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Thalamic Pain Syndrome(Central Post-Stroke Pain) in a patientpresenting with right upper limb pain:a case report Jeffrey R Tuling, BSc, DC*Eldon Tunks, MD, FRCP(C)** In the elderly, pain of a widespread nature can often be Les douleurs irradiantes, chez les personnes âgées, debilitating. It is not uncommon to attribute this peuvent souvent devenir incapacitantes. Il est fréquent widespread pain to osteoarthritis within the spinal d’attribuer ce type de douleur à l’arthrose, qui touche les column structures and peripheral joints or to other structures de la colonne vertébrale et les articulations musculoskeletal etiology. However, chiropractors should périphériques, ou encore à une autre étiologie musculo- remain wary regarding pain experienced by the elderly, squelettique. Cependant, les chiropraticiens devraient se especially if pain is widespread and exhibits neuropathic montrer circonspects devant les cas de douleur chez les features. Common features of neuropathic pain involve personnes âgées, surtout si celle-ci couvre une grande the presence of allodynia, hyperpathia and hyperalgesia. région et présente des caractéristiques neurologiques. This characteristic widespread pain can sometimes be Les cas de douleur neurologique sont habituellement the sequelae of a central nervous system lesion such as a associés à la présence d’allodynie, d’hyperpathie et “Thalamic Pain Syndrome”, or “Central Post-Stroke d’hyperalgésie. Ce type de douleur irradiante peut Pain”, which are terms commonly used to describe pain parfois être une séquelle d’une lésion du système that originates in the central nervous system. nerveux central, comme le syndrome de douleur Following is the case of a 90-year-old patient thalamique ou la douleur post-accident vasculaire presenting with widespread pain attributed to Thalamic central. Ces termes sont couramment utilisés pour Pain Syndrome or Central Post-Stroke Pain. Discussion désigner une douleur qui trouve son origine dans le of the characteristics of neuropathic pain and bedside testing techniques are presented to help the chiropractor Voici le cas d’un patient de 90 ans qui souffre de identify a patient who may be presenting with Central douleur irradiante, attribuée au syndrome de douleur thalamique ou à une douleur post-accident vasculaire central. Suit une discussion sur les caractéristiques de ladouleur neurologique et une présentation des techniquesd’évaluation au chevet des patients, dont l’objectif estd’aider le chiropraticien à repérer les personnes pouvantprésenter une douleur post-accident vasculaire central.
(JACC 1999; 43(4):243–248) K E Y W O R D S : thalamic diseases, cerebrovascular M O T S C L É S : maladies thalamiques, complications ou disorders/complications, chiropractic, osteoarthritis, troubles cérébro-vasculaires, chiropratique, arthrose, * Delamere Chiropractic Clinic, 40 Delamere Avenue, Stratford, Ontario N5A 4Z5. Tel: (519) 271-2562.
** Professor of Psychiatry, McMaster University, Chronic Pain Management Unit, Chedoke Rehabilitation Services, Holbrook Building, Room 65, Hamilton Health Sciences Corporation, Chedoke Site, Box 2000, Hamilton, Ontario L8N 3Z5.
Address reprints and all correspondence to J. Tuling.
In partial fulfillment of residency requirements.
Introduction
Chief complaints
In the elderly, it is not uncommon to attribute widespread Pain radiated from the left side of the neck to the fingers of pain to osteoarthritis within the spinal column structures the left hand. The left arm felt “numb” or “dead” when she and peripheral joints. In other cases, malignant processes awoke in the morning, and the left upper back and arm or other less common pathologies are the causes of wide- were oversensitive to stimulation. She experienced occa- spread pain. Chiropractors should remain wary of wide- sional headaches that did not occur daily (the headaches spread pain experienced by a geriatric patient. Central Post-Stroke Pain is one possible cause of widespread painafter a cerebrovascular accident. Clinically this syndrome Mental status examination
can be accompanied by musculoskeletal allodynia, hyper- Mental status examination was conducted by a psychia- trist, (without psychometric testing), which revealed aeuthymic individual. Memory recall was intact throughout Case report
the course of the interview. She was able to organize and A 90-year-old lady presented to a chronic pain clinic with relate her symptoms without any signs of disorientation.
severe pain of the left neck and left upper limb. She wascomplaining that her arm felt “numb” and “dead” in the Physical examination
morning. She had been referred by a rheumatologist.
On postural examination, she presented with marked ante-rior translation of her head with sloped shoulders. Active Past history
neck rotation to the right and left was limited to about half In 1972 she had fractured her left humerus and recovered of the expected range due to pain. Lateral flexion of the without complication. In 1988, while in Florida, she had neck was markedly limited due to pain. She was very pro- developed congestive heart failure and had been admitted tective of her left shoulder due to pain.
to hospital. During that episode she developed widespread On musculoskeletal examination, the patient related pain affecting the left side of her body (a diagnosis of this that the pain radiated into the third and fourth fingers of the pain was not made at that time). Subsequently she had a left hand. Upper limb deep tendon reflexes were normal series of admissions to hospital for related conditions which and symmetrical, and motor strength was normal. Assess- included congestive failure, arrhythmia and NSAID-in- ing with light touch induced pronounced amounts of pain duced gastrointestinal bleeding and anemia. There had also within the region being tested (allodynia) in the area of the been an episode of stroke involving her left face and arm left side of the neck, left supraclavicular area and all areas which was treated clinically (which was not investigated of the left upper limb. Light prick induced an exaggerated with imaging). In 1997 she had been referred to the rheuma- amount of pain (hyperalgesia) on the left side, compared to tologist with lateral epicondylitis. She was prescribed splint a normal response on the right. Areas of hyperalgesia in- therapy and cortisone injections and ultimately responded cluded the left side of the face, the left supraclavicular well to these therapies. Despite this improvement, she had area, left arm, the front of the chest and the back down to continued to complain of the left-sided widespread pain, the beltline all on the left side. Hyperalgesia was not which prompted referral to the pain clinic.
present distal to the beltline. Scratching with a pin alongthe upper arm produced a persistent “pricking” sensation Recent treatment
in the hand (hyperpathia). Scratching on the left face pro- Recent treatment for the neck and upper limb pain in- duced radiating sensations of sharpness (hyperpathia) sur- cluded a surgical collar which was worn during the day, rounding the area being scratched, in contrast to a normal with a towel worn at night producing equivocal benefit.
response on the right (pain did not spread). Once the pain She attended physiotherapy for laser, ultrasound and trac- was “stirred-up” in the left upper body and extremity, it tion of the neck with no resolution of symptoms. Soft tis- persisted for over a minute. Hyperpathia was also present sue therapy utilizing a vibrating modality over the neck by pin-pricking and scratching the back, the shoulder and and upper back musculature, and heat application at night the front of the chest. These noxious stimuli aggravated the yielded no abatement in pain sensation.
pain and also referred pain to the left arm. It was also aggravated by a firm hand grip over the left arm or pain. Reflex sympathetic dystrophy was not a possibility, given the complete lack of neurovascular changes, dystro-phy, sweating, coolness, or visible changes in the distal Diagnostic imaging and laboratory work-up
limb. Postherpetic neuralgia of such a distribution would Recent radiographic examination of the left shoulder and require a history of typical lesions, and would be accompa- cervical spine revealed moderate osteoarthritis and degen- nied by depigmented scars, which were not present.
erative disc disease with no definitive bony encroachmentof the intervertebral foramina. A mild anterior compres- Discussion
sion fracture of the C6 vertebral body of long standing was Chiropractors should be vigilant regarding pain experi- noted. A bone scan investigation did not reveal the pres- enced by the elderly, especially if the pain is of a ence of metastases. However, increased uptake was noted widespread and diffuse nature and is accompanied by throughout the cervical, thoracic and lumbar spinal col- neuropathic features. In this case, the plain film radiogra- umns, shoulder joints, distal right ulna, hands, knee joints, phy and bone scan results can inappropriately lead one to ankle joints and feet. The increased uptake was consistent conclude that the pain is related solely to osteoarthritis. As with osteoarthritis. Blood work revealed a high erythro- a result, a diagnosis of “osteoarthritis only” could then be cyte sedimentation rate of 71 mm/hr.
There are three points that this case report illustrates.
Clinical impression
First, the above case illustrates the fact that a patient ini- The features of this pain were consistent with a neuro- tially suffering from musculoskeletal pain may have some pathic type pain most likely arising from a stroke incident.
underlying pathology other than or in combination with The widespread nature of the pain on the left side of the musculoskeletal pain at a later presentation. Second, pain body suggested “thalamic syndrome”.
of neuropathic origin may be evident on a musculoskeletalexamination and masquerade as musculoskeletal pain Differential diagnoses
(since all tissue subserved by the neuropathic afflicted area Other conditions were considered, and indeed had been will hurt). Third, one should complement a musculoskel- considered by the referring rheumatologist. The patient etal examination by conducting a neurological screening had an elevated ESR of 71 mm/hr but did not meet diag- examination that will help determine whether or not there nostic criteria for polymyalgia rheumatica; proximal mus- are characteristics indicative of neuropathic origin pain.
cular pain and morning stiffness/weakness. Additionally, Thalamic Pain Syndrome or Central Post-Stroke Pain is the pain was unilateral despite onset in 1988 (and as it a term that is in common currency to describe widespread turned out later, responded to a low dose of anticonvul- pain of central nervous system origin. However, thalamic sant). ESR is a screening test with false positives and pain is not always attributed to a lesion within the thalamus negatives, and increases with age, female sex, various and its nuclei. Sites of involvement can also include le- inflammatory conditions, and in anemia, and by itself is sions within the dorsal horn, ascending pathways of the not confirmation of systemic disease. Blood work did not spinal cord, brainstem, subcortical white matter and cer- support the probable diagnoses of bony metastatic disease ebral cortex.1 As a result, Central Post-Stroke Pain (CPSP) or liver, kidney, or hematological disease.
is also a commonly used term to describe pain of central Whole-body bone scan had demonstrated multiple up- origin arising from lesions of the central nervous system as take in cervical, thoracic and lumbar spinal columns, a result of cerebrovascular accidents.
shoulders, bases of metacarpals, distal right ulna, knees, Strokes afflicting the central nervous system are one of ankles, and both feet. The bone scan findings were inter- the most common causes of central pain, followed by mul- preted as due to osteoarthritis which was consistent with tiple sclerosis, spinal cord injuries, traumatic brain inju- the clinical findings, and inconsistent with rheumatoid ar- ries, syringomyelia, and other neurological disorders.2–11 thritis or bony metastatic diseases. However, osteoarthritis About 85% of all central post-stroke pain (CPSP) can be could not explain the specific localization of left upper attributed to infarcts.2 In a prospective study, the incidence body pain and sensitivity, nor the neuropathic quality of of central pain occurred in as many as 8% of all stroke patients during the first year after experiencing a stroke.
ties such as burning, aching, lancinating, pricking, lacerat- Within that group of stroke patients, 63% experienced pain ing and pressing are commonly reported.18 within one month after onset of the stroke.10 The preceding There are many hypotheses that are invoked to help investigators were not aware of any subjects that might explain CPSP. A commonly held theory is that central pain have resolved spontaneously. Additionally, the study did arises due to lesions within the medial lemniscal pathway.
This results in the prevention of this pathway from provid- In Canada the stroke incidence is estimated to be 138 ing tonic inhibition upon the spinothalamic projection per 100 000 people.12 In a Statistics Canada survey of resi- zones responsible for pain and temperature.2 dents in health care institutions, the prevalence of stroke However, many patients with central pain exhibit nor- was estimated to be 4% for those aged 65 or older living in mal tactile and vibration sensibility. As a result, it is households and 22% for those living in institutions.13 thought that lesions within the spinothalamic pathways are Within the stroke population, there are many possible usually crucial for the development of central pain.2,19–21 disabilities that can involve cognitive impairments, lan- There are many studies that support the hypothesis that the guage difficulties, motor deficits, emotional changes and spinothalamic deficit is a necessary prerequisite for central other related disturbances. It can easily be conceived that pain.10,21 However, this explanation is not entirely com- pain is often forgotten and overlooked by the relatives and plete. A deficit in this tract (indicated by a disturbance or physicians of these patients.14 Since strokes contribute to loss of thermal sensation), can be found in greater than half disability within industrialized countries, it is important to of stroke patients, however these same patients do not nec- determine whether patients are experiencing neurological essarily experience pain.10 As a result, it is difficult to difficulties associated with post-stroke pain.
predict the development of central pain syndrome based Patients experiencing cerebrovascular lesions from strokes can experience pain immediately after the event, or The hypothesis remaining is that central pain is not due experience a few years delay between stroke and onset of to a particular characteristic mechanism but a multifaceted pain.11,15 The pain experienced can develop initially as a phenomenon. There may be several mechanisms at work sensory disturbance and muscle weakness or impairment that may contribute to central pain. There may be plastic and can then improve.16 However, the pain may often re- changes to the spared sensory fibres, the secondary path- main permanently, with varying intensities.17 In a patient ways, and spinothalamic pathways. Alternatively, there with central post-stroke pain, there are many external and may also be a loss of specific mechanisms which are part internal events that can evoke pain for extended periods of of the inhibitory process for the central nociceptive sys- time. These events include cutaneous stimuli (wearing tems. These changes could lead to an alteration of central clothes), body movements (changes in body position, sensory nuclei that results in abnormal firing patterns (cen- walking, extremity movements), visceral stimuli (full rec- tral sensitization) which are interpreted as pain.2,21 tum or urinary bladder), loud noise, bright light, emotions At present, there is no pathognomonic quality of pain associated with a specific mechanism causing the central Additionally, the area of pain in CPSP patients is often pain. Additionally, central pain may present as either con- diffuse in location.2 Many stroke patients can exhibit ex- tinuous, paroxysmal and spontaneous, or as paroxysms tensive pain afflicting the whole left or right side of the abnormally evoked. The pain can also be described as su- body or a body quadrant such as the body on one side perficial and/or deep.18 In some cases, the common pri- except the face, or the arm and/or the leg on one side, or the mary feature accompanying pain is a partial or complete face on one side and the extremities on the other side, or loss of afferent sensory information with the additional exclusively the face.2 Pain can also be restricted to smaller presence of hyperalgesic and hyperpathic phenomena within the painful area. Some patients may exhibit gross There may also be several differing qualities of pain sensory deficits while others may exhibit subtle sensory exhibited simultaneously. A wide variation in quality of deficits.14 Sensory loss can involve all the sensibilities, pain is reported from patient to patient, even with those with the spinothalamic functions (cold, warmth, pinprick) patients sharing the same lesions and diagnosis.15 Quali- being the most common modalities that are impacted.15 However, a clinical sensory deficit is not a necessary ac- been recognized because of the coexisting musculoskel- companying feature for pain to occur after a stroke.22 etal and medical problems. A chiropractic resident in the There are several characteristics found in CPSP patients clinic participated in the clinical bedside examination exhibiting pain. Simple bed-side examination techniques which finally defined this neurological component. By can be utilized to elucidate these neuropathic characteris- recognizing the neurological component in the diagnosis, tics. A classic feature is the presence of abnormally it was possible for the attending physician to prescribe evoked pain known as allodynia.14,18 Allodynia refers to carbamazepine, an anticonvulsant which has properties of the evocation of pain through applications of non-noxious reducing neuropathic pain. Fortunately in this patient’s stimuli. Non-noxious stimuli may include light, mechani- case, this treatment was very effective against the pain.
cal or thermal (cold or heat) stimuli.14 The presence of Other pharmacological treatments which might have allodynia can be determined clinically by lightly stroking been considered for chronic post-stroke pain include other with your fingertips or by gently squeezing the patient’s anticonvulsants, such as amitriptyline, or mexiletine.
region of complaint.14,23 If allodynia is present, then the However, central neuropathic pains of such chronic dura- patient will experience abnormal amounts of pain within tion are more often incompletely responsive to pharmaco- logical treatment, and residual muscular aching and A second characteristic is the presence of hyperalgesia.
reduced function would be common sequelae. In such a Hyperalgesia is an exaggerated response to normally pain- case, management of the stiffness and aching and improv- ful stimuli.14 Hyperalgesia can be determined clinically ing spine and limb function, offer good opportunities for by applying pin strokes to the region of complaint.
the chiropractic clinician to provide further relief and cor- These pin strokes should cause some discomfort of pain. If rection of disability. The role of the chiropractor in correct an exaggerated amount of pain is experienced, then the diagnosis, alerting the family physician, continued chiro- area of complaint is considered to be hyperalgesic to pin practic support of the patient in a primary care role, and following up with application of musculoskeletal treat- A third characteristic is the presence of hyperpathia.
ment for residual discomfort, can benefit patients who Hyperpathia arises when explosive cutaneous pain is expe- might otherwise continue to suffer pain and dysfunction.
rienced locally (and possibly also radiated elsewhere in thebody) as a result of noxious or non-noxious stimuli.23,24 Conclusion
The presence of hyperpathia can be determined by repeat- Central post-stroke pain is present within the stroke popu- edly lightly tapping a cutaneous region with a pin in one lation. As members of the health care profession, it is in- spot. While testing the area of complaint, one should ask cumbent upon us to recognize the common features of the patient “Does the pain travel elsewhere?”, “Does the Central Post-Stroke Pain (CPSP). These features are iden- pain worsen over time?”, “Does the pain continue after I tified through patients’ past histories and other clinical stop touching you?”, “What do the sensations feel like?”.
features such as allodynia, hyperalgesia or hyperpathia If there is pain present and it travels distally or proximally, which are suggestive of central origin pain.
and/or the pain worsens over time (the “windup effect”), This case report has illustrated the fact that a patient and/or the pain continues after stimulation, then it is sug- initially suffering from musculoskeletal pain may present gestive that hyperpathia is present.23 Hyperpathic pain can with another painful disorder other than or in combination continue long after the stimuli have been discontinued.
with musculoskeletal pain, at a later time. Second, pain of These phenomena are indicative that a neuropathic neuropathic origin may be evident on musculoskeletal ex- process is occurring which involves the central nervous amination and masquerade as musculoskeletal pain since all tissue subserved by the neuropathic afflicted area willhurt. Finally, a neurological screening examination (im- Treatment
plementing the aforementioned bedside techniques) This patient had been referred to a medical specialist at a should always complement the musculoskeletal examina- pain clinic. Despite repeated hospitalizations and workups tion for widespread or diffuse pain, to elucidate whether over 10 years, the neuropathic factors in the pain had not the pain is of neuropathic origin or due to centralized pain.
Once pain of central origin is identified, appropriate 11 Riddoch G. The clinical features of central pain. Lancet care involving other health care professionals can then be 1938; i:1093–8;1150–6;1205–1209.
12 Gordon M. Monograph Series on Aging-related Diseases: initiated which will ultimately benefit the patient.
III. Stroke (Cerebrovascular Disease). Chronic Diseases inCanada 1993; 14(3):64–89.
References
13 The National Population Health Survey of Residents of 1 Tasker R. Pain resulting from central nervous system Health Care Institutions. Statistics Canada, 1995.
pathology (central pain). In: Bonica JJ, ed. The 14 Jensen TS, Lenz FA. Central post-stroke pain: a challenge management of Pain, 2nd ed. Philadelphia: Lea and for the scientist and the clinician. Pain 1995; 61:161–164.
15 Leijon G, Boivie J, Johannson I. Central post-stroke pain- 2 Boivie J. Central Pain Syndromes. In: Campbell JN (Ed.) neurological symptoms and pain characteristics. Pain Pain 1996 – An Updated Review. Seattle: IASP Press, 16 Bowsher D. Central pain: clinical and physiological 3 Osterberg A, Boivie J, Holmgren KA, Thuomas K-A, characteristics. J Neurol Neurosurg Psychiatry 1996; Johansson I. The clinical characteristic and sensory abnormalities of patients with central pain caused by 17 Schott GD. From thalamic syndrome to central post-stroke multiple sclerosis. Proceedings of the 7th World Congress pain. J Neurol Neurosurg and Psychiatry; 1996; of Pain. In: Gebhart GF, Hammond DL, Jensen TS, eds.
Progress in Pain Research Management. Vol 2. Seattle: 18 Boivie J. Central pain. In: Wall PD, Melzack R, eds.
Textook of pain, 3rd ed. New York: Churchill Livingstone, 4 Seddall PJ, Taylor D, Cousins MJ. Pain associated with spinal cord injury. Curr Opin Neurol 1995; 8:447–450.
19 Pagni CA. Central pain due to spinal cord and brainstem 5 Marshall J. Sensory disturbances in cortical wounds with damage. In: Wall PD, Melzack R, eds. Textbook of Pain, special reference to pain. J Neurol Neurosurg Psychiatry 2nd ed. Edinburgh: Churchill Livingstone 1989: 634–655.
20 Boivie J. Pain syndromes in patients with CNS lesions and 6 Gates P, Nayernouri T, Sengupta RP. Epileptic pain: a a comparison with nociceptive pain. In: Bromm B, temporal focus. J Neurol Neurosurg Psychiatry 1984; Desmeth JE, eds. Advances in Pain Research and Therapy, Vol. 22. New York: Raven Press, 1995: 367–375.
7 Schott GD. Pain in Parkinson’s disease. Pain 1985; 21 Boivie J, Leijon G, Johansson L. Central post-stroke pain – a study of the mechanism through analysis of the sensory 8 Newrick PG, Langton-Hewer R. Pain in motor neuron abnormalities. Pain 1989; 37:173–185.
disease. J Neurol Neurosurg Psychiatry 1985; 48:838–840.
22 Vestergaard K, Nielsen J, Andersen G et al. Sensory 9 Schurch B, Wichmann W, Rossier AB. Post-traumatic abnormalities in consecutive, unselected patients with syringomyelia (cystic myelopathy): a prospective study of central post-stroke pain. Pain 1995; 61:177–186.
449 patients with spinal cord injury. J Neurol Neurosurg 23 Tunks E. Personal Communication. 1998.
24 Jensen TS, Rasmussen P. Phantom pain and related 10 Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen phenomena in amputation. In: Wall PD, Melzack R, eds.
TS. Incidence of central post-stroke pain. Pain 1995; Textbook of Pain 3rd ed. New York: Churchill Livingstone

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