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PubMed2005

Normal magnetic resonance imaging and medial temporal lobe epilepsy: the clinical syndrome of paradoxical temporal lobe epilepsy.

OBJECT: The syndrome of medial temporal lobe epilepsy (MTLE) may occur in patients in whom magnetic resonance (MR) images demonstrate normal findings. In these patients, there is no evidence of hippocampal sclerosis on neuroimaging, and histopathological examination of the resected hippocampus does not reveal significant neuron loss. In this paper the authors describe the distinct clinical features of this MTLE subtype, referred to as paradoxical temporal lobe epilepsy (PTLE). METHODS: The authors selected 12 consecutive patients with preoperative findings consistent with MTLE in whom MR imaging did not demonstrate any hippocampal abnormality. Onset of hippocampal seizure was confirmed by long-term intracranial monitoring. There were six female and six male patients with a mean age of 32 +/- 11 years, (mean +/- standard deviation [SD]) at presentation. These patients' seizure histories, available hippocampal volumetric measurements, and hippocampal cell densities in different subfields were reviewed. Sharp electrode recordings from dentate granule cells that had been maintained in hippocampal slices provided a measure of excitation and inhibition in the tissue. We compared these data with those of a cohort of 50 randomly selected patients who underwent anteromedial temporal resection for medial temporal sclerosis (MTS) during the same time period (1987-1999). The durations of follow up (means +/- SDs) for the PTLE and MTS groups were 51 +/- 59 months and 88 +/- 44 months, respectively. A history of febrile seizure was present less frequently in the PTLE group (8%) than in the MTS group (34%). Other risk factors for epilepsy such as trauma, meningoencephalitis, or perinatal injuries were present more frequently in the PTLE group (50%) than in the MTS cohort (36%). In patients in the PTLE group the first seizure occurred later in life (mean age at seizure onset 14 years in the PTLE group compared with 9 years in the MTS group, p = 0.09). Ten patients (83%) in the PTLE cohort and 23 patients (46%) in the MTLE cohort had secondary generalization of their seizures. Among patients with PTLE, volumetric measurements (five patients) and randomized blinded visual inspection (seven patients) of the bilateral hippocampi revealed no atrophy and no increased T2 signal change on preoperative MR images. All patients with PTLE underwent anteromedial temporal resection (amygdalohippocampectomy, in five patients on the left side and in seven on the right side). Electrophysiological studies of hippocampal slices demonstrated that dentate granule cells from patients with PTLE were significantly less excitable than those from patients with MTS. The mean pyramidal cell loss in the CAI subfield in patients in the PTLE group was 20% (range 0-59%) and that in patients in the MTS group was 75% (range 41-90%) (p < 0.001). Maximal neuron loss (mean loss 38%) occurred in the CA4 region in six patients with PTLE (end folium sclerosis). At the last follow-up examination, six patients (50%) in the PTLE group were seizure free compared with 38 patients (76%) in the MTS group. CONCLUSIONS: Clinical PTLE is a distinct syndrome with clinical features and surgical outcomes different from-those of MTS.

Adolescent↗

PubMed2002

Relations between brain pathology and temporal lobe epilepsy.

Temporal lobe epilepsy, the most common type of epilepsy in adult humans, is characterized clinically by the progressive development of spontaneous recurrent seizures of temporal lobe origin and pathologically by hippocampal neuronal loss and mossy fiber sprouting. In this study, we sought to test the prominent hypothesis that neuronal loss and mossy fiber sprouting play a critical role in the genesis and progression of temporal lobe epilepsy. Rats receiving a single kainic acid injection experienced a single sustained episode of epileptic status with massive neuronal loss and mossy fiber sprouting, whereas rats receiving triple kainic acid injections experienced two priming episodes and one sustained episode of epileptic status with no detectable neuronal loss and mossy fiber sprouting. Early in the process of chronic seizure development, primed rats that failed to show detectable neuronal loss and mossy fiber sprouting exhibited a starting date and a frequency of spontaneous recurrent seizures similar to those of nonprimed rats that showed massive neuronal loss and mossy fiber sprouting. However, nonprimed rats displayed significantly prolonged episodes of spontaneous recurrent seizures over the whole process of chronic seizure development and more frequent severe seizures later in the process. Similar results were observed in both Fischer-344 and Wistar rats as well as in the rat pilocarpine preparation of temporal lobe epilepsy. These results fail to reveal a relation between neuronal loss-mossy fiber sprouting and the genesis of temporal lobe epilepsy but suggest that neuronal loss, mossy fiber sprouting, or both contribute to the intensification of chronic seizures.

Animals↗

PubMed1995

Temporal lobe central benzodiazepine binding in unilateral mesial temporal lobe epilepsy.

PET-demonstrated decreases in [11C]flumazenil binding occur in anterior mesial temporal structures on the side of epileptogenesis in unilateral mesial temporal lobe epilepsy. We performed quantitative autoradiography on anterior mesial and lateral temporal specimens from 11 subjects with unilateral mesial temporal lobe epilepsy and six neurologically normal controls to identify the predominant in vitro correlates of the decreased [11C]flumazenil binding. In anterior mesial temporal regions exhibiting the greatest neuronal cell loss, decreases in agonist and antagonist binding to type 1 and 2 (central) benzodiazepine binding sites were highly correlated with neuronal cell counts. Cell loss and decreased binding were particularly prominent in the lateral portion of hippocampal region CA1, adjacent to CA2. Lateral temporal central benzodiazepine binding was diffusely increased, achieving statistical significance in cortical laminae V and VI. These findings suggest that the predominant source of PET-demonstrated decreases in [11C]flumazenil binding in mesial temporal epilepsy is hippocampal sclerosis, rather than down-regulation of central benzodiazepine binding sites on surviving hippocampal neurons.

Adult↗

PubMed2005

Is impairment in set-shifting specific to frontal-lobe dysfunction? Evidence from patients with frontal-lobe or temporal-lobe epilepsy.

Frontal-lobe epilepsy (FLE), temporal-lobe epilepsy (TLE), and matched-control subjects were administered the Trail Making Test (TMT) of the Delis-Kaplan Executive Function System (D-KEFS; Delis et al., 2001), which assesses set-shifting on a visuomotor sequencing task. Results indicated that patients with FLE were impaired in both speed and accuracy on the switching condition relative to patients with TLE and controls. The two patient groups did not differ from controls on the four baseline conditions of the test, which assess visual scanning, motor speed, number sequencing, and letter sequencing. In addition, seizure-related variables (i.e., age of seizure onset, duration of epilepsy, and seizure frequency) failed to correlate with set-shifting performance in patients with FLE. These results suggest that patients with FLE can be reliably distinguished from those with TLE and control subjects on set-shifting as measured by the DKEFS TMT.

Adult↗

PubMed2005

Response inhibition and set shifting in patients with frontal lobe epilepsy or temporal lobe epilepsy.

Patients with frontal lobe epilepsy (FLE), patients with temporal lobe epilepsy (TLE), and matched controls were administered a test of response inhibition and set shifting (switching) (Color Word Interference Test, CWIT). Patients with FLE were impaired relative to the controls across all conditions of the CWIT, with the FLE patients showing disproportionate impairment in the Inhibition and Inhibition/Switching conditions. In contrast, the TLE patients did not differ from controls. Further analysis of the patient groups revealed that patients with left FLE were impaired relative to those with right FLE, left TLE, and right TLE in the Inhibition condition. In the Inhibition/Switching condition, patients with left FLE and left TLE were impaired relative to their right-sided counterparts. Finally, performance by the TLE group in the Inhibition/Switching condition was correlated with seizure frequency. These data suggest that patients with FLE, but not TLE, show impaired inhibition and set shifting relative to controls. In addition, side of the seizure focus and seizure frequency may contribute to executive dysfunction in patients with epilepsy.

Adult↗

PubMed1991

Brain SPECT imaging in temporal lobe epilepsy.

Temporal lobe epilepsy is diagnosed by clinical symptoms and signs and by localization of an epileptogenic focus. A brain SPECT study of two patients with temporal lobe epilepsy, using 99mTc-HMPAO, was used to demonstrate a perfusion abnormality in the temporal lobe, while brain CT and MRI were non-contributory. The electroencephalogram, though abnormal, did not localize the diseased area. The potential role of the SPECT study in diagnosis and localization of temporal lobe epilepsy is discussed.

Adult↗

PubMed2005

Axonal sprouting of GABAergic interneurons in temporal lobe epilepsy.

Temporal lobe epilepsy is one of the most common forms of epilepsy. Numerous contributing factors and compensatory mechanisms have been associated with temporal lobe epilepsy. One feature found in both humans and animal models is sprouting of hippocampal principal cell axons, which suggests that axonal sprouting may be a general phenomenon associated with temporal lobe epilepsy. This article highlights the evidence showing that hippocampal GABAergic interneurons also undergo axonal sprouting in temporal lobe epilepsy. The caveats and unanswered questions associated with the current data and the potential physiological consequences of reorganizations in GABAergic circuits are discussed.

Axons↗

PubMed1999

Glial cell changes in the white matter in temporal lobe epilepsy.

Temporal lobe gliosis and neuronal loss are pathological hallmarks of complex partial seizures. However, the specificity of glial cell changes is not clear. To assess this we studied surgically resected temporal lobes containing either medial temporal sclerosis (MTS) or temporal lobe epilepsy with tumour (TLET) and compared them with idiopathic epilepsy cases and normal controls. We quantitatively assessed glial cell density and mean nuclear volume in the white matter of various temporal gyri and the deep white matter. There was an increase in mean glial cell nuclear volume in MTS and TLET cases in the white matter of superior temporal gyrus, parahippocampal gyrus and deep white matter but not in the white matter of the middle temporal gyrus. In contrast, the densities of glial cells immunopositive for glial fibrillary acidic protein in the MTS and TLET groups were reduced in all white matter regions when compared with the controls. These changes may indicate that glial cells in the white matter have an active role to play in epilepsy pathogenesis.

Adolescent↗

PubMed1994

The functional organization of the hippocampal dentate gyrus and its relevance to the pathogenesis of temporal lobe epilepsy.

Temporal lobe seizures are frequently associated with a characteristic pattern of hippocampal pathology (hippocampal sclerosis), as well as pathology in other temporal lobe structures. Despite more than a century of study, the relationship between pathology and epileptogenesis remains unclear. Endfolium sclerosis, which is characterized by the loss of dentate hilar neurons that are presumed to govern dentate granule cell excitability, is evident whenever hippocampal sclerosis exists and is the only temporal lobe pathology in some patients. Because prolonged seizures or head trauma produce endfolium sclerosis and granule cell hyperexcitability in experimental animals, hilar neuron loss may be the common pathological denominator and primary network defect underlying development of a hippocampal seizure "focus." Physiological studies suggest that vulnerable hilar mossy cells normally excite neurons that mediate granule cell inhibition. Recent anatomical studies indicate that the axons of mossy cells project longitudinally, out of the lamellar plane in which their cell bodies lie. If mossy cells in one lamella excite inhibitory neurons in surrounding lamellae, neocortical excitation of one segment of the granule cell layer may produce lateral inhibition and limit neocortical excitation to the targeted lamella. In patients who have had status epilepticus, prolonged febrile seizures, head trauma, or encephalitis, loss of dentate mossy cells may deafferent inhibitory neurons, render them "dormant," and thereby disinhibit an enlarged expanse of the granule cell layer. The selective loss of neurons that normally govern lateral inhibition in the dentate gyrus may cause functional delamination of the granule cell layer and result in synchronous, multilamellar discharges in response to cortical stimuli. Repetitive seizures may ultimately produce the full pattern of hippocampal and mesial temporal sclerosis by destroying cells within the seizure circuit that were not injured irreversibly by the initial insult. Thus, hippocampal pathology may be both the cause and effect of seizures that originate in the temporal lobe.

Animals↗

PubMedDate not supplied

Myxopapillary ependymoma of the temporal lobe--report of a rare case of temporal lobe epilepsy.

Myxopapillary ependymomas are a benign variant of ependymomas, occurring almost exclusively in the cauda equina region. We report an extremely rare case of myxopapillary ependymoma located in the left anterior temporal lobe. A 22-year-old man is presented with intractable seizures of 2 years duration with no focal neurologic deficits. Imaging of the brain revealed a well-circumscribed heterogeneous mass in the left anterior temporal pole with no connection to the ventricles. Imaging of the spine was normal. The patient underwent surgical removal of the tumor and at follow-up 4 months after surgery, there was improvement in his memory and speech along with complete cessation of seizures. Microscopic examination revealed the tumor to be a myxopapillary ependymoma, further confirmed by histochemical and immunohistochemical stains. To the best of our knowledge, this is the first documentation of myxopapillary ependymoma at this location and consequently, the first case to clinically present as intractable temporal lobe epilepsy.

Adult↗

PubMed2004

Preoperative clinical evaluation, outline of surgical technique and outcome in temporal lobe epilepsy.

Temporal lobe epilepsy (TLE) is the most common type of refractory epilepsy. The mechanisms of epileptogenesis and seizure semiology of the mesial and neocortical temporal lobe epilepsy are discussed. The evaluation and selection of patients for TLE surgery requires team work: the different clinical aspects of neuropsychological evaluation, magnetic resonance and functional imaging (positron emission tomography, single photon emission computed tomography and magnetoenephalography) are reviewed. In our programme of epilepsy surgery at Kuopio University Hospital, Finland, we have performed 230 temporal resections from 1988 until 2002. Preoperative diagnostic EEG-videotelemetry often required intracranial monitoring and it has proved to be safe and efficient. The indications and technique for tailored temporal lobe resection with amygdalohippocampectomy used in our institution, as well as the complications, are described. Our analysis of outcome after temporal lobe surgery included 140 consecutive adult patients between 1988 and 1999; one year after the operation in unilateral TLE the Engel I-II outcome was observed in 68% of the patients. Outcome of surgery improved significantly after introduction of the standardised MR imaging protocol from 1993; 74% of patients with unilateral TLE achieved Engel I-II outcome.

Electroencephalography↗

PubMed1994

Late-onset drop attacks in temporal lobe epilepsy: a reevaluation of the concept of temporal lobe syncope.

We report the clinical, radiologic, and EEG features of six patients with temporal lobe drop attacks (TLDA), all of whom underwent temporal resection. Postoperative follow-up of at least 1 year was available in all. TLDA were never the first manifestation but followed the onset of epilepsy after a long delay ranging from 7 to 43 years (mean, 24.4 years). Seizures were of unilateral temporal origin. In one patient, stereo EEG recording of TLDA showed rapid spread of the ictal discharge away from the temporal lobe in less than 1 second. Postoperatively, three patients were seizure free; one has had no TLDA but experiences sporadic auras; another, despite a reduction of more than 50%, continues to have complex partial seizures and TLDA; and the sixth has had sporadic secondarily generalized seizures upon reduction of antiepileptic medication. In conclusion, drop attacks may occur in temporal lobe epilepsy, usually long after the onset of epilepsy. They lead to increased disability and suggest a rapid spread of the ictal discharge and possible involvement of the pontine reticular formation rather than the presence of bitemporal foci or an extratemporal origin.

Adult↗

PubMed2003

[Yawning and temporal lobe epilepsy].

Temporal lobe epilepsy is a partial epileptic disorder in which mesial structures are responsible for the principal ictal symptoms. Its characteristic feature is the recurrence of simple and complex partial seizures, associated with postictal confusion and amnesia of the event. The facilitating effect of NREM sleep on the propagation of the seizure, as well as the sleep abnormalities provoked by epilepsy were evident in our two patients. Yawning is a physiological reflex induced by arousal and drowsiness and may appear in different neurological conditions. Its relation with epilepsy of limbic origin has been rarely reported. We describe in a 95 year old male patient, the occurrence of yawning followed by complex partial seizure during a state of drowsiness. His EEG showed independent bilateral interictal foci of temporal sharp waves and after being medicated with carbamazepine 400 mg/day, the episode did not recur. Another patient, a 17 year old female, displayed complex partial seizures and secondarily generalized seizures with yawning during the posictal period, after naps. The EEG was normal and her polysomnography showed bilateral synchronous temporal spikes and slow waves with secondarily generalization during stage 2 of NREM sleep that produce paroxysmal microarousals and increased stages 1 and 2 of NREM sleep and REM sleep diminished. After being medicated with divalproex sodium 750 mg/day, she suffered no further seizures. Temporal lobe epilepsy, sleep-wake cycles and yawning seem not only to share the same anatomic structures but also the same neurochemical mechanisms. The fact that endogenous opiods are considered as part of a protective system that stop and prevent seizures may allow us to postulate that yawning would be the expression of the endogenous opiods induced mechanisms that stop and prevent the recurrence of the temporal lobe epilepsy. Another hypothesis may be that this is only a particular form of temporal lobe epilepsy.

Adolescent↗

PubMed2000

Magnetic resonance imaging in temporal lobe epilepsy: usefulness for the etiological diagnosis of temporal lobe epilepsy.

With improvement in magnetic resonance (MR) imaging techniques, the ability to identify lesions responsible for temporal lobe epilepsy has increased. MR imaging has also enabled the in vivo diagnosis of hippocampal sclerosis. Brain tumors are responsible for 2-4% of epilepsies in adult population and 10-20% of medically intractable epilepsy. The sensitivity of MR imaging in the diagnosis of tumors and other lesions of the temporal lobe (vascular malformations, etc.) is around 90%. Both hippocampal sclerosis and other temporal lobe lesions are amenable to surgical therapy with excellent postsurgical seizure outcome. In this article, we characterize and underline distinguishing features of the different pathological entities. We also suggest an approach to reviewing the MR images of an epileptic patient.

Brain↗

PubMed1990

Frontal lobes, basal ganglia, temporal lobes--three sites for schizophrenia?

This special issue of the Schizophrenia Bulletin focuses on three brain areas hypothesized to play a role in the etiology of schizophrenia--the frontal lobes, the basal ganglia, and the temporal lobes. Contributors to the issue review evidence from brain-imaging, post-mortem, and psychopharmacological studies that support the involvement of each of these important brain areas in schizophrenia. It is concluded that theories emphasizing cortical/subcortical interconnections rather than a single brain area provide the greatest challenge, and also the greatest promise, to schizophrenia researchers.

Basal Ganglia↗

PubMed2000

Dipole source localization of interictal epileptiform activity in temporal lobe epilepsy with medial temporal lesion.

Dipole sources of interictal epileptiform activities recorded by conventional electroencephalogram (EEG) were estimated using the dipole tracing method. Four cases of temporal lobe epilepsy with medial temporal lesions were studied. Two patients with hippocampal sclerosis, one patient with granulation in the hippocampus and one patient with cavernous angioma were involved in the study. Interictal epileptiform activities were classified into two patterns according to the topography of spikes. They were widespread spikes over the parasagittal electrodes (parasagittal spikes) and restricted spikes at the temporal electrodes (temporal spikes). Dipole sources of parasagittal spikes were localized in the medio-basal temporal lobe with vertically orientated vector moment. Dipole sources of temporal spikes were localized in the medio-basal temporal lobe with horizontally orientated vector moment. Locations of dipoles and directions of vector moments were consistent with topography and polarity of spikes. The difference in the two patterns of interictal epileptiform activities was derived from the difference in the direction of the vector moment of dipole sources. There was no difference in the location of dipole sources. Both the dipole sources and the lesions were localized in the same medio-basal temporal lobe. Dipole tracing was very useful in localizing the dipole sources of interictal epileptiform activities and in understanding the neurophysiological background.

Adult↗

PubMed1976

Temporal lobe epilepsy and neuropathology. Histological findings in resected temporal lobes correlated to surgical results and clinical aspects.

Neuropathological findings were studied in 74 patients with drug-resistant temporal lobe epilepsy who underwent unilateral temporal lobe resection in 1960-1969 in Denmark. In 60 per cent of the patients a well-defined neuropathological abnormality was revealed (i.e. 13 cases of focal lesions, including four small tumours, 21 cases of gliosis, and 10 cases of perivascular infiltration), in 23 per cent the findings were either questionably abnormal or without structural abnormality, while in the last 18 per cent sequelae of a previous operation dominated the histology. The general trend was for the postoperative clinical outcome to be better, the more specific and circumscribed the histological abnormality. There was no correlation between the neuropathological findings and the preoperative types of seizures. Postoperative recurrence of seizures was more often observed in patients with gliosis than in those with other histological diagnoses. A positive correlation existed between a history of cerebral infection and the presence of perivascular lymphocytic and histiocytic infiltration, and gliosis was a frequent finding in patients with epilepsy of unknown aetiology. No other significant correlation was found between the neuropathological abnormalities and the clinical, hereditary, aetiological, and social aspects.

Adolescent↗

PubMed2003

[Temporal lobe epilepsy associated with cystic lesion in the temporal lobe and middle cranial fossa].

Four patients out of 52 patients with temporal lobe epilepsy (TLE), who underwent epilepsy surgery in our hospital since September of 1994, had cystic lesions in the temporal lobe and middle cranial fossa. Case 1 had old hematoma cavity in the inferior temporal gyrus and chronic subdural electrode recording revealed the ictal onset zone to be localized in the ipsilateral medial temporal region. Case 2 had cystic ganglioglioma in the temporal tip, and intraoperative electrocorticography demonstrated independent paroxysmal activities from medial temporal region and temporal tip near the cyst. Both area were resected and the patients became seizure free. Case 3 and 4 had arachnoid cysts in the middle cranial fossa. Chronic subdural electrode recording revealed that the ictal onset zone was localized in the ipsilateral inferior temporal gyrus (that had microdysgenesis) in Case 3 and contralateral medial temporal region (that had hippocampal sclerosis) in Case 4, respectively. These finding suggest that co-existence of extra-axial cyst such as Case 3 and 4 is incidental and that arachnoid cyst is less epileptogenic. However, intra-axial cyst such as Case 1 and 2 is epileptogenic and complicated physiological mechanism such as kindling phenomenon or secondary epileptogenesis may effect on the hippocampus. Comprehensive presurgical evaluation including electrocorticography is needed in the surgical treatment of TLE with cystic lesion.

Adolescent↗