Pain 123 (2006) 210–216

www.elsevier.com/locate/pain

Case report

Motor cortex stimulation for central pain following

a traumatic brain injury
a,*
Byung Chul Son , Sang Won Lee a, Eun Seok Choi b, Jae Hoon Sung a, Jae Taek Hong a

a
Department of Neurosurgery, St. Vincent’s Hospital, The Catholic University of Korea, Suwon, Republic of Korea
b
Department of Rehabilitation, Daejeon St. Mary’s Hospital, The Catholic University of Korea, Daejeon, Republic of Korea

Received 5 August 2005; received in revised form 18 January 2006; accepted 21 February 2006

Abstract

Central pain can occur in any lesions along the central nervous system affecting the spinothalamocortical pathway. Although
diverse etiologies have been reported to cause central pain, there are few reports on the occurrence and surgical treatment of central
pain following a traumatic brain injury (TBI). This paper describes the occurrence of central pain following a severe TBI, in which
the diagnosis of central pain was typically delayed due to the patient’s decreased ability to express his pain for severe aphasia as a
neurological sequela. The severe burning pain, deep pressure-like pain, and deep mechanical allodynia, which presented over the
contralateral side to the TBI, were successfully relieved with motor cortex stimulation (MCS). The analgesic effect of stimulation
was found to be long lasting and was still present at the 12-month follow up. As shown in this patient, the occurrence of central
pain syndrome should be considered by physicians caring for TBI patients, and a comprehensive, systematic study will be needed
to determine the prevalence of central pain after a TBI.
Ó 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.

Keywords: Central pain; Traumatic brain injury; Motor cortex stimulation

1. Introduction lower brainstem, and ventroposterior part of the thala-

In 1994, central pain was defined by the International
Association for the Study of Pain as ‘‘pain initiated or
caused by a primary lesion or a dysfunction within the
CNS’’ (Merskey and Bogduk, 1994). The reported caus-
es of central pain are vascular lesions in the brain and
spinal cord, multiple sclerosis, traumatic spinal cord
injury, traumatic brain injury, syringomyelia and syrin-
gobulbia, tumors, abscesses, viral and syphilitic myelitis,
epilepsy, and Parkinson’s disease. In addition to central
pain caused by spontaneous lesions, surgical lesions of
the central nervous system such as cordotomy also cause
central pain. The highest prevalence of central pain has
been observed to be a result of lesions in the spinal cord,
*
Corresponding author. Tel.: +82 031 249 8202; fax: +82 031 245
5208.
E-mail address: sbc@catholic.ac.kr (B.C. Son).
mus (Bonica, 1991; Boivie, 1992; Tsubokawa and
Katayama, 1998).
Considering that traumatic brain injury (TBI) is a
common cause of neurological morbidity around the
world, and the spinal cord is a known lesion location,
where the highest prevalence of central pain occurs, it
is surprising that there are very few reports on the occur-
rence of central pain after a TBI (Boivie, 1999). There
has been no clear explanation for this discrepancy of
occurrence of central pain between brain and the spinal
cord.
Motor cortex stimulation (MCS) was first proposed
for the treatment of central pain and has been shown
to be effective in relieving peripheral neuropathic pain
(e.g., trigeminal neuropathic pain, brachial plexus
avulsion, and phantom pain) (Myerson et al., 1993;
Tsubokawa et al., 1993; Nguyen et al., 1997; Tsubokawa
and Katayama, 1998; Saitoh et al., 2000). According to

0304-3959/$32.00 Ó 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
doi:10.1016/j.pain.2006.02.028
 B.C. Son et al. / Pain 123 (2006) 210–216
a review of the literature, Nguyen et al. (1997) reported
the result of MCS in one patient with central pain fol-
lowing a brain injury in 1997. However, the long-term
results at 12 months were unsuccessful and the details
were not reported. Because the report of central pain
following a TBI is extremely rare, and medically intrac-
table central pain conditions are notoriously resistant to
treatment, we report a patient whose intractable central
pain following TBI was successfully alleviated with
MCS.
2. Case report
2.1. History and examination
A 43-year-old right-handed man presented with a
severe spontaneous burning pain in his right hand, fore-
arm and right lower leg and foot, in addition to heavi-
ness and deep pressure-like pain in his right lower leg
including the foot. Two and a half years prior to admis-
sion, he fell from an electricity pole and sustained a
severe TBI. Initially, he was comatose as a result of an
acute subdural hematoma in his left convexity with mul-
tiple intracerebral contusions in his left temporal and
frontoparietal lobe, he underwent an emergency decom-
pressive craniectomy and an evacuation of the subdural
hematoma and intracerebral hemorrhagic contusion. He
was semicomatose after surgery and regained conscious-
ness over a 1-month period after the injury. However,
severe motor aphasia and a dense hemiplegia associated
with a hemisensory deficit developed. During the subse-
quent 6 months, he was taken to the rehabilitation unit.
His weakness progressively improved with active physi-
cal therapy, and finally he could stand and walk with
assistance.
Approximately 1 year after the accident, he could
walk by himself slowly with a cane and a short leg pros-
thesis. However, he was hesitant to perform active exer-
cise and finally refused to visit the rehabilitation unit.
His wife who had been caring for him finally disclosed
that he was suffering from a burning sensation and
heaviness in his right lower leg and his arm. Indeed,
he felt a gradually developing burning sensation in his
right foot 6 months after the injury, which ascended
slowly to the right upper leg, to the right inguinal area
during the following 6 months, and deep pressure-like
pain, heaviness, and crushing developed in his right
leg. Approximately, one year after the accident he began
to feel a burning pain in his right hand, which has
ascended to his right forearm, and another area of burn-
ing developed in his right lower back. He also felt a deep
pressure sensation in his right shoulder, which was
regarded as a type of musculoskeletal pain associated
with a frozen shoulder. Because of the progressive diffi-
culty in performing exercise and his withdrawal
response, he underwent a careful interview and sensory
211
examination. As a result, he was finally diagnosed with
a central pain following a TBI approximately 18 months
after the accident and 1 year after the development of
pain.
After the central pain had been diagnosed, the maxi-
mum medical treatment was provided for 3 months but,
his pain progressively worsened. The burning sensation
in his leg and arm was constant, and he experienced
an intermittent cramping pain. His pain was aggravated
as a result of exposure to cold temperatures, humidity,
and emotional upsets. During the 2 months prior to
referral, he could barely sleep at night, stroking his right
leg and right hand due to the severe heaviness and burn-
ing. His pain medication regimen at the time of referral
was as follows: gabapentin 2400 mg, paroxetine 20 mg,
tramadol 200 mg, trazodon 25 mg, oxycarbamazepine
600 mg, and amitryptyline 30 mg a day. At the time of
referral, his VAS was 75–85/100.
A physical examination showed that he had residual
motor weakness (grade 4/4) which was more severe in
the distal arm and leg. He showed a hemiplegic gait
and moderate rigidity in his arm and leg, he could walk
by himself slowly and carefully in a guarded fashion.
Hypesthesia to light touches in addition to pinprick
hypoalgesia, which was more severe in the painful areas,
was present on his right hemibody including face. In his
right arm and leg, i.e., the painful areas, there was
decreased thermal sensation, particularly cold. There
was a severe mechanical deep pressure allodynia in his
right leg and foot. However, no spontaneous paresthesia
and other types of mechanical allodynia, such as static,
dynamic, and cold allodynia were found. Fig. 1 shows
the distribution of his pain and sensory deficits. His
mentality was clear without confusion and disorienta-
tion. However, severe motor aphasia with stuttering
was noticed and his speech was difficult to understand.
He had difficulty in naming and showed some short-
term memory impairment. The magnetic resonance
imaging showed extensive damage to the left frontal,
temporal, insular, and parietal lobe (Fig. 2). Severe
encephalomalacic changes to the posterior part of inferi-
or frontal gyrus, were thought to be the cause of motor
aphasia.
2.2. Surgical procedure
An anatomical localization of the central sulcus was
performed using a three-dimensional image-guided nav-
igation system. After marking the course of the central
sulcus over the left convexity and the vertex, an approx-
imately 10-cm-long linear incision was carried out, and
an approximately 7-cm-diameter craniotomy was per-
formed under general anesthesia. The surgical procedure
performed in this patient was similar to those reported
previously (Nguyen et al., 1997; Katayama et al., 1998;
Tsubokawa and Katayama, 1998; Son et al., 2003).
212 B.C. Son et al. / Pain 123 (2006) 210–216
Fig. 1. Schematic diagram showing the distribution of central pain
after a TBI. The horizontally hatched areas indicate severe spontane-
ous burning pain. The obliquely hatched area shows heaviness and
pressure-like squeezing pain. Hypesthesia and hypoalgesia to a
pinprick were noted in the right side of the body including face.
We were unable to obtain an adequate motor contrac-
tion with direct cortical stimulation up to 18 mA used
to identify the neurophysiological somatotopy of the
precentral gyrus despite the discontinuation of the mus-
cle relaxant well before beginning the direct precentral
gyrus stimulation with a bipolar cortical stimulator.
Therefore, the location of the stimulating electrode
(Resume IIÒ, model 3587A, Medtronic Inc., Minneapo-
lis, MN) for the hand and forearm was determined
according to the anatomical imaging landmark indicat-
ing a motor hand area that was previously described
as a ‘hand knob’ (Yousry et al., 1997), and this electrode
was placed subdurally along the mediolateral somatoto-
py of the precentral gyrus because the overlying dura
mater was thickened as a result of previous trauma sur-
gery. Another electrode for stimulating the lower leg was
placed epidurally, parallel to the course of the superior
sagittal sinus, as recommended elsewhere (Fig. 3)
(Katayama et al., 1998; Tsubokawa and Katayama,
1998).
During the 7-day test stimulation period, significant
pain relief was observed when a 21 Hz, 210 ms,
0.8–1.2 V (‘‘0’’ negative, ‘‘3’’ positive, continuous mode)
for the forearm electrode and 30 Hz, 210 ms, 2.0–2.5 V
(‘‘0’’ negative, ‘‘2’’ positive, continuous mode) for the
leg and foot stimulation combinations were used.
During stimulation, a warm, vibrating paresthesia was
produced in his right hand, forearm, right lower trunk,
and his lower leg including the foot. Two pulse
generators (Itrel IIIÒ, model 7425, Medtronic Inc.,
Minneapolis, MN) were implanted in each side of the
upper chest after the induction of anesthesia (Fig. 3).
2.3. Results of pain relief
The level of stimulation was adjusted until satisfacto-
ry pain relief had been achieved by setting the electrodes
at 21–30 Hz, 210 ms, and 0.8–2.4 V. The post-stimula-
tion analgesic effect was estimated to last approximately
5 min, and a continuous mode of stimulation was deliv-
ered. Visual analogue scales, which were graduated from
0 to 100, were used to assess the extent of pain relief.
However, the McGill Pain Questionnaire could not be
assessed in this patient due to severe aphasia (Melzack,
1975). The effect of stimulation was evaluated preopera-
tively and 12 months post-operatively. The visual ana-
logue scale score improved 75–85 to 20–30 with
stimulation, and the spontaneous burning pain in the
right forearm, hand, and lower trunk improved by
90–95%. The burning pain, heaviness, and deep pres-
sure-like pain in his right leg improved by 70–80%.
However, the heaviness and deep pressure allodynia in
his foot improved by only 50%. The patient’s pain
changed minimally over the 12 months of follow up.
The shoulder pain previously believed to be a type of
musculoskeletal pain also improved and the range of
motion in his right shoulder increased much more with
the alleviation of pain, he could elevate his shoulder
again. An unwanted motor contraction and seizure
activity was not been observed. After 12 months of
stimulation, the patient’s medication was decreased to
900 mg gabapentin and 10 mg amitriptyline per day.
3. Discussion
Although head trauma had been reported to be a
cause of central pain, there are few reports on the
 B.C. Son et al. / Pain 123 (2006) 210–216 213

Fig. 2. Radiological findings showing the anatomical location of central pain following a TBI. (A) T1-weighted magnetic resonance image shows that
extensive damage to the insular cortex and perisylvian temporoparietal opercular areas. Note the severe loss of the insular cortex and the underlying
white matter, which interferes with the thalamocortical transfer of nociceptive information. (B) T1-weighted magnetic resonance image demonstrates
additional damage to the post-central gyrus and white matter in the parietal lobe.

occurrence of central pain after a TBI (Berthier et al.,
1988; Boivie, 1999; Yezierski, 2002). Until now, it
is uncertain why TBI causes central pain so rarely.
Fig. 3. Post-operative skull X-ray image showing the placement of the
two laminotomy electrodes in the left hemisphere. There are two
previous craniotomy sites on each side of the calvarium and a new
craniotomy for the placement of an electrode for motor cortex
stimulation.
However, it is possible that central pain itself is often
overlooked as a possibility in patients with a CNS disease
because of a lack of knowledge of its characteristics
(Boivie, 1999). This may cause puzzling symptoms when
several coexisting pains of an unusual nature exist. One
reason for the lack of knowledge of central pain is the
fact that relatively little systematic research has been
carried out on the clinical aspects of central pain. In
addition, the lack of experimental models for central
pain until recently hampered research into its mecha-
nisms (Boivie, 1999).
Burning pain and deep pressure-like pain in this
patient localized within the region of hypoesthesia and
he showed severe deficits in his ability to detect pain
and cold, as well as clear deficits in touch and proprio-
ception. Thus, this patient with central pain due to
TBI showed a clinical picture similar to CPSP. CPSP
patients generally have clear somatosensory deficits
and a paradoxical ongoing spontaneous pain that is felt
within the area of deficit. Central pain can be experi-
enced as superficial or deep pain, or both superficial
and deep components, but the high incidence of cutane-
ous hyperesthesias contributes to the impression that
superficial pain dominates, although deep pain is com-
mon too. In this particular patient, only mechanical
deep pressure allodynia was noted. In CPSP, cutaneous
hyperalgesia, allodynia, and/or hyperpathia are fre-
quently, but not invariably, present (Boivie and Leijon,
1991; Boivie, 1999). Recently, dissociation between cuta-
neous and deep sensibility in CPSP has been reported
(Mailis and Bennett, 2002).
Several areas of the brain, fronto-temporal and insu-
lar, and parietal lobes in this patient were severely dam-
aged (Fig. 2). Among them, the areas particularly
214 B.C. Son et al. / Pain 123 (2006) 210–216
related to the pathophysiology of central pain are the
insular and parietal lobes. The parietal or insular regions
have been shown to be associated with central pain
(Michel et al., 1990; Schmahmann and Leifer, 1992; Boi-
vie, 1999). Schmahmann and Leifer (1992) studied the
anatomic correlations in 6 patients with central pain as
a result of lesions of the parietal lobe, and reported that
the common area of involvement in their cases was the
white matter deep to both the caudal insula and the
opercular region of the posterior parietal cortex. They
suggested that a disruption of the interconnections
between these cerebral cortical areas (including the sec-
ond somatosensory representation, SII) and the thala-
mus, particularly the intralaminar and ventroposterior
nuclei, might be responsible for the occurrence of central
pain syndrome namely, parietal pseudothalamic pain
syndrome. The extensive area of damage to the insula
in this patient was consistent with those reported by
Schmahmann and Leifer (1992).
The middle/posterior insular cortex is known to be
the area where discriminative thermosensory sensation
is represented in humans (Craig et al., 2000). The func-
tional anatomy in monkeys indicates that a dedicated
thalamic nucleus relays the topographic, discriminative
thermoreceptive-specific, and nociceptive-specific lami-
na I spino- and trigeminospecific projections to the dor-
sal margin of the middle/posterior insular cortex (Craig
et al., 1994, 1999). Data from a PET imaging study of a
thermal grill illusion of pain and an fMRI study indicate
that a strong innocuous cool stimulation (20 °C) acti-
vates the contralateral insular cortex, but not the parie-
tal cortex (Craig et al., 1996; Davis et al., 1999). These
findings support the proposal that central pain results
from loss of the normal inhibition of pain by cold (Craig
et al., 1994, 2000), because the lesions involving the insu-
la can produce central pain (Schmahmann and Leifer,
1992).
The parietal opercular area including the SII was also
damaged in our patient (Fig. 2B). Lesions of the SII and
the insula produce asymbolia for pain, suggesting that
the SII is an important cortical locus for the conscious
perception of noxious stimuli (Biemond, 1956; Mesulam
and Mufson, 1985; Berthier et al., 1988). The anatomical
and electrophysiological data show that in monkeys,
these regions receive direct nociceptive input (Ploner
et al., 1999; Craig et al., 2000). Experimental and lesion
data in humans suggest these areas are associated with
the motivational-affective aspects of pain and the senso-
ry-discriminative components of pain perception (Vogt
et al., 1993; Craig et al., 1996; Rainville et al., 1997;
Ploner et al., 1999).
Although MCS has been proven to be a promising
treatment for various central and peripheral neuropath-
ic pain, the precise analgesic mechanism of MCS is still
unclear (Garcı́a-Larrea et al., 1997; Nguyen et al., 1997;
Katayama et al., 1998). Tsubokawa and Katayama
have suggested that MCS might produce an analgesic
effect through the orthodromic and/or antidromic acti-
vation of the fourth-order antinociceptive neurons,
which secondarily results in the inhibition of hyperac-
tive nociceptive cortical neurons, that restores the
inhibitory surrounding field around the restricted area
of excited neurons in the somatosensory cortex
(Tsubokawa et al., 1993). However, MCS has not been
shown to produce any significant cerebral blood flow
(CBF) changes in the parietal cortex, suggesting that
the sensory cortex is not the key structure (Peyron
et al., 1995; Garcı́a-Larrea et al., 1999; Nguyen et al.,
1999). On the other hand, positron emission tomogra-
phy (PET) studies suggest that the thalamus is an
important structure in the mediation of the functional
MCS effects, and MCS exerts its analgesic effect by
modulating the thalamic activity (Nguyen et al., 1999;
Son et al., 2003; Saitoh et al., 2004).
Studies on groups of patients with intractable pain
with various origins have confirmed the existence of sig-
nificant CBF increases during MCS in the lateral and
medial thalamus, anterior cingulate-orbitofrontal cortex
(BA32), the anterior insula-medial temporal lobe, and
the upper brainstem (Garcı́a-Larrea et al., 1997). The
thalamic area showing the most significant CBF changes
are the ventrolateral and ventroanterior nuclei, i.e., the
thalamic regions directly connected to the motor and
premotor cortices. However, these clinical and PET
studies could not explain how MCS relieves the CPSP,
which has a damaged thalamus, where the substrate
for the functioning MCS has already been destroyed
by the stroke.
Recently, Saitoh et al. (2004) showed in a patient with
CPSP that was caused by a thalamic hemorrhage that a
successful MCS induced a significant CBF increase in
the contralateral hemisphere (thalamus, gyrus rectus,
and superior frontal cortex) compared with the
stimulated one, suggesting that the efficacy of MCS
was mainly related to the increased synaptic activity in
the thalamus. As an explanation for the contralateral
thalamic activation, they suggested that the reorganiza-
tion of the major thalamic function to the contralateral
side and the contralateral thalamus in the dominant
hemisphere might play a more important role in their
particular patient. It has already been reported that
right post-stroke pain disappeared after an additional
contralateral left parietal lobe lesion (Helmchen et al.,
2002).
It is now known that only approximately 1/2 of the
pyramidal tract fibers, which are those constituting the
corticospinal tract itself, actually terminate in the spinal
cord (Wisendanger, 1969; Davidoff, 1990). Many pyra-
midal tract axons terminate in, or send collateral branch-
es to, a number of supraspinal structures that are
generally considered to be sensory in function (e.g.,
sensory and motor nuclei of the thalamus, trigeminal
 B.C. Son et al. / Pain 123 (2006) 210–216
nucleus, dorsal column nuclei, striatum, red nucleus,
pontine nuclei, midbrain and bulbar reticular formation,
and inferior olive) (Wisendanger, 1969; Armand, 1982).
Indeed, physiological studies indicate that the pyramidal
tract contains many fibers of a cortical origin that affect
the sensory input and somatosensory transmission at
each synaptic relay at both spinal and subcortical levels.
The pyramidal tract can be regarded as an internuncial
pathway intercalated between the subcortical structures,
the cortical structures, and the afferent inputs from the
peripheral sensory receptors and spinal motoneurons,
and provides a pathway for the corticofugal regulation
of various sensory relays. This control of the sensory
inflow into the central structures can influence the type
and amount of somesthetic and proprioceptive informa-
tion carried to both the sensory receiving cortex and the
association cortex (Davidoff, 1990).
4. Conclusion
Motor cortex stimulation was found to be effective in
this particular patient with central pain following a TBI.
As shown in our case, it is possible that doctors engaged
in the the treatment and rehabilitation of a TBI might
overlook the occurrence of central pain. Further
detailed studies will be needed to determine the patho-
genesis of central pain and the systematic analysis of
the prevalence of central pain after a TBI.
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