This document contains a written report on Fibromyalgia, Bell's Palsy, and Parkinson's Disease submitted by a physical therapy intern. For Fibromyalgia, it provides definitions, characteristics, prevalence, diagnostic criteria, contributing factors, and management approaches. For Bell's Palsy, it describes the anatomy of the facial nerve, signs and symptoms, prognosis, and physical therapy management. For Parkinson's Disease, it outlines the anatomy of the basal ganglia and striatal motor system involved.

1. Davao Doctors College
Gen. Malvar St. Davao City 8000
PHYSICAL THERAPY DEPARTMENT
A WRITTEN REPORT ON
FIBROMYALGIA,
BELL'S PALSY and
PARKINSON'S DISEASE
Submitted by:
ARTEMIO L. GORDONAS, JR.
DDC PT- Intern '14
Submitted to:
Mindanao Orthopedic, Sports and Rehabilitation Clinic
-NOVEMBER 2013-

2. FIBROMYALGIA
Is now recognized as one of many central pain-related syndromes that are common in
the general population. Research advances have lead to the conclusion that disturbances
within the central nervous system (CNS) known as central sensitization represent the most
likely source.
Fibromyalgia, as defined by the American College of Rheumatology, is a chronic
condition characterized by widespread pain that covers half the body (right or left half, upper
or lower half) and has lasted for more than 3 months. Additional symptoms include 11 of 18
tender points at specific sites throughout the body nonrestorative sleep, and morning
stiffness. A final common problem is fatigue with subsequent diminished exercise tolerance.
Over the last two decades, rheumatologists generally have adopted a redefinition of
fibrositis. In 1981, Smythe, who initiated this redefinition, listed his updated diagnostic criteria
for fibrositis: (1) Widespread aching of more than 3 months duration; (2) local tender-ness at
12 or more of 14 specific sites; (3) skin-roll tender-ness over the upper scapular region; and
(4) disturbed sleep with morning fatigue and stiffness. ( David G. Simons, M.D. UST- Hospital
Manila)
Characteristics of FM
The characteristics of FM include the following.
➢ The first symptoms of FM can occur at any age but usually appear during early to
middle adulthood.
➢ For more than 30% of those diagnosed, the symptoms develop after physical trauma
such as a motor vehicle accident or a viral infection.
➢ Although the symptoms vary from individual to individual, there are several hallmark
complaints. Pain is usually described as muscular in origin and is predominantly
reported to be in the scapula, head, neck, chest, and low back.
➢ Another common report is a significant fluctuation in symptoms. Some days an
individual may be pain-free, whereas other days the pain is markedly increased. Most
individuals report that when they are in a cycle where the symptoms are diminished
they try to do as much as possible. This is usually followed by several days of
worsening symptoms and an inability to carry out their normal daily activities. This is

3. often the response to exercise.
➢ Individuals with FM have a higher incidence of tendonitis, headaches, irritable bowel,
temporal mandibular joint dysfunction, restless leg syndrome, mitral valve prolapse,
anxiety, depression, and memory problems.
Contributing Factors to a Flare
Although FM is a noninflammatory, nondegenerative, nonprogressive disorder, several factors
may affect the severity of symptoms. These factors include environmental stresses, physical
stresses, and emotional stresses. FM is not caused by these various stresses, but it is
aggravated by them.
➢ Environmental stresses include weather changes, especially significant changes in
barometric pressure, cold, dampness, fog, and rain. An additional environmental stress
is fluorescent lights.
➢ Physical stresses include repetitive activities, such as typing, playing piano,
vacuuming; prolonged periods of sitting and/or standing; and working rotating shifts.
➢ Emotional stresses are any normal life stresses.
Prevalence
The prevalence of fibromyalgia ranges from 2-6% of the population. Fibromyalgia is more
prevalent among women and the vast majority of those with fibromyalgia are women. Below
are the prevalence and percentage of fibromyalgia patients distributed between the sexes:
Prevalence:
Women (3.4%)
Men(0.5%)
Percentage of Fibromyalgia Patients: Women (75-90%) Men (10-25)
Although most diagnoses of fibromyalgia are made during middle-age, prevalence of the
disorder increases with age.
Characteristics/Clinical Presentation
Those with fibromyalgia can present with a host of symptoms that can make diagnosing the
disorder difficult. Below is an extensive but not exclusive list of common patient symptoms
and presentations created from several sources:

4. •Morning stiffness
•Tingling or numbness in hands and feet
•Headaches, migraines
•Constipation, diarrhea
•Thinking and memory abnormalities (“fibro fog”)
•Painful menstrual periods
•Fatigue
•Trouble sleeping
•Jaw Pain
•Abnormal muscle pain and malaise after exercise
•Dizziness or lightheadedness
•Skin and chemical sensitivities
•Deep, aching, throbbing, shooting, radiating, stabbing pain
•Non-cardiac chest pain, heart palpitations, shortness of air, profuse sweating
•Feeling of swollen extremities
•Sensitivities to all the senses (loud noises, bright lights, some foods, odors, etc…)
Systemic Involvement
Fibromyalgia has the potential to involve several systems as mentioned previously under the.
Characteristics/Clinical Presentation section. Fibromyalgia may involve any or all of the
following systems:
•Musculoskeletal
•Urogenital
•Gastrointestinal
•Neurological/Cognitive
•Immune
Diagnostic Tests/Lab Tests/Lab Values
A diagnosis of fibromyalgia is generally made based upon the results of a physical
examination and ruling out other similar conditions. It takes an average of 5 years from the
time a person begins experiencing symptoms to the time they are diagnosed with

5. fibromyalgia.First, a candidate for the diagnosis has to be diagnosed with chronic pain.
Chronic pain is described as pain that lasts for at least three months, pain that is both above
and below the waist and pain that is present on both sides of the body.
The introduction of the American College of Rheumatology (ACR) fibromyalgia
classification criteria 20 years ago began an era of increased recognition of the syndrome.
The criteria required tenderness on pressure (tender points) in at least 11 of 18 specified sites
and the presence of widespread pain for diagnosis. Widespread pain was defined as axial
pain, left- and right-sided pain, and upper and lower segment pain.
Similarities and differences between Fibromyalgia and Myofascial Pain Syndrome
FIBROMYALGIA
MYOFASCIAL PAIN SYNDROME
Similarities
✔ Pain in muscles
✔ Decreased ROM
✔ Postural stresses
Differences
✗
Tender points
✗
Trigger points on muscles
✗
Poor sleep
✗
Referred patterns of pain
✗
No referred patterns of pain
✗
Tight band of muscle
✗
Fatigue
Management—Fibromyalgia
Research supports the use of exercise, particularly aerobic exercise, to reduce the most
common symptoms associated with FM.
In addition to exercise, interventions include:
➢ Prescription medication
➢ Over-the-counter medication
➢ Instruction in pacing activities, in an attempt to avoid fluctuations in symptoms
➢ Avoidance of stress factors
➢ Decreasing alcohol and caffeine consumption
➢ Diet modification

6. BELL'S PALSY
Other names of Bell's palsy:
1. idiopathic facial paralysis
2. peripheral facial paralysis
3. refrigeration palsy
4. prosoplegia
DEFINITION: a facial paralysis of acute onset presumed to be due to a non-suppurative
inflammation of unknown etiology of the facial nerve within its canal above the stylomastoid
foramen.
Anatomy
COMPONENT
PRIMARY CELL
COURSE
PERIPHERAL
BODY
Brachial motor
TERMINATION
Facial nucles
Temporal bone facial Muscles of expression
side
Visceral motor
Superior
hyoid elevators
salivary a. greater superficial a. glands of nose,
nucleus
petrosal
to palate, lacrimal
sphenopalatine
b. submaxillary and
ganglion
sublingual glands
b. chorda tympani to
submaxillary ganglion
Visceral sensory
Geniculate ganglion
Internal
acoustic Anterior taste buds
meatus
INCIDENCE
 75% of lesions of the facial nerve fall into category of Bell's palsy
 occurs at all times of the year
 occurs at all ages but most frequent in young adults.
 Male>F

7. ETIOLOGY
It is due to an acute inflammation and edema involving the nerve within its canal. It
may be caused by any of the following:
1. exposure to cold and chill
2. secondary to viral infection (herpes simplex, herpes zoster)
3. Rubella infection
4. Diabetes
5. acute respiratory tract infection
6. tumor which invade the temporal bone
7. fractures of the temporal bone
8. lymphocytes-mediated hypersensitivity phenomenon
9. middle ear infection
10. meningits
11. hemorrhage
12. infectious disease
13. middle ear surgery
Theories regarding the cause:
1.
hereditary – due to the size of the diameter of the facial canal
2.
vascular ischemic theory
3.
viral theory
Pathogenic Process
From the course of the illness, it is presumed that the acute non-suppurative
inflammation of unknown etiology cause swelling and / or edema and hyperemia of the
sheath, with compression of the axons in the narrow facial canal, ths strangulating them.
Onset
Within a day or two after exposure, they may be slight fever, pain behind the ear, and
pain and stiffness in the neck. The onset is sudden or acute, and often, the patient awakens
to find the face paralyzed. A feeling of stiffness and numbness but sensory testing is normal.
About ½ of the cases attain maximum paralysis in 48 hours and practically all cases in 5
days.

8. Signs and Symptoms
These depends upon the location of the lesion:
A. Lesion 1. Outside the stylomastoid foramen. As it is LMNL, the muscles of both lower and
upper part of the ipsilateral face are involved in aflaccid paralysis forehead cannot be
wrinkled.
1.
widened palpebral fissure due to paralysis of the orbicularis palpebrum
2.
upper eyelid closes slowly due to pull of gravity
3.
Bell's phenomenon – the eyeball rotates upward and outward when attempting to close
the eye
4.
blink or corneal reflex is lost in the ipsilateral side
5.
oculogyric auricular reflex is lost in the ipsilateral side.
6.
Tear's are roll down the cheek
7.
obliterated nasolabial fold, unwrinkled brow, angle of the mouth sags and the side of
the face is expressionless.
8.
Mouth is drawn to the opposite side
9.
saliva may dribble from the mouth and food gathers between the cheeks and the gums
10.
Paralyzed lip may give an asymmetric appearance and push the tongue to the
opposite side
11.
atrophy is present, although rarely apparent because muscle bulk is small
12.
electrical reaction of degeneration appears in 10-14 days, depends upon the extent of
damage.
B. Lesion 2. In facial canal involving the chorda tympani, all signs of lesion 1 are present as
well as:
1.
loss of taste in the anterior 2/3 of tongue
2.
reduced salivation on the affected side. This is because the preganglionic
parasympathetic secreto-motor innervation of the sublingual and maxillary glands enter the
chorda tympani before finally ending in the maxillary ganglion
C.
Lesion 3. Higher is the fascial canal involving the stapedius muscle. Plus all signs of
lesion 1 and 2.
Hyperacusis – painful sensitivity to loud sounds; increased acuity of hearing

9. D.
Lesion 4. Higher involving the geniculate ganglion. Plus all signs of lesion 1,2 and 3
–
pain behind and within the ear
–
herpes of the tympanum and concha may precede the palsy
Ramsay hunt syndrome – Bell's palsy associated with herpes zoster of the geniculate
ganglion; facial paralysis and ipsilateral deafness.
E. Lesion 5. In the internal auditory meatus. Plus all signs of lesions 1-4.
Lesion will present:
1.
signs of Bell's palsy
2.
deafness (CN 8 involvement)
3.
tinnitus
4.
defective vestibular response
F. Lesion 6. At the emergence of the facial nerve from the pons.
–
involvement of CN 5 & 8
–
may also involve CN 6, 11 & 12
1. Marcus-Gunn or jaw winking phenomenon- seen in congenital ptosis; is the elevation of a
ptotic eyelid on movement of the jaw to the contralateral side.
2. Marin Amat Syndrome- observed after peripheral facial paralysis; referred to as an inverted
Marcus Mann; closure of the eye occurs when the patient opens the mouth forcefully &
maximally
POINT OF COMPARISON
Bell's palsy
ETIOLOGY
Unknown
Central palsy paralysis
CVA,
tumors,
vascular
lesions, UMNL
UMNL/LMNL
LMNL
UMNL
TYPES OF LESION
Peripheral or nuclear
Central or supernuclear
DISTRIBUTION
One side, ipsilateral
One side, contralateral
PARALYSIS
Upper and lower quadrant
Lower quadrant
NERVE AFFECTED
Facial nerve
No specific nerve
SKIN CONDITION
Dry
dry

10. Prognosis:
–
depends on the severity of the lesion
–
total actual deficit may not be determined for about 7 to 10 days because damaged
fibers may conduct during the process of degeneration, and undestroyed fibers may not
function temporarily.
–
Spontaneous recovery may take place in mild cases
Good prognostic signs:
1.
recovery of taste in the first week
2.
incomplete paralysis in the first 5 to 7 days- most favorable prognostic sign
3.
if within after a few days after onset, EMG shows there are motor units under voluntary
control in the facial muscles and if facial nerve conduction remains normal or only slightly
slow.
4.
Return of voluntary motor power at the end of 3 weeks from onset.
Poor prognostic signs or with patients are high risk of not recovering completely:
1.
age greater than 60 years old
2.
hypertension
3.
diabetes mellitus
4.
hyperacusis
5.
diminished lacrimation
Recovery
–
taste precedes recovery of motor function
–
electrical reaction of degeneration taken after 10 days indicates the time required for
recovery usual order of return of fucntion.
1.
buccinator
2.
zygomatic
3.
inferior levator
4.
orbicularis oculi
5.
frontalis

11. Complications
1.
contracture or state of overtoning
2.
synkinesis or associated movements – attempt to move one group of facial muscle
results in contraction of all.
3.
Crocodile tears- unilateral lacrimation on eating
4.
Hemifacial spasm- may be due to irritative facial nerve; usually begins orbicularis oculi
PT MANAGEMENT
1.
infrared rays
2.
electrical stimulation
3.
facial massage
4.
facial exercise
5.
taping

12. PARKINSON'S DISEASE
Anatomy
I.
Basal ganglia- consist of subcortical nuclei (gray matter) located within the cerebral
hemisphere.
A. components
1. caudate nucleus
2. putamen
3. globus pallidus
4. amygdala
5. claustrum
B. groupings of the basal ganglia
1.
striatum (neostriatum) – consists of the caudate nucleus and the putamen which are
similar in structure and connections ad have common embryological origin.
2.
lentiform nucleus – consists of the putamen and globus pallidus
3.
corpus striatum – consists of the lentiform nucleus and the caudare nucleus.
II.
Striatal motor system

a.k.a extrapyramidal motor systematic

plays a role in the initiation and execution of somatic motor activity, especially voluntary
movements

involved in automatic stereotyped motor activity of a postural and reflex nature

exerts its influence on motor activities via the thalamus, motor, cortex, coticobulbar and
conticospinal systems
A. component of striatal system

consists of the following nuclei
1. striatum (caudatoputamen or neostriatum)
a. caudate nucleus
b. putamen
2. globus pallidus (pallidum or paleostriatum)
a. medial (internal) segment - adjacent to the internal capsule

13. b. lateral (external) segment – adjacent to the putamen
3. subthalamus
a. zone incerta
b. Forel's tegmental field H
c. Subthalamic nucleus
4.
thalamus
a. ventral anterior nucleus
b. ventral lateral nucleus
c. centromedian nucleus / intralaminar nucleus
5.
substantia nigra
a. pars compacta- contains dopaminergic neurons which contain the pigment melanin
b. pars reticularis- contains GABA-ergic neurons
6.
pedunculopontine tegmental nucleus- lies in the lateral tegmentum of the caudal
midbrain.
B. major connection of the striatal system
1.
striatum- receives its largest input from the neocortex, from virtually all neocortical
areas
2.
globus pallidus- receives input from the striatum & subthalamic nucles
3.
Subthalamic nucleus- receives input from the globus pallidus and the motor cortex
4.
thalamus
- input to the thalamus
a. globus pallidus
b. substantia nigra
5.
substantia nigra- receives input from striatum
6.
pedunculopontine tegmental nucleus- receives input from globus pallidus
C.
Major neurotransmitter of the neurons of the striatal system
1.
glutamate-containing neurons – project from the cerebral cortex to the striatum; from
subthalamic nucleus to the globus pallidus; excite striatal GABA-ergic and cholinergic

14. neurons.
2.
GABA (gamma-amino-butyric acid) – containing neuro
- predominant neurons of the striatal system
- degenerate in “Huntingtons's disease”
3.
dopamine (DA) – containing nucleus
- local circuit neurons in the striatum
4.
neuropeptide-containing neurons
-includes enkephalin, dynorphin, subtance P, somatostain, neurotensin, neuropeptide Y and
cholectystokinin
-also found in the basal ganglia
DEFINITION: It is progressive degenerative disease of the extrapyramidal system (basal
ganglia and its related structures) that is caused by decrease in dopamine.
Incidence
 onset of the disease is usually between 50-60 y/o but may occur as early as 20-40 y/o
 peak onset: 6th decade of life
 mean age of onset: 58-60 y/o
 M F 3:2 ratio
 ranks 3rd behind CVA & arthritis as the most common disease pf late adulthood
Etiology
3 groups
1. idiopathic parkinsonism
- most common
-M=F
- unknown etiology
-theories: 1. premature or accelerated aging; 2. metabolic defect
2. secondary / acquired parkinsonisim
-may be caused by:
a. use of drugs: (Reserpine- depletes DA stored in the striatum, Neuroleptics- blocks
post-synaptic dopamine receptors; Metodopramide; Tetrabenazine

15. b. toxins – Mn, CO
c. postencephalitis- rarely seen today
d. vascular lesion – caused by infarction or trauma to the head (e.g. as in boxers)
3. parkinson's plus
- a group of multi-system degenerative diseases that exhibits signs of parkinson's
disease along with other neurologic deficits.
-may occur in association with:
a. Supranuclear palsy
b. Olivopontocerebellar palsy
c. Shy-Drager syndrome – type of PD associated with hypotension, fainting and urinary
incontinence.
PATHOLOGY
1. There is loss of pigmented cells in the substantia nigra (zona compacta) which are
responsible for the production of dopamine.
2. Degeneration of the nigrostriatal pathway
3. Microscopically, there is the presence of neuronal dropout and gliosis, Lewy bodies
(appears as an unusual cytoplasmic inclusion)
4. Loss of dopamine causes an alternation in the relation of dopamine with the other
neurotransmitter.
Signs and Symptoms
1. Tremors
 most common symptoms
 affects 2/3 of the cases
 3-6 Hz; 4-7 oscillations / second; resting type; “pill-rolling”
 suppressed by activity
 enhanced by fatigue, stress, excitement or even movement of the opposite limb
 loss of DA lead to loss of inhibition to the striatal cholinergic system,allowing
excessive excitation to the oscillatory loops in the thalamocortical system.
 EMG shows ryhthmic alternating bursts in both the agonist & antagonist muscle

16. 2. Rigidity
Types:
▪ Leadpipe - (+) resistance to passive movement of both the extensor and flexor muscle
groups throughout the range of motion.
▪ Cogwheel – alternating give and resistance
3. Bradykinesia
 slowness of movement
 reduction of the rotatory component of movement results in one plane of motion
 accounts for many disabling characteristic of PD:
a. masked faces – expressionless face
b. staring expression – due to loss of blinking; 5-10 blink/min (normal: 20blink/min)
c. slight widening of the palpebral fissures (Stelwag sign)
d. decrease swallowing- drooling (e.g. sialorrhea)
e. micrographia- small cramped handwriting
f. slow speech & low volume
g. difficulty rising from a chair & turning in bed
h. difficulties with ambulation
 all aspects of movement are affected:
1. initiation
2. execution
3. ability to stop movement once iniatiated
Akinesia- inability to move
“kinesia paradoxica” - ability to make rapid movement when experiencing surge of emotional
energu (e.g patient is able to cath a ball when thrown to him but is not able to do so when
asked to do so)
4. Posture
 simian posture
 stooped posture due to dominance of the progravity flexor muscle (trunkal rigidity)
 chin towards the chest
 kyphotic
 shoulders protracted & internally rotated
 elbows, hips and knees are flexed- to lower the COG this improving stability

17.  seldom crosses the legs when seated
 rarely adjusts body posture
 slow from rising from chair to upright position
5. Ambulation
 shuffling gait – small steps with the absence of arm swing
 festinating gait- patient leans forward with an increasingly faster steps to catch up with
his COG
 lack of postural reflexes – lateral pulsion & retropulsion
 loss on normal heel-toe pattern
 “En block movemen” - gait pattern with difficulty in turning.
 Freezes on passing through narrow passages
 stair climbing – not as difficulties
 tricks to overcome freezing attacks:
a. marching to command
b. stepping over objects
c. walking to music or clapping
d. shifting body weight
e. rocking movements
6. Postural instability
 least specific but most disabling feature
7. Deterioration in intellect – seen as disease progresses
a. bradyphrenia- slownes of thought process
b. dementia and depression- seen in 2/3 of the cases
c. personality changes
d. diminished memory
8. Signs of Autonomic Dysfunction
a. othostasis
b. Central Horner's Syndrome- miosis (pupillary constriction), enophthalmus (backward
displacement of the eyeball into the orbit) and ptosis due to paralysis of cervical
sympathetic nerves particulary the 1st thoracic segment
c. increase salivation and drooling
d. increase perspiration- seborrhea with oily skin

18. e. bladder incontinence- hyperreflexic in nature
f. decrease GI peristalsis.
g. constipation- represent inactivity, side effect of anticholinergic medication
9. Cranial Nerve dysfunction
a. chewing difficulties
b. dysphagia
c. decrease blinking due to bradykinesia if muscles innervated by CN III, VII & IX
d. coughing when eating
e. expressionless face with reduced eye blinking; ocular problems, Parinaud's
syndrome – paralysis of upward gaze, loss of convergence, blepharospasminvoluntary closure of eyelids, blepharoclonus – fluttering of closed eyelids.
Voice volume-reduced
speech- monotone & poor pronounced with rapid staccato pattern
Diagnosis
1. Patient amy present with usual signs and symptoms of PD patient.
2. Onset of symptoms- unilateral
3. may initially complain of tremor, fatigue, minor clumsiness of an arm, dragging of a leg,
simulation of a hemiparetic patient but with an exaggerated DTR & normal sensory exam.
4. abnormal reflexes – not specific to PD; Myerson sign- exaggerated glabellar reflex
5. Things to include in the assessment:
a. specific joint limitation
b. chest expansion
c. equilibrium
d. gait
e. action and reaction time
Course of Prognosis

over 5-15 years, overall function diminishes
 tremor not as disabling as rigidity and bradykinesia
 earlier onset of tremor progress more slowly
 (+) akinesia – more rapidly progressing disease
 mortality rate- reduces dramatically with the introduction of L-dopa

19. TREATMENT

no known cure for PD patients

overall management: keep the patient functioning independently as long as possible
while minimizing disability

methods:
a. pharmacology
b. rehabilitation
c. neurosurgery procedures
Pharmacology
a. L-dopa
b. anticholinergic
c. Amantidine
d. Dopamine receptor agonist
e. Deprenyl

initiated when symptomatology restricts normal activity

has been found to improve quality & quantity of life for PD patients

L-dopa – initial use should be reserved until symptomatology restric functional activity
REHABILITATION

may not reverse the progressive nature of the disease but:
1. teach patient compensatory mechanism
2. helps prevent complications
3. enhances the quality of patient's life
PHYSICAL THERAPY MANAGEMENT
1.
relaxation technique
2.
slow, rhythmic rotational movement
3.
gentle, prolonged passive stretching & flexibility exercises
4.
functional activity training
5.
postural control
6.
facilitatory techniques

20. 7.
breathing exercise
8.
gait training
9.
reciprocal motion
10.
aerobic conditioning exercises
NEUROSURGICAL PROCEDURES

Stereotaxic surgery- used to allevaite the symptoms of parkinsonism in certain patients

involves producing destructive lesions in basal ganglia or thalamus by cryosurgery or
chemosurgery

does not improve crippling effect of bradykinesia

principal effects: a. decrease or abolish tremor, b. reduce rigidity
REFERENCES:
1.Kisner C, Colby L. Therapeutic Exercise. 5th Ed. F.A . Davis Company. 2007: 316-318
2. Young M, Tiquis A, et. al. CONCEPTs Basic and Clinical Notes for Physical Therapst
1st ed,