Evidence for reflex activation of experiential complex partial seizures
O. Martinez, MD;,
R. Reisin, MD;,
F. Andermann, MD, FRCPC;,
B.G. Zifkin, MD, CM, FRCPC and
G. Sevlever, MD, PhD
From the Hospital Britanico de Buenos Aires (Drs. Martinez, Reisin, and Sevlever), Argentina; Faculty of Medicine (Dr. Andermann), McGill University and Montréal Neurological Hospital and Institute, Montréal; and Epilepsy Clinic (Dr. Zifkin), Montréal Neurological Hospital; and Département des Sciences Neurologiques, Hôpital du Sacré-Coeur de Montréal and Faculté de Médicine, Université de Montréal, Quebec, Canada.
Address correspondence to Dr. Frederick Andermann, Montréal Neurological Hospital and Institute, 3801 rue Université, Montréal, PQ, Canada H3A 2B4.
Reflex activation of seizures by thoughts or mental images issuggested by patients but has not been objectively demonstrated.The authors present a report of a man with experiential complexpartial seizures reliably activated by thinking about his familyhome. During monitoring, such seizures were repeatedly inducedin this way. Seizures were refractory to antiepileptic drugs,but ceased after left temporal resection. Pathologic examinationshowed cortical dysplasia.
Patients often say that they can bring about seizures by certainthoughts, and even more frequently imply that they can interruptor prevent attacks by breaking a train of thought. Such experientialreflex activation, though suspected, has only rarely been studiedand, to our knowledge, never documented. We present a case reportof a man who could reliably induce temporal lobe seizures bythinking about his family home, and whose reflex attacks wererecorded during video monitoring.
This 36-year-old, right-handed man with no risk factors hadintractable complex partial seizures that began at age 14. Hehad a rising epigastric sensation, an ill-defined feeling inhis head, or a feeling of warmth followed by altered consciousness,lip smacking, and gestural automatisms. The seizures lastedabout 1 to1.5 minutes. Postictally, he was drowsy and confused.There were no precipitating factors in the first several years,but he noted later that seizures were reliably precipitatedby the thought of his family home, where he lived from birthto age 18, and more specifically by thinking of his father lookingat him. He reported that about 90% of all seizures were triggeredby this thought, and that the thought would always trigger aseizure. Seizures would occur if he thought spontaneously aboutit, or if he was asked to describe or recall it. He stated thathe could also trigger seizures voluntarily by thinking abouthis family home. These were heralded by a feeling of fear. Henoted that just after the triggering thought occurred, he wouldexperience seeing his father, the rooms in the home, and othermembers of his family. He avoided walking by or visiting hisparents’ home because this would always trigger an attack.He described his childhood as happy, and recalling other childhoodevents or viewing photographs of his father, family, friends,or home did not precipitate seizures. Seeing or speaking tohis father did not trigger attacks. He did not have seizuresinduced by mental stress without this thought. He found theseizures unpleasant and tried to avoid them by diverting hisattention from the thought. He claimed to be able to abort someseizures in this way.
Several seizures occurred during interviews during which hewas questioned about the seizure trigger. Neurologic examinationwas unremarkable. He was treated with several antiepilepticdrugs in various combinations without success.
Routine EEG showed only sporadic left temporal slow activity.Neuropsychological evaluation showed mild verbal memory deficits,suggesting left temporal dysfunction. MRI with volumetric studyof the temporal lobes showed no significant lateralized hippocampalatrophy. However, gray–white matter differentiation wasindistinct in the left temporal lobe. Interictal SPECT showedmild left temporal lobe hypoperfusion. Ictal SPECT showed increasedblood flow in the left temporal region.
Four typical seizures were recorded during video–EEG monitoringwith scalp and sphenoidal electrodes ( figure). All were triggeredduring interviews in which he was being asked about the seizuretrigger or when he was talking about it. He reported his aura,and the seizures then occurred with staring, lip smacking, alteredconsciousness, and automatisms. The EEG showed ictal epileptiformactivity initially over the left sphenoidal electrode and lefttemporal convexity. Just after the aura of one of these seizures,elicited while he was explaining what could trigger an attack,he said that he would have a seizure if he continued to thinkabout it and then immediately repeated "la casa, la casa." Hethen said that the attack was coming, and then stared as theclinically evident seizure began.
Figure. EEG of a reflex experiential seizure induced during video monitoring. Scalp and sphenoidal electrode recording. Seizure onset with ictal rhythmic activity seen on the EEG after the patient is asked (arrow) to think about his family home. Continuous tracing. Vertical marker = 50 uv; horizontal marker = 1 second.
He had a left temporal resection extending 5 cm from the temporalpole, including the amygdala and hippocampus. Pathologic examinationshowed cortical laminar disorganization, irregular clusteringof neurons, balloon cells, occasional binucleate cells, andneurons showing abnormal polarity with misdirected apical dendrites.The amygdala and hippocampus were removed by aspiration andcould not be studied pathologically. Adjacent white matter showednonspecific astroglial changes.
He has had no seizures since the operation in May 1998, andtakes 300 mg oxcarbazepine three times a day. He has been ableto visit the family home and think about it spontaneously andon command without ill effects.
The unusual feature of this patient’s attacks is thatalmost all of his seizures were of an experiential nature, andfor many years prior to surgery were generated by an actionof mind, a quite specific recollection of emotionally meaningfulpeople and images, the thought of his family home. There werealso features of forced thinking in the triggering of his attacks.He reported that he could abort some seizures by willfully divertinghis thoughts from the trigger. Mental stress alone was not aneffective trigger. After surgery he could think about the familyhome, view photographs of it, and visit with no ill effects.He was convinced that the triggering thought was the cause ofthe seizure and not a part of it. His ability to trigger seizuresvoluntarily, the sensitivity to the trigger seen during monitoring,and the results of surgery suggest that he was correct.
This patient had reflex seizures arising in the left temporallobe with a cortical dysplastic lesion and has remained seizure-freesince left temporal resection. The pattern of complex partialseizures and the history of seeing family members or the roomsof the home just before the visible seizure, as well as hisexclamation during monitoring, confirm an experiential aura,classically associated with temporal cortical ictal discharge.
Patients often report that they can start or stop seizures byan act of mind, but documentation is scanty.1 When specificallyquestioned, 22% of patients in a specialized epilepsy clinicclaimed to be able to induce a seizure voluntarily by thoughtsor moods, and 53% said that they could stop a seizure. The roleof photosensitivity was not explored. Nonepileptic seizureswere said to have been carefully excluded, but no EEG studieswere reported.1 It has been reported that 16% of children withrefractory seizures in a specialized clinic could produce aseizure on demand, but EEG confirmation was not provided.2 Aurainterruption, which this patient used at times to prevent afull-blown seizure, is well described and discovered by patientson their own.3 Seizures induced by an act of mind have beendescribed as psychogenic1, a term that has become attached tononepileptic seizures. Although entirely correct, this termis best avoided at this time to prevent ambiguity and confusion.Reflex experiential seizures might be a better term to describethese attacks.
Dysplastic gray matter is inherently epileptogenic4,5 and mayhave abnormal or reorganized connections with surrounding brain.6-8The hyperexcitable dysplastic region may have been easily triggeredby afferents from normal limbic structures involved in bringingthe critical memory to consciousness, and thus this dysplasticregion could recruit temporolimbic tissue to discharge abnormallyand produce a clinical complex partial seizure. However, aninitial role for an abnormal hippocampus triggering a hyperexcitabledysplastic lesion is also plausible and cannot be excluded withoutdepth electrode study and pathologic evidence. When dysplasticlesions are found, "dual pathology" commonly involves the hippocampusin the presence of neuronal migration disorders or gliosis.9The aura of fear and experiential phenomena is sometimes localizedto mesial temporal structures, especially the amygdala; buttemporal isocortex has also been implicated in experientialphenomena. Gloor, studying experiential auras, pointed out thatdifferent stimulation methods may account for this, but alsosuggested the existence of distributed neuronal networks withreciprocal connections between temporal limbic structures andisocortex. These psychical symptoms "could presumably be elicitedfrom different locations within the temporal lobe, includingtemporal isocortex and various limbic structures."10 A hyperexcitableand abnormally connected dysplastic region within such a networkcould well be involved in reflex seizures.
This documentation of such reflex seizures should lend credenceto patients’ statements that they can bring on seizuresby thinking about certain, often emotional, scenes or events;or inhibit seizures by changing their train of thought or interruptingforced thinking. Such activating or interrupting mechanismsmay be more common than previously suspected.
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Received April 26, 2000.
Accepted in final form August 24, 2000.
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