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Pages243-248
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 beLes douleurs irradiantes, chez les personnes âgées,debilitating. It is not uncommon to attribute thispeuvent souvent devenir incapacitantes. Il est fréquentwidespread pain to osteoarthritis within the spinald’attribuer ce type de douleur à l’arthrose, qui touche lescolumn structures and peripheral joints or to otherstructures de la colonne vertébrale et les articulationsmusculoskeletal etiology. However, chiropractors shouldpériphériques, ou encore à une autre étiologie musculo-remain wary regarding pain experienced by the elderly,squelettique. Cependant, les chiropraticiens devraient seespecially if pain is widespread and exhibits neuropathicmontrer circonspects devant les cas de douleur chez lesfeatures. Common features of neuropathic pain involvepersonnes âgées, surtout si celle-ci couvre une grandethe presence of allodynia, hyperpathia and hyperalgesia.région et présente des caractéristiques neurologiques.This characteristic widespread pain can sometimes beLes cas de douleur neurologique sont habituellementthe sequelae of a central nervous system lesion such as aassociés à la présence d’allodynie, d’hyperpathie et“Thalamic Pain Syndrome”, or “Central Post-Stroked’hyperalgésie. Ce type de douleur irradiante peutPain”, which are terms commonly used to describe painparfois être une séquelle d’une lésion du systèmethat originates in the central nervous system.nerveux central, comme le syndrome de douleurFollowing is the case of a 90-year-old patientthalamique ou la douleur post-accident vasculairepresenting with widespread pain attributed to Thalamiccentral. Ces termes sont couramment utilisés pourPain Syndrome or Central Post-Stroke Pain. Discussiondésigner une douleur qui trouve son origine dans leof the characteristics of neuropathic pain and bedsidetesting techniques are presented to help the chiropractorVoici le cas d’un patient de 90 ans qui souffre deidentify a patient who may be presenting with Centraldouleur irradiante, attribuée au syndrome de douleurthalamique ou à une douleur post-accident vasculairecentral. 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:
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III. Stroke (Cerebrovascular Disease). Chronic Diseases inCanada 1993; 14(3):64–89. References
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1 Tasker R. Pain resulting from central nervous system
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