Mesial Temporal Atrophy Research Articles

Reappraisal of epileptic pain as a rare symptom of seizures.

To draw attention to epileptic pain which is a rare seizure symptom mostly causing wrong diagnosis and delayed treatment. We present nine patients in whom pain was a prominent initial or early ictal symptom. We reviewed the records of 4736 patients, and found nine patients who had pain as an aura or an early prominent symptom of their seizures. Seizure semiology, EEG, and cranial imaging features were evaluated retrospectively. Age at seizure onset ranged from 6 months to 50 years, and the mean age during the study was 37.7±11.9 years. Pain was predominantly peripherally localized in four patients, whereas cephalic pain was detected in three patients, and abdominal pain was detected in two patients. Electroencephalography (EEG) revealed epileptic abnormalities on the temporoparietal and frontotemporal regions in three patients each. Photosensitive generalized epileptic discharges were detected in one and diffuse background slowing in the remaining two other patients. Electroencephalography abnormalities were lateralized to the contralateral site of the pain in four patients with strictly localized pain. Three patients revealed no abnormality on the cranial MR imaging, whereas others showed different types of abnormality such as heterotopias (n:1), mesial temporal lobe atrophy (n:1), white and gray matter sequela lesions (n:1), diffuse white matter lesion (n:1), chronic encephalomalacia and gliosis (n:1), and perivascular space dilatation (n:1). Epileptic pain is a neglected, but important, semiologic symptom with localization and lateralization value in the patients with somatosensorial seizures of parietal as well as temporal lobe origin. It occurs mainly as peripherally localized, cephalic, or abdominal pain and is usually associated with a symptomatic etiology. Awareness of epileptic pain is important to avoid misdiagnosis and delayed treatment.

A Survey of Alzheimer’s disease using Fuzzy Neural Network

Alzheimer disease is one of the most common diseases in the aging population, ranking as the fourth most common cause of death and it is a progressive neurodegenerative disorder characterized by the gradual onset of dementia. Magnetic resonance imaging (MRI) is a preferred neuro imaging examination for Alzheimer disease diagnosis. It allows accurate 3-dimensional (3D) volume measurement of brain structures. The primary role of MRI in the diagnosis of Alzheimer disease is the assessment of volume change in characteristic locations. The diagnosis should be made on the basis of two features: mesial temporal lobe atrophy and temporoparietal cortical atrophy. Computer implementations increased the accuracy and performance of detecting undergoing changes in affected brain areas. It uses Image Segmentation and integrating of its algorithms provides simpler guidance for the diagnosis process. This paper provides a survey of existing techniques of image segmentation and a comparison of the K-means and neuro-fuzzy algorithms are also given.

Young-onset frontotemporal dementia in a homozygous tau R406W mutation carrier.

Microtubule-associated protein tau mutations result in 10-20% of cases of genetic frontotemporal lobar degeneration. Tau mutation carriers typically develop behavioral variant frontotemporal dementia with or without parkinsonism. Unlike most frontotemporal dementia gene mutations, heterozygous R406W tau mutation carriers most often develop clinical Alzheimer's disease. We report a homozygous tau R406W mutation carrier with behavioral variant frontotemporal dementia who developed symptoms 20years before mean family symptom onset. Voxel-based morphometry showed frontoinsular, frontal, and mesial temporal cortical atrophy. Homozygous tau R406W mutations appear to accelerate symptom onset and drive a behavioral variant frontotemporal dementia syndrome.

Mixed tau and TDP-43 pathology in a patient with unclassifiable primary progressive aphasia

Classifying primary progressive aphasia (PPA) into variants that may predict the underlying pathology is important. However, some PPA patients cannot be classified. A 78-year-old woman had unclassifiable PPA characterized by anomia, dysarthria, and apraxia of speech without agrammatism. Magnetic resonance imaging revealed left mesial temporal atrophy and 18-flourodeoxy-glucose positron emission tomography showed left anterior temporal and posterior frontal (premotor) hypometabolism. Autopsy revealed a mixed tauopathy (argyrophilic grain disease) and transactive response-DNA-binding-protein-43 proteinopathy. Dual pathologies may explain the difficulty classifying some PPA patients and recognizing this will be important as new imaging techniques (particularly tau-positron emission tomography) are introduced and patients begin enrollment in clinical trials targeting the underlying proteinopathy.

A Brief History of Voxel-Based Grey Matter Analysis in Alzheimer's Disease

Voxel-based morphometry (VBM) and cortical thickness measurement are common techniques to identify regional atrophy in neurodegenerative diseases such as Alzheimer's disease (AD). Because studies employing these methods draw conclusions regarding patterns of regional cortical degeneration, it is important to be aware of their possible limitations. To evaluate the effect of different VBM versions, we performed voxel-based analyses through successive versions-from SPM99 to SPM8-as well as FSL-VBM on n = 20 AD patients and n = 20 controls. Reproducibility was assessed in an independent sample, again of n = 20 per group, from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Further, we tested the hypothesis that VBM can sensitively detect hippocampal atrophy, but is relatively insensitive to changes in the cortical ribbon, by contrasting VBM with FreeSurfer cortical thickness measurements. The results with both datasets confirmed that VBM preferentially identifies grey matter lesions in the mesial temporal lobe but is largely insensitive to isocortical atrophy. In contrast, FreeSurfer identified thinning of cortical ribbon association cortex more significant in post- rather than pre-Rolandic areas and with relative preservation of primary sensory-motor regions-in other words precisely as would be expected in AD. The results highlight a bias that VBM has toward detecting mesial temporal lobe atrophy. This finding has important implications for interpretation of clinical and cognitive studies in AD.

Asymmetric cortical surface area and morphology changes in mesial temporal lobe epilepsy with hippocampal sclerosis

To date, magnetic resonance imaging (MRI)-based studies of the cerebral cortex in mesial temporal lobe epilepsy (MTLE) have focused primarily on investigating cortical volume and thickness. However, volume is a composite of surface area and thickness, each reflecting distinct neurobiologic and genetic processes. The goal of this study was to investigate cerebral cortex (1) surface area, (2) surface geometric distortion, and (3) thickness in MTLE with hippocampal sclerosis (HS). Seventy patients with "sporadic" unilateral MTLE + HS and 40 healthy controls underwent T(1) -weighted MRI. Processing MR images using an automated cortical surface reconstruction method (FreeSurfer), we quantified cortical surface area, surface geometric distortion (metric distortion), and thickness at each vertex across the entire cortex. Differences between patients and controls were determined using generalized linear models. Separate linear regression models were employed to assess the relationship between cortical surface area and hippocampal volume as well as a series of important clinical features of the condition. We detected an asymmetric reduction in cortical surface area, predominantly in ipsilateral mesial and anterior temporal lobe subregions, of patients with MTLE + HS. Changes in surface geometric features were also evident and closely mirrored surface area patterns. In contrast, cortical thinning appeared dispersed across the cortex bilaterally. The regression models revealed that ipsilateral hippocampal volume was a significant predictor of temporal lobe surface area changes. Our findings indicate that contraction in surface area, rather than cortical thinning, explains ipsilateral mesial and anterior temporal lobe atrophy in patients with MTLE with HS. Furthermore, the alterations in surface geometry indicate folding abnormality involving the same regions. Cortical surface changes may represent sequelae of the disease or deviant cortical development.

13 Neuroimaging correlates of vascular cognitive impairment: prevalence and clinical relevance of mesial temporal lobe atrophy in a stroke service cohort

ObjectivesVascular cognitive impairment and Alzheimer's disease (AD) may interact and co-exist. We investigated the prevalence and impact of mesial temporal lobe atrophy (MTA), a radiological marker for AD, in a...

Potential Predictors of Hippocampal Atrophy in Alzheimerʼs Disease

The hippocampus is a vulnerable and plastic brain structure that is damaged by a variety of stimuli, e.g. hypoxia, hypoperfusion, hypoglycaemia, stress and seizures. Alzheimer's disease is a common and important disorder in which hippocampal atrophy is reported. Indeed, the available evidence suggests that hippocampal atrophy is the starting point of the pathogenesis of Alzheimer's disease and a significant number of patients with hippocampal atrophy will develop Alzheimer's disease. Studies indicate that hippocampal atrophy has functional consequences, e.g. cognitive impairment. Deposition of tau protein, formation of neurofibrillary tangles and accumulation of β-amyloid (Aβ) contributes to hippocampal atrophy together with damage caused by several other factors. Some of the factors associated with the development of hippocampal atrophy in Alzheimer's disease have been identified, e.g. hypertension, diabetes mellitus, hyperlipidaemia, seizures, affective disturbances and stress, and more is being learnt about other factors. Hypertension can potentially damage the hippocampus through ischaemia caused by atherosclerosis and cerebral amyloid angiopathy. Diabetes can produce hippocampal lesions via both vascular and non-vascular pathologies and can reduce the threshold for hippocampal damage. Carriers of the apolipoprotein E (ApoE)-ε4 genotype have been shown to have greater mesial temporal atrophy and poorer memory functions than non-carriers. In addition to giving rise to abnormal lipid metabolism, the ApoE-ε4 allele can affect the course of Alzheimer's disease via both Aβ-dependent and -independent pathways. Repetitive seizures can increase Aβ-peptide production and cause neurotransmission dysfunction and cytoskeletal abnormalities or a combination of these. Affective disturbances and stress are proposed to increase corticosteroid-induced hippocampal damage in many different ways. In the absence of any specific markers for predicting Alzheimer's disease progression, it seems appropriate to learn more about the various predictors of hippocampal atrophy that determine the progression of Alzheimer's disease from mild cognitive impairment (MCI), and then attempt to address these. It would be interesting to know to what extent these predictors play a role in the development of MCI or hasten the conversion of MCI to full-blown Alzheimer's disease. Finally, it would be useful to know the extent to which these predictors can worsen or aggravate existing Alzheimer's disease. Of the clinically used drugs in Alzheimer's disease, anticholinesterases have been shown to slow down the rate of progression of hippocampal atrophy. One study observed that the neuroprotective effect of these agents is possibly due to an anti-Aβ effect produced by cholinergic stimulation. Similarly, antihypertensive and antihyperglycaemic drugs (pioglitazone and insulin) have been shown to reduce the risk of Alzheimer's disease or disease progression. Currently, there are no disease-modifying therapies available for Alzheimer's disease. It has been suggested that for treatment to be most effective, the regimen must be started before significant downstream damage has occurred (i.e. before the clinical diagnosis of Alzheimer's disease, at the stage of MCI or earlier). Since the hippocampus is a plastic structure and atrophy of this structure is closely related to the pathophysiology of Alzheimer's disease, if we could control blood pressure, regulate blood sugar, treat behavioural and psychological symptoms, achieve satisfactory lipid lowering and maintain a seizure-free state in patients with Alzheimer's disease, this may not only improve disease control but could also potentially affect the rate of disease progression.

Nutrition and Alzheimer's disease.

Alzheimer's disease begins with cognitive deficiencies that gradually become worse with the extension of cerebral lesions. Other troubles arise such as loss of independence, orientation impairments, disordered eating behavior, and weight loss. This weight loss increases the risk of infections, skin ulcers, and falls and consequently decreases quality of life in Alzheimer's patients. Various hypotheses (increased energy expenditure, mesial temporal cortex atrophy) were suggested to explain weight loss. We set up a Health Promotion Program that aims to prevent weight loss in patients with Alzheimer's disease. This program uses various tools (nutrition calendar, Mini Nutritional Assessment, nutrition education sessions) described in this article.

High frequency oscillations in intracranial EEGs mark epileptogenicity rather than lesion type

High frequency oscillations (HFOs) called ripples (80-250 Hz) and fast ripples (FR, 250-500 Hz) can be recorded from intracerebral EEG macroelectrodes in patients with intractable epilepsy. HFOs occur predominantly in the seizure onset zone (SOZ) but their relationship to the underlying pathology is unknown. It was the aim of this study to investigate whether HFOs are specific to the SOZ or result from pathologically changed tissue, whether or not it is epileptogenic. Patients with different lesion types, namely mesial temporal atrophy (MTA), focal cortical dysplasia (FCD) and nodular heterotopias (NH) were investigated. Intracranial EEG was recorded from depth macroelectrodes with a sampling rate of 2000 Hz. Ripples (80-250 Hz) and Fast Ripples (250-500 Hz) were visually marked in 12 patients: five with MTA, four with FCD and three with NH. Rates of events were statistically compared in channels in four areas: lesional SOZ, non-lesional SOZ, lesional non-SOZ and non-lesional non-SOZ. HFO rates were clearly more linked to the SOZ than to the lesion. They were highest in areas in which lesion and SOZ overlap, but in patients with a SOZ outside the lesion, such as in NHs, HFO rates were clearly higher in the non-lesional SOZ than in the inactive lesions. No specific HFO pattern could be identified for the different lesion types. The findings suggest that HFOs represent a marker for SOZ areas independent of the underlying pathology and that pathologic tissue changes alone do not lead to high rates of HFOs.

Surgical treatment of independent bitemporal lobe epilepsy defined by invasive recordings

Objectives: Bitemporal lobe epilepsy is commonly encountered in the evaluation of pharmacoresistant epilepsy. Yet the role of surgery in the management of these patients is unclear. This study evaluates the...

Memory impairment in multiple sclerosis: correlation with deep grey matter and mesial temporal atrophy

Background:MRI research in multiple sclerosis (MS) samples reveals pathology in both the cerebral cortex and deep grey matter (DGM). The classical subcortical dementia hypothesis has been ascribed to MS and...

The role of MRI in localisation of epileptogenic foci: how far have we come?

Published online: 26 August 2005 Springer-Verlag 2005 During the last decade, MR imaging has changed dramatically, from identification of gross structural abnormalities to in-depth analysis of ‘‘cryptogenic lesions’’— their anatomical extent as well as their functional significance. Newly developed MR methods such as voxel based morphometry (VBM) have expanded our knowledge about partial epileptic syndromes. For example, structural involvement of the entorhinal cortex in mesial temporal epilepsy [7] (TLE)—the most common cause of refractory epilepsy—was recently identified. Ongoing seizures seem to correlate with progressive mesial temporal atrophy as demonstrated in longitudinal MR [4]. In addition, development of neocortical atrophy is related to seizure frequency, interpreted as seizure-induced neuronal loss, as well as involvement of extensive neocortical neuronal networks [3]. Malformations of cortical development (MCD) are increasingly recognised as pathological substrate, and are currently the second most common cause for refractory partial epilepsy in adults. These lesions are hardly visible in routine MRI, but voxel-based 3-D MRI has the potential to increase the sensitivity to detect a MCD [5] by more than 30%. Whilst grey-matter abnormalities are preferentially delineated by VBM, associated white-matter changes are probably best depicted by diffusion tensor imaging (DTI). DTI provides information about the directionality and magnitude of the molecular motion of water, and is a promising method for delineating the extent of a cortical dysplasia into white matter [6]. The article ‘‘Evaluating functional MRI procedures for assessing hemispheric language dominance in neurosurgical patients’’ by Baciu and colleagues in this issue highlights the significance of functional neuroimaging in the presurgical evaluation of refractory epilepsy patients. FMRI has been widely used to identify eloquent areas in order to prevent language and memory impairment after removal of the epileptogenic focus. The authors have used four different language paradigms to delineate eloquent regions in patients with partial epilepsies. The sensitivity of two different methods quantifying the HLD were investigated. These results were subsequently compared to various tests, such as WADA, electrocortical stimulation and surgical outcome as gold standards. By using the lateralisation index instead of predefined average magnitude measures of the BOLD signal, concordant fMRI predictions of HLD were achieved in 73% of all patients. According to Baciu et al. [2] the most sensitive parameter for HLDNeuroradiology (2005) 47: 803–804 DOI 10.1007/s00234-005-1442-0 EDITORIAL

New-onset mesial temporal lobe epilepsy in a 90-year-old: clinical and EEG features

Although there is a peak in the incidence of epilepsy in the elderly compared with the general population, complex partial seizures represent less than 15% of the seizure types reported. We report on a 92-year-old woman with a 2-year history of daily complex partial seizures. Prolonged video/EEG recording showed bilateral anterior mesial temporal interictal spikes, which predominated on the left, and two typical seizures arising from the left temporal area. Cranial MRI scanning showed multiple lacunar infarcts without temporal lobe involvement or mesial temporal atrophy. Our case appears to be oldest patient in the literature with newly diagnosed mesial temporal lobe epilepsy confirmed by video/EEG recording.

Intermetamorphosis in a Patient With Alzheimer's Disease

Back to table of contents Previous article Next article LetterFull AccessIntermetamorphosis in a Patient With Alzheimer's DiseaseFrédéric Assal, M.D., and Mario F. Mendez, M.D., Ph.D., Frédéric AssalSearch for more papers by this author, M.D., and Mario F. MendezSearch for more papers by this author, M.D., Ph.D., VA Greater Los Angeles and UCLA Alzheimer's disease Center, Los Angeles, CA (f.a., m.f.m.); VA Greater Los Angeles Neurobehavior Unit and Department of Neurology and Psychiatry, UCLA, Los Angeles, CA (m.f.m.)Published Online:1 May 2003AboutSectionsView EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: Intermetamorphosis is a misidentification syndrome in which familiar persons are believed to have exchanged identities.1 We report a patient with clinically probable Alzheimer's disease who developed intermetamorphosis for several members of his family. Analysis of this patient's disturbance suggests abnormal processing between the normal face recognition units and the person identity node in the inferior temporal lobe.2–4Case ReportA 76-year-old right-handed man had a 3-year history of progressive decline in memory and cognition. His medical history was remarkable only for prior ethanol abuse. The patient had undergone an evaluation for dementia, including neurological examination, laboratory tests, and neuroimaging. Magnetic resonance imaging was significant only for prominence of the temporal horns of the lateral ventricles, suggesting bilateral mesial temporal atrophy, and he was diagnosed with clinically probable Alzheimer's disease.About 2 years into his illness he began misidentifying family members. Initially, he misidentified his wife as his deceased mother and, later, as his living sister. His substitution of his sister for his wife became firmly established and could not be corrected with explanation. When confronted, he subsequently claimed that he had never been married or that his wife had left him. Gradually, the patient began misidentifying his son as his brother, his daughter as another sister, and his granddaughter as his daughter. These misidentifications persisted even on the telephone. Moreover, on different clinic visits he described the hospital as a meeting hall or a church where he visited to socialize or to help out.On examination he was cooperative, attentive, and euthymic. His Mini-Mental State Examination Score was 16 (out of 30), and his examination showed deficits in verbal fluency, confrontation naming, delayed recall, complex constructions, and abstractions. The elementary neurological examination was otherwise normal.We tested the patient with photographs of familiar persons from a photo album. Positive responses were counted when the photo subjects were positively identified or named. The control was his wife, who scored 100% correct answers. The results showed 100% misidentification of his wife as his sister in photographs with 100% persistence of the misidentification over the past without a retrograde gradient, and correct identification of himself through different ages. He did not have prosopagnosia (he recognized 80% of the photographs) and could recognize his own face in a mirror.CommentWe present a rarely described intermetamorphosis syndrome occurring in a patient with Alzheimer's disease. The patient did not have facial recognition difficulty, a temporal memory gradient for recalling familiar faces, or a failure to integrate prior memories of familiar faces with currently perceived faces. The misidentifications were not limited to the visual modality, as they occurred with the persons' voices as well. This points to a preservation of the abnormal “person identity nodes” across time and across modalities.These findings, as well as the reduplicative misidentification of the hospital, suggest an inability to correctly identify the source of his sense of familiarity for family members as a result of temporal lobe disease. Frontal lobe dysfunction also may contribute to his misattribution of identity.5References1 Courbon P, Tusques J: Illusions d'intermétamorphose et de charme. Ann Médico Psychol 1932; 90:401-405Google Scholar2 Ellis HD, Young AW: Accounting for delusional misidentifications. Br J Psychiatry 1990; 157:239-248Crossref, Medline, Google Scholar3 Breen N, Caine D, Coltheart M: Models of face recognition and delusional misidentification: a critical review. Cogn Neuropschychol 2000; 17:55-71Crossref, Medline, Google Scholar4 Hudson AJ, Grace GM: Misidentification syndromes related to face specific area in the fusiform gyrus. J Neurol Neurosurg Psychiatry 2000; 69:645-648Crossref, Medline, Google Scholar5 Tomita H, Ohbayashi M, Nakahara K, et al: Top-down signal from prefrontal cortex in executive control of memory retrieval. Nature 1999; 401:699-703Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited byPsychiatry and Clinical Psychopharmacology, Vol. 28, No. 1Neuropsychologia, Vol. 45, No. 13 Volume 15Issue 2 May 2003Pages 246-247 Metrics History Published online 1 May 2003 Published in print 1 May 2003

Wisconsin Card Sorting performance in patients with temporal lobe epilepsy: clinical and neuroanatomical correlates.

A sizable proportion of patients with temporal lobe epilepsy (TLE) display impairments on tests of executive function. Previous studies have suggested several factors that may explain such performance, including the presence of hippocampal sclerosis, electrophysiological disruption to extratemporal regions, and early age of seizure onset. However, no clear determinants have been found that consistently explain such executive dysfunction. The present study investigated the contribution of several clinical variables and temporal lobe neuroanatomic features to performance on the Wisconsin Card Sorting Test (WCST) in a series of patients with TLE. Eighty-nine patients with lateralized TLE (47 left, 42 right) were examined. Seventy-two patients from this series underwent anterior temporal lobectomy (ATL). Regression analysis was used to examine the effects of age, education, age at seizure onset, seizure duration, seizure laterality, history of secondary generalized seizures, and MRI-based volumes of the right and left hippocampi on preoperative WCST performance (number of categories completed, perseverative errors). Further univariate analyses examined whether the presence of bilateral hippocampal sclerosis, mesial temporal lobe abnormalities beyond the hippocampus, or temporal neocortical abnormalities affected preoperative WCST performance. In addition, we examined whether becoming seizure free after ATL affected change in WCST performance. Overall regression analysis was not significant. However, an examination of individual partial correlations revealed that patients with a history of secondary generalized seizures performed more poorly on the preoperative WCST than did patients without such history. In addition, patients who were seizure free after ATL did not exhibit better WCST outcome than patients who did not become seizure free. The presence of bilateral hippocampal sclerosis, extrahippocampal mesial temporal atrophy, or temporal neocortical lesions did not affect WCST performance. These results indicate that the presence of temporal lobe structural abnormalities do not significantly affect executive function as measured by the WCST. The present study does suggests that the critical determinants of WCST performance in patients with TLE lie outside the temporal lobe and likely relate to metabolic disruption to frontostriatal neural network systems.

Interictal EEG and ictal scalp EEG propagation are highly predictive of surgical outcome in mesial temporal lobe epilepsy.

Surgical outcome in patients with mesial temporal lobe sclerosis (MTS) is worse than that in patients with temporal lobe activity (TLE) with tumors. Previous studies of the ictal EEG focused on ictal EEG onset in scalp EEG or ictal EEG propagation in invasive recordings. Ictal EEG propagation with scalp electrodes has not been reported. Ictal scalp EEG propagation patterns were studied in 347 seizures of 58 patients with MTS or nonlesional TLE. Interictal epileptiform discharges (IEDs) and the presence of unilateral mesial temporal lobe atrophy in magnetic resonance imaging (MRI) also were studied in these 58 patients. Forty-nine patients were operated on (minimal follow-up of 1 year). Postoperatively, seizure-free outcome was seen in (a) 82.8% of patients with regionalized EEG seizure without contralateral propagation, but in only 45.5% of patients with contralateral propagation (p = 0.007); (b) 84.6% of patients with 100% IED lateralized to one temporal lobe, but in only 52.2% with <100% unitemporal IED (p = 0.015); (c) 88.9% with 100% unitemporal IED and regionalized ictal EEG combined, 73.7% with one of both variables, and only 33.3% with <100% ipsitemporal IED combined with contralateral ictal EEG propagation (p = 0.007). Switch of lateralization or bitemporal asynchrony in the ictal scalp EEG and bitemporal IED are most probably an index of bitemporal epileptogenicity in MTS and are associated with a worse outcome.

Clinical patterns of patients with temporal lobe epilepsy and pure amygdalar atrophy.

MRI volumetric measurements (MRIvol) have been proven reliable in determining mesial temporal atrophy in patients with TLE. We attempted to correlate the clinical features with different patterns of hippocampal formation (HF) and amygdala (AM) atrophy in patients with TLE without foreign tissue lesion. We studied 65 patients with refractory TLE. They were divided into five groups according to MRIvol results: pure AM atrophy (n = 11, 10 unilateral and one bilateral), unilateral HF atrophy (n = 16), bilateral HF atrophy (n = 12), unilateral AM + HF atrophy (n = 13), and patients with normal volumes of AM and HF (n = 13). MRIvol of AM and HF were performed by using a protocol previously described by Watson et al. (Neurology 1992;42:1743-50). Patients with AM atrophy had later onset of seizures compared with those with unilateral HF atrophy (p < 0.01). History of febrile convulsions (p < 0.0001) and frequent secondarily generalized tonic-clonic seizures (GTCSs) were more often found in patients with HF atrophy compared with those with pure AM atrophy and those with normal volumes (p = 0.04). Prolonged postictal confusion was more often found with AM atrophy (p = 0.05). Memory impairment was more severe in patients with HF atrophy than in those with AM atrophy only or in those with normal volumes (p = 0.03). There were no significant differences among the five groups in the following parameters: age, duration of epilepsy, seizure frequency, and presence and type of aura. Prolonged postictal confusion appeared to be related to AM atrophy, in keeping with previous clinical observations. These patients also had a lower incidence of early febrile convulsions, older age at epilepsy onset, lower frequency of secondary GTCS, and lesser memory dysfunction compared with patients with hippocampal atrophy.

Nocturnal temporal lobe epilepsy.

To analyze clinical, electrophysiologic, and neuroradiologic characteristics and prognostic factors in a group of patients with temporal lobe epilepsy (TLE) and complex partial seizures (CPS) occurring exclusively or predominantly after they fall asleep or before they awaken. CPS arising during sleep are classically identified with frontal lobe epilepsy. TLE associated with seizures occurring only or predominantly during sleep (nocturnal TLE) is less common. From a series of patients with refractory TLE studied between 1980 and 1996, the authors identified 26 patients (15 men) with nonlesional nocturnal TLE (mean age, 40 years). Clinical and laboratory characteristics of these individuals were studied and compared with a group of 72 age-matched, randomly selected patients with nonlesional TLE and predominantly diurnal seizures (diurnal TLE). Mean age at seizure onset was similar for both groups (16.3 versus 18.7 years). In the nocturnal TLE group, 2 of 26 patients had a positive family history of epilepsy, 18 reported an aura, 4 presented with CPS in clusters, 11 had unilateral and 15 bilateral temporal EEG abnormalities, and 14 of 21 studied had unilateral mesial temporal atrophy. None of these factors differed significantly in the two groups except for higher frequency of the following in the diurnal TLE group compared with the nocturnal TLE group: positive family history for epilepsy (33% versus 8%, p=0.01), estimated frequency of seizures (median, 14 versus 2 per month; p < 0.01), and presence of antecedent febrile convulsions (33% versus 11%, p=0.04). In the nocturnal TLE group, eight patients underwent surgical therapy and became seizure free (follow-up, > 12 months). Only two were seizure free on medication. Infrequent and nonclustered seizures, rare family history of epilepsy, and low prevalence of childhood febrile convulsions characterize nocturnal TLE. Within the TLEs, the nocturnal TLE form seems to have a better surgical prognosis.

Bilateral temporal hypometabolism in epilepsy.

Positron emission tomography (PET) has proven useful in epilepsy surgery for its ability to identify unilateral temporal hypometabolism (UTH), which is predictive of good surgical outcome. The significance of bilateral temporal hypometabolism (BTH) is not known. We identified all patients who had marked bilateral reduction in temporal lobe metabolism relative to the cerebellar hemispheres and compared their clinical features and treatment outcomes with those of control patients with UTH. BTH was evident in 10% of PET scans for epilepsy at our institution. We compared these patients with age-matched controls with UTH. The BTH patients had a higher percentage of generalized seizures; were more likely to have bilateral, diffuse or extratemporal seizure onsets; and had bilateral or diffuse magnetic resonance imaging (MRI) findings. UTH patients were more likely to have unilateral mesial temporal atrophy on MRI. Even when electrical seizure onsets were well localized, surgical outcomes were markedly worse in these patients than in controls. Medical treatment was also less successful. Social and cognitive functioning was worse in the BTH group. The only death occurred in the group with BTH. Patients with BTH have features distinct from those with UTH and have a worse prognosis for seizure remission after surgery.