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Clinical commentary with video sequencesEpileptic Disord 2013; 15 (1): 67-71

Post-traumatic epilepsy withisolated memory flashbacksChusak Limotai 1, Seyed M. Mirsattari 1,2,3,4

1 Department of Clinical Neurological Sciences,2 Department of Medical Biophysics,3 Department of Medical Imaging,4 Department of Psychology, Western University, London, Ontario, Canada

Received January 9, 2012; Accepted January 9, 2013

ABSTRACT – Some traumatic events can cause both post-traumatic stressdisorder and epileptic seizures. We report the case of a woman who expe-rienced a severe head injury which subsequently led to the developmentof paroxysmal episodes of isolated memory flashbacks related to the injury.

ng with video-EEG telemetry record-en these two conditions. [Published

raumatic stress disorder

lision (MVC) one and a half yearsago. At the time, she presentedwith an initial Glasgow Coma Scale(GCS) of 11/15 (E3V3M5). She wasperseverative and confused uponher arrival to the hospital. She wasunable to move her left arm and hada left-sided, upper motor neuron-type facial weakness. She was foundto have an acute traumatic subarach-noid haemorrhage, diffuse axonalinjury, minimal right hemothorax,and multiple fractures including thetransverse process of C7 vertebraand left acetabular bone. She wasamnestic to the events surround-ing the MVC, one week beforeand one week afterwards. Approxi-mately within a month after herMVC, she developed stereotyped

orrespondence:

Detailed analysis of her symptoms aloings was helpful to distinguish betwewith video sequences]

Key words: memory flashback, post-t

Reminiscence of past traumaticevents in a “flashback” manner(i.e. intrusive memories) has beencommonly recognised as a symp-tom of post-traumatic stress dis-order (PTSD) (American PsychiatricAssociation, 2000). However, otherpotential causes, such as epilepticseizures, may be overlooked. Someepileptic seizures may manifest withexperiential hallucinations of pastexperience (Gloor, 1990; Vignal et al.,2007).We report a patient with post-traumatic epilepsy whose seizuresconsisted of isolated memory flash-backs. This case illustrates that adetailed clinical assessment andvideo-EEG telemetry may be helpfulto differentiate between epileptic

pileptic Disord, Vol. 15, No. 1, March 2013 67

eyed M Mirsattariepartments of Clinical Neurologicalciences,edical Biophysics, Medical Imaging,

nd Psychology,estern University,

10-110, 339 Windermere Rd,ondon, Ontario N6A 5A5, Canadasmirsat2@uwo.ca>

seizures and PTSD.

Case study

A 43-year-old, right-handed womanwas involved in a motor vehicle col-

paroxysmal episodes of perceiving“awful feelings” that were, at times,associated with flashback memo-ries related to her MVC. Theseepisodes were consistently associat-ed with migraine-like headaches.During such episodes, she would

6

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. Limotai, S.M. Mirsattari

eel hot, flushed, sweaty, and “awful”. The latter wasoorly defined but was characterised by the per-eption of bad experiences from her MVC, such asntubation or insertion of a chest tube while she wasn the intensive care unit or during her hospitalisationt a rehabilitation centre. She would recognise thesepisodes as unreal thoughts without seeing or hear-

ng anything related to the events. The episodes eachasted for a few minutes.nitially, she was treated with valproic acid but thisid not help relieve her episodes or headache. Sub-equently, valproic acid was discontinued and topi-amate, at 150 mg daily, was started; this providedelief for her headaches and reduced the number ofpisodes.er neurological examination at the time of her admis-

ion for prolonged scalp video-EEG telemetry wasemarkable for generalised hyperreflexia, which was

8

ore pronounced on the left side. Her cranial MRIhowed diffuse axonal injury with scattered tiny spotsf increased signal intensity on T2-weighted and Fluidttenuated Inversion Recovery (FLAIR) sequences,hich were most prominent in the right subcortical

erebral white matter and haemosiderin deposits inhe left superior frontal region and splenium of the

A B

C D

igure 1. (A) Fluid Attenuated Inversion Recovery (FLAIR) sequence shainly in right subcortical white matter. (B and C) Gradient echo s

aemosiderin deposits noted in the left superior frontal region andetected in bilateral temporal regions including bilateral hippocampi

flpsiH2e

orpus callosum (figure 1). No abnormality was seenn the temporal lobes, particularly the hippocampi.outine outpatient EEGs revealed a few interictalpileptiform discharges (IEDs) in the right temporalegions and bilateral intermittent delta slow in theemporal areas. Scalp video-EEG telemetry revealednfrequent sequential IEDs in the right hemisphere,

aximum at F8-T4-M2, with minimal spread to F4-C4.nterestingly, no focal slow wave was seen with topira-

ate, but was evident in the bilateral temporal regionsfter a reduction in topiramate, which resulted in aluster of 19 clinical seizures.he seizures were semiologically and electrophysio-

ogically similar, but varied in duration. During theseeizures, she reported feeling hot, flushed, and light-eaded, with headache and “awful feelings”, butithout motor manifestations. On two occasions, she

tated that “I am having bad thoughts” referring to

Epileptic Disord, Vol. 15, No. 1, March 2013

owing scattered tiny spots of increased signal intensity, observedequence revealed evidence of diffuse axonal injury, showingright-sided splenium, respectively. (D) No abnormalities were

.

ashback memories of being in the rehabilitation hos-ital, which she was normally amnestic to (see videoequence). She could not describe these awful feel-ngs in further detail, other than being “unpleasant”.er recorded seizures varied in duration from 40 to

20 seconds. She was unresponsive during the longerpisodes.

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lectrographically, her seizures started with a build-p of subtle repetitive small-amplitude, 2-Hz spikest F8-M2 (clearly discernible in our montage contain-ng A1-A2 and F7-F8 derivations in which A1 referredo M1 [mandibular electrode] and A2 referred to M2).his was followed by diffuse, semi-rhythmic, 5-6-Hzaves with right hemispheric predominance for 30

econds. For the longer seizures, they would beollowed by 0.5-0.8-Hz, higher amplitude, repetitivepikes at M2-F8, with minimal spread to T4. These werentermingled with right hemispheric, semi-rhythmic,-5-Hz waves and generalised, low-amplitude, fastctivity with right-sided predominance for another0-150 seconds (figure 2).

iscussion

e herein report a case with temporal lobe seizures,s evidenced by video-EEG, manifesting with memoryashbacks. The immediate occurrence of thesepisodes after the patient’s severe head injury and

ack of typical characteristics of temporal lobe seizuresed, for several months, to the misinterpretation ofTSD.he DSM-IV-TR (American Psychiatric Association,000) includes the term “dissociative flashbackpisodes” as one of the diagnostic features of PTSD.he criteria emphasize a response which includesvoidance behaviour associated with symptoms ofncreased arousal, e.g. difficultly falling asleep, exag-erated startle response, and functional disturbance.he re-experienced event may include recurrent and

ntrusive distressing recollections of the event, suchs images, thoughts, perceptions, or recurrent dis-ressing dreams of the event. Among the clustersf symptoms required for the diagnosis of PTSD,voidance or numbing is reported to be a strongeterminant or marker (Ehlers et al., 1998; North etl., 2005). The present case did not present with anyymptoms applicable to this cluster. During thesepisodes, the patient did not express fear nor did shexhibit avoidance behaviour during or in between herpisodes.Flashbacks” have been reported with epilepticeizures (Gloor et al., 1982; Bancaud et al., 1994;arbeau et al., 2005; Vignal et al., 2007). However, theserevious cases were more consistent with “dreamytates” as they described recollection of visual scenes

pileptic Disord, Vol. 15, No. 1, March 2013

r fragments of scenes. In these cases, the patientsescribed the visual scenes as if they were specta-

ors (Vignal et al., 2007). Our patient, on the otherand, did not see or hear anything related to herVC and her episodes were based only on her feel-

ngs. Vignal et al. (2007) proposed the semiologicalontinuity between the phenomenon of déjà vu and

dpaeorc

Memory flashbacks

uch complex visual hallucinations, given the recipro-al connections between the amygdala/hippocampusnd other cortical areas, including the primary andssociation visual and auditory cortices.he International League Against Epilepsy (ILAE) Taskorce on Classification and Terminology classifiedexperiential aura” as affective, mnemonic, halluci-atory, and illusive perceptions (Blume et al., 2001).enfield and Perot distinguished “dreamy state” asither interpretive response or seizure and experien-ial hallucination (Penfield and Perot, 1963). The formereferred to perceptual illusion (visual and auditory),éjà vu, and emotion, in the sense of false interpreta-

ion of the present. The latter was memory flashback,oted as a sudden re-experience of the past. Mostf these were elicited from the temporal neocortex.loor (1990) used the term “experiential” in theroader sense, to encompass perceptual, mnemonic,nd affective features. The mnemonic phenomenaeferred to the actual recall of a past event or situa-ion (flashback) and a feeling of recognition, familiarity,r reminiscence. Experiential responses were elicitedy stimulation of the limbic structures of the tempo-al lobe, for which the amygdala showed the highestncidence of positive responses, compared to the tem-oral neocortex (Gloor, 1990). This is in line withstereoelectroencephalographic (SEEG) study which

howed a role for the amygdala and hippocampus inecall of recent and distant memories (Vignal et al.,007). Bancaud et al. (1994) demonstrated that bothesial and lateral temporal neocortices are involved

n this phenomenon. Bartolomei et al. (2004) studiedhe role of the anterior subhippocampal structures (i.e.hinal cortices) in eliciting déjà vu sensation. Based onheir study, they suggested that déjà vu phenomenon isikely triggered in the anterior subhippocampal struc-ures and requires transient functional coupling withther mesial temporal structures, which eventuallyesults in recollection (Bartolomei et al., 2004; Guedjt al., 2010; Bartolomei et al., 2012). This phenomenoneflects positive expression of the function of temporalobe structures. Once stimulated or elicited seizuresccur, the epileptic discharges may strengthen inter-onnectivity of the neurons among these structuresGloor, 1990; Vignal et al., 2007).

ith regards to the underlying pathophysiology ofTSD, aside from psychological factors and persona-

ity characteristics that contribute to the developmentf PTSD, functional imaging and neurochemical stu-

69

ies have implicated a role of the amygdala, mesialrefrontal cortex (PFC), hippocampus, epinephrine,nd cortisol. Acute stress can cause an increase inpinephrine secretion, which facilitates the encodingf emotionally arousing information in the amygdala,esulting in some form of implicit memory. A highoncentration of epinephrine impairs PFC function

70 Epileptic Disord, Vol. 15, No. 1, March 2013

C. Limotai, S.M. Mirsattari

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1 sec03/13/2011 11:49:04EEG onset

Figure 2. (A) Initial EEG onset, starting with a build-up of subtle, repetitive, low-amplitude spikes at 2 Hz, observed at F8-M2 (clearlydiscernible on special montage containing A1-A2 and F7-F8 derivations; A1 referred to M1 [mandibular electrode] and A2 referred toM2). (B and C) Subsequent ictal EEG changes.

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Penfield W, Perot P. The brain’s record of auditory and

hrough �-1 adrenergic receptor activation. Given thenhibitory effects of PFC on the amygdala via itseciprocal connections, PFC dysfunction could beelated to the inability of PTSD patients to inhibitntrusive memories (Elzinga and Bremner, 2002). Thisould thus implicate disinhibition of the mesial tem-oral structures, particularly the amygdala, in PTSD,

n contrast to their direct stimulation during epilepticeizures or electrical stimulation.

onclusion

n summary, prolonged scalp video-EEG recordingsonfirmed that our patient’s episodes of isolatedemory flashbacks were epileptic seizures, arising

rom the right temporal region. An absence of typicaleatures of temporal lobe seizures (altered aware-ess, automatisms, or typical auras) made it difficult toifferentiate between epileptic seizures and PTSDn clinical grounds. A shorter duration of attacks,ssociated headache or autonomic symptoms, andbsence of the avoidance/numbing symptom clusteray serve as possible clues for epileptic seizures in

atients with isolated memory flashbacks, which cane confirmed by video-EEG telemetry. �

isclosures.one of the authors has any conflict of interest or financial

upport to disclose.

Legend for video sequence

Video recording of a seizure in which the patientdescribed “head pounding” and “awful thought” atapproximately two and three minutes after EEG off-set. Of note, the initial part of ictal EEG was obscuredby muscle and movement artefacts. The first clearlyobserved ictal EEG change was semi-rhythmic dis-charge of 6-7 Hz observed at F8-M2 (A2 referred toM2), which was noted at approximately 30 secondsafter the beginning of this recording.

Key words for video researchon www.epilepticdisorders.com

pileptic Disord, Vol. 15, No. 1, March 2013

Syndrome: focal non-idiopathic temporal (tle)Etiology: head traumaPhenomenology: hallucinations (visual);nonepileptic paroxysmal eventLocalization: temporal lobe (right)

v1

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Memory flashbacks

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