlusion of the internal carotid artery (ICA) or the middle cerebral artery (MCA) were treated with hyperbaric oxygenation (HO). EEG analyses were performed regularly in order to assess the course of the cerebral lesion. Patients in an early post-stroke stage (III B) and patients in a chronic post-stroke stage (IV) had the changes in EEG analysis and neurological distributed evenly between these two groups.     

Spinal Cord Injury and Anti-NGF Treatment Results in Changes in CGRP Density and Distribution in the Dorsal Horn in the Rat

Spinal cord injury (SCI) results in chronic pain states in which the underlying mechanism is poorly understood. To begin to explore possible mechanisms, calcitonin gene-related peptide (CGRP), a neuropeptide confined to fine primary afferent terminals in laminae I and II in the dorsal horn of the spinal cord and implicated in pain transmission, was selected. Immunocytochemical techniques were used to examine the temporal and spatial distribution of CGRP in the spinal cord following T-13 spinal cord hemisection in adult male Sprague–Dawley rats compared to that seen in sham controls. Spinal cords from both hemisected and sham control groups (N = 5, per time point) were examined on postoperative day (POD) 3, 5, 7, 14, and 108 following surgery. Sham operated rats displayed CGRP immunoreaction product in laminae I and II outer, Lissauer's tract, dorsal roots, and motor neurons of the ventral horn. In the hemisected group, densiometric data demonstrated an increased deposition of reaction product that was statistically significant, in laminae III and IV, both ipsilateral and contralateral to the lesion that extended at least two segments rostral and caudal to the hemisection site by POD 14, and remained significantly elevated as long as POD 108. Since upregulation alone of CGRP would occur in an acute temporal window (by 2 to 3 days following spinal injury), these results are interpreted to be invasion of laminae III and IV by sprouting of CGRP containing fine primary afferents. Intrathecal delivery of antibodies against purified 2.5S nerve growth factor for 14 days to the hemisected group resulted in CGRP density in laminae I through IV that was significantly less than that seen in untreated or vehicle treated hemisected groups and to sham controls. These data indicate changes in density and distribution of CGRP following spinal hemisection that can be manipulated by changes in endogenous levels of NGF. These observations suggest possible strategies for intervention in the development of various pain states in human SCI.     

Striatopallidonigral degeneration in Pick's disease: a clinicopathological study of 41 cases

Summary The frequency and degree of stiatopallidonigral (SPN) degeneration were examined in 41 autopsy cases of Pick's disease. Based on the degree of SPN degeneration, these cases were arranged into four groups: 1) group I (severely degenerate; 19.5%), 2) group II (moderately degenerate; 22.0%), 3) group III (mildly degenerate; 36.5%), and 4) group IV (non-degenerate; 22.0%). 17 of the 41 cases had a definite (moderate to severe) SPN degeneration. The striatum, especially the caudate nucleus, was most frequently and most severely affected, while the internal segment of the globus pallidus was least frequently and least severely affected. In general, the oral portions of the SPN nuclei were more severely involved. In addition, in the putamen and globus pallidus the dorsomedial portions adjacent to the internal capsule were apt to be affected more markedly than the other portions. In the substantia nigra the degeneration tended to be more predominant in the pars reticulata than in the pars compacta, although both were usually involved. In addition, the medial to central portions of the substantia nigra were more vulnerable. In comparing the severely and moderately degenerate groups (groups I and II) with the mildly and non degenerate groups (groups III and IV), the former had more female cases, longer duration of illness, and more third-stage cases. In addition, the former contained more cases with lower brain weight and (predominant) frontal atrophy type, and more atypical cases without Pick bodies, or with symmetrical pyramidal tract degeneration or with combined traumatic lesions. It is notable that in all cases with definite SPN degeneration no extrapyramidal involuntary movements had been detected.     

An EEG study of Wilson's disease. Findings in patients and heterozygous relatives

The correlation of clinical and EEG findings was studied in 40 patients with Wilson's disease and their 57 heterozygous relations (25 children, 30 parents and 2 siblings). EEG changes in Wilson's disease were found in 84% (50% mild, 34% moderate) with but a slight predominance in patients with neurological involvement. The relatively high rate of pathological EEG findings in the hepatic or asymptomatic forms suggested the presence of subclinical CNS damage even in these cases. Diffuse episodic abnormalities were a dominant feature in all the groups under observation. As for the heterozygous relatives, a significant increase in pathological EEG findings (80-28% mild, 52% moderate to severe) was found in the heterozygous children. The changes often correlated with the clinical detection of minimal brain damage. The grossest EEG changes were seen in the youngest age group (under 10 years of age) with a subsequent tendency to abatement. In 2 cases there was an extinction of specific epileptic graphoelements which may have been the result of long-term penicillamine administration. In the adult heterozygous population (parents and siblings) there was no significant increase in the rate of pathological EEG findings compared with our control group. The authors discuss the problem of control mechanisms which have a role to play in the normalization of biochemical and probably also clinical and EEG findings in the heterozygotes.     

Relationship between metabolic recovery and the EEG prolonged ischemia of cat brain

In normothermic cats, cerebral blood flow was arrested for 1 hour followed by blood recirculation for 5-6 hours. Functional recovery was evaluated by qualitative and quantitative EEG analysis, and metabolic recovery by measuring metabolite and electrolyte levels in tissue samples taken from the cerebral cortex. In 5 out of 12 animals EEG activity did not recover after ischemia (group I); in 3 animals, intermittent EEG activity (group II) and in 4 animals continuous EEG activity returned during the observation period (group III). In group I the energy state was severely disturbed and an increase of calcium was detected, in group II this disturbance was much less pronounced, and in group III changes in energy metabolism and ion concentration were absent with the only exception of lower ADP levels. During recovery, the total intensity of EEG correlated positively with ATP (p less than 0.01) and inversely with lactate (p less than 0.05), and the intensity of the delta band inversely with sodium content (p less than 0.05). The results obtained demonstrate that electrophysiological recovery after prolonged ischemia is closely correlated with the restoration of the energy state and of electrolyte homeostasis of the brain. The inverse relationship of EEG intensity with lactate and sodium are interpreted as evidence for the adverse effects of ongoing post-ischemic glycolysis, resulting in the activation of the H+/Na+ antiporter for the regulation of intracellular pH.     

Effects of moderate hypothermia on leukocyte- endothelium interaction in the rat pial microvasculature after transient middle cerebral artery occlusion.

Background and Purpose--It has been demonstrated that moderate hypothermia attenuates brain damage, but the mechanism whereby this is achieved has not been clearly shown. Recently, the role of leukocytes as mediators of secondary brain damage after brain ischemia has been discussed. The aim of this study is to examine the effects of moderate hypothermia on leukocyte-endothelium interaction in the rat pial microvasculature after transient middle cerebral artery occlusion (MCAO). Methods--Rhodamine 6G-labeled leukocytes in brain surface were visualized with intravital fluorescence videomicroscopy through a closed cranial window. We analyzed the number of leukocytes adhering to the venular and arteriolar endothelium before ischemic insult and up to 3 hours after reperfusion. Rats were divided into 4 experimental groups. Group I (n=6) consisted of sham-operated animals. Groups II (n=6) and III (n=6) received left MCAO for 1 hour under normothermia (36 degrees C to 37 degrees C, group II) and under moderate hypothermia (30 degrees C to 32 degrees C, group III). Group IV (n=4) received left common carotid artery occlusion for 1 hour under normothermia. Results--The number of adhering leukocytes in venules in groups II and IV increased significantly (P<0.001) after reperfusion compared with the group I, but that in group III did not increase significantly (P>0.05). The number of adhering leukocytes in arterioles in group II increased significantly (P<0.01) compared with the other groups, although the adhering leukocytes were not as numerous as those seen in venules. Conclusions--It is demonstrated that hypothermia attenuates adhering leukocytes in venules and arterioles after reperfusion of MCAO. The inhibition of the leukocyte function may be an important factor in the neuroprotective effect of hypothermia.     

Mitochondrial dysfunction and ultrastructural damage in the hippocampus during kainic acid-induced status epilepticus in the rat

PURPOSE: Prolonged and continuous epileptic seizure (status epilepticus) results in cellular changes that lead to neuronal damage. We investigated whether these cellular changes entail mitochondrial dysfunction and ultrastructural damage in the hippocampus, by using a kainic acid (KA)-induced experimental status epilepticus model. METHODS: In Sprague-Dawley rats maintained under chloral hydrate anesthesia, KA (0.5 nmol) was microinjected unilaterally into the CA3 subfield of the hippocampus to induce seizure-like hippocampal EEG activity. The activity of key mitochondrial respiratory chain enzymes in the dentate gyrus (DG), or CA1 or CA3 subfield of the hippocampus was measured 30 or 180 min after application of KA. Ultrastructure of mitochondria in those three hippocampal subfields during KA-induced status epilepticus also was examined with electron microscopy. RESULTS: Microinjection of KA into the CA3 subfield of the hippocampus elicited progressive build-up of seizure-like hippocampal EEG activity. Enzyme assay revealed significant depression of the activity of nicotinamide adenine dinucleotide cytochrome c reductase (marker for Complexes I+III) in the DG, or CA1 or CA3 subfields 180 min after KA-elicited temporal lobe status epilepticus. Conversely, the activities of succinate cytochrome c reductase (marker for Complexes II+III) and cytochrome c oxidase (marker for Complex IV) remained unaltered. Discernible mitochondrial ultrastructural damage, varying from swelling to disruption of membrane integrity, also was observed in the hippocampus 180 min after hippocampal application of KA. CONCLUSIONS: Our results demonstrated that dysfunction of Complex I respiratory chain enzyme and mitochondrial ultrastructural damage in the hippocampus are associated with prolonged seizure during experimental temporal lobe status epilepticus.     

Effects of gamma-hydroxybutyrate on cerebrospinal fluid lactate and glucose levels after spinal cord trauma.

This study aims to evaluate the effects of gamma-hydroxybutyrate (GHB) after spinal cord trauma (SCT). Twenty rabbits were divided equally into four groups: group I was the sham-operated group, group II suffered from SCT but received no treatment, group III was given a dose of 400 mg/kg of GHB intravenously before SCT and group IV received the same dose after SCT. Cerebrospinal fluid (CSF) samples were obtained 30 min before SCT (T(0)), at 60 (T(1)) and 120 min (T(2)) after SCT. There was a threefold increase in lactate levels from baseline value at T(2) in group II, while statistically significant elevation of the lactate levels were not observed in groups III and IV. Glucose levels at T(1) and T(2) were significantly lower in groups III and IV compared with the control group. The findings of this study demonstrate that GHB can control the increase of CSF lactate and glucose levels following SCT and that this metabolic effect may be associated with neuroprotective physiological changes.     

Clinical,radiological and neurophysiological spectrum of JEV encephalitis and other non-specific encephalitis during post-monsoon period in India

AIMS: To study the spectrum of encephalitis during the post-monsoon period in a tertiary care centre of India. METHODS: Clinical, neurophysiological and radiological features of patients with encephalitis are reported in this communication. The patients were subjected to clinical examination, CT or MRI scan, EEG, motor and somatosensory evoked potentials in both upper and lower limbs bilaterally and concentric needle electromyography. The laboratory studies for Japanese encephalitis (JE) comprised virus isolated, IgM capture ELISA, mercaptoethanol test and hemagglutination inhibition titre in paired sera against JE virus. Patients were classified into JEV encephalitis and non-specific encephalitis. On the basis of radiological features, they were classified into group I (thalamic or basal ganglia involvement), group II (brainstem involvement only) and group III (normal MRI). The outcome was defined into poor (bedridden), partial (dependent for daily activities) and complete (independent) recovery at the end of 3 months. RESULTS: Out of 26 patients (Age 7-70 years, mean 24.8 years), laboratory evidences of JEV infection was present in 14 patients and one patient had herpes simplex encephalitis. The patients with JEV encephalitis had more severe illness as evidenced by lower GCS score, higher frequency of anterior horn cell involvement, movement disorders and more extensive MRI changes. The EEG and MEP changes were also more frequently abnormal in the JEV group. On radiology, 15 patients had thalamic or basal ganglia involvement (group I), 3 isolated midbrain involvement (group II) and 8 had normal MRI (group III). Laboratory evidence consistent with JE were present in 11 out of 12 patients in group I and 3 out of 8 in group III, however, there was no laboratory evidence of JE virus infection in patients with isolated brainstem involvement. There was overlap in the neurologic and systemic manifestations in all the 3 radiological groups as well as in the groups with and without laboratory evidences of JEV infection. CONCLUSION: The observed overlap in neurological and systemic involvement in different subgroups of encephalitis may be due to JE or JE-like viral infection. The possibility of strain variation, change in virulence of organism or immunity of host needs further studies.     

The calculation of the first positive Lyapunov exponent in sleep EEG data

To help determine if the EEG is quasiperiodic or chaotic we performed a new analysis by calculating the first positive Lyapunov exponent L₁ from sleep EEG data. Lyapunov exponents measure the mean exponential expansion or contraction of a flow in phase space. L₁ is zero for periodic as well as quasiperiodic processes, but positive in case of chaotic processes expressing the sensitive dependence on initial conditions. We calculated L₁ for sleep EEG segments of 15 healthy male subjects corresponding to sleep stages I, II, III, IV and REM (according to Rechtschaffen and Kales). Our investigations support the assumption that EEG signals are neither quasiperiodic waves nor simple noise. Moreover, we found statistically significant differences between the values of L₁ for different sleep stages.     

Functional respiratory chain studies in subjects with chronic progressive external ophthalmoplegia and large heteroplasmic mitochondrial DNA deletions.

The functional consequences of large heteroplasmic mtDNA deletions were investigated in a group of 6 patients with chronic progressive external ophthalmoplegia (CPEO) syndromes. State III respiration rates corrected for age were low with site I and II substrates in all cases and cytochrome oxidase activity was depressed. The severity of impairment varied and is consistent with inclusion of a variable percentage of non-functioning mitochondria (with deleted mtDNA) in the pellet. Western blot studies with a holocomplex antibody battery revealed no abnormalities in subunit content of complexes III and IV. A deficiency of several complex I subunits in 3 cases suggests that abnormal nuclear-mitochondrial regulation of complex I assembly may follow large mtDNA deletions.     

Immunohistochemical expression of fibroblast growth factor‐2 in developing human cerebrum and epilepsy‐associated malformations of cortical development

To elucidate the biological significance of fibroblast growth factor‐2 (FGF‐2) expression in epilepsy‐associated malformations of cortical development, immunohistochemical expression of FGF‐2 was investigated in the developing human cerebral mantles obtained from 30 autopsy cases of fetuses, stillborn infants and children ranging from 12 weeks gestation to 15 years old, and 70 surgically‐resected corticectomy specimens from patients with medically intractable epilepsy, including: group I, 12 tubers of tuberous sclerosis; group II, 24 cases of focal cortical dysplasia (FCD) with balloon cells (BC); group III, 11 FCD without BC; group IV, 23 histologically normal‐appearing neocortices from patients with Rasmussen encephalitis, cystic‐gliotic encephalopathy, temporal lobe epilepsy; and group V, 14 normal‐appearing neocortices adjacent to dysplastic lesions from groups I and II. FGF‐2 expression was detected in a population of matrix cells and/or neuroblasts within the ventricular zone in fetuses younger than 19 weeks gestation. Nuclei of glioblasts and immature astrocytes were also positive for FGF‐2 in cases older than 18 weeks gestation. FGF‐2 expression was not detected in immature cortical plate neurons. Astrocytes and ependymal cells were positive for FGF‐2 in the postnatal brains. Choroid plexus epithelium was strongly positive for FGF‐2 in all cases examined. Among the corticectomy specimens, the cytoplasms and/or nuclei of dysmorphic neurons (DNs) and BCs in groups I and II were variably positive for FGF‐2. The proportions of FGF‐2 immunoreactive cells (FGF‐2‐IR%) was significantly higher in groups I (36.9 ± 9.6) and II (45.1 ± 7.0) than in groups III (21.0 ± 5.7), IV (14.4 ± 4.7) and V (24.3 ± 10.3), and that in group V was higher than in group IV (P < 0.01). These results indicate that FGF‐2 upregulation in DNs and BCs is an important feature common to groups I and II, and suggest that BCs and DNs in these groups represent disturbed gliogenesis from matrix cells and disturbed maturation of cortical neurons from migrating neuroblasts, respectively.     

Ictal source localization in presurgical patients with refractory epilepsy.

Source localization of epileptic foci using ictal spatiotemporal dipole modeling (ISDM) yields reliable anatomic information in presurgical candidates. It requires substantial resources from EEG and neuroimaging laboratories. The profile and number of patients who may benefit from it are currently unknown. The purpose of this study is to demonstrate the clinical usefulness of source localization in a prospectively analyzed series. One hundred patients (51 male and 49 female patients) with mean age of 31 years (range, 2 to 63 years) and mean duration of refractory epilepsy of 20 years (range, 1 to 49 years) were enrolled consecutively in a presurgical protocol. Ictal EEG was available in 93 patients. ISDM was performed when suitable ictal EEG files were available. The clinical applicability of ISDM was examined in three patients groups: 37 patients in whom ictal EEG recording and MRI were congruent (group I), 30 patients in whom results were not completely congruent but not incongruent (group II), and 26 patients in whom the results were incongruent (group III). ISDM could be performed in 31 of 100 patients: 11 in group I, 8 in group II, and 12 in group III. ISDM influenced decision making in none of the patients in group I, in 4 of 8 patients in group II, and in 10 of 12 patients in group III. Typically, the results of ISDM directed avoiding intracranial EEG recordings in what appeared to be unsuitable candidates for resection by clearly confirming the incongruency between ictal EEG and MRI findings. In this series of 100 presurgical candidates, ictal source localization could be performed in 31% of patients. In 14% of patients, it proved to be a key element in the surgical decision process.     

Epilepsy surgery in patients with bilateral temporal lobe seizures: A systematic review

We explored the association between magnetic resonance imaging (MRI) lesion, degree of seizure laterality on intracranial electroencephalography (iEEG), and seizure outcome in patients with ambiguous or presumed bilateral temporal lobe epilepsy (BiTLE) on scalp EEG. We systematically reviewed the literature using Embase and MEDLINE up to May 31, 2012. Patients with bilateral iEEG, temporal lobe surgery, and follow‐up ≥1 year were included. We undertook three separate analyses on patients whose scalp EEG showed ambiguous onset or BiTLE (1) group data of those whose iEEG demonstrated unilateral TLE, (2) group data of those whose iEEG demonstrated BiTLE, (3) individual patient analysis in those with BiTLE for whom iEEG seizure laterality data were provided. Of 1,403 patients with ambiguous or presumed BiTLE on scalp EEG, 1,027 (73%) proved to have unilateral TLE on iEEG and contributed to the first analysis. Of these, 58% had Engel class I and 9% Engel class II outcomes. Of 132 patients in the second analysis (true BiTLE), Engel class I and II outcomes were achieved in 23% and 14%, respectively. Of 41 patients in the third analysis, 66% and 2% had Engel class I and II outcomes, respectively. The median proportion of seizures ipsilateral to the resection on iEEG did not differ between BiTLE patients with Engel class I–II (76%) and Engel III–IV (78%) outcomes (p = 0.87). Patients with ambiguous or independent bitemporal seizure onset on scalp EEG achieved good surgical outcomes. Overall, a significantly higher proportion of patients achieved good outcomes when iEEG showed unilateral TLE (67%) than when it showed true BiTLE (45%). However, the degree of seizure lateralization in those with BiTLE was not associated with seizure outcome, and it has a limited role in selecting the side of surgery.