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-

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

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:

•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

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

✗ Poor sleep

✗ No referred patterns of pain

✗ Fatigue

✗ Trigger points on muscles

✗ Referred patterns of pain

✗ Tight band of muscle

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

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

BODY

COURSE PERIPHERAL

TERMINATION

Brachial motor Facial nucles Temporal bone facial

side

Muscles of expression

hyoid elevators

Visceral motor Superior salivary

nucleus

a. greater superficial

petrosal to

sphenopalatine

ganglion

b. chorda tympani to

submaxillary ganglion

a. glands of nose,

palate, lacrimal

b. submaxillary and

sublingual glands

Visceral sensory Geniculate ganglion Internal acoustic

meatus

Anterior taste buds

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

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.

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

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 Central palsy paralysis

ETIOLOGY Unknown 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

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

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

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

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

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

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

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

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

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, blepharospasm-

involuntary 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

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

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,