1

Traumatic Medial Temporal Lobe Epilepsy

Associated with a Subcortical Lesion in the
Internal Capsule A Case Report
Nobutaka Mukae
1)
, Takato Morioka
1)
, Tetsuro Sayama
1)
, Takeshi Hamamura
1)
, Kosuke Makihara
2)
,
Hiroshi Shigeto
3)
, Tomio Sasaki
4)

Although there is no universally accepted
definition, traumatic medial temporal lobe ep-
ilepsy (traumatic MTLE) can be generally de-
fined as a type of post-traumatic epilepsy with
medial temporal epileptogenicity. Previous
studies have demonstrated that patients with
traumatic MTLE frequently have hippocampal
sclerosis (HS) coexisting with traumatic neo-
cortical lesions. We report a 39-year-old
MTLE patient with a subcortical lesion in the
internal capsule, suspected to be caused by
mild diffuse axonal injury. The results of pre-
surgical examinations and intraoperative elec-
trocorticograms were consistent with a diag-
nosis of MTLE. Therefore, an anterior tem-
poral lobectomy with hippocampectomy was
performed. A 3D short tau inversion recovery
3-Tesla MRI scan clearly depicted possibly
Wallerian degeneration in the temporal stem,
which was continuous with the subcortical
Correspondence: Takato Morioka, M.D., Ph.D.
Department of Neurosurgery, Kyushu Rosai Hospital, 1-1 Sone-Kita, Kokuraminami-ku, Kitakyushu, 800-0296, Japan
Tel: +81-93-471-1121; Fax: +81-93-473-0627 E-mail: takato@med.kyushu-u.ac.jp
Epilepsy & Seizure
Journal of Japan Epilepsy Society
Vol.6 No.1 (2013) pp.1-9
1
Department of Neurosurgery, Kyushu Rosai Hospital, Kitakyushu, Japan
2
Department of Surgical Pathology, Kyushu Rosai Hospital, Kitakyushu, Japan
3
Department of Neurology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
4
Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
Abstract
Accepted March 12, 2011Published online March 13, 2013
Case Report
Key words: temporal lobe epilepsy, trauma, hippocampal sclerosis, subcortical lesion,
Wallerian degeneration
2
lesion. We speculate that Wallerian degenera-
tion in the temporal stem could potentially
involve the hippocampus, eventually leading
to HS.

Introduction
Although there is no universally accepted
definition, traumatic medial temporal lobe
epilepsy (traumatic MTLE) can be generally
defined as a type of post-traumatic epilepsy
with medial temporal epileptogenicity [1-3].
Previous studies have demonstrated that hip-
pocampal sclerosis (HS) frequently coexists
with traumatic neocortical damage [1-5]. We
report a case of MTLE associated with a sub-
cortical lesion in the internal capsule, sus-
pected to be the result of mild diffuse axonal
injury.

Case report
A 39-year-old right-handed man was eval-
uated for epilepsy surgery because of refrac-
tory seizures. At 3 months of age, he was hit
on the head over the left temporal region by
the door of a car. Following this head trauma,
he suffered weakness in his right extremities.
From 3 years of age, he started having sei-
zures in the right extremities accompanied by
secondary generalized tonic-clonic seizures.
Although his seizures were almost complete-
ly controlled with antiepileptic drugs, they
recurred at 9 years of age. His seizures began
with abdominal discomfort, followed by
cloudy consciousness and motor automatism
of his right hand and dystonic posture of his
left hand. Secondary generalized tonic-clonic
seizures were often observed. He was pre-
scribed various drug treatments, but the sei-
zures became medically intractable. At opti-
mal dosages of carbamazepine, phenytoin,
valproate, clonazepam and clobazam, daily
occurrence of complex partial seizures per-
sisted.
A presurgical evaluation was performed.
Neurologically, mild left hemiparesis was
noted. He also had mild disturbances of
memory function (verbal memory of 77 and
visual memory of 90 on the WMS-R). His
total IQ was 77 (PIQ of 83 and VIQ of 76).
Interictal EEG recordings depicted frequent
paroxysmal activities in the right fronto-
temporal region. Long-term video-EEG mon-
itoring captured five episodes of habitual sei-
zures and revealed that ictal discharges began
in the right frontotemporal region.
Magnetic resonance imaging (MRI) was
performed using a 3-Tesla (3T) machine, as
described previously [6]. Images obtained
with the fluid-attenuated inversion recovery
sequence (FLAIR) depicted hyperintensity
and atrophy of the right hippocampus (Fig.
1A, B) as well as a small area of hyperinten-
sity in the posterior limb of the right internal
capsule (Fig. 1C, D). A 3D short tau inver-
sion recovery MRI scan clearly demonstrated
low intensity bands in the temporal stem (Fig.
2 white arrows) as well as in the cerebral pe-
duncle (Fig. 2 black arrows), which were
continuous with the low intensity lesion in
the posterior limb of the internal capsule. The
low intensity band in the cerebral peduncle
Traumatic MTLE with Subcortical Lesion Nobutaka Mukae, et al.
3
was accompanied by shrinkage of the ipsilat-
eral cerebral peduncle, suggesting the pres-
ence of Wallerian degeneration.
Positron emission tomography with [
18
F]
fluorodeoxyglucose (FDG-PET)

[7] indicated
hypometabolism in the right temporal lobe
(Fig. 1E, F). Because the findings of the pre-
surgical examination were consistent with a
diagnosis of right MTLE, epilepsy surgery of
the right medial temporal lobe was scheduled.
Through a right frontotemporoparietal cra-
niotomy, the cortical surface of the temporal
lobe was exposed and the arachnoid mem-
brane on the Sylvian fissure was found to be
cloudy (Fig. 3A). Intraoperative electrocorti-
cographic (ECoG) recordings from the medi-
al, basal and lateral aspects of the temporal
lobe (Fig. 3B) demonstrated frequent parox-
ysmal activities over the medial temporal
lobe (Fig. 3C). Resection of the middle and
inferior temporal gyri was performed at 4.0
cm from the temporal apex, and the inferior
horn of the lateral ventricle was exposed (Fig.
4A). An EEG recorded from the hippocam-
pus

[6,8] showed frequent paroxysmal activi-
ties (Fig. 4B, C), and a hippocampectomy
was performed. The hippocampal resection
was extended to 2.0 cm from the hippocam-
pal tip to include the focus of paroxysmal ac-
tivity, which was located 1.5 cm from the
hippocampal tip (Fig. 4C).
The patient was seizure-free during the
first 30 postoperative months. Histopatholog-
ical analyses of the resected hippocampal tis-
sue demonstrated severe cell loss in the py-
ramidal cell layers of CA1 (Fig. 5A) and
CA3, and in the hilar region of the dentate
gyrus (Fig. 5B). As a result, HS was diag-
nosed. Prominent astrogliosis was also ob-
served in the lateral temporal lobe (Fig. 5C).

Discussion
The pathophysiological mechanisms of
traumatic MTLE are unclear [1,2,4,5,9]. It is
generally accepted that direct injury is one of
the major factors in the development of post-
traumatic epileptogenesis [10]. However, the
clinical characteristics of traumatic MTLE
are different from other types of post-
traumatic epilepsy [10]. Direct injury to the
hippocampus as a result of traumatic brain
injury is uncommon. In this regard, Diaz-
Arrastia et al.

[1] demonstrated that HS re-
sulted from secondary effects of traumatic
brain injury. In a rodent model of traumatic
brain injury induced by fluid percussion, the
complete profile of classic HS is not ob-
served. Instead, damage to the hippocampal
formation is restricted primarily to the hilar
region of the dentate gyrus and occasionally
CA3, with little cell loss in CA1 [11]. In our
patient, severe cell loss was observed in CA1
and CA3 as well as in the dentate hilus, indi-
cating a classic case of HS.
Another possible mechanism of traumatic
MTLE is temporal evolution from traumatic
neocortical epilepsy originating from a trau-
matic neocortical lesion, resulting in dual pa-
thology with MTLE. Although dual patholo-
gy is common in MTLE, past discussions on
dual pathology have emphasized congenital
migration disorders or neoplasias and have
Epilepsy & Seizure Vol.6 No.1 2013
4
not focused on traumatic lesion [12]. Previ-
ous studies of traumatic MTLE have de-
scribed the coexistence of neocortical damage
and HS [1-5]. Schwartz et al.

[9] examined 21
traumatic MTLE patients and found that 8
patients had cystic change or encephalomala-
cia in the ipsilateral neocortex on preopera-
tive MRI. Additionally, temporal neocortical
pathology such as hemosiderin deposits was
universally present. In rodents, DAmbrosio
et al.

[13] clearly demonstrated that fluid per-
cussion injury induced frontal-parietal neo-
cortical epilepsy at the injury site, and that
this progressed to MTLE with dual pathology
as demonstrated both electrophysiologically
and pathologically. In our case, however, in-
stead of neocortical lesion, subcortical lesion
was noted in the ipsilateral internal capsule.
Although traumatic lesion in the internal cap-
sule with direct coup and contra-coup injury
is quite rare, a recent diffusion tensor imag-
ing study clearly demonstrated that diffuse
axonal injury, even in mild traumatic brain
injury, produced subcortical lesions in corpus
callosum and internal capsule [14].
Recent development of the 3T-MR system
has improved the quality of morphological
and functional neuroimaging. Specifically,
the development of 3DSTIR imaging using
the 3T-MR system has improved the anatom-
ical resolution of routine clinical images to a
level equivalent to that used in general pa-
thology, and this technique has been used for
imaging epileptogenic lesions [6]. In the 3D-
STIR images of the present case, Wallerian
degeneration of the pyramidal tract was ob-
served as an abnormally low signal intensity,
which was continuous with the lesion in the
posterior limb of the internal capsule, accom-
panied by shrinkage of the ipsilateral cerebral
peduncle [15]. Furthermore, a similar low
signal intensity band was also noted in the
temporal stem. The temporal stem is a major
white matter region containing several major
pathways that connect the temporal lobe to
the rest of the brain [16]. Since the temporal
stem tracts contain both afferent and efferent
connections to the hippocampus [17], we
speculate that Wallerian degeneration of the
temporal stem tracts could potentially involve
the hippocampus, eventually leading to HS.
Conversely, in a recent diffusion tensor MRI
study of non-traumatic MTLE with HS,
Schoene-Bake et al.

[18] reported disrupted
white matter tracts in the temporal stem fol-
lowing selective hippocampectomy. In our
histological analysis, prominent astrogliosis
was observed in the lateral temporal lobe,
thus supporting our speculation.
Many previous studies have found no sig-
nificant differences in postoperative outcome
between traumatic and non-traumatic MTLE
patients, despite the high frequency of wide-
spread cerebral hemispheric injury in trau-
matic MTLE cases [1-4]. In the present case,
findings from preoperative examinations and
intraoperative ECoG were consistent with
typical MTLE. Based on this diagnosis, ante-
rior temporal lobectomy with hippocam-
pectomy was performed. The patient
achieved good seizure control during the first
30 postoperative months, although long-term
Traumatic MTLE with Subcortical Lesion Nobutaka Mukae, et al.
5
follow-up should be performed. Although
firm conclusions cannot be drawn from a sin-
gle case report, we believe that good seizure
outcome can be obtained by surgical treat-
ment following extensive presurgical exami-
nation, even in traumatic MTLE patients with
subcortical lesions.
We thank Ms. Kuniko Yamamoto and To-
momi Kido, Clinical Laboratory, Kyushu Ro-
sai Hospital, and Ms. Ayumi Sakata, Depart-
ment of Clinical Chemistry and Laboratory
Medicine, Kyushu University Hospital, for
supporting our study.

Fig.1. Oblique (along the long axis of the hippocampus) [A, C] and coronal [B, D] views of MRI scans with the
fluid-attenuated inversion recovery sequence (FLAIR) demonstrate hyperintensity and atrophy in the
right hippocampus [A, C], and a small region of hyperintensity in the posterior limb of the internal
capsule [C, D: white arrows]. Positron emission tomography with [
18
F] fluorodeoxyglucose (FDG-PET)
[E, F] at a comparable level to that of [A] and [B], respectively, depicts hypometabolism in the right
temporal lobe.
Epilepsy & Seizure Vol.6 No.1 2013
6
Traumatic MTLE with Subcortical Lesion Nobutaka Mukae, et al.
Fig. 2. Serial coronal images of 3D short tau inversion recovery MRI clearly demonstrate low intensity bands in the
temporal stem (white arrows) as well as in the cerebral peduncle (black arrows), which are continuous with
the low intensity lesion in the posterior limb of the internal capsule.
Fig. 3. [A]: An intraoperative photograph shows the cloudy arachnoid membrane on the Sylvian fissure (Syl.).
Temp; temporal lobe, Front; frontal lobe.
[B]: Intraoperative electrocorticographic recordings from electrodes placed on the medial (M), basal (B) and
lateral (L) aspects of the right temporal lobe are shown.
[C]: The recording sites are indicated on a coronal section of a FLAIR image. Intraoperative ECoG with a
nasion reference shows frequent paroxysmal discharges on the medial temporal lobe.
7
Fig. 4. [A]: An intraoperative photograph shows the exposed hippocampus following resection of the lateral temporal lobe.
[B]: A strip electrode is placed on the hippocampus.
[C]: An intraoperative EEG recording of the hippocampus is shown. The numbers indicate the distance of the record-
ing electrodes from the hippocampal tip. The upper five tracings are monopolar recordings with a nasion refer-
ence and the lower three tracings are bipolar recordings. Frequent paroxysmal discharges are observed, with the
highest voltage in the monopolar recording and phase reversal in the bipolar recording at 1.5 cm posterior to the
hippocampal tip.
Fig. 5. [A]: A coronal section of the resected hippocampus shows pyramidal cell loss in the CA1 region
(original magnification 20, H&E staining).
[B]: Cell loss is also noted in the dentate hilus (original magnification 10, H&E staining).
[C]: Histology of the resected lateral temporal lobe demonstrates prominent astrogliosis
(original magnification 40, glial fibrillary acidic protein staining).
Epilepsy & Seizure Vol.6 No.1 2013
8
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