A case report about focal status epilepticus as first presentation in Alzheimer’s disease: finding the culprit
Astrid DevulderGreet VanderlindenEvy CleerenValerie GoovaertsTom TheysKoen Van LaereWim Van Paesschen
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We prospectively studied 535 newborn infants who had been monitored during labour with scalp electrodes. Daily examination of scalp changes showed frequent transient mild lacerations, while severe complications were rare: seven (1.3%) had scalp ulceration and one (0.2%) developed scalp abscess.
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To evaluate the prevalence and mechanism of ictal speech in patients with language-dominant, left temporal lobe seizures.We retrospectively reviewed the video-EEG telemetry records for the presence of ictal speech in 96 patients with surgically proven left temporal lobe epilepsy and studied the seizure-propagation patterns in three patients who required intracranial EEG recordings for seizure localization.Ictal speech preservation was observed in five patients. One patient's seizures demonstrated rapid propagation of the ictal discharges to the contralateral temporal area where the seizure evolved, resembling a nondominant temporal lobe seizure. The other two patients had ictal discharges that remained confined to the inferomesial temporal areas, sparing language cortex.Preservation of speech in complex partial seizures of language-dominant, left temporal lobe origin is rare. Based on intracranial EEG recordings, the likely mechanism underlying this potentially misleading clinical finding is the preservation of language areas due to limited seizure-propagation patterns.
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Status epilepticus has been defined as `seizures so severe as to constitute a fixed and lasting condition. Prevention of status epilepticus is one of the reasons given for administering anticonvulsant drugs to children. Because status epilepticus is widely believed to be capable of producing neurologic deficit, seizures are believed to require emergency treatment to prevent status epilepticus that might cause brain damage. However, when was the last time you saw a child with status epilepticus who died or had residual encephalopathy? Certainly, there was the child who nearly drowned; the drowning caused both damage to the brain and status epilepticus. I would attribute the residual brain damage to the drowning, not to the status epilepticus.
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Status epilepticus has been defined as `seizures so severe as to constitute a fixed and lasting condition." Prevention of status epilepticus is one of the reasons given for administering anticonvulsant drugs to children. Because status epilepticus is widely believed to be capable of producing neurologic deficit, seizures are believed to require emergency treatment to prevent status epilepticus that might cause brain damage. However, when was the last time you saw a child with status epilepticus who died or had residual encephalopathy? Certainly, there was the child who nearly drowned; the drowning caused both damage to the brain and status epilepticus. I would attribute the residual brain damage to the drowning, not to the status epilepticus.
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A patient in status epilepticus has continuous or rapidly repeating seizures. Although the danger of this pattern of seizure activity has been recognized since antiquity, our understanding of the pathophysiology of status epilepticus is incomplete. The frequency of cases in the United States is approximately 102,000 to 152,000 per year, and roughly 55,000 deaths are associated with status epilepticus annually.1 Twelve to 30 percent of adult patients with a new diagnosis of epilepsy first present in status epilepticus.2,3 This review focuses on generalized status epilepticus, which is the most common form of the disorder.1,4 This is a life-threatening . . .
Pathophysiology
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The Hippocampus and Cortex Together Generate the Scalp EEG Ictal Discharge in Temporal Lobe Epilepsy
The scalp EEG ictal discharge in temporal lobe epilepsy is reportedly visible only after the intracranial discharge becomes well synchronized and present over 10 to 30 cm of cortex. We investigated the role of the hippocampal formation in the generation of the scalp EEG ictal discharge.Intracranial EEG video monitors were recorded using simultaneous scalp, stereotaxic depth, and subdural strip electrodes in 19 subjects with temporal lobe epilepsy. The location, frequency, morphology, and timing of the initial ictal discharge, and subsequent ictal patterns, were examined in hippocampal formation, medial paleocortex, and lateral temporal neocortex electrocorticographic and scalp temporal EEG recordings.In every subject, a scalp ictal discharge was visible only after the intracranial ictal discharge had spread to involve the whole temporal lobe (hippocampal formation, medial paleocortex, and lateral temporal neocortex). Beta/gamma frequency and decremental electrocorticographic ictal discharges were never visualized in the EEG. The scalp EEG ictal discharge frequency was 2.4 to 10 Hz and appeared a median of 18 seconds after a faster frequency electrocorticographic initial ictal discharge, once the intracranial discharge slowed to an alpha, theta, or delta frequency.In temporal lobe epilepsy, an ictal pattern is not readily visible in the scalp EEG until the intracranial ictal discharge is ≤10 Hz and has propagated from its site of onset to involve the hippocampus, medial paleocortex, and lateral temporal neocortex.
Neocortex
Electrocorticography
Stereoelectroencephalography
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Hippocampal sclerosis
Stereoelectroencephalography
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OBJECTIVES
The phenomenon of interictal regional slow activity (IRSA) in temporal lobe epilepsy and its relation with cerebral glucose metabolism, clinical data, MRI, and histopathological findings was studied.METHODS
Interictal18F-fluorodeoxyglucose positron emission tomography (FDG PET) was performed under continuous scalp EEG monitoring in 28 patients with temporal lobe epilepsy not associated with intracranial foreign tissue lesions, all of whom subsequently underwent resective surgery. Regions of interest (ROIs) were drawn according to a standard template. IRSA was considered lateralised when showing a 4:1 or greater ratio of predominance on one side.RESULTS
Sixteen patients (57%) had lateralised IRSA which was always ipsilateral to the resection and of maximal amplitude over the temporal areas. Its presence was significantly related to the presence of hypometabolism in the lateral temporal neocortex (p=0.0009). Logistic regression of the asymmetry indices for all measured cerebral regions confirmed a strong association between IRSA and decreased metabolism of the posterior lateral temporal neocortex only (p=0.009). No significant relation could be shown between slow activity and age at onset, duration of the epilepsy, seizure frequency, and MRI evidence for hippocampal atrophy. Furthermore, IRSA was not specifically related to mesial temporal sclerosis or any other pathology.CONCLUSIONS
Interictal regional slowing in patients with temporal lobe epilepsy not associated with a mass lesion is topographically related to the epileptogenic area and therefore has a reliable lateralising, and possibly localising, value. Its presence is irrelevant to the severity or chronicity of the epilepsy as well as to lateral deactivation secondary to neuronal loss in the mesial temporal structures. Although slow EEG activity is generally considered as a non-specific sign of functional disturbance, interictal regional slowing in temporal lobe epilepsy should be conceptualised as a distinct electrographic phenomenon which is directly related to the epileptogenic abnormality. The strong correlation between interictal regional slowing and lateral temporal hypometabolism suggests in turn that the second may delineate a field of reduced neuronal inhibition which can receive interictal and ictal propagation.Hippocampal sclerosis
Neocortex
Fluorodeoxyglucose
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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.
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Nonconvulsive status epilepticus includes three clinical situations: complex partial status epilepticus; absence status epilepticus; and obtundation in the presence of electrographic status epilepticus. Animal models that provide information helpful to clinical management exist for both complex partial and absence status epilepticus. In models of complex partial status epilepticus (pilocarpine, kainic acid, and various protocols using electrical stimulation), neuronal damage in discrete neuronal populations follows an episode of status epilepticus. Hippocampal populations are particularly susceptible to neuropathologic sequelae. Although it is difficult in some cases to distinguish whether the inducing agent or the status epilepticus causes neuropathology, the similar patterns of damage caused by different inducing stimuli provide converging lines of evidence suggesting that the neuropathologic consequences stem at least in part from status epilepticus. In models of absence status epilepticus (genetic mutants, pentylenetetrazole), there is relatively scarce neuropathology that can be attributed directly to status epilepticus. Together these data from animal models suggest that neuropathologic consequences from complex partial status epilepticus may be more severe than those from absence status epilepticus. If these findings translate to patients, then nonconvulsive status epilepticus of the complex partial type should be managed more aggressively than nonconvulsive status epilepticus of the absence type.
Neuropathology
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