Introduction
A disorder that is singularly resistant to celiac plexus block
is chronic pancreatitis. This has been a puzzle to pain
management specialists for many years. Because the pain of
pancreatic carcinoma usually responds dramatically to
celiac plexus blockade, it would seem logical that chronic
pancreatitis should respond well. Oddly enough, patients
with chronic pancreatitis, no matter what the cause, usually
get no relief or very brief or partial relief from celiac plexus
block
14). Recent studies have demonstrated significant
involvement of dorsal column pathways in transmission of
visceral pain syndrome
3-5). Application of spinal cord
stimulation (SCS) for the neuropathic pain, such as failed
back surgery syndrome, angina pectoris, peripheral nerve
injury pain, causalgia, reflex sympathetic dystrophy have
been shown good outcome
3-5,7,8,16). In addition, spinal cord
stimulation suppresses visceral response to colon distension
in an animal model 3,12,13,16). Case series in the literature
report an effective outcome of SCS on intractable visceral
pain
3-5,16).
In this paper we present that SCS treatment could be the
alternative option for intractable visceral pain due to chronic
pancreatitis.
CASE REPORT
A 51 -year-old man presented with 3 years history of
abdominal pain with diffuse upper thoracic area. The
patient had a history of nonalcoholic chronic pancreatitis,
cholecystitis, multiple emergency room visits and repeated
hospitalization, including multiple abdominal work-ups,
endoscopic retrograde cholangiopancreatographies and
biliary internal stent insertion. Pain control could not be
achieved medically or by other interventional procedures.
Medications included intravenous injection of 10 mg of
morphine every 12 hrs, 60 mg of oxycontin peroral, intra-
venous injection of 50 mg of pethidine every 6 hrs, fentanyl
citrate patch, intravenous injection of 50 mg of tridol every
6 hrs, 370 mg of talniflumate (somalgen) every 8 hrs peroral
and 20 mg of amitriptyline. These drugs could not reduce
pain intensity sufficiently. Nerve block was performed twice
with no significant result. The patient suffered from squee-
• Received : December 17, 2008 •Revised : Februaty 11, 2009
• Accepted : August 4, 2009
• Address for reprints : Jung-Kyo Lee, M.D. Ph.D.
Department of Neurosurgery, Asan Medical Center, University of Ulsan
College of Medicine, 388-1 Pungnap 2-dong, Songpa-gu, Seoul
138-736, Korea
Tel : +82-2-3010-3553, Fax : +82-2-476-6738
E-mail :
[email protected]
online © ML Comm
zing epigastric pain that was either intermittent or conti-
nuous. Although these were treatment trials, pain scores
were displayed at 7 -10 point in VAS score. In Korean
McGill Pain Questionnaire, pain rating index (PRI) was
rated at 44/75 and present pain intensity score (PPI) was
rated at 5/5. Functional disability was rated at 45/70
according to Korean Brief Pain Inventory.
The relatively non-invasive and non-destructive method
is preferred as the first choice of pain treatment. Therefore,
he underwent a SCS trial with placement of a eight -
electrode percutaneous lead (Octrode lead, Advanced
Neuromodulation Systems, Plano, TX, USA) at the midline
of T7-8 level. The stimulation parameters were pulse width
of 500-microsec, amplitude of 2.3 mA and frequency of 60
Hz. During trial, the patient reported excellent coverage of
his usual pain and using temporal leads had excellent pain
control. In order to prevent migration of electrode, a surgical
permanent electrode (Lamitrode 88C Lead, Advanced
Neuromodulation Systems, Plano, TX, USA) was placed at
T6-8 after total laminectomy of T7 (Fig. 1). The patient
experienced a decrease in VAS scores for pain intensity,
amount of opioid consumed and other pain medications
intake. There was a gradual reduction in preoperative pain
medication intake. There was no considerable change in
the parameter during the follow-up period. Postoperative
medication included 30 mg of oxycontin at last follow up.
The patient was followed up for more than 14 months, and
he presented good outcome without complication. Pain
scores decreased, from 10/10 to 5/10 in VAS, from 44/75
to 36/75 in PRI and from 45/70 to 42/70 in functional
disability. He was a white-collar worker. He returned back
to his work without further hospitalization.
Discussion
The visceral pain is originated from damage or injury of
internal organ, such as thorax, abdomen and pelvis4,5,12,16).
Most cases cannot even be clearly explained the charac -
teristics of pain, which is considered to be deep, dull and
vague sensation. The visceral pain afferents receive the
signal through the sympathetic and parasympathetic
system, and the signal travels to the spinal cord and higher
cortical centers
3,5). The sympathetic pain pathway, which
carry nociceptive information in small fiber, can be blocked
by SCS
3,5,11).
However, recent evidence indicates that chronic visceral
pain may, in fact, not be nociceptive in nature, but a neuro-
pathic pain syndrome. As the treatment method of intrac-
table pain, SCS has been developed on basis of the gate
control theory
5,7-9,13,15). SCS has been employed for visceral
pain due to pancreatitis, endometriosis and irritable bowel
syndrome
3-5,16). The mechanism of pain relief by SCS still
remains unclear. However, the gate control theory of pain is
widely accepted among many mechanism theories.
According to this theory, cell associated with central trans-
mission of pain in DC is controlled by the afferent activity
of large-fiber or small-fiber in the peripheral nerve system
9).
This gate closes when an excess of large-fiber activity. The
other theoretical basis of mechanisms in SCS include
neural conduction blockade, activation of putative supras-
pinal pain centers, supraspinal or intraspinal sympathetic
blockade and release of putative neuromodulators
3,5-8,15).
DC lesion leads to decrease activation of thalamic and
gracile neurons by visceral stimuli and to prevent potentia-
tion of visceromotor reflex evoked by colorectal distention
under inflammatory conditions in animal model experi-
ments
3,12,13). Pain control through SCS may mediate direct
effects on DC lesion. Kapural et al. 3,4) reported one case
and 6 case -series published efficacy of SCS on various
visceral pains. Tiede et al.16) applied SCS on two visceral
pain patients and obtained good outcomes.
Nauta et al.10) suggested that punctate midline myelotomy
could control visceral pain. The theory is that there is an
ascending midline dorsal column visceral pain pathway in
humans and that its interruption may provide a way to
relieve midline visceral pain syndrome. The benefit was
probably derived not from the interruption of the crossing
spinothalamic fibers but from the coincidental damage to
the midline region of the dorsal columns
10). That benefit
could be regarded as a pain control mechanism of SCS for
visceral pain. Both procedures could reduce pain via inter-
ruption of the spinothalamic fibers, but punctate midline
myelotomy is an ablative procedure with the possibility of
J Korean Neurosurg Soc 46| August 2009
166
Fig. 1. Anteroposterior radiograph showing a surgical permanent electrode
(Lamitrode 88C Lead, Advanced Neuromodulation Systems, Plano, TX,
USA) at T6-8 after total laminectomy of T7.
moderate to severe complication. SCS is a less invasive
procedure with minimal complications.
Krames et al. 6) suggested that chronic pain of visceral
origin travels within the spinothalamic tracts and may be
amplified by the postsynaptic dorsal column pathways.
Thus, both procedures could be controlled at the spinal
cord level by SCS and explain the efficacy of SCS for
visceral painful disorder.
The incidence of chronic pancreatitis is reported to be
approximately 13-75 cases per 100,000 patients per year
1,2).
In Korea, the exact prevalence is not known, but it is on the
rise in Japan due to increased alcohol abuses. The charac-
teristic pain of chronic pancreatitis is recurrent or permanent,
and it leads to major socioeconomic problems such as
narcotic addiction, physical and emotional disability
1). In
chronic pancreatitis, causes of sustained pain can be visceral
inflammation, pancreatic ischemia, inflammatory injury to
the nerve sheaths, and pancreatic-independent mechanism
including plastic changes in the nervous system
1,2). This
pain has been difficult to be controlled medically or surgically
and hypogastric plexus block has shown long term effect of
only 10% patients
3,4). There are only two articles regarding
SCS treatment for chronic pancreatitis at present. The
largest study was reported by Khan et al.
5) with five clinical
cases. In this study, the target area was the T5-T6 level in
the midline according to the dermatomal distribution of
pain and its corresponding spinal levels. The pain relief for
all patients achieved more than 50% and reduction of 4-5
point in VAS scores was observed 6-8 months after SCS.
Kapural et al.
4) also presented the good outcome with
reduction of 7 point in one patient. Their target area was
same as Khan et al.
5) In our study, the patient was moni-
tored for more than 10 months and presented a reduction
of 4 point in VAS score without complication.
The most common complication of percutaneous SCS is
electrode migration (11.7-21.5%)
7,8,15). T o prevent migration
of electrode in percutaneous type, several methods were
attempted such as combination with the each type of
anchors such as short butterfly and long anchor and using
the brace for immobilization during 4-6 weeks after ope-
ration. In contrast to percutaneous lead, surgical leads have
technical advantages
17). North et al. 11) showed a broader
stimulation pattern and lower stimulation requirements of
surgical electrodes. Also, surgical electrodes appeared to be
associated with better long -term effectiveness. Other
complications that have been reported with following inci-
dences; hardware malfunction (8.1%), fractured electrode
(2.9-5.9%), subcutaneous hematoma (4.4%), infection (3.4-
3.9%), discomfort at the pulse generator site (1.2%), foreign
body reaction (1%), rotation of the pulse generator (0.7%),
cerebrospinal fluid leak (0.5%)
7,8,15).
Conclusion
We report the application of SCS for the treatment option
of intractable visceral pain. SCS can provide moderate pain
relief with improved quality of life and less consumption of
medication for patient with chronic pancreatitis.
References
1. Dimcevski G, Sami SA, Funch-Jensen P, Le Pera D, Valeriani M,
Arendt-Nielsen L, et al. : Pain in chronic pancreatitis : the role of
reorganization in the central nervous system. Gastroenterology 132:
1546-1556, 2007
2. Fregni F, Pascual-Leone A, Freedman SD : Pain in chronic pancreatitis :
a salutogenic mechanism or a maladaptive brain response? Pancrea-
tology 7: 411-422, 2007
3. Kapural L, Narouze SN, Janicki TI, Mekhail N : Spinal cord stimula-
tion is an effective treatment for the chronic intractable visceral pelvic
pain. Pain Med 7: 440-443, 2006
4. Kapural L, Rakic M : Spinal cord stimulation for chronic visceral pain
secondary to chronic non-alcoholic pancreatitis. J Clin Gastroenterol
42 : 750-751, 2008
5. Khan YN, Raza SS, Khan EA : Application of Spinal Cord Stimula-
tion for the Treatment of Abdominal Visceral Pain Syndromes : Case
Reports. Neuromodulation 8: 14-27, 2005
6. Krames ES, Foreman R : Spinal Cord Stimulation Modulates Visceral
Nociception and Hyperalgesia via the Spinothalamic Tracts and the
Postsynaptic Dorsal Column Pathways : A Literature Review and
Hypothesis. Neuromodulation 10: 224-237, 2007
7. Kumar K, Hunter G, Demeria D : Spinal cord stimulation in treatment
of chronic benign pain : challenges in treatment planning and present
status, a 22-year experience. Neurosurgery 58: 481-496; discussion
481-496, 2006
8. Lee AW, Pilitsis JG: Spinal cord stimulation : indications and outcomes.
Neurosurg Focus 21: E3, 2006
9. Melzack R, Wall PD : Pain mechanisms : a new theory. Science 150:
971-979, 1965
10. Nauta HJ, Soukup VM, Fabian RH, Lin JT, Grady JJ, Williams
CG, et al. : Punctate midline myelotomy for the relief of visceral cancer
pain. J Neurosurg (2 Suppl) 92: 125-130, 2000
11. North RB, Kidd DH, Olin JC, Sieracki JM : Spinal cord stimulation
electrode design : prospective, randomized, controlled trial comparing
percutaneous and laminectomy electrodes-part I : technical outcomes.
Neurosurgery 51: 381-389; discussion 389-390, 2002
12. Palecek J : The role of dorsal columns pathway in visceral pain.
Physiol Res 53 Suppl 1: S125-S130, 2004
13. Qin C, Lehew RT, Khan KA, Wienecke GM, Foreman RD : Spinal
cord stimulation modulates intraspinal colorectal visceroreceptive
transmission in rats. Neurosci Res 58: 58-66, 2007
14. Stacey B, colantonio A, Vookles JL, Sibell D, Kulawiak L : Manage-
ment of pain by anesthetic techniques, in Winn HR (ed) : Youmans
Neurological Surgery Fifth edition : Saunders, 2004, Vol 3, p 2983
15. Sundaraj SR, Johnstone C, Noore F, Wynn P, Castro M : Spinal cord
stimulation : a seven-year audit. J Clin Neurosci 12: 264-270, 2005
16. Tiede JM, Ghazi SM, Lamer TJ, Obray JB : The use of spinal cord
stimulation in refractory abdominal visceral pain: case reports and
literature review. Pain Pract 6: 197-202, 2006
17. Villavicencio AT, Leveque JC, Rubin L, Bulsara K, Gorecki JP :
Laminectomy versus percutaneous electrode placement for spinal cord
stimulation. Neurosurgery 46: 399-405; discussion 405-406, 2000
Spinal Cord Stimulation for Chronic Pancreatitis| JK Kim, et al.
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