Mesial Temporal Sclerosis

Impaired and facilitated functional networks in temporal lobe epilepsy

“…A few previous studies of functional connectivity in TLE have focused on intrahemispheric effects (Bettus et al, 2009, 2010), while others have noted decreased connectivity between medial temporal regions (Pittau et al, 2012), but typically without extending the scope to the temporal neocortex. As with local changes described above, decoupling of the medial temporal region at the functional level may in part reflect the cellular pathophysiologic changes observed in some TLE patients manifesting as hippocampal atrophy and mesial temporal sclerosis (Hogan, 2001), some of which reflects neuronal cell loss. In our study, we defined regions of interest based on the individually segmented anatomy of each participant, with the specific objective of reducing the effect of atrophy on measured functional coupling.…”

“…Patients were screened for enrollment based on reported clinical semiology of their seizures and confirmed unilateral temporal lobe epilepsy by video-EEG monitoring. Clinical semiology for study inclusion included auras of epigastric rising, experiential phenomena (most commonly fear) and gustatory or olfactory sensations (Hogan, 2001). Subjects with auras suggestive of lateral temporal onset seizures, including auditory hallucinations, visual misperceptions, or language disturbance, were excluded from the study group (Commission on Classification and Terminology of the International League Against Epilepsy, 1989).…”

“…Temporal lobe epilepsy (TLE) is a well-characterized example of focal epilepsy, with seizures that typically originate in the medial temporal region. From a structural/pathologic standpoint, TLE can often be associated with specific structural and metabolic abnormalities, including hippocampal atrophy and/or sclerosis (Margerison and Corsellis, 1966; Van Paesschen et al, 1997; Hogan, 2001) and medial temporal hypometabolism (Theodore et al, 1992; Arnold et al, 1996; Carne et al, 2004). Yet localized structural and/or metabolic abnormalities extend beyond the medial temporal region to multiple, non-limbic brain regions, most prominently lateral temporal and frontal regions, as noted via structural magnetic resonance imaging (Bernhardt et al, 2010), positron emission tomography (Theodore et al, 1992; Arnold et al, 1996), magnetic resonance spectroscopy (Stanley et al, 1998; Miller et al, 2000), and pathologic studies (Margerison and Corsellis, 1966).…”

Impaired and facilitated functional networks in temporal lobe epilepsy

“…A few previous studies of functional connectivity in TLE have focused on intrahemispheric effects (Bettus et al, 2009, 2010), while others have noted decreased connectivity between medial temporal regions (Pittau et al, 2012), but typically without extending the scope to the temporal neocortex. As with local changes described above, decoupling of the medial temporal region at the functional level may in part reflect the cellular pathophysiologic changes observed in some TLE patients manifesting as hippocampal atrophy and mesial temporal sclerosis (Hogan, 2001), some of which reflects neuronal cell loss. In our study, we defined regions of interest based on the individually segmented anatomy of each participant, with the specific objective of reducing the effect of atrophy on measured functional coupling.…”

“…Patients were screened for enrollment based on reported clinical semiology of their seizures and confirmed unilateral temporal lobe epilepsy by video-EEG monitoring. Clinical semiology for study inclusion included auras of epigastric rising, experiential phenomena (most commonly fear) and gustatory or olfactory sensations (Hogan, 2001). Subjects with auras suggestive of lateral temporal onset seizures, including auditory hallucinations, visual misperceptions, or language disturbance, were excluded from the study group (Commission on Classification and Terminology of the International League Against Epilepsy, 1989).…”

“…Temporal lobe epilepsy (TLE) is a well-characterized example of focal epilepsy, with seizures that typically originate in the medial temporal region. From a structural/pathologic standpoint, TLE can often be associated with specific structural and metabolic abnormalities, including hippocampal atrophy and/or sclerosis (Margerison and Corsellis, 1966; Van Paesschen et al, 1997; Hogan, 2001) and medial temporal hypometabolism (Theodore et al, 1992; Arnold et al, 1996; Carne et al, 2004). Yet localized structural and/or metabolic abnormalities extend beyond the medial temporal region to multiple, non-limbic brain regions, most prominently lateral temporal and frontal regions, as noted via structural magnetic resonance imaging (Bernhardt et al, 2010), positron emission tomography (Theodore et al, 1992; Arnold et al, 1996), magnetic resonance spectroscopy (Stanley et al, 1998; Miller et al, 2000), and pathologic studies (Margerison and Corsellis, 1966).…”

Intractable Epilepsy Secondary to Cyclosporine Toxicity in Children Undergoing Allogeneic Hematopoietic Bone Marrow Transplantation

“…18,19 In fact, febrile or repeated seizures, together with other hypoxic events during this period of life, can cause irreversible injury at the level of some cortical regions, in particular mesial temporal areas, which are particularly sensitive to these events. [20][21][22][23][24] The third possible risk factor for the evolution to epilepsy is prolonged cyclosporine administration, likely associated with other neurologic risk factors, as in the case of the two children with hemophagocytic lymphohistiocytosis in which central nervous system involvement can occur. 25 As for the clinical and EEG data, we believe that the temporal localization observed in three of the four epileptic children can be considered secondary to the mesial temporal sclerosis, 26 whereas in the child with multifocal epilepsy and secondary generalization, the mesial temporal sclerosis is probably only an epiphenomenon associated with but not determining the epilepsy.…”

Adolescent Seizures and Epilepsy Syndromes

“…Recent volumetric MRI studies have suggested that hippocampal sclerosis is a progressive disorder with a risk for cognitive dysfunction (64). The characteristic clinical features and an ability to identify hippocampal disturbances noninvasively with modern MRI have allowed MTLE to be established as a discrete epileptic syndrome (65–69).…”

Impaired and facilitated functional networks in temporal lobe epilepsy

“…A few previous studies of functional connectivity in TLE have focused on intrahemispheric effects (Bettus et al, 2009, 2010), while others have noted decreased connectivity between medial temporal regions (Pittau et al, 2012), but typically without extending the scope to the temporal neocortex. As with local changes described above, decoupling of the medial temporal region at the functional level may in part reflect the cellular pathophysiologic changes observed in some TLE patients manifesting as hippocampal atrophy and mesial temporal sclerosis (Hogan, 2001), some of which reflects neuronal cell loss. In our study, we defined regions of interest based on the individually segmented anatomy of each participant, with the specific objective of reducing the effect of atrophy on measured functional coupling.…”

“…Patients were screened for enrollment based on reported clinical semiology of their seizures and confirmed unilateral temporal lobe epilepsy by video-EEG monitoring. Clinical semiology for study inclusion included auras of epigastric rising, experiential phenomena (most commonly fear) and gustatory or olfactory sensations (Hogan, 2001). Subjects with auras suggestive of lateral temporal onset seizures, including auditory hallucinations, visual misperceptions, or language disturbance, were excluded from the study group (Commission on Classification and Terminology of the International League Against Epilepsy, 1989).…”

“…Temporal lobe epilepsy (TLE) is a well-characterized example of focal epilepsy, with seizures that typically originate in the medial temporal region. From a structural/pathologic standpoint, TLE can often be associated with specific structural and metabolic abnormalities, including hippocampal atrophy and/or sclerosis (Margerison and Corsellis, 1966; Van Paesschen et al, 1997; Hogan, 2001) and medial temporal hypometabolism (Theodore et al, 1992; Arnold et al, 1996; Carne et al, 2004). Yet localized structural and/or metabolic abnormalities extend beyond the medial temporal region to multiple, non-limbic brain regions, most prominently lateral temporal and frontal regions, as noted via structural magnetic resonance imaging (Bernhardt et al, 2010), positron emission tomography (Theodore et al, 1992; Arnold et al, 1996), magnetic resonance spectroscopy (Stanley et al, 1998; Miller et al, 2000), and pathologic studies (Margerison and Corsellis, 1966).…”

Intractable Epilepsy Secondary to Cyclosporine Toxicity in Children Undergoing Allogeneic Hematopoietic Bone Marrow Transplantation

“…18,19 In fact, febrile or repeated seizures, together with other hypoxic events during this period of life, can cause irreversible injury at the level of some cortical regions, in particular mesial temporal areas, which are particularly sensitive to these events. [20][21][22][23][24] The third possible risk factor for the evolution to epilepsy is prolonged cyclosporine administration, likely associated with other neurologic risk factors, as in the case of the two children with hemophagocytic lymphohistiocytosis in which central nervous system involvement can occur. 25 As for the clinical and EEG data, we believe that the temporal localization observed in three of the four epileptic children can be considered secondary to the mesial temporal sclerosis, 26 whereas in the child with multifocal epilepsy and secondary generalization, the mesial temporal sclerosis is probably only an epiphenomenon associated with but not determining the epilepsy.…”

Adolescent Seizures and Epilepsy Syndromes

“…Recent volumetric MRI studies have suggested that hippocampal sclerosis is a progressive disorder with a risk for cognitive dysfunction (64). The characteristic clinical features and an ability to identify hippocampal disturbances noninvasively with modern MRI have allowed MTLE to be established as a discrete epileptic syndrome (65–69).…”

Impaired and facilitated functional networks in temporal lobe epilepsy

“…A few previous studies of functional connectivity in TLE have focused on intrahemispheric effects (Bettus et al, 2009, 2010), while others have noted decreased connectivity between medial temporal regions (Pittau et al, 2012), but typically without extending the scope to the temporal neocortex. As with local changes described above, decoupling of the medial temporal region at the functional level may in part reflect the cellular pathophysiologic changes observed in some TLE patients manifesting as hippocampal atrophy and mesial temporal sclerosis (Hogan, 2001), some of which reflects neuronal cell loss. In our study, we defined regions of interest based on the individually segmented anatomy of each participant, with the specific objective of reducing the effect of atrophy on measured functional coupling.…”

“…Patients were screened for enrollment based on reported clinical semiology of their seizures and confirmed unilateral temporal lobe epilepsy by video-EEG monitoring. Clinical semiology for study inclusion included auras of epigastric rising, experiential phenomena (most commonly fear) and gustatory or olfactory sensations (Hogan, 2001). Subjects with auras suggestive of lateral temporal onset seizures, including auditory hallucinations, visual misperceptions, or language disturbance, were excluded from the study group (Commission on Classification and Terminology of the International League Against Epilepsy, 1989).…”

“…Temporal lobe epilepsy (TLE) is a well-characterized example of focal epilepsy, with seizures that typically originate in the medial temporal region. From a structural/pathologic standpoint, TLE can often be associated with specific structural and metabolic abnormalities, including hippocampal atrophy and/or sclerosis (Margerison and Corsellis, 1966; Van Paesschen et al, 1997; Hogan, 2001) and medial temporal hypometabolism (Theodore et al, 1992; Arnold et al, 1996; Carne et al, 2004). Yet localized structural and/or metabolic abnormalities extend beyond the medial temporal region to multiple, non-limbic brain regions, most prominently lateral temporal and frontal regions, as noted via structural magnetic resonance imaging (Bernhardt et al, 2010), positron emission tomography (Theodore et al, 1992; Arnold et al, 1996), magnetic resonance spectroscopy (Stanley et al, 1998; Miller et al, 2000), and pathologic studies (Margerison and Corsellis, 1966).…”

Intractable Epilepsy Secondary to Cyclosporine Toxicity in Children Undergoing Allogeneic Hematopoietic Bone Marrow Transplantation

“…18,19 In fact, febrile or repeated seizures, together with other hypoxic events during this period of life, can cause irreversible injury at the level of some cortical regions, in particular mesial temporal areas, which are particularly sensitive to these events. [20][21][22][23][24] The third possible risk factor for the evolution to epilepsy is prolonged cyclosporine administration, likely associated with other neurologic risk factors, as in the case of the two children with hemophagocytic lymphohistiocytosis in which central nervous system involvement can occur. 25 As for the clinical and EEG data, we believe that the temporal localization observed in three of the four epileptic children can be considered secondary to the mesial temporal sclerosis, 26 whereas in the child with multifocal epilepsy and secondary generalization, the mesial temporal sclerosis is probably only an epiphenomenon associated with but not determining the epilepsy.…”

Adolescent Seizures and Epilepsy Syndromes

“…Recent volumetric MRI studies have suggested that hippocampal sclerosis is a progressive disorder with a risk for cognitive dysfunction (64). The characteristic clinical features and an ability to identify hippocampal disturbances noninvasively with modern MRI have allowed MTLE to be established as a discrete epileptic syndrome (65–69).…”