PRESENTED BY…
M0HD JAVED QUERAISHI
STUDENT PHYSIOTHERAPIST
Pt.J.N.M.MEDICAL COLLEGE,RAIPUR (C.G.)
Marsden in 1994 has defined Parkinson’s Disease as “ A clinical syndrome dominated by a disorder of
movement consisting of Tremor at rest , Rigidity ,
elements of Bradykinesia ( Slowness of movement ),
Hypokinesia ( reduced movement ) , Akinesia (loss of
movement) & Postural abnormalities associated with a
distinctive pathology consisting of degeneration of
pigmented brain stem nuclei , including the
Dopaminergic Substantia Nigra Pars compacta (SNPc)
with the presence of Lewy bodies in the remaining nerve
cells .
( Adapted from Fahn S & Jankovic J in 1992)
(1) Primary or Idiopathic Parkinsonism
(2) Secondary or Acuired or Symptomatic Pakinsonism
(3) Parkinsonism plus syndrome or Parkinsonian
syndrome.
It is a Progressive, Disabling, Primary
Neurodegenerative disorder. There are four cardinal
signs:( A ) Tremor
( B ) Rigidity
( C ) Bradykinesia
( D ) Postural instability
(A B C are together called as Classical Triad)
It is the collective term for a group of conditions that includes
PD as well as several other degenerative brain disorders. The
signs & symptoms includes the four cardinal signs of PD.
Parkinsonism results from a variety of causes that include
infections,toxins,drugs,vascular leisons, tumors & trauma.
(Neuroleptic Drugs are considered to be the commonest cause
of Secondary Parkinsonism today.)
It constitute of heterogenous group of multifaceted disorders
characterised by Parkinsonian features, with various combinations
of Pyramidal , Cerebellar & Autonomic dysfunctions.
( The most common form of Parkinsonism seen by Neurologists
today is the Idiopathic variety of Parkinson’s disease)
(1) In 1817 , James Parkinson first described the PD. His description of
the disorder was as follws :-
“ Involuntary tremulous motion , with lessened muscular power, in parts
not in action & even when supported , with a propensity to bend the trunk
forward, & to pass from a walking to a running paces ; the senses &
intellects being uninjured.”
(2) In 1867, Trousseau noted the muscular rigidity & cog wheeling
appearance.
(3)In 1877, Charcot named first disease as Parkinson’s Disease & he noted the
absence of facial expression (Masked Facies) as a feature of disorder.
(4) In 1880, Charcot listed PD as the 5th most common disease.
(5) In 1888, Gower noted that , the malady usually commences after 40 yrs of
age.
(6) In 1898, Purves Stewart , recognised dystonic posturing of the feet , usually
provoked by exercise but occasionally relieved by walking & which could be the
first symptom of malady.
(7)In 1913 , Lewy first described the concentric hyaline cytoplasmic inclusion &
called it as LEWY BODY.It is observed in the nucleus of Substantia Innominata.
(8) In 1919, Tretiakoff was the first to observe the characteristic leisons of
Substantia Nigra ie. Depletion of pigmented cells.
(9) In 1937, Hassler described the anatomy of Substantia Nigra & in 1938
noticed pathological process of PD for the ventrolateral Pars compacta cell
group.
(10) In 1957, Carlsson showed that cerebral Dopamine was concentrated in the
striatum.
(11) In 1960 , Ehringer & Hornykiewicz demonstrated that in PD Dopamine was
markedly reduced in the Substantia Nigra , Caudate nucleus & Putamen.
(12) In 1967 , Cotzias shows the clinical benefits of high doses of Levo-Dopa in
chronic patient with PD.
(1) PD occurs in about 1% of the population older than 55 yrs of
age.
(2) Males are slightly more at risk for developing PD than
females.
(3) In 10 % cases PD occurs before the age of 40 yrs.
(4) Mainly found in Western countries.
.
(A) It consists of regular , rhythmic , alternate contraction antagonist & agonist
muscles @ 4-6 times / second.
(B)The tremors occurs due to uninhibited activity of the basal ganglia-cortico-thalamus
circuit as a result of degeneration of the striatonigral pathway.
(C) It is a rhythmic involuntary movement normally affecting the limbs.
(D) It is the 1st complain of the patient but in some patient Bradykinesia is usually the
first recognised symptom.
(E) Resting tremor present mainly PIN / PILL rolling type as like pin / pill rolls between
the thumb & index fingure.
(F) Frequency is 4-6 times / second in early stage & 6-8 times/ second in later stage.
( G ) Maximal at periphery & affects the arm more frequently than the leg.
(H) Tremor is increased by stress & disappeared during sleep & goal directed
movements.
( I ) The hand which is most affected assumes a posture of flexion of the MCP joints
with extension of the more distal joints.
(A) Rigidity is defined as resistance to passive motion that is not velocity dependent.
(B) It is manifested as cocontraction of agonist & antagonist muscles due an increase in the
supraspinal influences on the normal spinal system causing increase tone in the agonist & the
antagonist.There is an increased discharge of gamma motor neurons.
(C) The patient usually complains of rigidity as a sensation of heaviness or stiffness of the limbs.
(D) Present in almost all cases of PD.
(E) Cog wheel type rigidity is present. There is intermittent resistance throughout ROM.
Lead pipe rigidity is also seen in some cases. There is constant resistance throughout ROM.
(F) It affects proximal muscles first, mainly shoulders & neck and then progresse to face &
extremities and then the whole body.
(G) As the disease progresses ; Rigidity becomes more severe.
(H) Rigidity decreases the ability of patients to move easily. For eg; loss of bed mobility , loss of
reciprocal arm swing during gait.
(I) Mental concentration & Emotional tension may increase the amount of rigidity present.
(J) Prolonged rigidity results in decreased available ROM & serious secondary complications of
contracture & postural deformity.
(K) Rigidity also has a direct impact on increasing Resting Energy Expenditure (REE) &
fatigue levels.
(A) Bradykinesia refers to slowness & difficulty in maintaining movements.It is
theoretically presumed that it could be because of difficulty to the basal ganglia to
integrate sensory information.
(B) Movements are typically reduced in speed,range & amplitude ; termed hypokinesia.
(C) Pateint with PD typically demonstrate micrographia ; an abnormally small hand
writing that is difficult to read.
(D) Pateint feels difficulties in ADL such as bathing,dressing, rising from a chair,turning
over in bed,loss of dexterity & making buttoning etc.
(E) Pateint experiences difficulty in integrating two motor programmes at the same time
(F) Pateint feels hesitation on initiation of movements & early fatigue.
(A) Simians posture or Stooped posture.
(B) Head protuted forward , flexion at neck , trunk , elbow , hip & knee.
(C) Tandem stance :- walking on a single line with narrow BOS.
(D) Balance is poor & patient fall if encounters even minor postural
perturbation ( a slight push ) due to loss of postural reflexes.
(A) Parkinsonian gait / Freezing / Festinating / Shuffling / Toe –heel / Hurrying gait.
(B) Pateint takes small steps on walking.
(C) Pt. feels difficulty in initiating movement & to stop walking once started .
(D) There is loss of normal heel toe progression . The toe strikes first.
(E) The forward leaning of the trunk moves the body’s COG forward , thus causing the
patient to hasten his/her pace in order to catch up COG.
(F) Loss of arm swing & pelvic rotation.
(G) Stride length decreases & speed increased therefore called as festinating gait.
(H) Stance phase & double support time are lengthened while the period of
single limb support is shortened.
(I) Pt. are able to stop only when they come in contact with an object or a wall.
(J) Turning or changing direction is particularly difficult.
(A) Lack of facial expression.
(B) Subsequent loss of blinking.
(C) Smiling may be possible only on command or volitional effort.
(D) This can have a significant impact on social interaction & social disability.
(A) Rotational movement are reduced, resulting in movements that are basically
uniplanar (in one plane of of motion ) eg; flexion–extension in saggital plane.
(B) There is an overall decrease in total number of movements.
(C) Movement impoverishment can lead to mental fatigue & loss of motivation.
(A) In a patient of PD fatigue is one of the symptom.
(B) The pt. has difficulty in sustaining activity & experiences increasing weakness.
(C) Repetitive motor acts may start out strong but decrease in strength as the activity
progresses.
(D) The 1st few words spoken may be loud & strong but diminish rapidly as speech
progresses.
(A) Pt. Shows the effects of generalized musculoskeletal deconditioning.
(B) The more chronic & generalised the disease becomes , the greater the level of
muscle weakness & fatigue.
(C) Loss of flexibility.
(D) Lack of movement in any body segement leads to contracture development of both
contractile & noncontractile tissue.
(E) Contarctures mainly developes in hip & knee flexors,hip rotators & adductors,
plantarflexors, dorsal spine & neck flexors, shoulders adductors & internal rotators, and
elbow flexors.
(F) Kyphosis is the most common postural deformity.
(G) Some pt. may develop Scoliosis from leanning consistently to one side when sitting or
walking.
(H) Scoliosis generally results from unequal distribution of rigidity in the trunk.
(I) Older pt. with reduced activity levels & poor diet are likely to develop osteoporosis.
(A) Dysphagia ,impaired swallowing, is present in 50-90 % of pt.
(B) Dysphagia can lead to choking or aspiration pnuemonia & impaired nutrition.
(C) Dysphagia is the result of rigidity,reduced mobility& restricted range of movement.
(D) Pt. experiences problems in all four stages of swallowing;- oral preparatory,
oral,pharyngeal & esophageal.
(E) Pt. typically experiences excessive drooling (sialorrhea) as a result of increased
salivary production & decreased spontaneous swallowing.
(A) Speech is impaired in in 50- 73 % of pt.
(B) Hypokinetic Dysarthria; which is characterised by decreased volume , monotone or
monopitch speech, imprecise or distorted disarticulation& uncontrolled speech rate.
(C) Speech difficulties are also result of rigidity & bradykinesia.
(D) Patients experiences reduced mobility , restricted range of movement& uncontrolled
rate of movement of muscles controlling respiration , phonation , resonation &
articulation.
(A) Visual disturbances are common in PD. These can include blurring of vision &
difficulty in reading which is not coeected by glasses .
(B) Conjugate gaze & saccadic eye movements may also be impaired.
(C) Eye movements may have a jerky & cog wheeling quality.
(D) Pupillary abnormalities are also possible with decreased reflex responses to light &
nocciceptive stimuli.
(E) 50% patient experiences paresthesias & pain.This can include sensations of
numbness ,tingling, abnormal temperature & pain that is cramp like & poorly localized.
(F) Postural stress syndrome.
(G) Akathisia; it is often described as painful and interferes with relaxation & sleep
(A) Dementia occurs in approximately 1/3rd of the patients with PD.
(B) Bradyphrenia, a disorder of intellectual function, is common in pt. It is characterised
by a slowing of thaught processes with lack of cocentration & attention.
(C) Pt. May also demonstrate learning deficits.
(D) Perceptual deficits also present.
(E) Deficits have been reported in vertical perception, topographic orientation, body
shceme and spatial relations.
(A) Depression is the most common,occuring in25-40% of pt.
(B) Pt. may demonstrate symptoms of major depression ,including apathy, passivity,loss
of ambition or enthusiasm & changes in appetite,sleep and dependency. Suicidal
thaughts may be present.
(C) Dysthymic disorder characterised by variability in dysphoric mood, or typical
depression characterised by intermittent episodes of severe anxiety.
(D) Drug related psychoses can occur.
(A)Dysautonomia ; autonomic nervous system dysfunction occurs in pt.
(B) Commons problems includes excessive perspiration,greasy skin,increased
salivation,thermoregulatory abnormalities(including uncomfertable sensations of heat or
cold).
(C) Bladder dysfunction includes urinary frequecy, urgency & nocturia.
(D)Sexual dysfunction includes impotence.
(E) Patient have low appetites & decreased motility of the GIT.
(F) Constipation is also problem seen in pt.
(A) Pulmonary function impairement is reported in 84% of pateints.
(B) Orthostatic hypotension & low resting blood presure.Cardiac arrhythmias can also
occurs as aresult of L-Dopa .
(C) Airway obstruction leads to pulmonary failure.
(D) Bradykinetic disorganisation of of respiratory movements.
(E)Restrictive dysfunction due to decreased chest expansion that occurs as a result of
rigidity of trunk muscles , loss of musculoskeletal flexibility & kyphotic posture.
(F) Decrease in FVC , FEV1 & increase in RV , RAW (airway resistance).
(G) In long standing disease, the lower extremities may exhibit circulatory changes owing to
venous pooling as a result of decreased mobility & prolonged sitting. Thus pt. can present with
mild to moderate edema of the feet & ankles , which usually subsides during sleep
.
(A)Dermatitis can occur due to increased secretion by sweat &
sebaceous glands.
(A) Tapping forehead causes repititive blinking.
(A) It is present in 75 – 90 % of pt.
DEFINITION :The term Basal Ganglia is applied to group of nuclei
(mass of gray matter) in the fore brain & upper part of the
brain stem that have motor function of great importance . It is
the primary motor area in lower animals ( reptiles & birds).
The BG includes :(1) Caudate nucleus – it possesses a head and a tail.
(2) Putamen – a Latin word for shell.
(3) Globus pallidus or Pallidium or Paleostriatum- it is subdivided into external &
internal segment.
(4) Subthalamic nucleus (BODY OF LUYS) – it is located in the diencephalon ventral
to the thalamus & lateral to the hypothalamus.
(5) Substantia nigra – it has two parts ; (a) dorsomedial part is Pars compacta
(b) ventrolateral part is Pars reticulata.
(Substantia Nigra Pars compacta{SNPc} contains Dopaminergic neurons which
produces the Dopamine. Dopamine has inhibitory action.
The scheme of subdivisions of the BG components is shown as follows :-
(1) Putamen + Caudate nucleus = Neostriatum or striatum.
(2) Putamen + Globus pallidus = Lentiform nucleus.
(3) Lentiform nucleus + Caudate nucleus = Corpus striatum.
(A)The corpus striatum has a rich concentration of Acetylcholine (Ach).
(B) Ach is synthesized & released by small striatal neurons, upon which it has
an Exitatory effect.
(C) Dopamine (DA) is synthesized by the pigmented neurons of SNPc & it has
Inhibitory effect on striatal neurons.
(D) Dopamine is transported from SNPc to Corpus striatum via Nigrostriatal or
Dopminergic tract.
(E) There is functional equilibrium exists in the striatum between Ach &
Dopamine in the normal physiological condition.
(F) In PD , there is a loss of pigmented neurons (neuromelanin) in SNPc. As a result ,
the DA cocentration in the corpus striatum is markedly decreased.
(G) There is formation of Lewy Bodies in the remaining neurons.
(H) LEWY BODIES are characteristic intracytoplasmic , eosinophilic inclusion bodies.
These are circular in shape with the dens central “core” & clear peripheral “halo”.
(I) There may also be a decrease in other Neurotransmitter like noradrenaline(NA),
5hydroxytryptamine(5HT),gamma –aminobutyric acid (GABA),Enkephalins &
substance-P.
(J) Involvement of non nigrostriatal system :Cell loss outside the Substantia Nigra involves the following major neuron
groups :-
(1) Midbrain– ventral tegmental area.
(2) Pons– noradrenergic locus coeruleus.
(3) Midbrain– serotonergic dorsal raphe nuclei.
(4) Basal forebrain – cholinergic nucleus basalis of Meynert in substantia innominata.
(5) Brainstem– peptidergic nuclei
(K) Alteration in noradrenergic & serotonergic system results in
Depression in pt.
(L) Neuronal loss in the nucleus basalis , locus coeruleus & ventral
tegmental area causes Dementia.
(M) Loss of somatostatin neurons in the cortex results in Alzheimer
disease.
(1) IDIOPATHIC.
(2) INFECTIONS :- encephalitis lethargica , AIDS, cryptococcal meningitis
and Jacob-Creutzfeldt disease.
(3) NEUROTOXINS :- 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)
manganese carbonmonoxide, carbondisulphide, cyanide, methanol.
(4) DRUGS TOXICITY :(a) Neuroleptic drugs.
(b) Antidepressant drugs.
(c) Antihypertensive drugs.
(5) METABOLIC DISORDERS :- disturbed calcium metabolism result in
calcification in BG.
(6) VASCULAR DISORDERS :- atherosclerosis , hypertension.
(7) HEAD INJURY :- RTA , punch boxers syndrome.
(8) MULTIPLE SYSTEM DEGENERATION :$ Alzheimer disease
$ Shy Drager syndrome
$ Progressive supranuclear palsy.
$ Wilsosn’s disease
$ Amyotrophic lateral sclerosis.
$ Olivopontocerebellar atrophy.
$ Huntington’s disease
$ Hallervorden – Spatz disease.
$ Strionigral degeneration.
$ Cortico-basalganglionic degeneration.
(A) The diagnosis of PD is based on the clinical symptoms & signs.
(B) Blood & CSF examination and cerbral imagin such as CT Scan , MRI are
non cotributory in making the diagnosis of PD.
(C) Positron Emission Tomography (PET) using fluorodopa has been useful in
detecting loss of dopa uptake in the striatum . It shows 60% reduction of
fluorodopa uptake.
(D) Single Photon Emission Computerised Tomography (SPECT).
(E) DNA Analysis :- mitochondrial complex 1 activity is reduced, alterations in
DNA, Monoamine oxidase-B (MAO-B) activity increased.
(F) The diagnosis is usually made on the basis of history & clinical examination.
Handwriting samples, speech analysis, interview questions that focus on developing
symptomatology & physical examination are used in the preclinical stage to detect early
manifestations of the disease.
(G) The diagnosis of PD can be made if atleast two of the cardinal features are present.
(H) EMG may done to find out the level of rigidity & also to know the increase in the
reaction time & movement time.
(A) PD is a progressive disorder but its rate of progression is variable.
(B) Before L-dopa therapy 28% of pt. became severely disabled or died with in
5 yrs of diagnosis , 61% with in 10 yrs & 83% with in 15 yrs.
(C) Following L-dopa therapy only 9% became disabled or had died at 5 yrs ,
21% at 10 yrs & 37.5% at 15 yrs.
(D) Death may occur from aspiration pneumonia ,septicemia from UTI,
decubitus ulcer or from secondary causes like vascukar disease or neoplasia.
PHARMACOLOGICAL TREATMENT
(A) Anticholinergics – Trihexyphenidyl , Bentropine.
(B) Dopamine replacement – Levedopa , Carbidopa , Sinemet , Sinemet CR.
(C) Dopamine agonists – Pergolide , Bromocriptine .
(D) Amantadine.
(E) MAOI-B – Seligiline.
(A) STERIOTAXIC SUEGERY :- started in 1950 before levo dopa not in use.
(B) PALLIDOTOMY :- clearing of destructive leisons in globus pallidus
internus (Gpi).
(C) THALAMOTOMY :- clearing of destructive leison in the ventral
intermidius nucleus of thalamus.
(D) DEEP BRAIN STIMULATION (DBS):- started in 1997 by using
implantation of electrodes in brain specifically in ventral interomedial nucleus
of thalamus.
(E) TRANSPLANTATION TECHNIQUE :- grafting of foetal cells ,
autotranplantation with patient’s own adrenal medullary cells.
(A) PATIENT HISTORY.
(B) GENERAL EXAMINATION.
(C) NEUROLOGICAL EXAMINATION.
(D) CARDIORESPIRATORY ENDURANCE.
(E) OTHER ASSESSMENT :(1) Functional status.
(2) General health measures.
(3) Skin integrity & condition.
(1) COGNITION :memory function , conceptual reasoning , problem solving ability , attention
and concentration are reduced.
Assessment instrument – Mini Mental Status Exam (MMSE).
(2) AFFECTIVE & PSYCHOSOCIAL FUNCTIONING :stress , anxiety , sadness , apathy , passivity , insomnia , aprexia , wt. loss ,
inactivity , suicidal thaugts may present.
Assessment instrument – Geriatric Dpression Scale.
Beck Depression Inventory.
(3) VISUAL FUNCTION :-Visual acuity , peripheral vision , accomodation , light & dark adaptation are reduced.
- Depth perception , blurring of vision , cataract , glaucoma , may present.
- Senile macular degeneration , diabetic retinopathy , homonymous hemianopsia may
present.
(4) DYSPHAGIA & SPEECH IMPAIREMENT :- Dysphagia , sialorrhea ( drooling) present.
-Hypokinetic dysarthria .
-Mutism.
Assessment instruments – The verbal learning test.
- The verbal comprehension test.
(5) MUSCLE PERFORMANCE :- Spasticity
- Strenght reduced.
- Endurance decreased.
Assessment Instrument – MMT
- Modified Asworth scale.
- Isokinetic Dynamometers.
- Hand Held Dynamometers.
(6) RIGIDITY :-Present in trunk , neck , extremities & face.
(7) BRADYKINESIA :- Slowness of movement.
- Increased Reaction Time (RT).
- Increased Movement Time (MT).
Assessment instrument – Timed test for Rapid Alternating Movement (RAM).
- EMG for RT & MT.
(8) JOINT RANGE OF MOTION :- AROM & PROM both decreased.
- Loss of hip & knee extension , shoulder flexion , elbow extension ,dorsal spine &
neck extension and axial rotation of spine.
Assessment instrument – Goniometers.
(9) TREMORS :- Resting tremors.
- Mainly in periphrey of upper limbs.
(10) SENSORY INTEGRITY :- Blunting of touch sensations.
- Loss of propioception more in lower extremities than upper , distal than proximal.
- Paresthesias ( sensation of numbness or tingling ).
(11) PAIN :- Mild aching & cramp like.
- Poorly localised.
- Potural stress syndrome.
Assessment Instrument – The Mc Gill Pain Questionnaire.
- The Visual Analogue Scale.
(12) POSTURAL INSTABILITY :- Disturbed balance.
- Greater problem in single limb stance.
Assessment instrument – Timed up & go test.
- Berg balance test.
- Functional reach.
- Clinical Test for Sensory Interaction in Balance (CTSIB).
- Tinetti’s Performance Oriented Mobility Assessment(POMA)
(13) POSTURE :- Flexed or stooped.
- Kyphosis & cervical lordosis.
Assessment instrument – Postural grids or Plumb lines.
- Still photogarphy.
- Videotapes.
(14) GAIT :- Freezing episodes.
- Shuffling gait pattern.
- Stride length , step width decreases.
- Cadence increased.
( Gait should be examined during all move,ent directions ; forwrad , backward ,
sideward ).
(15) AUTONOMIC CHANGES :- Excessive drooling ( salivation).
- Excessive sweating.
- Greasy skin.
Cardiorespiratory endurance may be reduced from impaired respiratory functions
& long standing inactivity.
(1)ABNORMAL BREATHING PATTERNS :-
- Ribcage compliance & chest wall mobility decreases.
- Restrictive breathing.
- Kyphosis present.
(2) ALTERED LUNG VOLUMES & CAPACITIES :- FVC , FEV ,decreased.
- RV , RAW increased.
- TLC , VC decreased.
(3) ALTERED VITAL SIGNS :- HRmax reduced.
- Respiratory rate increased.
- PaO2 is decreased.
- BP decreased ( orthstatic hypotension).
Assessment instrument – PFT
- 6 Minute walking test.
- Exercise tolerance test.
- Sphygnomannometer.
(1) FUNCTIONAL STATUS :- Difficulty in performing ADL.
- Activities having a rotational component is reduced or absent.
Assessment instrument – The functional independence measure ( FIM).
- Katz index of independece in activities of daily life.
(2) GENERAL HEALTH MEASURES :-
- Decrease in physical & social function.
- Decrease in emotional well being.
Assessment instrument – Rand 36 item health survey SF 36
- Sickness impact profile.
(3) SKIN INTEGRITY & CONDITION :- Bruising & skin breakdown.
- Pressure sore may be present in patient confined to bed.
(4) FINGER DEXTERITY :-
- Pt. May unable to button up three shirt buttons upto 3 minutes.
(1) HOEN & YAHR SCALE ( 1967).
(2) THE UNIFIED PARKINSON’S DISEASE RATING
SCALE –UPDRS (1987).
(3) THE PARKINSON’S DISEASE QUESTIONNAIRE
(PDQ-39).
STAGE 1 – Disability or functional impairement is usually absent or minimal.
- If present , unilateral involvement.
STAGE 2 – Bilateral or midline involvement.
- Balance not disturbed.
STAGE 3 – Impaired righting reflexes.
- Functionally restricted in some activities but pt. can live independently.
- Disabilty is mild to moderate.
STAGE 4 – All symptoms present & severly disabled.
- Standing & walking possible only with assistance.
STAGE 5 – Confined to wheelchair or bed.
(1) It is a rating tool to follow the longitudinal course of PD.
(2) It is made up of :(a) Mentation , Behaviour & Mood.
(b) ADL.
(C) Motor sections.
(3) These are evaluated by interviewing the pt.
(4) A total of 199 points are possible.
(5) 199 points represents the worst ( total disability) & 0 point represnts no
disability.
(A) The PDQ is a 39 items questionnaires.
(B) It focuses on the subjective reports of the impact of PD on daily life.
(C) These are interviewed with patients.
( D) Scored are given & summarised as Parkinson’s Disease Summary Index
(PDSI).
(1) TO DECREASE THE RIGIDITY.
(2) TO MAINTAIN THE MUSCULOSKELETAL
FLEXIBLITY.
(3) TO INCREASE THE JOINT MOBILITY.
(4) TO IMPROVE THE BALANCE.
(5) TO IMPROVE THE MOTOR LEARNING.
(6) TO IMPROVE THE CARDIORESPIRATORY
FUNCTIONS.
(7) TO IMPROVE THE GAIT.
(8) TO IMPROVE THE PSYCHOSOCIAL WELL BEING.
(1) Gentle rocking exercises & rotational exercises in slow &
rhythmic patterns.
(2) PNF (Rhythmic Initiation ) technique in which movement
progresses from passive to active assisted & then to active
movements.
(A) SUPINE:- slow side to side head rotations.
(B) SUPINE :- bilateral symmetrical D2F( flexion,abduction,external rotation)
& its reversal D2E pattern ( extension,adduction,internal rotation)
(C) Hooklying :- lower trunk rotations.
(D) Side lying :- upper & lower trunk rotations.
(E) Side lying :- trunk rotations combined with scapular patterns (shoulder
protraction with elevation & retraction with depression).
(3) Deep breathing exercises can be incorporated into rotational exercises
to enhance relaxation.
(A) Bilateral symmetrical D2F (BS D2F) patterns can be combined with inspiration.
(B) Bilateral symmetrical D2E (BS D2E) patterns can be combined with expiration.
(4) Meditation techniques.
(5) Jacobson’s progressive relaxation techniques.
(6) Relaxation audiotapes home exercise programmes.
(7) Feldenkrais relaxation techniques.
(1) Both active & passive ROM exercises.
(A) Exercises should focus on strengthening the patient weak , elongated
extensor muscles while ranging the shortened , tight flexors muscles.
(B) ROM exercise should be also emphasize restoring range in the neck &
trunk and can be performed in combination with rotational exercises to promote
relaxation.
(2) PNF pattern :- muscle inhibition techniques Hold Relax or
Contract Relax. Contract Relax is the preferred technique because
it combines autogenic inhibition from isometric contraction of the
tight agonist muscles with active rotation of the limb.
(A) For U/L –BSD2F & L/L – hip and knee extension in a D1 pattren (hip
extension , abduction & internal rotation.
(3) TRADITIONAL STRETCHING TECHNIQUES :(A) Gentle stretching of elbow flexors , hip ,knee flexors & ankle plantarflexors.
(B) Stretching can be combined with joint mobilisation techniques to reduce tightness
of the joints capsule or of ligaments around a joint.
(C) Autostretching or Selfstretching.
(D) Maintain the stretch force atleast 15 – 30 seconds. Ideally the stretches are repeated
atleast 3-5 times.
(E) Ballistic stretches ( high intensity bounding stretches) & aggressive stretch should
be avoided.
(F) Braces may be used for prolonged stretching of tight muscles.
(G) Calisthenics exercises in supine , sitting & stand.
(H) Standing erect with arms in elevation (over head ) against a wall or corner of the
room & the patient should try to stretch out his body.
(I) Lie supine with pillow under the upper thorax.
(4) PASSIVE POSITIONING :- it is long duration technique to improve
flexiblity .
(A) To avoid Phantom Pillow Posture pt.should be positioned in prone position.
(B) The pt with a developing lateral curvature can be positioned in side lying with a
small pillow under the lateral trunk.
(C) Mechanical low load stretching can also be used . This approach utilizes a weight
pulley & traction set up with low load wt. ( eg. 5 – 15 lbs or 5 – 10 % of body wt.) .
Time duration is 20 –30 minutes.
(D) Mechanical stretching can be achieved through the use of tilt table . The pt is
positioned with fixed leg straps to reduce hip & knee flexion contractures or toe wedge
to reduce plantarflexion contracture.
(E) Braces can be used for prolonged stretching of tight muscles.
(1) The overall focus is on improving mobility / controlled
mobility function with specific emphasis on improving segmental
mobility of the head , trunk & proximal segments ( hips &
shoulders ) . Relaxation exercises are important pre-requisites to
all mobility training.
(A) For thorax & neck extension :- prone on elbow , prone extension , standing
wall push ups or corner push ups.
(B) For extremities PNF techniques of Rhythmic Initiation.
(C) Bed mobility activities ( rolling , supine to sit etc ).
(D) Pelvic mobility ( anterior , posterior & side to side tilt ) exercises on Swiss ball.
(E) Wt shifting exercises & upper extremities reaching activities . Reaching should be
practised in all directions with emphasis on promoting rotational movement of trunk.
(2) PNF patterns for upper extremity in sitting :(A) D2F & D2E patterns are ideal because they expand the restricted chest while
promoting upper trunk extension.
(B) A lift / reverse lift patterns or chop / reverse chop pattern can be used to promote
upper trunk extension with rotation in sitting.
(C) Static –dynamic activities for the lower trunk & pelvis in sitting include crossing
one leg over the other or scooting.
(3) The pt can be instructed to practise lip pursing ,movement of tounge,
swallowing & facial movement such as smiling , frowing etc. A mirror
can be used to provide visual feedback.
(4) Movements of opening & closing of mouth , chewing should be
combined with neck stabilisation in a neutral position.
(5) Pool exercises or Hydrotherapy.
(1) The balancing training should always be begin from of lower
COG to higher COG.
(2) Training should begin with weight shifts in both sitting &
standing in order to help the pt develop an appreciation of his
limits of stability.
(3) By giving the slight the push to pt. Patient try to maintain the
balance.
(4) Reaching activities.
(5) Activities on Swiss ball.
(6) Kitchen shink exercises:- the pt can be instructed in standing heel rises toe offs
, partial wall squats and chair rises , single limb stance with side kicks or back kicks &
marching in place , all while maintaining light touch down support of the hands.
(1) To teach the pt to do one movement at a time because he feels
difficulty in carrying out simultaneous movements ( dual task).
(2) The combination of movements results in slowing of
movements.
(3) Teach the pt rolling , supine to sitting , sitting to standing etc.
(4) Avoid the movements where attention is divided ; because
learning activities is also become difficult. For eg for a pt sitting
on chair don’t ask him to walk , first ask him to stand up from
chair & then walk.
(1) Diaphragmatic & Segmental breathing exercises.
(2) Air shifting techniques.
(3) Deep breathing execises to improve chest wall mobility &
vital capacity.
(4) Chest mobility exercises.
(5) PNF :- BSD2F & BSD2E patterns of upper extremitise for
chest mobility. Execises are performed in sitting position to
promote trunk stabilisation.
(6) Incentive spirometry .
(7) Balloon blowing.
(8) Aerobic execises eg. Daily walking for short distance , ergometry etc.
(1) The major goals are to lengthen stride , broaden BOS ,
improve stepping , improve heel–toe gait pattern , increase
contralateral movement & arm swing and provide a programme of
regular walking.
(2) Weight transfer ; standing on single limb.
(3) High stepping to strengthen the flexors.
(4) Side stepping or crossed stepping with or without support.
(5) PNF activity of braiding , which combines side to side stepping with
alternate crossed stepping to improve the lower trunk rotation with
stepping movement.
(6) Normal heel-toe progression.
(7) To overcome shuffling pattern , draw foot marks or parallel lines with
red or yellow colours ; then ask the pt to walk on it.
(8) The pt should be practised stopping , starting , changing direction &
turning. Turning of 180degree should be practised first then 360.
(9) Two wands or sticks ( held by pt & therapist one in each hand ) can
be used to facilitate reciprocal arm swing during gait. The therapist uses
his arm swing to assist the patient.
(10) Gait can be vey well trained by using audiovisual cues/ commands.
(11) Auditory cues can be effective in improving gait & reducing
episodes of freezing ( gait block). Pt responds positively to brisk march
music or other similar types of rhythmic music.
(12) Metronome stimulation was found to significantly reduce the
number of freezing episodes & lenthen strides.
(13) Use of walker or parallel bar is not advisable in treatment of PD
because the confined nature of this gait training only increases the
freezing.
.(1)Active participation of family members is required. Patient
counselling to increase the confident & independency.
(2) Feeling of hopelessness , dependency & depression should be
reduced.
(3) Self management skills should be promoted.
(4) Regular participation of patient into various social activities
should be encouraged.
(5) Coping skills ( to compete with the variety of social &
environmental factors ) can be facilitated.
(1) Teach the pt for Relaxation , Flexibility , Strengthening ,
Mobility & Breathing exercises.
(2) Avoid prolonged periods of inactivity.
(3) The pt should be cautioned agianst over doing activity , which
could result in excessive fatigue.
(4) Early morning warm-up& Callisthenics execises.
(5) Compensatory techniques or triggering maneuvers to
overcome the crippling effects of bradykinesia & freezing.
(6) Wall pulleys can be used to improve upper extremity ROM.
(7) Hanging from an overhead bar can be used to maintain stretch on the
upper trunk and extremity flexors.
(8) In standing , a countertop or sturdy chair should be used to assist in
stabilisation during calisthenics & balance activities.
(9) Make the pt to sleep in the prone position.
(1) NATIONAL PARKINSON FOUNDATION (NPF) , MIAMI.
WEBSITE : - www.parkinson.org
(2) PARKINSON’S DISEASE FOUNDATION (PDF) , NEW YORK
(USA).
WEBSITE : - www.pdf.org
(3) AMERICAN PARKINSON’S DISEASE ASSOCIATION (APDA),
NEWYORK (USA).
WEBSITE : - www.apdaparkinson.com
(4) CHARTED SOCIETY OF PHYSIOTHERAPY (CSP) , LONDON (U.K.)
WEBSITE : - www.csp.org.uk
(5) AMERICAN PHYSICAL THERAPIST ASSOCIATION (APTA) U.S.A.
WEBSITE : - www.apta.org
(6) MOHD JAVED QUERAISHI , STUDENT PHYSIOTHERAPIST.
Pt.J.N.M.MEDICAL COLLEGE RAIPUR , C.G.
E -MAIL :- javed_physio@yahoo.co.in