Cardiac asystole during a temporal lobe seizure

The association between temporal lobe seizures and cardiac arrhythmias has been anecdotally reported in the literature. Ictal bradycardia and cardiac asystole are rare, and maybe underestimated. The physiological mechanism is poorly understood. We report a patient with left temporal lobe seizures who developed ictal bradycardia and cardiac asystole during a complex partial seizure and required a subsequent placement of a pacemaker.     

Ictal asystole mimicking seizure deterioration in temporal lobe epilepsy

We report on a patient with temporal lobe epilepsy, secondary to a left lateral temporal cavernoma, in whom the change in seizure semiology suggested recurrence of secondary generalized seizures. Anticonvulsive medication previously controlled secondary generalized seizures over a period of years but focal seizures continued at a lower rate. Continuous video‐EEG monitoring revealed ictal asystole associated with myoclonic syncope and falls during focal seizures arising from the left temporal lobe. After implantation of a cardiac pacemaker, no more falls occurred during the focal seizures. In conclusion, recurrence of seizure‐associated falls is typically attributed to recurrence of secondary generalized seizures, however, ictal asystole should be considered in selected epilepsy patients as a differential diagnosis of falls. [Published with video sequence]     

Clinical cues for detecting ictal asystole

Objective The occurrence of asystole during an epileptic seizure is the most dramatic manifestation of ictal bradycardia. Recognition of ictal asystole is important as treatment with both antiepileptic drugs and cardiac pacing may be necessary. The purpose of this study was to identify clinical cues to aid in the detection of ictal asystole. Methods We analyzed the clinical and electrophysiologic features of all recorded seizures in consecutive patients diagnosed with ictal bradycardia and asystole on prolonged video-EEG/ECG monitoring over a 14 year period. Results Twenty-nine seizures with ictal bradycardia were identified in 13 patients. Of these, 11 seizures in seven patients were associated with asystole. Bilateral transient limb movements consisting of asymmetric posturing or jerking occurred during eight episodes of ictal asystole, and loss of muscle tone occurred during four. In contrast, neither bilateral limb movement nor loss of muscle tone was observed in any of the non-asystolic seizures, whether ictal bradycardia was present or not. All patients with ictal asystole reported a history of seizure-related falls and brief body and limb jerking. Conclusions The presence of loss of muscle tone or bilateral asymmetric jerky limb movements during a seizure suggests the possibility of ictal asystole. Video-EEG/ECG monitoring should be considered in patients with epilepsy demonstrating these clinical features to determine if ictal asystole is present.     

Cardiac asystole during right frontal lobe seizures: a case report

Abstract The association between partial seizures and cardiac asystole has rarely been reported in the literature. This potentially life-threatening symptom has been observed principally in left-sided epilepsies, in particular during seizures originating in temporal lobe. We describe a case with ictal bradycardia followed by cardiac asystole during right frontal lobe seizures. Video-EEG monitoring recorded two partial seizures with electro-clinical findings suggestive of a right frontal lobe origin, associated with ictal bradycardia followed by prolonged asystole. The brain MRI showed a lesion located in the cingulate gyrus of the right frontal lobe. The patient required a subsequent placement of a pacemaker. In conclusion, cardiac asystole may be a potentially life-threatening symptom during seizures of frontal lobe origin. The right fronto-mesial structures may play a role in autonomic regulation of cardiovascular responses.     

Ictal tachycardia: its discriminating potential between temporal and extratemporal seizure foci.

A wide variety of CNS lesions have been associated with changes in heart rate (HR). However, in epileptic patients their value to lateralize seizure onset remains controversial. This study aims to assess if HR changes associated with partial onset seizures could be useful in lateralizing seizure onset. We analysed HR changes on 100 seizures from 38 consecutive patients (mean age: 27.5 years) admitted for video-EEG telemetry monitoring. We evaluated the R-R interval 30 seconds before the seizure onset and 10, 20 and 120 seconds after the onset. We assessed whether there was a correlation between HR changes and seizure type, left/right differences and different semiological components for each seizure. We recorded 100 seizures. Three non-lateralized seizures were excluded from the analysis; 63/97 (65%) had left hemisphere onset, mainly from the temporal lobe (57.7%). The mean baseline HR was 77 beats per minute Ictal tachycardia (HR: > or = 107.06 beats per minute) was detected in 32 seizures, with ictal onset from the mesial temporal lobe structures in 23/32; 16/32 occurred during the first 10 seconds and 16/32 during the next 20 seconds from the seizure onset independently of the site of origin. Among the different semiological components for each seizure, only dystonic posturing and automatism correlated with HR increments. We did not find bradycardia in our series. Ictal tachycardia occurs most frequently with seizures arising from the mesial temporal lobe and it may not reliably predict the lateralization of seizure onset.     

The association of cardiac asystole with partial seizures: does it result from ictal or interictal activity?

Bradycardia or asystole that occur during some seizures may be life threatening as a leading cause of SUDEP. A patient with right and left temporal lobe onset seizures and preceding bardycardia or asystole is presented. He had bilateral hippocampal atrophy on MRI. The unreliability of ictal bradycardia or asystole as a lateralizing sign in patients with partial epilepsy and the role of interictal autonomic activity in heart rate changes during seizures are discussed.     

Focal semiologic and electroencephalographic features in patients with juvenile myoclonic epilepsy

PURPOSE: A few reports have described focal electroencephalographic or clinical features or both of juvenile myoclonic epilepsy (JME), but without video-EEG documentation. We examined focal clinical and EEG features in patients with JME who underwent video-EEG monitoring. METHODS: Twenty-six patients (nine males and 17 females) who had seizures recorded during video-EEG monitoring were included. Age at seizure onset was 0 to 22 years (mean, 12.3 years), and age at monitoring was 12 to 44 years (mean, 26.5 years). In one patient with left parietooccipital epilepsy, primary generalized tonic-clonic seizures developed after resection of the parietal tumor. Two patients had both temporal lobe epilepsy and JME. Videotaped seizures in each patient were analyzed. Interictal and ictal EEG also were analyzed for any focal features. RESULTS: Focal semiologic features were observed in 12 (46%) of 26 patients. Six patients had focal myoclonic seizures, and two had Figure 4 sign: one with version to the left, and another had left version followed by Figure 4 sign, and left arm clonic seizure. Their ictal EEGs were generalized at onset but with a lateralized evolution over the right hemisphere. The patient who had both JME and left parietooccipital epilepsy, right arm clonic seizure, and Figure 4 sign was seen during a generalized EEG seizure. Interictally, one patient had temporal sharp waves, and another had run of spikes in the right frontal region. CONCLUSIONS: Fourteen (54%) of 26 patients with JME exhibited focal semiologic or electroencephalographic features or both. Video-EEG was essential in reaching a correct diagnosis and choosing an appropriate antiepileptic drug regimen.     

Early seizure termination in ictal asystole

To evaluate the association between cerebral hypoperfusion and seizure termination, we compared seizure duration in seven patients with syncopal ictal asystole (IA), seven with non-syncopal ictal bradycardia, and ten with non-bradycardic seizures. Mean seizure duration was 34.4±13 s in IA, 67±28.9 s in ictal bradycardia, and 82.1±31.1 in non-bradycardic seizures. These were significantly different (ANOVA, p<0.02). This suggests cerebral hypoxia-ischemia favors seizure termination.     

Bradycardia and asystole during generalised interictal EEG discharges

Few studies have investigated the effects of interictal epileptic discharges on the cardiac autonomic system. This study reports the case of a 37‐year‐old man with refractory generalised epilepsy, who recently reported an increase in frequency of nocturnal tonic‐clonic seizures, not responding to treatment. During the nocturnal video study, in non‐rapid eye movements sleep, we recorded 106 generalised sharp‐ and polyspike‐waves lasting for 3 to 7 seconds, associated with bradycardia and asystole, without behavioural changes and without increase in deltoid muscle activity. The asystole had a duration of between 3 and 8 seconds. In one case, a 7 second asystole was associated with a tonic‐clonic generalised seizure. A 24‐hour electrocardiographic study revealed a bradycardia and a Wenckebach atrioventricular block. Heart rate analysis at the time of the interictal epileptic discharges revealed an abrupt increase in the RR interval, occurring simultaneously with the onset of interictal epileptic discharges and followed by a return to values below baseline value. A cardiac pacemaker was installed with a reduction of asystole length during the interictal epileptic discharges. Our findings indicate, for the first time, the role of interictal generalised discharges in EEG‐related asystole and bradycardia. These data support the hypothesis that some patients with epilepsy may be predisposed to disturbances of the autonomic cardiac system.     

Cardiac asystole in epilepsy: clinical and neurophysiologic features

PURPOSE: Cardiac asystole provoked by epileptic seizures is a rare but important complication in epilepsy and is supposed to be relevant to the pathogenesis of sudden unexplained death in epilepsy (SUDEP). We sought to determine the frequency of this complication in a population of patients with medically intractable epilepsy and to analyze the correlation between EEG, electrocardiogram (ECG), and clinical features obtained from long-term video-EEG monitoring. METHODS: Retrospective analysis of the clinical records of hospitalized patients from May 1992 to June 2001 who underwent long-term video-/EEG monitoring. RESULTS: Of a total of 1,244 patients, five patients had cardiac asystole in the course of ictal events. In these patients, 11 asystolic events, between 4 and 60 s long in a total of 19 seizures, were registered. All seizures had a focal origin with simple partial seizures (n = 13), complex partial seizures (n = 4), and secondarily generalized seizures (n = 2). One patient showed the longest asystole ever reported (60 s) because of a seizure. Cardiac asystole occurred in two patients with left-sided temporal lobe epilepsy (TLE) and in three patients with frontal lobe epilepsy (FLE; two left-sided, one bifrontal). Two patients reported previous cardiac disease, but only one had a pathologic ECG by the time of admission. Two patients had a simultaneous central ictal apnea during the asystole. None of the patients had ongoing deficits due to the asystole. CONCLUSIONS: These findings confirm that seizure-induced asystole is a rare complication. The event appeared only in focal epilepsies (frontal and temporal) with a lateralization to the left side. A newly diagnosed or known cardiac disorder could be a risk factor for ictal asystole. Abnormally long postictal periods with altered consciousness might point to reduced cerebral perfusion during the event because of ictal asystole. Central ictal apnea could be a frequent associated phenomenon.     

Ictal central apnea as a predictor for sudden unexpected death in epilepsy

Epidemiological evidence associating ictal hypoventilation during focal seizures with a heightened risk for subsequent sudden unexpected death in epilepsy (SUDEP) is lacking. We describe a patient with temporal lobe epilepsy with two focal seizures recorded in the epilepsy monitoring unit that were associated with central apnea lasting 57 and 58 seconds. During these events, she demonstrated oxygen desaturation down to 68 and 62%. The patient subsequently died at home from autopsy-confirmed SUDEP. The family was not alerted of any seizure activity by the auditory alarm system in her room nor by sleeping in the adjacent room with open doors. This case emphasizes the fact that ictal hypoxia and SUDEP may occur in seizures without noticeable convulsive activity. The report gives credibility to the growing body of literature suggesting that epilepsies affecting the autonomic nervous system may predispose to SUDEP independent of the effects of a secondary generalized convulsion.     

Postictal central apnea as a cause of SUDEP: evidence from near-SUDEP incident

While undergoing video-EEG monitoring, a 20-year-old woman had a 56-second convulsive seizure, after which she developed persistent apnea. The rhythm of the electrocardiogram complexes was unimpaired for approximately 10 seconds, after which it gradually and progressively slowed until it stopped 57 seconds later. Evaluation after successful cardio-respiratory resuscitation showed no evidence of airway obstruction or pulmonary edema. The patient had a previous cardio-respiratory arrest after a complex partial seizure without secondary generalization. Although epileptic seizures are known to be potentially arrhythmogenic to the heart, our observations strongly suggest that one probable mechanism of sudden unexplained death in epilepsy is the marked central suppression of respiratory activity after seizures.     

Entorhinal-Hippocampal Interactions in Medial Temporal Lobe Epilepsy

Summary: Experimental studies suggest important interactions between hippocampus and entorhinal cerebral cortex in generation of temporal lobe seizure activity. We studied electrical expression of spontaneous temporallobe ictal activity in hippocampus and entorhinal cortex in 9 medically refractory epileptic patients who had intracranial depth and subdural electrodes implanted during surgical evaluation. All 9 patients subsequently under-went anteromedial temporal lobectomy with hippocam-pectomy, all had >50% decrease in neuronal cell density in hippocampal CA1 and CA3, and all had good to excellent seizure outcome after operation. Two to 10 spontaneous seizures were analyzed per patient (total 41 seizures). Nine patients had variable onset of seizure activity recorded in hippocampus, entorhinal cortex, or both simultaneously. Low-voltage fast activity was observed in either location and varied among seizures in an individual patient. Periodic preictal spikes, when present, were often synchronous in both locations, but were noted independently only in hippocampus. Our data suggest that preictal spikes and low-voltage fast seizure discharges have anatomically distinct origins, and that some syndromes of medial temporal lobe epilepsy involve interactions between entorhinal and hippocampal regions that act together to produce and propagate the seizures in such patients.     

Postictal language assessment and lateralization of complex partial seizures

We performed a prospective study of ictal and postictal language function after 105 temporal lobe complex partial seizures in 26 patients. Seizure localization was verified by a greater than 90% reduction in seizure frequency after temporal lobectomy. At the time of the seizure, the patient was asked to read a test phrase aloud until it was read correctly and clearly. In all 62 seizures originating from the left temporal lobe, the patient took more than 68 seconds to read the test phrase correctly (mean, 321.9 seconds); in 42 of 43 seizures from the right temporal lobe, the patient read the test phrase in less than 54 seconds (mean, 19.7 seconds). Postictal paraphasias occurred in 46 of 62 seizures from the left temporal lobe (11 of 14 patients). In this study, quantifying the time delay in reading a test phrase lateralized seizure onset in all 26 patients tested, proving significantly more accurate than any other single noninvasive presurgical test.     

Hippocampal dysgenesis associated with temporal lobe hypoplasia and arachnoid cyst of the middle cranial fossa

We describe two children with left hippocampal dysgenesis in association with temporal lobe hypoplasia and arachnoid cyst of the middle cranial fossa. The hippocampus showed an abnormal globular shape and blurred internal structure in both patients. One of the patients had juvenile myoclonic epilepsy without evidence of seizure onset in the abnormal temporal region. The other patient did not have epilepsy; however, he showed developmental language disorder with a probable relationship to the left temporal abnormalities.     

Clustering syncope in a young male with temporal lobe seizures

We report the case of a male aged 2 years 6 months with left temporal lobe epilepsy who presented with ictal bradycardia syndrome leading to asystole. The clinical presentation was remarkable for the occurrence of clustering syncope. A seizure was recorded on a video electroencephalogram- electrocardiogram and analyzed. A cardiac pacemaker was implanted and antiepileptic drug treatment was initiated. We suggest that clustering of syncope is an important feature in the presentation of epilepsy in a young child.     

The ictal bradycardia syndrome: localization and lateralization

PURPOSE: Previous studies have established the importance of the insular cortex and temporal lobe in cardiovascular autonomic modulation. Some investigators, based on the results of cortical stimulation response, functional imaging, EEG recordings of seizures, and lesional studies, have suggested that cardiac sympathetic and parasympathetic function may be lateralized, with sympathetic representation lateralized to the right insula, and parasympathetic, to the left. These studies have suggested that ictal bradycardia is most commonly a manifestation of activation of the left temporal and insular cortex. However, the evidence for this is inconsistent. We sought to assess critically the predictable value of ictal bradycardia for seizure localization and lateralization. METHODS: In this study, we reviewed the localization of seizure activity in 13 consecutive patients with ictal bradycardia diagnosed during prolonged video-EEG monitoring at Mayo Clinic Rochester. The localization of electrographic seizure activity at seizure onset and bradycardia onset was identified in all patients. In addition, we performed a comprehensive review of the ictal bradycardia literature focusing on localization of seizure activity in ictal bradycardia cases. RESULTS: All occurrences of ictal bradycardia in the 13 identified patients were associated with temporal lobe-onset seizures. However, no consistent lateralization of seizure activity was found at onset of seizure activity or at onset of bradycardia in this population. Seizure activity was bilateral at bradycardia onset in nine of 13 patients. The results from the literature review also showed that a predominance of patients had bilateral activity at bradycardia onset; however, more of the ictal bradycardia cases from the literature had left hemispheric localization of seizure onset. CONCLUSIONS: Ictal bradycardia most often occurs in association with bilateral hemispheric seizure activity and is not a consistent lateralizing sign in localizing seizure onset. Our data do not support the existence of a strictly unilateral parasympathetic cardiomotor representation in the left hemisphere, as has been suggested.     

Ictal asystolia in the differential diagnosis of dizziness

Frequently, epileptic seizures are accompanied by changes in the heart rate. They are usually transient and irrelevant for the patient's symptoms and the patient recorders his usually baseline rhythm in second or a few minutes. In this report we present a case of a patient diagnosed previously of epilepsy who presented episodes of dizziness and presyncope. During the video-EEG study we recorded one of these spells. The diagnosis of this spell was a focal seizure associated with asystole: the seizure was almost asymptomatic, and only when the asystole developed (40 seconds after the EEG ictal changes) the patient complained about dizziness. Recovery was fast, but treatment with pacemaker must be considered.     

Effect of spinal cord lesions on convulsive activity induced by intrathecal morphine

Non-specific convulsive behavior induced by intrathecal (IT) morphine microinjection appears to be tonically modulated by centrifugal pathways originating within the brain since the frequency of IT morphine-induced hindlimb seizures and myoclonic twitches are both increased following spinal transection. These effects on convulsant activity are dissociable by selective neural lesions. Bilateral dorsolateral funiculus lesions potentiate seizure activity whereas ventral funiculus lesions and, to a lesser extent, interruption of cerebral cortical influences enhance myoclinic twitch activity. These initial studies indicate that distinct supraspinal centers differentially modulate myoclinic and seizure activity and suggest that an understanding of these systems may have clinical implications for the control of convulsant activity.     

From swelling to sclerosis: acute change in mesial hippocampus after prolonged febrile seizure.

Mesial temporal sclerosis (MTS) has been linked to prolonged febrile seizures. The sequence of changes in the temporal lobe/hippocampus following prolonged febrile seizures and status epilepticus is beginning to be elucidated. We obtained repeated magnetic resonance imaging (MRI) volumetric analysis of the hippocampi in a 23-month-old boy after a prolonged focal febrile seizure. Three days after a prolonged left focal febrile seizure, brain MRI showed increased T2 weighted signal and increased volume (swelling) of the right hippocampus. Repeat MRI 2 months later demonstrated sclerosis of the right hippocampus. Review of the literature shows four other children with prolonged focal seizures associated with the MRI sequence of temporal lobe swelling followed by sclerosis. All had left focal seizures followed by right MTS. Our patient demonstrates a shorter interval for the radiologic development of hippocampal sclerosis compared to other reports.