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PubMedDate not supplied

Auditory processing in patients with temporal lobe epilepsy.

UNLABELLED: Temporal epilepsy, one of the most common presentation of this pathology, causes excessive electrical discharges in the area where we have the final station of the auditory pathway. Both the anatomical and functional integrity of the auditory pathway structures are essential for the correct processing of auditory stimuli. AIM: to check the Auditory Processing in patients with temporal lobe epilepsy regarding the auditory mechanisms of discrimination from sequential sounds and tone patterns, discrimination of the sound source direction and selective attention to verbal and nonverbal sounds. METHOD: eight individuals with temporal lobe epilepsy were assessed, after excluding those with non-confirmed diagnosis or with the focus of discharges not limited to this lobe. The evaluation was carried out through special auditory tests: Sound Localization Test, Duration Pattern Test, Digits Dichotic Test and Non-Verbal Dichotic Test. Their performances were compared to the performances of individuals without neurological diseases (case-control study). RESULTS: similar performances were observed between patients with temporal lobe epilepsy and the control group regarding the auditory mechanism of sound source direction discrimination. Comparing the other auditory mechanisms assessed, the patients with temporal lobe epilepsy presented worse results. CONCLUSION: individuals with temporal lobe epilepsy had more deficits in auditory processing than those without cortical damage.

Acoustic Stimulation↗

PubMed2006

Present practice and perspective of evaluation and surgery for temporal lobe epilepsy.

Surgery for temporal lobe epilepsy refractory to medical treatment is a promising treatment option. After a short overview of historical developments in this field, we describe the present practice of presurgical evaluation and resection strategies as practiced at our institution and review the corresponding publications from other centers. We will be trying to outline major future developments for the surgical therapy of temporal lobe epilepsy based on present trends.

Anticonvulsants↗

PubMed2004

Abnormal behavior in children with temporal lobe epilepsy and ganglioglioma.

Temporal lobe epilepsy in childhood is characterized by great clinical, electroencephalographic, and etiological diversity. The prognosis after temporal lobe epilepsy surgery in childhood is usually good, with most patients achieving complete seizure control. However, in some children behavior deteriorates postoperatively. We report two girls (2 and 6 years of age) with refractory seizures due to temporal lobe ganglioglioma. They exhibited aggression and hyperactivity since the beginning of their epilepsy. In both patients, behavioral disturbances worsened postoperatively, despite complete seizure control. Patients and parents should be advised about possible behavioral disturbances after epilepsy surgery, especially in the presence of a temporal lobe developmental tumor, even when seizure control is achieved postoperatively.

Anticonvulsants↗

PubMed1969

Clinical aspects of temporal lobe epilepsy--a review.

Temporal lobe epilepsy appears to be of increasing concern to psychiatrists, pediatricians and lawyers as an explanation for some aspects of behavior. There is a high incidence of structural abnormality associated with temporal lobe epilepsy, the most common being mesial temporal sclerosis. Depth electrode studies have shown that the most common focus for the clinical seizure is in the hippocampus or hippocampal gyrus. The first line of treatment continues to be attempt at control with anticonvulsant agents. Surgical treatment can be offered, in many instances, when drug therapy has failed.

Age Factors↗

PubMed2000

Pediatric candidates for temporal lobe epilepsy surgery.

Temporal lobectomy is an under-valued and effective therapy for selected children with temporal lobe seizures. This article details three components of the identification and evaluation of such children. The ictal symptoms and signs remains an essential component. This includes an aura suggesting limbic system involvement, and the nature of automatisms and other motor phenomena which may have lateralising value. Electroencephalography continues to accurately identify a principally epileptogenic focus in children and adults. The value of high quality magnetic resonance imaging is emphasized. Invasive studies are required in only a minority of cases. Several studies have revealed that 73-100% of carefully selected children receive benefit from this procedure whereas significant neurosurgical complications rarely occur.

Child↗

PubMed2000

Mitochondrial complex I deficiency in the epileptic focus of patients with temporal lobe epilepsy.

Mitochondria are cellular organelles crucial for energy supply and calcium homeostasis in neuronal cells, and their dysfunction causes seizure activity in some rare human epilepsies. To directly test whether mitochondrial respiratory chain enzymes are abnormal in the most common form of chronic epilepsy, temporal lobe epilepsy (TLE), living human brain specimens from 57 epileptic patients and 2 nonepileptic controls were investigated. In TLE patients with a hippocampal epileptic focus, we demonstrated a specific deficiency of complex I of the mitochondrial respiratory chain in the hippocampal CA3 region. In contrast, TLE patients with a parahippocampal epileptic focus showed reduced complex I activity only in parahippocampal tissue. Inhibitor titrations of the maximal respiration rate of intact human brain slices revealed that the observed reduction in complex I activity is sufficient to affect the adenosine triphosphate production rate. The abnormal complex I activity in the hippocampal CA3 region was paralleled by increased succinate dehydrogenase staining of neurons and marked ultrastructural abnormalities of mitochondria. Therefore, mitochondrial dysfunction is suggested to be specific for the epileptic focus and may constitute a pathomechanism contributing to altered excitability and selective neuronal vulnerability in TLE.

Adolescent↗

PubMed1997

Decrease in somatostatin-immunoreactive neurons in the rat amygdaloid complex in a kindling model of temporal lobe epilepsy.

In human temporal lobe epilepsy, seizures can begin in the hippocampus, amygdala, or surrounding cortical areas. Histologically, the seizure-induced selective neuronal damage and synaptic reorganization are best documented in the hippocampus. Little information is available about the damage in the other temporal lobe structures or whether the distribution of damage depends on the location of the primary seizure focus. We used an amygdala-kindling model of temporal lobe epilepsy to study whether seizures of amygdaloid origin cause damage to the amygdala and hippocampus. All rats experienced five class 5 generalized seizures. Neuronal damage was assessed by counting the density of GABA-immunoreactive (GABA-ir) and somatostatin-immunoreactive (SOM-ir) neurons in the amygdala and hilus of the dentate gyrus six months after the last seizure. We found that the density of GABA-ir neurons did not differ from that in controls in the contralateral amygdala. The density of SOM-ir neurons was, however, decreased in the lateral (69% of neurons remaining, P < 0.01), basal (67% remaining, P < 0.05), and accessory basal (68% remaining, P < 0.05) nuclei. In the hilus, the densities of GABA-ir and SOM-ir neurons were similar to that in controls. According to our data, a few seizures of amygdaloid origin may cause more severe damage to SOM-ir neurons in the amygdala than in the hilus. Such decrease in SOM-ir neurons which form one subpopulation of GABAergic inhibitory interneurons may increase the local excitability in the amygdala and, therefore, contribute to epileptogenesis.

Amygdala↗

PubMed1982

Neuroendocrine dysfunction in temporal lobe epilepsy.

Since medial temporal lobe structures are involved in the modulation of endocrine function and temporal lobe epileptics commonly show personality changes that resemble endocrine disorders, the existence of neuroendocrine dysfunction in temporal lobe epileptics was investigated by comparing the response of serum luteinizing hormone levels with intravenous luteinizing hormone-releasing hormone infusion in patients and normal controls. Five of seven consecutive patients had response curves that fell almost entirely outside of the normal control range, and all seven had either baseline or peak values that were outside of the normal range. These findings suggest that hypothalamic-pituitary control of gonadotropin secretion may be altered among patients with temporal lobe epilepsy.

Adult↗

PubMed1996

Characteristics of temporal lobe epilepsy with mesial temporal sclerosis, with special reference to psychotic episodes.

This study investigates the histories and the clinical course of 111 patients who had nonlesional temporal lobe epilepsy. We compared 61 patients with unilateral hippocampal sclerosis (UHS group) and 50 patients with minimal change (MRI negative group) assessed on the basis of MRI. In agreement with previous reports, we confirmed statistically that patients in the UHS group strongly tended to have had febrile convulsive status during early childhood or infancy and that habitual seizures tended to begin at a younger age than the other subset of nonlesional temporal lobe epilepsy. Strikingly, episodes of psychoses, especially postictal psychoses, occurred significantly more often in the UHS group than in the MRI negative group. Additional involvement of temporal neocortex further augmented this association. We stress the role of mesial temporal pathology, and its linkage to the temporal neocortex, in the genesis of postictal psychoses.

Adult↗

PubMed1993

Mesiobasal versus lateral temporal lobe epilepsy: metabolic differences in the temporal lobe shown by interictal 18F-FDG positron emission tomography.

Metabolic abnormalities in the temporal lobe (TL) of 25 patients suffering from temporal lobe epilepsy of mesiobasal or lateral TL origin have been investigated using interictal [18F]-fluorodeoxyglucose (FDG) positron emission tomography (PET). The epileptogenic area was determined by ictal EEG recordings using foramen ovale and scalp electrodes in 20 patients, and by the use of stereo-electroencephalography in one patient. Four patients with structural lesions on their MRIs had noninvasive ictal surface EEG recordings. Sixteen patients had a clear-cut mesiobasal seizure onset, and in five patients the seizures originated from the lateral temporal neocortex. Twenty-four patients underwent selective surgery. Patients with temporal limbic seizures associated with mesial gliosis (n = 15) had the lowest FDG uptake in the entire TL, followed by patients with lateral temporal seizure origin (n = 5). Patients with tumors located in the mesiobasal TL (n = 5) showed, in general, only a slight decrease of glucose metabolism in all TL structures. There was no clear-cut correlation between the degree of hypometabolism and the location of EEG-defined epileptogenic focus. The metabolic pattern, however, differed between the patient groups and allowed a discrimination between patients of mesial temporal and lateral temporal seizure onset.

Adolescent↗

PubMed1998

The relationship between sleep and epilepsy in frontal and temporal lobe epilepsies: practical and physiopathologic considerations.

PURPOSE: The influence of sleep on the incidence of seizures and the reciprocal effects of epilepsy on sleep were analyzed in 30 patients with intractable partial seizures, all candidates for surgery. METHODS: The patients were classified into two groups of 15 patients according to the documented site of the epileptogenic zone: frontal lobe epilepsy (FLE) and medial temporal lobe epilepsy (TLE). Frequency and waking-sleep distribution of seizures were evaluated by continuous video-EEG monitoring for 5 days, under defined antiepileptic drug (AED), sleep, and sleep deprivation regimens. Sleep organization was analyzed by polysomnography prior to the presurgical protocol. RESULTS: Significant differences were found between the two groups in sleeping-waking distribution of seizures under varied conditions, and in the quality of sleep organization. In FLE patients, seizures most often occurred during sleep, although sleep organization was normal. In TLE patients, most seizures occurred while patients were awake, and sleep organization was characterized by a low efficiency index. The difference in seizure distribution between FLE and TLE persisted under all conditions investigated, i.e., after AED discontinuation and sleep deprivation. CONCLUSIONS: Sleep recording may be useful for diagnosis of FLE, and monitoring after sleep deprivation for that of TLE. We speculate that sleep-related seizures in FLE may depend on interaction between frontal lobe areas with the thalamus cortical synchronization system and the acetylcholine regulatory system of waking.

Adult↗

PubMed1985

Autonomic responsiveness to affective visual stimulation in temporal lobe epilepsy.

Patients with temporal lobe epilepsy (TLE) have been posited by some to manifest a syndrome of interictal personality and behavioral change. Furthermore, this syndrome has been attributed to an underlying mechanism--enhanced affective responsiveness. The purpose of this investigation was to determine whether patients with TLE manifest increased emotional responsiveness relative to appropriate controls. Patients with TLE (n = 23) were compared with non-TLE (n = 7) and healthy controls (n = 16) as to their autonomic nervous system responsiveness to an emotionally stressing film. No differences were found among the groups. These results are related to the larger literature concerning epilepsy and psychopathology.

Adult↗

PubMed1990

Hyperprolactinemia and temporal lobe epilepsy in a woman: concomitant and persistent prolactin suppression and temporal lobe epilepsy relief.

It has been reported that hyperprolactinemia may be associated with increased temporal lobe activity. Coexisting hyperprolactinemia (97.5 +/- 3.2 ng/ml) related to a pituitary tumefaction (8 mm) and Temporal Lobe Epilepsy (TLE), were observed in a 37-year-old woman. Carbamazepin (CBZ) therapy induced a marked improvement in TLE symptoms and EEG recordings, but did not influence hyperprolactinemia and related symptoms. Long-lasting (27 months) normoprolactinemia (19.4 +/- 0.6 ng/ml) and TLE relief were achieved on a dopamine (DA) agonist medication, e.g. pergolide mesylate, 25-50 micrograms/day given over 8 months, and persisted as long as 27 months after drug withdrawal. Posttreatment CT scans showed progressive shrinkage of the pituitary tumor (2 mm) associated with an empty-sella. It is proposed that, whenever TLE and hyperprolactinemia coexist, therapy with a DA agonist such as pergolide mesylate, resulting in normoprolactinemia, may be beneficial in TLE control.

Adult↗

PubMed2002

Immature-like astrocytes are associated with dentate granule cell migration in human temporal lobe epilepsy.

In human temporal lobe epilepsy, a dispersion of dentate granule cells is frequently described in adults who had an early risk factor. To elucidate the role of glia in this phenomenon, we investigated neuronal dispersion, astrocyte organization and expression of intermediate filaments of mature and immature astrocytes (i.e. glial fibrillary acidic protein (GFAP) and vimentin, respectively) in seven subjects with early febrile seizures (F(+)) and five subjects with other etiologies than febrile seizures (F(-)). Compared to F(-) patients, a majority of F(+) subjects showed neuronal dispersion and vimentin expression in radial glia. However, in two patients with the maximal dispersion, radial processes expressed only GFAP. We suggest that granule cell migration that occurs in adult epileptic focus results from the transient occurrence of immature-like glia throughout the granular layer.

Adult↗

PubMed1993

Dormancy of inhibitory interneurons in a model of temporal lobe epilepsy.

In humans temporal lobe epilepsy (TLE) is characterized by recurrent seizures, neuronal hyperexcitability, and selective loss of certain neuronal populations in the hippocampus. Animal models of the condition indicate that a diminution of inhibition mediated by gamma-aminobutyric acid (GABA) accounts for the altered function, and it has been hypothesized that the diminution arises because GABAergic basket interneurons are "dormant" as a result of their being disconnected from excitatory inputs. In hippocampal slices, inhibitory postsynaptic potentials (IPSPs) were elicited in CA1 pyramidal cells by activation of basket cells; responses from an animal model of TLE were compared to those from control tissue. IPSPs evoked indirectly by activation of terminals that then excited basket cells were reduced in the epileptic tissue, whereas IPSPs evoked by direct activation of basket cells, when excitatory neurotransmission was blocked, were not different from controls. These results provide support for the "dormant basket cell" hypothesis and have implications for the pathophysiology and treatment of human TLE.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2000

Surviving granule cells of the sclerotic human hippocampus have reduced Ca(2+) influx because of a loss of calbindin-D(28k) in temporal lobe epilepsy.

In mesial temporal lobe epilepsy (mTLE), the predominant form of epilepsy in adults, and in animal models of the disease, there is a conspicuous loss of the intracellular Ca(2+)-binding protein calbindin-D(28k) (CB) from granule cells (GCs) of the dentate gyrus. The role of this protein in nerve cell function is controversial, but here we provide evidence for its role in controlling Ca(2+) influx into human neurons. In patients with Ammon's horn sclerosis (AHS), the loss of CB from GCs markedly increased the Ca(2+)-dependent inactivation of voltage-dependent Ca(2+) currents (I(Ca)), thereby diminishing Ca(2+) influx during repetitive neuronal firing. Introducing purified CB into GCs restored Ca(2+) current inactivation to levels observed in cells with normal CB content harvested from mTLE patients without AHS. Our data are consistent with the possibility of neuroprotection secondary to the CB loss. By limiting Ca(2+) influx through an enhanced Ca(2+)-dependent inactivation of voltage-dependent Ca(2+) channels during prolonged neuronal discharges, the loss of CB may contribute to the resistance of surviving human granule cells in AHS.

Action Potentials↗

PubMed2004

[Place of surgery in the treatment of adult temporal lobe epilepsy].

Surgery for temporal lobe epilepsy has made significant progress during the past twenty years: in addition to traditional factors (frequency of partial seizures and relative resistance to medical treatment), the possibilities offered by MRI in a large number of cases to detect the responsible lesion (hippocampal sclerosis in the majority of cases) has led to an increase in the use of surgical methods. Furthermore, other examinations (EEG-video, SPECT Depth-electrode recording) now permit precise localization of the epileptic focus. Surgical techniques have likewise been considerably modified: in parallel to classical temporal lobectomy, new surgical methods offer more restricted resection of the lateral cortex. The results are, on the whole, quite satisfactory, as three-quarters of patients can be considered cured or greatly improved. The length of post-operative follow-up does not seem to influence the quality of the results, as observed by the end of the second year.

Electroencephalography↗

PubMed2002

Decrease of sympathetic cardiovascular modulation after temporal lobe epilepsy surgery.

In temporal lobe epilepsy (TLE), there is evidence of ictal and interictal autonomic dysregulation, predominantly with sympathetic overactivity. The effects of TLE surgery on autonomic cardiovascular control and on baroreflex sensitivity (BRS) have not been studied. To evaluate such effects, we monitored heart rate (HR), systolic blood pressure (BP(sys)) and respiration in 18 TLE patients 3-4 months before and after TLE surgery. We used Blackman-Tukey spectral analysis to assess sympathetic and parasympathetic modulation as powers of HR and BP(sys) oscillations in the low frequency (LF, 0.04-0.15 Hz) and high frequency (HF, 0.15-0.5 Hz) bands. BRS was determined as the LF transfer function gain between BP and HR. After surgery, HR, BP(sys), respiration and HF powers remained unchanged, while LF powers of HR (1.57 +/- 1.54 bpm(2)) and BP(sys) (2.19 +/- 1.34 mmHg(2)) and BRS (0.68 +/- 0.31 bpm/mmHg) were smaller than pre-surgical LF powers of HR (3.87 +/- 3.26 bpm(2)) and BP(sys) (4.80 +/- 3.84 mmHg(2)) and BRS (1.12 +/- 0.39 bpm/mmHg; P < 0.05). After TLE surgery, there is a reduction of sympathetic cardiovascular modulation and BRS that might result from decreased influences of interictal epileptogenic discharges on brain areas involved in cardiovascular autonomic control. TLE surgery seems to stabilize the cardiovascular control in epilepsy patients by reducing the risk of sympathetically mediated tachyarrhythmias and excessive bradycardiac counter-regulation, both of which might be relevant for the pathophysiology of sudden unexpected death in epilepsy patients (SUDEP). Thus, TLE surgery might contribute to reducing the risk of SUDEP.

Adrenergic Fibers↗