A 52-year-old male with a history of focal epilepsy was diagnosed at the age of 14. He has no history of febrile seizures, meningitis, encephalitis, significant head trauma or developmental delay. The patient does not have a history of violent behavior independent of his seizures.
The patient has two types of seizures. He experiences focal seizures with alteration of awareness associated with a sense of deja vu followed by an unpleasant feeling in his stomach, inability to speak and alteration in awareness with post-ictal fatigue. In addition, he experiences focal to bilateral tonic-clonic seizures with post-ictal fatigue lasting for several hours.
In 2008, he was noted to have an increase in seizure frequency, up to one convlsive seizure a month, and began experiencing aggressive outbursts associated with violence in the post-ictal period. At that time, he was taking valproic acid and lamotrigine for seizure management. The first aggressive outburst presented with aggressive behavior and suicidal delusions. During this event he assaulted his neighbor and threatened to harm his children. He was found to have Enterococcus faecium bacteremia and it was assumed that his aggressive behavior was related to delirium asscoiated with infection. Later that year; however, he presented to medical attention with a second event. He had experienced three seizures in one day and soon after became psychotic with delusional thinking and combative behavior which lasted for several hours. Since this time the patient continued to have episodic aggressive behavior which was consistently observed in the post-ictal period. Aggression and violence were typically observed after clusters of multiple seizures or tonic-clonic seizureswithin hours after the seizures lasting for several hours. During one episode of postictal violence, he presented to the Emergency Room. An EEG performed at this time documented a brief right temporal electrographic seizure which was not associated with any obvious ictal clinical manifestations, aside from the agitated state as the reason that the patient presented to the Emergency Room. A formal psychiatric evaluation was performed during the admission with the psychiatrist providing an axis 1 diagnosis of post-ictal psychosis.
During the following two years, his valproic acid dose and lamotrigine were increased, yet he still had inadequate seizure control. The patient was subsequently trialed on lacosamide which was not associated with any improvement in seizure control.
In 2010, he was admitted to the University of Alberta epilepsy monitoring unit for prolonged video-EEG telemetry. During that time, he demonstrated seizures associated with alteration of awareness arising from the right temporal lobe. Neuropsychological assessment demonstrated normal intelligence with intact verbal memory and mild to moderately impaired figural memory consistent with right mesial temporal lobe dysfunction. MRI of the brain did not show any obvious structural abnormality. Specifically, there was no evidence of hippocampal sclerosis or any other temporal lobe structural lesions. Based on the absence of an obvious structural lesion, intracranial EEG evaluation was suggested; however, the patient declined this investigation due to reluctance for surgical intervention.
From 2010 to 2015 carbamazepine and clobazam were introduced without any improvement in seizure control. The change in the patient's antiseizure drugs was not associated with any psychiatric symptoms. He continued to experience seizures two to three times a month despite medical therapy associated with prominent agitation and aggressive behavior leading to frequent trips to the emergency room. It was noted that his aggressive behavior was undirected and unintentional but was exacerbated when attempts were made to restrain or control him. During one of these aggressive episodes, he got into a conflict with the police assaulting an officer and was subsequently arrested.
Based on the ongoing issues with postictal aggression, he reconsidered the option of epilepsy surgery and in 2016 he was admitted to the epilepsy monitoring unit for intracranial video-EEG monitoring. Bitemporal depth electrodes were implanted with the deepest contacts targeted at the amygdala and hippocampus (Fig. 1). Interictal EEG demonstrated independent interictal epileptifrom discharges from the amygdala and hippocampus bilaterally. Ictal onset was documented independently from the deepest electrode contacts (amygdala and hippocampus) of both the right and left temporal electrodes (Fig. 2). During the 16-day intracranial video-EEG evaluation, twenty seizures were recorded. Twelve focal seizures with alteration in consciousness were recorded with focal ictal onset in the right amygdala and hippocampus and six were recorded originating from the left amygdala and hippocampus (Fig. 2). The remaining two seizures associated with focal to bilateral tonic-clonic seizures demonstrated bitemporal ictal EEG activity at onset without clear evidence of lateralization. With regard to seizure semiology, with the exception of ictal aphasia indicating left temporal seizures, most of the patient's recorded seizures were not associated with lateralizing ictal semiology. During one seizure, the patient had significant post-ictal agitation and pulled the depth electrodes out. Based on the demonstration of independent bitemporal ictal onset along with the lack of clear lateralization for two focal to bilateral tonic-clonic seizures, the patient was deemed to be a poor surgical candidate. He continued to experience extreme events with postictal rage and aggressive behavior occurring every two to three months.
As the episodes of violence continued to be a major problem, having led to charges of assaulting a police officer and marital discord, psychiatry was consulted regarding possible pharmacological approaches to manage the violent behavior independent of seizure control. Based on the successful use of beta blockers in management of violent behavior in patients with brain injury, pindolol was trialed at 10 mg twice daily dosing assuming that this patient's postictal violence could have a similar underlying pathogenesis. Following the introduction of pindolol the patient has continued to experience seizures on a monthly basis including convulsions occurring at a similar rate compared to before pindolol was started. Despite experiencing similar seizure frequency and severity, the patient has not experienced any episodes of postictal aggression and violence in over two years since pindolol was initiated.