Neuroscience Letters 380 (2005) 75–79
Hemodynamic response to emotional memory recall with eye movement
Toshiyuki Ohtani
a,∗
, Koji Matsuo
a
, Kiyoto Kasai
a
, Tadafumi Kato
b
, Nobumasa Kato
a
a
DepartmentofNeuropsychiatry,GraduateSchoolofMedicine,UniversityofTokyo,7-3-1Hongo,Bunkyo-ku,Tokyo113-8655,Japan
b
LaboratoryforMolecularDynamicsofMentalDisorders,BrainScienceInstitute,RIKEN,2-1HirosawaWakoCity,Saitama351-0198,Japan
Received 19 November 2004; received in revised form 4 January 2005; accepted 7 January 2005
Abstract
Previous studies on rapid eye movement sleep have demonstrated the effect of eye movement on emotional memory. However, the brain
mechanism involved in the influence of the eye movement on the emotional recall remains unclear. We investigated the prefrontal response
during an emotional memory recall with and without eye movement. Ten healthy volunteers were recruited. The changes in concentration
of oxygenated hemoglobin ([oxy-Hb]) in the prefrontal cortex were examined using near-infrared spectroscopy (NIRS) during a task that
involved emotional recall with and without eye movement. Six participants demonstrated a significant increase in [oxy-Hb] during emotional
recall, and the level of increase was reduced through repeated emotional recall with eye movement. The results suggest that eye movement is
associated with a reduction in the hemodynamic response to emotional memory recall.
© 2005 Elsevier Ireland Ltd. All rights reserved.
Keywords: Eye movement; Emotional recall; Near-infrared spectroscopy; Prefrontal cortex
Recent studies have reported a selective activation of the
amygdala, which is a decisive factor in the processing of emo-
tional stimuli, during rapid eye movement (REM) sleep. REM
sleep is supposed to have a memory consolidation function
[4] and plays an important role in the formation of emotional
memory [24]. It has also been reported that while visualizing
the most salient aspect of a traumatic memory, saccadic eye
movements result in changes in the cognitive assessment of
the memory and cessation of intrusive thoughts [20]. This ef-
fect of eye movement, namely, eye movement desensitization
and reprocessing (EMDR), was one of the treatments of the
anxiety associated with traumatic memories and a wide range
of experientially based disorders [21,22]. The repetitive redi-
rection of attention in EMDR induces a neurobiological state
that is optimally configured to support the cortical integra-
tion of traumatic memories into general semantic networks,
similar to that occurring during REM sleep [23]. However,
the brain mechanism involved in these phenomena has not
been elucidated.
∗
Corresponding author.
E-mailaddress: otanit-tky@umin.ac.jp (T. Ohtani).
Neuroimaging studies on emotion in healthy subjects re-
vealed the relationship between emotion and the limbic sys-
tem [10,13,16]. For instance, fear induction was strongly as-
sociated with the amygdala [17]. The prefrontal cortex has
significant direct and indirect connections with the amyg-
dala, which can mediate inhibitory influences [1,10], and the
medial prefrontal cortex may play a general role in emo-
tional processing [8,9,18]. Activation of the prefrontal cor-
tex by trauma-related stimuli in posttraumatic stress disorder
(PTSD) was reported in a study using single photon emission
computerized tomography (SPECT) [12] and near-infrared
spectroscopy (NIRS) [14]. A case report indicated that, upon
recall of the traumatic memory during SPECT scanning, the
left frontal lobe was hyperactive post-EMDR treatment rela-
tive to pretreatment [11]. We noticed the activation of the pre-
frontal cortex during emotional memory recall and predicted
that eye movement has an effect on the prefrontal cortex acti-
vation during emotional memory recall. In order to examine
the effect of eye movement on the brain response, the changes
in oxygenated hemoglobin concentration ([oxy-Hb]) in the
prefrontal cortex during emotional memory recall with and
without eye movement were investigated using NIRS. We
hypothesize that hemodynamic response to memory recall
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doi:10.1016/j.neulet.2005.01.020