Epilepsie und Schläfenlappen

Stauder, K. H.

doi:10.1007/bf01814225

Cited by 58 publications

(11 citation statements)

References 37 publications

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“…Vessels pass into the hippo¬ campus through a pial cleft, and the enter¬ ing vessels are illustrated in the same figure and in many of the others. They do not Plate 2.-Higher magnifications of the ventral hippocampus in the same four animals illus¬ trated in Plate 1 (9,40,42, and 60 days), in addition to another cat, which lived 177 days.…”

Section: Resultsmentioning

confidence: 99%

Experimentally Induced Epilepsy in the Cat with Injury of Cornu Ammonis

GREEN¹

1957

Arch NeurPsych

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Section: Resultsmentioning

confidence: 99%

Experimentally Induced Epilepsy in the Cat with Injury of Cornu Ammonis

GREEN¹

1957

Arch NeurPsych

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“…In cases with this symptomatology, small focal lesions were found in the anterior temporal lobe, and in particular, in the hippocampus, but he did not go as far as to link AHS with TLE. Stauder (1935) was the first to correlate AHS with seizures of temporal lobe semiology (49). In his autopsy study he showed a clear correlation of the clinical signs of TLE and AHS that was identified in 33 of 36 cases.…”

Section: Hs: Association With Temporal Lobe Epilepsy (Tle) and The Sumentioning

confidence: 98%

Hippocampal Sclerosis: Progress Since Sommer

Thom

2009

Brain Pathology

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Hippocampal sclerosis (HS) continues to be the most common pathology identified in patients with refractory temporal lobe epilepsy undergoing surgery. Wilhelm Sommer described this characteristic pattern of neuronal loss over 120 years ago through his post-mortem studies on patients with epilepsy. Neuropathological post-mortem studies in the 20th century proceeded to contribute significantly to the understanding of this disease process, with regard to the varying patterns of HS and involvement of adjacent limbic structures. From studies of surgical temporal lobe specimens from the 1950s onwards it was recognized that an early cerebral injury could act as the precipitant for the sclerosis and epilepsy. Modern neuropathological studies have focused on aspects of neuronal injury, loss of specific neuronal groups and cellular reorganization to address mechanisms of epileptogenesis and the enigma of how specific hippocampal neuronal vulnerabilities and glial proliferation are both the effect and the cause of seizures.

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“…He confirmed the hypothesis that Ammon's horn sclerosis was frequently encountered in epileptic patients [6]. These early studies demonstrated a possible linkage of hippocampal pathology with seizures, but several decades then passed before two autopsy studies demontrated a link between hippocampal sclerosis and complex partial seizures [21,33]. In 1968 Falconer reported a series of patients who underwent en bloc resection for intractable temporal lobe seizures.…”

Section: Introductionmentioning

confidence: 56%

Dysgenetic mesial temporal sclerosis: an unrecognized entity

Vernet¹,

Farmer

Montes

et al. 2000

Child's Nerv Syst

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Mesial temporal sclerosis (MTS) is the most frequently encountered lesion in adult patients with intractable temporal epilepsy; it is found in isolation in approximately two-thirds of surgically treated cases. Whereas the exact etiology of MTS is still controversial, several reports suggest that this pathologic lesion is both the cause and the consequence of chronic seizures and develops progressively during childhood secondary to recurrent seizures. In order to evaluate the clinical importance of MTS in children, we retrospectively reviewed the clinical charts of children who underwent surgery for medically intractable temporal epilepsy and report cases presenting an amygdalo-hippocampic dual pathology. Six children aged 1.5-16 years (mean +/- SD: 7.5 +/- 3 years) presenting with partial complex seizures (5 cases) or extension spasms (1 case), with onset from 6 months to the age of 8.5 years (mean seizure onset +/- SD: 3 +/- 5 years) underwent anterior temporal lobectomy including resection of the amygdala and hippocampus. All patients exhibited variable degrees of severity of neuronal loss and gliosis in the amygdala and/or hippocampus. The pathological picture of MTS was not isolated, however. Careful pathological examination has thus shown foci of amygdalo-hippocampic neuronal dysplasia in six patients, with concomitant bilaminated fascia dentata in two cases. Postoperatively, no mortality or morbidity was encountered. After a mean follow-up of 2.5 years, four patients are seizure free. One patient had a 80% rate of improvement in seizure frequency, though still having occasional febrile convulsions. In another patient, complex partial seizures resolved, but rare episodes of absence were still observed. These data are in keeping with the hypothesis that MTS could be secondary to repeated seizures. The analysis of this series of patients could suggest that mesiotemporal dysplastic lesions within the amygdalo-hippocampic structures induce seizures, which, in turn, will favor the development of MTS during childhood. MTS could then lead to synaptic reorganization, which can express abnormal hyperexcitability and result in more recurrent seizures. In this way a vicious circle is set up, which may explain the progression of seizures in some patients.

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Epilepsie und Schläfenlappen

Cited by 58 publications

References 37 publications

Experimentally Induced Epilepsy in the Cat with Injury of Cornu Ammonis

Experimentally Induced Epilepsy in the Cat with Injury of Cornu Ammonis

Hippocampal Sclerosis: Progress Since Sommer

Dysgenetic mesial temporal sclerosis: an unrecognized entity

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