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  • 1
    ISSN: 1437-2320
    Keywords: Key words Cavernous malformations ; Epilepsy ; Lesionectomy ; Epilepsy surgery ; Dual pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Cerebral cavernous malformations (CM) are well-circumscribed vascular malformations that often present with epileptic seizures. Although patients may initially benefit from antiepileptic drugs, surgical treatment may become necessary due to medically intractable seizures. However, it is unclear whether lesionectomy alone or tailored epilepsy surgery with previous invasive monitoring is the optimal strategy in such cases. We report two patients with epileptic seizures due to CM. One patient with few seizures prior to surgery became seizure-free following resection of the CM and the surrounding tissue. In the second patient with long-lasting epilepsy, lesionectomy was performed because of the proximity to a functioning left hippocampus. This limited resection failed and the patient still had seizures. Subsequently, invasive monitoring with intracranial depth and strip electrodes was performed in order to localize the epileptogenic area and determine whether the left hippocampus could be spared. The invasive study showed the seizure origin in the tissue around the former CM but no epileptic discharges in the hippocampus. In a second operation, an anterior temporal resection was performed with removal of the epileptogenic surrounding tissue and the patient became seizure-free without cognitive deficits. The optimal surgical strategy for CM presenting with epileptic seizures must take into account various factors such as underlying mechanisms and duration of epilepsy, and location of the lesion.
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  • 2
    ISSN: 1432-0533
    Keywords: Key words Neurodegeneration ; Epilepsy ; Kainic acid ; fos ; Gliosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Periodic acid-Schiff (PAS)-positive deposits have been demonstrated in the central nervous system (CNS) of patients suffering from a wide variety of neurodegenerative disorders including Alzheimer's disease, presenile dementia, Parkinson's disease, diabetes mellitus, myoclonic epilepsy, and cerebral palsy. The etiology of these deposits and their relationship to mechanisms of progressive neurodegeneration is unknown. In the present study, we demonstrate that the kainic acid model of limbic status epilepticus provides a useful system for the study of PAS-positive staining. The relationship between PAS-positive deposition, induction of fos-like immunoreactivity (FLI), neuronal necrosis, reactive gliosis, and blood-brain barrier breakdown following the kainic acid induction of status epilepticus was investigated. Epileptiform activity was elicited in rats by intraperitoneal administration of 10 mg/kg kainic acid and brains were examined 3, 5, 12, 24, 72, and 168 h after drug injection. Four distinct types of PAS-positive staining in rat brain were observed: type 1, extracellular matrix (ECM) or blood vessel associated-material; type 2, granular deposits; type 3, glial labelling; and type 4, neuronal labelling. Results demonstrated that the four types of PAS-positive staining were differentially associated with specific markers of neuropathology: (1) type 1 ECM staining and type 3 glia were preferentially localized to edematous tissue; (2) the majority of type 3 glia were identified as reactive astrocytes, while a minority of appeared to be proliferating microglia; (3) type 1 blood vessels labelled hemorrhaging vasculature; (4) early deposition of type 2 granules was predictive of subsequent cell loss; (5) chronic type 2 granular deposits and type 4 neuronal labelling not associated with cell death could be predicted by early changes in FLI; and (6) chronic deposition of all four forms of PAS-positive material was correlated with earlier, transient blood-brain barrier compromise. The results support the growing literature that local carbohydrate metabolism may be one of a constellation of parameters important to the development of progressive neurodegeneration.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Neurodegeneration ; Epilepsy ; Kainic acid fos ; Gliosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Periodic acid-Schiff (PAS)-positive deposits have been demonstrated in the central nervous system (CNS) of patients suffering from a wide variety of neurodegenerative disorders including Alzheimer's disease, presenile dementia, Parkinson's disease, diabetes mellitus, myoclonic epilepsy, and cerebral palsy. The etiology of these deposits and their relationship to mechanisms of progressive neurodegeneration is unknown. In the present study, we demonstrate that the kainic acid model of limbic status epilepticus provides a useful system for the study of PAS-positive staining. The relationship between PAS-positive deposition, induction of fos-like immunoreactivity (FLI), neuronal necrosis, reactive gliosis, and blood-brain barrier breakdown following the kainic acid induction of status epilepticus was investigated. Epileptiform activity was elicited in rats by intraperitoneal administration of 10 mg/kg kainic acid and brains were examined 3, 5, 12, 24, 72, and 168 h after drug injection. Four distinct types of PAS-positive staining in rat brain were observed: type 1, extracellular matrix (ECM) or blood vessel associated-material; type 2, granular deposits; type 3, glial labelling; and type 4, neuronal labelling. Results demonstrated that the four types of PAS-positive staining were differentially associated with specific markers of neuropathology: (1) type 1 ECM staining and type 3 glia were preferentially localized to edematous tissue; (2) the majority of type 3 glia were identified as reactive astrocytes, while a minority of appeared to be proliferating microglia; (3) type 1 blood vessels labelled hemorrhaging vasculature; (4) early deposition of type 2 granules was predictive of subsequent cell loss; (5) chronic type 2 granular deposits and type 4 neuronal labelling not associated with cell death could be predicted by early changes in FLI; and (6) chronic deposition of all four forms of PAS-positive material was correlated with earlier, transient blood-brain barrier compromise. The results support the growing literature that local carbohydrate metabolism may be one of a constellation of parameters important to the development of progressive neurodegeneration.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2072
    Keywords: Conditioned taste aversion ; Morphine ; d-Amphetamine ; 6-OHDA ; Noradrenaline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stereotaxically placed microinjections of 6-hydroxydopamine (6-OHDA) into the dorsal tegmental noradrenergic (NA) pathway extensively depleted NA in the hippocampus and cortex of rats. This treatment severely attenuated the conditioned taste aversion (CTA) to saccharin normally produced by repeated pairings with 10 mg/kg morphine. This is interpreted as a specific change in the punishing properties of morphine and not a deficit in the ability of 6-OHDA-treated animals to learn a CTA, since identical lesions in other groups of rats failed to affect the CTA induced by 0.5 or 1.0 mg/kgd-amphetamine.
    Type of Medium: Electronic Resource
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