International Journal of Osteopathic Medicine (2014) 17, 272e278

www.elsevier.com/ijos

CASE REPORT

A prodromal, musculoskeletal
presentation of Parkinsons disease:
A case report
Peter Simpson

British School of Osteopathy, London, UK

Received 14 November 2013; revised 15 March 2014; accepted 11 June 2014

KEYWORDS Abstract This is the case report of a 79-year-old female patient (Mrs X), referred for
Acromioclavicular; assessment and osteopathic treatment of her left shoulder pain and restricted range
Adhesive capsulitis; of motion. Seven months later Mrs X was diagnosed with left hemi Parkinsons disease
Diagnosis; (PD). The report reflects on whether or not the left shoulder signs and symptoms were
Evaluation; prodromal of PD, the diagnostic reasoning and evaluation of this patient prior to the
Glenohumeral; diagnosis of PD, the challenges to musculoskeletal practitioners associated with po-
Osteopathic; tential prodromal musculoskeletal presentations of PD and the prospect of increasing
Parkinsonism; numbers of such presentations with the projected rise in PD cases in years to come.
Parkinsons disease; 2014 Elsevier Ltd. All rights reserved.
Prodromal

Implications for clinical practice Introduction

 The report highlights the predicted increase
in prevalence of Parkinsons disease in the
next two decades.
 The report raises practitioner awareness of
Adhesive Capsulitis as a potential indicator of
Parkinsons disease.
 The report highlights the uncertainty inherent
in diagnosis of shoulder dysfunction in an
aging population particularly where known
orthopaedic diagnostic tests have limited
clinical applicability.
Parkinsons Disease (PD) is a progressive neurode-
generative condition resulting from the death of
the dopamine-generating cells of the substantia
nigra of the midbrain. Its onset is insidious and
sufferers classically present with the symptoms
and signs associated with Parkinsonism, namely
slowness of movement, rigidity and rest tremor.
The mean age of onset of PD is 65 years and it may
progress to cause significant disability and hand-
icap with impaired quality of life for the affected
person.1

E-mail addresses: simppete@googlemail.com, p.simpson@bso.ac.uk.

http://dx.doi.org/10.1016/j.ijosm.2014.06.001
1746-0689/ 2014 Elsevier Ltd. All rights reserved.
A prodromal, musculoskeletal presentation of Parkinsons disease
Prevalence estimates for the UK and Europe vary,
depending on the study population, between 121
and 200 per 100,000 persons.2,3 UK and European
incidence estimates vary between 12 and 26 per
100,000 persons.3 PD primarily affects the over
50s. Prevalence and incidence rates increase with
age4 and are highest over the age of 80.3 In
Western Europes five and the worlds ten most
populous nations the number of individuals over
50 with PD is projected to double to between 8.7
and 9.3 million by 2030.5
Musculoskeletal problems, mainly pain experi-
enced in the legs, back and shoulders,6 are
common in PD groups7e11 with a significantly
higher prevalence compared to matched con-
trols.12 A significantly higher incidence of a history
of shoulder complaints and adhesive capsulitis
was found in one PD population.13 Adhesive
capsulitis is one of the most common presenting
musculoskeletal conditions associated with PD7,14
and may be a presenting sign of the disease.13,15
One study revealed that 19 out of 320 patients
with PD were found to have a history consistent
with adhesive capsulitis prior to diagnosis of PD,16
the diagnosis of adhesive capsulitis being made
retrospectively using PD sufferers responses to
questions regarding their history of shoulder pain
and restricted movement rather than clinically.
Oversight of adhesive capsulitis as an early sign of PD
may lead to diagnostic confusion15 and unnecessary
diagnostic procedures whilst delaying the
treatment of PD symptoms contributing to poor
quality of life.16 From this viewpoint a patient
over 50 with a shoulder problem resembling
adhesive capsulitis represents a potential clinical
challenge to the osteopathic practitioner. This age
group is amongst the most likely to develop
adhesive capsulitis.14 In its early stages adhesive
capsulitis can appear clinically similar to a number
of other shoulder conditions14 and the adhesive
capsulitis presentation may be a prodromal
symptom of another disorder (e.g. PD)7,13e15 the
clinical signs of which have yet to manifest. Typical
symptoms of PD can be very subtle, hard to discern
and can take up to 2 years to develop.7,16
Conversely, early treatment of PD is contingent
upon early and accurate diagnosis of clinical fea-
tures and the experience of the practitioner.4
In the elderly female population prevalence of
shoulder pain is estimated between 18 and 23%,17
significantly greater than the prevalence of PD,
and the GP is likely to be the initial primary care
contact when a patient seeks help. The current
report presents the case of Mrs Xs where there
were no clinical signs of PD at the time of
presentation. The case history, signs and
273
symptoms were consistent with a musculoskeletal
presentation and her case was managed as such
pending any emergent evidence to the contrary
whilst in my care.
The osteopathic evaluation
Mrs X was referred with a preliminary diagnosis of
left adhesive capsulitis. An X-ray report from
March 2011 noted minor osteoarthritic changes to
the left acromioclavicular joint (ACJ) and degen-
erative changes in the lower cervical spine
(C4eC7). Mrs X is right handed. Her left shoulder
symptoms are presented in Table 1.
At 79 years of age, Mrs X was outside the expected
age range for adhesive capsulitis14,18 although her
symptoms were not unlike those of an inflamed joint
capsule. Minor osteoarthritic changes in the left
ACJ could have explained Mrs Xs symptoms but
radiographic findings are not considered reliable as
predictors of pain since many patients with
observable radiographic changes may be symptom
free.19,20 Mrs X may have had partial or full thickness
tears of the rotator cuff tendons since prevalence of
tendinopathy increases from 40 years onwards to as
much as 50% by the age of 60 years.21,22 Several of
Mrs Xs symptoms were consistent with those of ro-
tator cuff tendinopathy.23
The degenerative changes in the cervical spine
could also explain the shoulder symptoms as
degenerative cervical spondylosis is the
most common cause of cervical myelopathy.24
Symptoms of cervical myelopathy include shoul-
der and arm pain associated with muscle weak-
ness, numbness and paraesthesia depending on the
nerve(s) affected.24 However, in Mrs Xs case there
were no neurological symptoms.
The ageing effects on Mrs Xs musculature also
required consideration. Sarcopenia increases with
age25 and can affect over 50% of persons over 80
years of age.26 The main symptoms of sarcopenia
are weakness, leading to disability, lack of stamina
and frailty25 with risk factors being age, chronic
inflammation, atrophy of motor neurons secondary
to cervical spondylosis and immobility.27 However,
Mrs X remained active domestically, socially and
walked the dog regularly perhaps reducing the
likelihood of age related sarcopenia. At this point
in Mrs Xs evaluation I was not considering any
neurodegenerative diseases.
Clinical examination
The clinical examination findings are presented in
Table 2.
274
Table 1 Presenting shoulder symptoms.
Onset Symptoms Progression of
symptoms
Four months ago Pain and Worsening
No apparent limitation of
reason active
movement.
Burning pain,
dissipating over
several minutes,
in the shoulder
joint following
traction
Stiffness after
static postures
The findings regarding the ACJ were contradic-
tory. Pain was reproduced in the left shoulder
when Mrs X adducted her left arm from a flexed
position which suggests ACJ pathology.28 However,
no pain was elicited on palpation of the ACJ which
is a high sensitivity screen for ACJ pathology when
negative.28 The active and passive movement
findings for the glenohumeral (GH) joint were not
consistent with the capsular pattern of restriction
of the GH joint wherein external rotation is more
limited than abduction which is more limited than
internal rotation.29 Passive left GH ROM was
greater than active and less painful implying that
the dysfunction causing symptoms was located in
the periarticular structures rather than the GH
joint itself. If capsulitis were present, the active
and passive ROM would be expected to be equally
limited and equally painful.14 This was not the
case.
The restricted ROM in Mrs Xs left GH joint limited
the special tests that could be applied to evaluate
the rotator cuff tendons e.g., the Empty Can
test28,30 for supraspinatus. The HawkinseKennedy
test for sub-acromial impingement was feasible but
lacks specificity and could only be recommended as
a screening test for impingement in conjunction
with the Empty Can test.28,30
What, however, would be the clinical value of
evaluating individual muscles of the rotator cuff?
The likelihood, at Mrs Xs age, of degeneration,
partial and full thickness tears was high21,22 and
although the supraspinatus is more vulnerable,
particularly in the elderly,22 the likelihood of any
single muscle injury is small. Crepitus, evident on
passive articulation of the left GH joint, offered
some diagnostic insight into the degenerative sta-
tus of the rotator cuff but also lacked sensitivity
and specificity. Since only a small number of
P. Simpson
Aggravating Relieving factors Daily pattern
factors
Abduction Almost pain free Greater shoulder
Adduction from a when the arm stiffness more
flexed position was in a neutral difficult but not
Medial rotation position by her necessarily more
Lying on her left side painful, to move
side at night in the morning
Traction on the
arm when
walking the dog
Moving after
being static
clinical tests were feasible in Mrs Xs case, diag-
nosis relied on the few clinical findings and the
case history. Accuracy was therefore unlikely
although systematic reviews of shoulder assess-
ment tests inform us that few are diagnostic28,31 or
reliable,32 although some authors disagree.33 Had
further special testing been feasible it was likely
that any diagnosis may still have lacked accuracy.
During the case history, Mrs X had reported
some weakness in her left wrist and experienced
occasional difficulties gripping utensils which she
attributed to the colder weather. No apparent
weakness was elicited in the upper extremity C5,
6, 7, 8 and T1 myotomes using a modified Medical
Research Council (MRC) grading system34 which has
been shown to be reliable.35 In resisted isometric
muscle testing of shoulder flexors, extensors, ab-
ductors, adductors, medial and lateral rotators
with the arms in a neutral position, Mrs X scored 4
in both shoulders, according to the MRC grade
criteria, since she could move against gravity and
moderate resistance. There was no discernible
difference in power between the left and right
shoulders. Muscle tone appeared normal on pas-
sive movement of the upper extremities and the
deep tendon reflexes elicited were slight, pre-
sent36 and equal to the right. The finger nose test
of coordination was only possible on Mrs Xs right
side but appeared normal.
Diagnosis
Although adhesive capsulitis appeared less likely,
there was the probability of rotator cuff tendin-
opathy predisposed by her age, the presence of
inflammation,37 the shoulder girdle posture, sub-
acromial impingement,23 and degenerative
change in the GH and AC joints (again predisposed

Table 2 Clinical examination findings.
Postural observation
Thoracic spine and rib cage Moderate kyphosis
Structural thoracic scoliosis
concave R and rotated L
Left rib angles prominent
posteriorly
Scapulae Elevated on the left.
Protracted on the left (A
possible compensation for
the shape of the thorax?)
Acromioclavicular joints
(ACJ)
Cervical spine More approximated to the
scapula on the left side due
to the elevation of the
shoulder girdle and the
apparent incline of the
cervical spine to the left
Glenohumeral joints (GH) Positioned in external
rotation on the left
Anteriorised humeral head
Palpatory findings
A rigid feel.
No tender points
Left periscapular muscle tone
was generally elevated,
particularly the upper fibres
of trapezius (UFT) and levator
scapulae which was tender to
palpation around its insertion
into the superior angle of the
scapula
Elevated tone in the
infraspinatus and teres minor
muscles on the left
The rotator cuff and
periscapular muscles
appeared slightly atrophied
and felt thin and fibrous
bilaterally
No pain on palpation of the
left ACJ. No heat or swelling
in the left ACJ
Increased tone in the left
UFT, lower cervical erector
spinae, levator scapulae and
scalenii muscles
Left GH was not hot or
swollen
The left long head of biceps
was tender to palpate
A prodromal, musculoskeletal presentation of Parkinsons disease
Active movement Passive movement
examination examination
A general restriction to A general restriction to
motion motion
Limited in elevation and
retraction on the left. A likely
consequence of shortening in
the left pectoral musculature
and serratus anterior,
secondary to the thoracic
kypho-scoliosis
Reasonable movement. Pain
was reproduced in adduction
Limited in all ranges
No reproduction of left
shoulder symptoms
Left markedly limited by Passive range of movement
sub-acromial pain in was found to greater than the
Abduction 45e50 . Flexion active in all ranges
45e50 .
Medial rotation 50 Extension
15e20 Lateral rotation full
pain free
275
276
by age). Essentially, the posture and function of
Mrs Xs left shoulder were compromised and
her tissues were aged and less likely to repair
quickly.
Prognosis
Taking into account Mrs Xs age, tissue state and
degree of shoulder dysfunction it was difficult to
say, confidently, whether treatment might help
and, if so, how many would be required to achieve
an acceptable improvement in her ROM or a
reduction in pain. Anticipating such an explanation
Mrs X agreed to try four treatment sessions, with
some accompanying home exercises of gentle
traction and circumduction to improve synovial
fluid distribution in the joint,38 and review the
outcome after that time.
Treatment outcome
During April and May 2011, Mrs X reported a slow
improvement in her range of motion, a reduction
in pain and, although the exercises made her
shoulder a bit sore, she persevered with them.
An ultrasound (US) scan of the left shoulder
requested by the GP showed marked ACJ degen-
eration, subacromial bursitis and supraspinatus
tendonosis. Chronic capsulitis was diagnosed
given the thickening along the rotator interval
and the subacromial, subdeltoid and subscapularis
bursal thickening.
Following the scan, Mrs X opted to continue
with osteopathy rather than undergo a hydro-
distension and intra-articular steroid injection
procedure.
In early June 2011, after eight treatment ses-
sions plus exercises, Mrs Xs GH movement
appeared smoother with an objective increase in
her ROM. She was able to lift her arm to reach her
hair at the top and back of her head and reach up
behind her back without the assistance of the
other arm. Passive GH abduction, adduction in
flexion and scapular thoracic function were also
increased and provoked less pain.
The development of Parkinsons disease
At a follow up consultation in September 2011, Mrs
X complained of weakness in her left thumb. She
had become embarrassed about eating in restau-
rants because she could not, sufficiently, pierce
foodstuffs using a fork, especially meats, and
would often drop food. Squeezy ball exercises to
strengthen her hand had resulted in cramp so she
gave them up.
P. Simpson
She had been feeling generally unwell. She was
tired and her back, legs and arms hurt.
When she undressed she was having more diffi-
culty with buttons. Once undressed, it was clear
Mrs X had lost a lot of weight. She remarked that
she couldnt be bothered to eat sometimes! She
was also becoming more kyphotic and her lower
extremities, especially the left, had become
oedematous.
On examination, Mrs X had a very slight tremor
in both her hands at rest which was no longer
apparent when she moved her arm and hand. She
was able, on active movement of her left arm, to
put her left hand to her mouth demonstrating that
she was capable of that movement albeit slowly.
However, passive placement of the left arm into a
position mimicking that of eating revealed inter-
mittent resistance or rigidity. Her left upper ex-
tremity myotomes appeared weaker than her right
which represented a change since her last assess-
ment where power was equal. Reflexes were
unchanged in comparison to the previous assess-
ment. Her ability to coordinate hand eye move-
ments appeared unchanged but again her
movements appeared slow. Rapid alternate
movements of forearm pronation and supination
appeared slow suggesting dysdiadochokinesia. This
bradykinesia was apparent bilaterally but more
pronounced on the left. A negative Adsonsa test
indicated that a compromise of the neurovascular
supply at the thoracic outlet was unlikely but this
may not have been a reliable finding.39 Symptoms
in the arm were unaffected by cervical spine
movement.
Mrs X was referred, by her GP, to a neurologist
for further tests regarding her left arm and a
cardiologist for assessment of the lower extremity
oedema. The neurologist concluded that Mrs Xs
symptoms and clinical signs were indicative of a
diagnosis of left hemi Parkinsons without the
classical tremor but with bradykinesia and rigidity.
Reflections following Mrs Xs diagnosis of
Parkinsons disease
Whilst gratified that my neurological assessment
had been thorough and consistent with that of the
neurologist, could the bigger clinical picture of
PD been better constructed and arrived at sooner?
I had not observed Mrs Xs handwriting to comment
on any micrographia or noted any change in her
facial expressions, which at the time were not
mask like (Hypomimia)40 but I had observed her
tremor, her lack of dexterity which, at the time, I
viewed as a function of age, and her shuffling gait
which I had attributed to the osteoarthritis in her
A prodromal, musculoskeletal presentation of Parkinsons disease
hip joints and the developing oedema in her legs
and ankles.
I missed an opportunity to follow up on Mrs Xs
statement that she couldnt be bothered to eat
sometimes! when I had noticed her weight loss
on her follow up visit in September 2011. She
may have been having difficulty swallowing;
another sign of PD,40 or perhaps eating or pre-
paring food was becoming too difficult to manage
physically.
Had I been aware that adhesive capsulitis like
symptoms are a common prodromal presentation
of PD7,14 and that a kyphotica scoliotic posture, or
spinal deformity, is often associated with PD8 I may
have considered PD in my initial differential diag-
nosis. Mrs X had complained of wrist weakness in
the initial consultation but no objective sign of
weakness or upper motor neuron dysfunction was
elicited during peripheral neurological assessment
and had I included PD in my differential diagnosis I
may have been dissuaded from reasoning along
those lines based on my clinical findings. Had signs
of upper motor neuron dysfunction e.g. rigidity
been observed then an expedited diagnosis of PD
may have enabled Mrs X to access the appropriate
treatment sooner.15
Mrs X had had X-rays and an US scan confirming
what was clinically suspected regarding the
shoulder structures. These were requested by the
GP when the case was being managed as a
musculoskeletal problem. Following the imaging,
Mrs X elected to continue with osteopathy rather
than undergo a surgical procedure.
It could be argued that the imaging was unnec-
essary since her treatment management remained
unchanged. The imaging did not contribute toward
the diagnosis of PD and could be considered an
unnecessary intervention15,16 following the
wrong diagnostic route.15,16 However, imaging
did serve to confirm the presence of chronic
capsular thickening rather than adhesive capsulitis
and enabled Mrs X to make an informed decision
about her ongoing care whilst her case was being
managed as a musculoskeletal presentation.
Mrs X responded positively to osteopathic
treatment, an unlikely scenario if the symptoms
were prodromal of PD, and was extremely grateful
for the improvement in her functional capacity
irrespective of a lack of a tissue specific diagnosis
and the developing neurological deficit of PD.
It remains possible, because of Mrs Xs positive
response to osteopathic treatment before any
dopamine medication16 had been prescribed that
her shoulder symptoms were not prodromal of PD
and may have emerged irrespective of it and as a
consequence of her age.17
277
Conclusion
In conclusion, my advice to my fellow osteopathic
practitioners is to be aware of prodromal muscu-
loskeletal presentations in practice, in particular
with reference to PD which is likely to increase in
incidence and prevalence as the population in-
creases in age5 and be vigilant toward emergent
signs and symptoms in your patients.
Author contribution statement
This work was originally drafted by me as an original
case presentation for my M.Sc. The conception,
design, drafting of the manuscript and revision is
all my own work. There were no other parties
involved.
I give my approval to the final version of the
manuscript submitted for consideration to publish.
Acknowledgements
I would like to thank my M.Sc. course supervisor,
Ms Shireen Ismail, for her encouragement to sub-
mit this manuscript and for her proof reading.
Thanks also to the British School of Osteopathy
for their support in my academic development.
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