Irogue Seminar Presentation October 2010

PHYSIOTHERAPY IN THE MANAGEMENT OF PARKINSONS PARKINSONS DISEASE
Presented by IROGUE.EGHOSA. KENNEDY MRH/2005/024 Student Physiotherapist Department Of Medical Rehabilitation Faculty of Basic Medical Science,O.A.U Ile Ife SPECIAL TOPIC SEMINAR MRH 507
PRESENTATION OBJECTIVES

To define key issues in the management of Parkinsons disease (PD) relating to physiotherapy treatment. treatment.
To inform our knowledge of current evidenceevidencebased recommendations of physiotherapy in Parkinson's disease.
OUTLINE

Definition Classification Background / History Diagnosis Differential diagnosis Pathophysiology Epidemiology Clinical features / presentation. Prognostic factor Managements of Parkinsons disease Medical therapy Surgical therapy Physiotherapy
Overview of Parkinsons disease

Also known as : Paralysis agitans Shaking palsy.
Why Parkinsons disease ?

The evidence available to practitioners with regards to appropriate physiotherapy intervention for people with Parkinson's disease up till the RESCUE Project randomised control trial has either been of poor quality or absent. Physiotherapy has therefore had to rely absent. on unsubstantiated anecdotal reports from professionals, people with Parkinsons or carers regarding the effectiveness of input. An input. effectiveness bulletin on neurological conditions (Chartered Society of Physiotherapy 2001) concluded that many areas of 2001) physiotherapy had yet to be sufficiently evaluated. evaluated.
In neurological problems, Parkinsons disease is the most common disorder leading to gait disturbance and falls (Stolze et al, 2005). 2005) Despite advances in pharmacological treatments and surgical techniques, gait and balance deficits still persist and are associated with loss of independence, immobility and high cost for healthcare systems. systems. (Grimbergen et al., 2004). al. 2004) Other mobility deficits, includes difficulties with transfers and posture. posture.
This frequently leads to loss of independence, (fear of) falls, injuries, and inactivity, resulting in social isolation and an increased risk of osteoporosis or cardiovascular disease. (Bloem, et al., 2001; Garrett, et al., 2004). Consequently, costs increase (Pressley, et al., 2003) and quality of life decreases (Schrag, et al., 2000). These mobility deficits are difficult to treat with drugs or neurosurgery. (Schrag et al., 2002; Bloem et al., 1996) Physical therapy is often prescribed next to medical treatment (Keus, et al., 2004). Therefore, the awareness and application of rehabilitation approaches that work in conjunction with current treatment is important to manage these problems.
However, there is presently the first evidence-based evidenceinternational guideline for physical therapy in Parkinsons disease developed according to international standards of guideline development with practical recommendations graded according to scientific evidence. This is the KNGF guidelines for physical therapy in patients with Parkinsons disease. The guidelines identify six core areas of physiotherapy practice: physical capacity and prevention of inactivity; transfers; gait; posture; reaching and grasping; and balance and falls. To this guideline we based current physiotherapy management on Parkinsons disease
In Africa, Nigeria to be precise a recent research on the clinical profile of Parkinsons disease patients shows that it is the same with other population but characterised by delayed presentation as has been reported in other developing countries. Young-onset Parkinsons disease countries. Youngoccurs but may be less commonly encountered and frequency of positive family history is lower than in western population (Okubadejo et al., 2010).physiotherapy al. 2010) is therefore advocated in combination with optimal timing of medications(Morris et al.,1998) al. 1998)
DEFINITION
Marsden (1994) defined parkinsons disease as a 1994) clinical syndrome of movement consisting of tremor at rest, rigidity, elements of bradykinesia (slowness of movement), akinesia(loss of movement) and postural abnormalities associated with a distinctive pathology consisting of degeneration of pigmented brain stem nuclei, including the dopaminergic Substantia Nigra Par Compacta(SNPC) with the presence of lewy bodies in the remaining nerve cells. cells.
HISTORY/BACKGROUND

In 1817, James Parkinson first described the 1817, Parkinson disease. His description of the disease disease. was as follows. follows.
Involuntary
tremulous
motion,
with
lessened
muscular power in parts not in action and even when supported with a propensity to bend the trunk forward and to pass from a walking to running paces; paces; the senses and intellects being uninjured. uninjured.
In 1867, Trousseau noted the muscular rigidity and cog wheeling appearance.
In 1877, Charcot named first disease as Parkinsons disease as he noted the absence of facial expression (masked faces) as a feature of the disorder.
In 1880, Charcot listed PD as the 5th most common disease.
In 1888, Gower noted that, the malady usually commences after 40years of age.
In
1898, 1898,
Purves
Stewart,
recognized
distinct
positioning of the feet, usually provoked by exercise but occasionally relieved by walking and which could be the first symptom of the malady. malady.

In 1913, lewy first described the concentric hyaline 1913, cytoplasmic inclusion and called it as lewy body. It is body. observed in the nucleus of substantia innominata. innominata.
In 1919, Tretiakoff was the first to observe the 1919, characteristic lesions of substantia nigra i.e depletion of pigmented cells. cells.
In 1937, Hassler described the anatomy of substantia 1937, nigra and in 1938, noticed pathological processes of PD 1938, for the ventrolateral pars compacta cell group. group.
In 1957, Carlson showed that cerebral dopamine was 1957, concentrated in the striatum. striatum.
In 1960, Ehinger and Honykiewicz demonstrated that in 1960, PD, dopamine was markedly reduced in the substantia Nigra caudate nucleus and putamen. putamen.
In 1967, Cotzias shows the clinical benefits of high dose 1967, of levo-dopa in chronic patients with PD. levoPD.
CLASSIFICATION BASED ON AETIOLOGY

Primary or idiopathic Parkinsons disease Secondary or acquired or symptomatic Parkinsons disease
Parkinsons plus syndrome. (adapted from syndrome. Fahn and Jankovic 1992) 1992)
PRIMARY OR IDIOPATHIC PARKINSONS DISEASE

It is a progressive, disabling, primary neurodegenerative disorder. There are four signs:

Rest tremor Rigidity Bradykinesia Postural instability
(The first three are together called the classical triad)
SECONDARY OR SYMPTOMATIC OR ACQUIRED PARKINSONISM

It is the collective term for a group of conditions that indicate PD as well as several other degenerative brain disorders. disorders. The signs and symptoms includes the four cardinal signs of PD. Parkinson results from a variety PD. of causes that include infections, toxins, drugs, vascular lesions, tumor and trauma. (neuropeptic trauma. drugs are considered to be the commonest cause of secondary Parkinson today)
PARKINSONPARKINSON-PLUS SYNDROME OR PARKINSONISM SYNDROME It constitutes of heterogeneous group of multifaceted disorder characterised by
parkinsonia features, with various combinations of pyramidal, cerebella, and autonomic
dysfunctions. dysfunctions. (The most common form of Parkinsonism seen by neurologists today is the idiopathic variety of Parkinsons disease). disease).
Examples of Parkinson-plus syndrome are: Parkinson1) PROGRESSIVE SUPRANUCLEAR PALSY:

Early postural instability and falls Vertical gaze palsy Rigidity of trunk Speech and swallowing problem Unusual tremor Symmetrical onset
Examples of Parkinson-plus syndrome: Parkinson2) MULTIPLE SYSTEMIC ATROPHY

Early autonomic features (postural BP decrease and bladder dysfunction) dysfunction) Cerebella pyramidal sign Rigidity>tremors

3) LEWY BODY DEMENTIA 4) VASCULAR PARKINSONISM 5) PUGILISTIC ENCEPHALOPATHY (TRAUMA)
Examples of Parkinson-plus syndrome: Parkinson6) POST ENCEPHALOPATHY

7) DRUG INDUCED E.G NEUROLEPTICS, PROCHLORPERAZINE AND METOCLOPRAMIDE. 8) TOXIN INDUCED E.G MANGANESE, COPPER (WILSONS DISEASE)
DIAGNOSIS
a)
The diagnosis of PD is based on the clinical symptoms & signs.
b)
Blood & CSF examination and cerebral imaging such as CT Scan, MRI are non contributory 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).
DIAGNOSIS

DNA Analysis: - mitochondrial complex 1 activity is reduced, alterations in DNA, Monoamine oxidase-B oxidase(MAO(MAO-B) activity increased. 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. The diagnosis of PD can be made if at least two of the cardinal features are present.
DIAGNOSIS
g)
EMG may be done to find out the level of rigidity & also to know the increase in the reaction time & movement time.
A TYPICAL EMG
DIFFERENTIAL DIAGNOSIS
PATHOPHYSIOLOGY
Guttman, M. et al. CMAJ 2003;168:293-301
Fig. 1: Coronal section of the brain, showing nigrostriatal pathways and location of selective dopaminergic degeneration in patients with Parkinson's disease
PATHOPHYSIOLOGY
In Parkinsons disease, there is degeneration of dopaminergic neuron in the substantial Nigra par compacta associated with lewy body; causing decreased striatal dopamine (putamen and caudate nucleus) level. This is thought to be related to mitochondrial DNA dysfunction.
EPIDEMIOLOGY
PREVALENCE: Worldwide, Worldwide, based on the available prevalence studies, there are likely more than 6 Million people with PD. However, due to many people with PD remaining undiagnosed, there may be millions more. In China alone there are more than 1.7Million people with PD.
EPIDEMIOLOGY
Decreasing order of prevalence : Amish community>Brescia>Nebraska,> Persia By country per 100,000 of population 100, USA-329-107, USA-329-107, Japan 193-76Nigeria 67Korea 193-76 67Korea 19, Ethiopia 7 19, Prevalence of PS/PD is rising slowly with aging population
EPIDEMIOLOGY
INCIDENCE RATES Sweden 22.5-7.9>faroes Island>USA 20.3-13.0 22.5-7.9>faroes 20.3.England 12.. Libya 45.
AGE DISTRIBUTION: In 1875, Henri Huchaud(1844-1911) detailed the first Huchaud(1844case Juvenile Parkinsons disease. He described a 3 year old who had all the clinical features of PD.
EPIDEMIOLOGY
The youngest reported case of PD. The youngest reported case of PD since then is that of a 10 year old girl from Oklahoma who showed her first symptoms of PD at only 2years old. However, its very uncommon for people under the age of 30 to develop PD.
EPIDEMIOLOGY PD usually occurs when people are significantly older than that and becomes increasingly more common with age.

The average age at which symptoms usually begin differs from country to country, with the oldest average onset being in Sweden 65.6 and Estonia 66.9.
EPIDEMIOLOGY

In Nigeria, mean age of onset for idiopathic PD was 55.6 years (Osuntokun, 1979) 55. 1979)
Recently, Recently, mean age of onset for PD in Nigeria was discovered to be 61.5 years 61. (Okubadejo et al., 2010) al. 2010)
EPIDEMIOLOGY

There is likelihood of Parkinsons disease increasing sharply at the age of 60, and peaks in 60, those aged 85-89 years old. 85old.
The likelihood of developing PD starts to decline at 90 years of age and reduces even further after that PD is very rare amongst the very old-those oldpeople over 100 and even in those people over 110 to 119 years old. old.
EPIDEMIOLOGY
GENDER DISTRIBUTION The ratio of males to females differs a lot according to the country. country. There is a stark contrast between a clear Male dominance in Nigeria and Japan where Women dominate in PD. PD. RATIO OF MEN TO FEMALE: FEMALE: Nigeria 3.3, Tanzania 2.72, U.S.A 1.91-1.0 e.t.c 72, 91-
EPIDEMIOLOGY
RACIAL DIFEFRENCES: DIFEFRENCES:

The risk of PD increases according to Hair colour. colour. People with Black hair were found to be least prone to PD. PD.
People with brown hair are 40% more likely to 40% develop PD. And, those with blonde hair 60% more PD. 60% likely to develop PD. PD.
EPIDEMIOLOGY
Worst at risk are people with Red hair which are twice at risk. risk. PD and hair colour share some biochemistry. biochemistry. OCCUPATIONAL DIFFERENCES PD is far more common amongst Welders. Prevalence is Welders. significantly higher amongst Physicians, Dentist, Teaches, Lawyers, Scientists, and Religion-related jobs. Religionjobs.
CLINICAL PRESENTATION OF PARKINSONS DISEASE

NATURAL COURSE OF PARKINSONS DISEASE Relatively little is known about the natural course of PD. Although always progressive, the natural course is very variable. (Poewe, 1998). The first symptoms are usually unilateral. (Olanow, et al., 2001). Around three 2001). years after the first symptoms present, it typically develops into a bilateral disorder, usually still with intact balance. (Muller, et al., 2000) balance.

Problems with balance develop about two to three years later, although some patients reach this stage only seventeen years after the start of the disease. (Muller, et al., 2000) Recurrent falling starts on average ten years after the first symptoms. (Wenning, (Wenning, et al., 1999) Eventually, nearly all patients will have impaired balance and will fall repeatedly. repeatedly.

This forms a threat to quality of life. (Schrag, et al., life. al. 2000) 2000) Initially, patients with balance problems can stand and walk on their own, but on average after eight years, falling becomes, in combination with the other symptoms, a more severe problem. Eventually problem. the balance impairment can become so severe that the patient is permanently confined to a wheelchair or bed, if he has no help of others. others.

Less than five percent of patients with PD are confined to a wheelchair or bed eventually (Global Parkinson Disease Survey Steering Committee, 2002). In later stages non motor symptoms may arise, such as dementia. In geriatric patients PD is often accompanied by depression.

1)
(a)
TREMORS:
It consists of regular , rhythmic , alternate contraction antagonist & agonist muscles @ 4-6 times / second. 4-
(b)
The tremors occurs due to uninhibited activity of the basal ganglia-corticoganglia-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 recognized symptom.
e)
Resting tremor present mainly PIN / PILL rolling type as like pin / pill rolls between the thumb & index finger.
f)
Frequency is 4-6 times / second in early stage & 6-8 times/ 46second 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.
2) RIGIDITY
a)
Rigidity is defined as resistance to passive motion that is not velocity dependent.

b)
It is manifested as co contraction of agonist & antagonist muscles due to 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. neurons.
c)
The patient usually complains of rigidity as a sensation of heaviness or stiffness of the limbs. 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 progress to face & extremities and then the whole body.
g) h)
As the disease progresses ; Rigidity becomes more severe. severe. Mental concentration & Emotional tension may increase the amount of rigidity present. present.

i)
Rigidity decreases the ability of patients to move easily. For e.g.; loss of bed mobility , loss of reciprocal arm swing during gait. gait.
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.

3) BRADYKINESIA
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)
Patient with PD typically demonstrate micrographia ; an abnormally small hand writing that is difficult to read.
d)
Patient feels difficulties in ADL such as bathing, dressing, rising from a chair, turning over in bed, loss of dexterity & making buttoning etc.
e)
Patient experiences difficulty in integrating two motor programmes at the same time.(dual tasking)
f)
Patient feels hesitation on initiation of movements & early fatigue.

4) POSTURAL INSTABILITY
a) b)
Simians posture or Stooped posture. Head protruded forward , flexion at neck , trunk , elbow , hip & knee.
c) d)
Tandem stance :- walking on a single line with narrow BOS. :Balance is poor & patient fall if encounters even minor postural perturbation ( a slight push ) due to loss of postural reflexes.

5) GAIT
a)
Parkinsonian gait / Freezing / Festinating / Shuffling / Toe heel / Hurrying gait.
b) c)
Patient takes small steps on walking. walking. Patient feels difficulty in initiating movement & to stop walking once started.
d)
There is loss of normal heel toe progression. The toe strikes first.
e)
Loss of arm swing & pelvic rotation.

f)
The forward leaning of the trunk moves the bodys COG forward thus causing the patient to hasten his/her pace in order to catch up COG.
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) j)
Turning or changing direction is particularly difficult. Patient are able to stop only when they come in contact with an object or a wall.

INDIRECT IMPAIREMENTS & COMPLICATIONS 1) MASKED FACE
a) b) c) d)
Lack of facial expression. Subsequent loss of blinking. blinking. Smiling may be possible only on command or volitional effort. This can have a significant impact on social interaction & social disability.

2) POVERTY OF MOVEMENT
a)
Rotational movement are reduced, resulting in movements that are basically uniplanar (in one plane of motion ) e.g.; flexion flexionextension in sagital plane.
b)
There is an overall decrease in total number of movements. movements.
c)
Movement impoverishment can lead to mental fatigue & loss of motivation.

3) FATIGUE
a) b)
In a patient of PD fatigue is one of the symptom. The patient 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.(palilalia)

4) MUSCULOSKELETAL CHANGES
a)
Patient shows the effects of generalized musculoskeletal deconditioning.
b)
The more chronic & generalized the disease becomes , the greater the level of muscle weakness & fatigue.
c) d)
Loss of flexibility. Lack of movement in any body segment leads to contracture development of both contractile & non -contractile tissue.

e)
Contractures mainly develops in hip & knee flexors, hip rotators & adductors, plantar flexors, dorsal spine & neck flexors, shoulders adductors & internal rotators, and elbow flexors.
f) g)
Kyphosis is the most common postural deformity. Some pt. may develop Scoliosis from leaning consistently to one side when sitting or walking.
h)
Scoliosis generally results from unequal distribution of rigidity in the trunk.

i)
Older patient with reduced activity levels & poor diet are likely to develop osteoporosis.
5) SWALLOWING DYSFUNCTION
a) b)
Dysphagia ,impaired swallowing, is present in 50-90 % of pt. 50Dysphagia can lead to choking or aspiration pnuemonia & impaired nutrition.
c)
Dysphagia is the result of rigidity,reduced mobility& restricted range of movement.

d)
Patient experiences problems in all four stages of swallowing; oral preparatory, oral, pharyngeal & esophageal.
e)
Patient typically experiences excessive drooling (sialorrhea) as a result of increased salivary production & decreased spontaneous swallowing.
6) COMMUNICATION DYSFUNCTION
a) b)
Speech is impaired in 50- 73 % of patient. 50Speech difficulties are also result of rigidity & bradykinesia. bradykinesia.

c)
Hypokinetic Dysarthria; which is characterised by decreased volume , monotone or monopitch speech, imprecise or distorted disarticulation & uncontrolled speech rate.
d)
Patients experiences reduced mobility , restricted range of movement& uncontrolled rate of movement of muscles controlling respiration , phonation , resonation & articulation.
7) VISUAL & SENSORIMOTOR DISTURBANCES

a)
Conjugate gaze & saccadic eye movements may also be impaired. impaired.

b)
Visual disturbances are common in PD. These can include blurring of vision & difficulty in reading which can not be corrected by glasses.
c) d)
Eye movements may have a jerky & cog wheeling quality. Pupillary abnormalities are also possible with decreased reflex responses to light & nociceptive stimuli.
e)
Akathisia; it is often described as painful and interferes with relaxation & sleep. sleep.

f)
50% patient experiences paresthesias & pain. This can include sensations of numbness ,tingling, abnormal temperature & pain that is cramp-like & poorly localized. cramp-
g)
Postural stress syndrome.
8) COGNITIVE DYSFUNCTION
a)
Dementia occurs in approximately 1/3rd of the patients with PD.

b)
Bradyphrenia, Bradyphrenia, a disorder of intellectual function, is common in pt. It is characterised by a slowing of thought processes with lack of concentration & attention.
c) d) e)
Patient May also demonstrate learning deficits. Perceptual deficits also present. Deficits have been reported in vertical perception, topographic orientation, body scheme and spatial relations.

9) BEHAVIOURAL DYSFUNCTION
a) b)
Depression is the most common, occurring in25-40% of patient. in25Patient may demonstrate symptoms of major depression ,including apathy, passivity, loss of ambition or enthusiasm & changes in appetite, sleep and dependency. Suicidal thoughts may be present. present.
c)
Dysrhythmic disorder characterised by variability in dysphoric mood, or typical depression characterised by intermittent episodes of severe anxiety.

d)
Drug related psychoses can occur.
10) AUTONOMIC DYSFUNCTION

a)
Dysautonomia ; autonomic nervous system dysfunction occurs in patient.
b)
Commons problems includes excessive perspiration,greasy skin,increased salivation,thermoregulatory abnormalities(including uncomfortable sensation of heat or cold). cold).

c)
Bladder dysfunction includes urinary frequency, urgency & nocturia. Sexual dysfunction includes impotence. Patient have low appetites & decreased motility of the GIT. Constipation is also problem seen in patient.
d) e) f)
11) CARDIOPULMONARY DYSFUNCTION

a) b)
Pulmonary function impairment is reported in 84% of patients. Airway obstruction leads to pulmonary failure.

c)
Orthostatic hypotension & low resting blood pressure. Cardiac arrhythmias can also occurs as a result of L-Dopa . L-
d) e)
Bradykinetic disorganization of respiratory movements. 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.
12) SKIN INFECTIONS

a)
Dermatitis can occur due to increased secretion by sweat & sebaceous glands.

13) GLABELLAR TAP SIGN
a)
Tapping forehead causes repetitive blinking.
14) OLFACTORY DYSFUNCTION

a)
It is present in 75 90 % of patient.
PROGNOSTIC FACTOR OF PARKINSONS DISEASE

According to KNGF guideline development group of Parkinson's disease 2004, physical therapy influences physical inability and falling as prognostic in Parkinsons disease. Jankovic et al., distinguish TREMOR DOMINANT TYPE of Parkinson's disease and AKINETIC RIGID TYPE
TREMOR DOMINANT TYPE 1) Tremor is the initial symptom. 2) Process often develop more slowly. 3) Characterized by problems of balance gate and freezing. AKINETIC RIGID TYPE Rigidity and hypokinesia are the initial symptoms. More rapid course of Parkinsons disease in motor and cognitive areas. Characterize by less frequent dominant and cognition impairment.

In patients of young age cognition functions and postural reflexes often remain unimpaired.
Patients with recurrent falls and with insufficient physical activity has an unfavourable prognosis. prognosis.
PD is a progressive disorder but its rate of progression is variable.
Before L-dopa therapy 28% of pt. became severely disabled or Ldied with in 5 yrs of diagnosis , 61% with in 10 yrs & 83% with in 15 yrs. yrs.

Following L-dopa therapy only 9% became Ldisabled or had died at 5 yrs , 21% at 10 yrs & 37.5% at 15 yrs.
Death may occur from aspiration pneumonia ,septicemia from UTI, decubitus ulcer or from secondary causes like vascular disease or neoplasia.
MANAGEMENT OF PARKINSONS DISEASE

The management of PD follows the multidisciplinary approach. approach. This involve the MULTIDISCIPLINARY TEAM that includes: includes:

Neurologist A rehabilitation Physician A physical therapist An occupational therapist A speech therapist A neuropsychologist A recreational activities supervisor A social work A PD specialist Nurse
MANAGEMENT OF PARKINSONS DISEASE MEDICAL THERAPY
MEDICAL THERAPY
MEDICAL THERAPY
MEDICAL THERAPY

MEDICAL THERAPY
Treatment algorithm for the management of the early stages of Parkinsons disease. As shown below

SURGICAL THERAPY
A.
Stereotactic surgery is done on the basal ganglia by ruling out part of the region (-tomy) as in: (-
Pallidotomy: clearing of destructive lesion in globus pallidus internus, decrease dyskinesia.
Thalamotomy: Clearing of destructive lesion in the ventral intermedius nucleus of the thalamus, decreases tremor.
Stereotactic surgery started in 1950 before Levo-dopa not in use. Levo-
SURGICAL THERAPY
B.
Deep Brains Stimulator(DBS) : started in 1997, stimulation takes place by implantation of electrode in the brain, specifically in ventral intermedius nucleus of the thalamus to a pacemaker.
Complications might occur as a consequence:

By intervention itself(by damaging the surrounding tissue) The applied equipment( e.g. infection) The lesion or stimulation (among others falling problems paraesthesia and headache).
SURGICAL THERAPY
C.
Transplantation technique: grafting of foetal cells, auto transplantation with patients own adrenal medullary cells.
MOTOR FEATURES OF PD

Initiation problems movements under scaled motor instability slowing deterioration with simultaneous tasks Tremor
NONNON-MOTOR FEATURES OF PD

Sleep: Bowels Bladder Pain Postural hypotension * Sexual dysfunction Sweating

PHYSIOTHERAPY
Physiotherapy intervention is broadly divided into two processes:

Diagnostic process Therapeutic process (KNGF, 2004)
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE

DIAGNOSTIC PROCESS
This involves ASSESSMENTS and CLINICAL IMPRESSION.

Subjective Assessment Objective Assessment Analysis of finding Plan of treatment Goals of treatment

Therapeutic process This involves:

Means of treatment Evaluation and follow up Reporting The objectives or aims of physiotherapy are based on the outcome from these two processes.
For a patient with PD, the major objectives of physiotherapy are:

To improve the quality of life

To maintain the patients independence, safety, and well being. To improve functional activity. To reduce or delay limitation in activities (disability).
ASSESSMENT

REFERRAL Early referral (immediately after diagnosis) to a physical therapist is recommended to prevent or decrease complication as a result of falls and inactivity. (Plant et al., 2000; Morris, 2000; Chesson, 1998 ) Chesson,

Henvel et al., stated the following information needed from the referring physician:

Name, date of birth and address of the patient. Date of referral Diagnosis Is other forms of parkinsonism excluded? CoCo-morbidity Course of the health problem Reason for referral Name, address and signature of the physic

HISTORY TAKING To get an accurate picture of the patient problem.

Patient specific complaints questionnaire; for performance of activities and assessment of the treatment goal .it determines the functional status of individual patient.

history of falling questionnaire freezing of gait questionnaire (FOG): This is used for patient who have recently experienced that their feet seemed glued or stocked to the ground.

For inventory of evaluation of falling or near falling

fall efficacy scale fall diary LASA physical activity questionnaire; measure physical activity of the elderly.

Analysis to formulate the objective to be tested: Based on the information obtained while taking the medical history, a number of problems is formulated, these are to be tested in physical examination. Possible objective are:
1. 2. 3. 4.
Physical capacity Transfer Reaching and grasping Balance and gait

Physical Examination Physical therapist should determine if the patient is in ON OR OFF period. For structured physical examination.
QUICK REFERENCE CARD CAN BE USE.
NEUROLOGICAL ASSESSMENT
(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 thoughts may present.
Assessment instrument Geriatric Depressions Scale Beck Depression Inventory.

(3) VISUAL FUNCTION:FUNCTION:
Visual acuity, peripheral vision, accommodation, light & dark adaptation are reduced.
Depth perception, blurring of vision, cataract, glaucoma, may present.
Senile macular degeneration, diabetic retinopathy, homonymous hemianopia may present.

(4) DYSPHAGIA & SPEECH IMPAIREMENT:IMPAIREMENT:
Dysphagia , sialorrhea ( drooling) present. Hypokinetic dysarthria . Mutism.
Assessment instruments: The verbal learning test. The verbal comprehension test. (5) MUSCLE PERFORMANCE:PERFORMANCE:
Spasticity

Strength reduced. Endurance decreased.
Assessment Instrument: Manual Muscle grading Modified Ashworth 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: Goniometer (9) TREMORS ::
Resting tremors. Mainly in periphery of upper limbs.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE (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 localized. Postural stress syndrome.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Assessment Instruments: The Mc Gill Pain Questionnaire. The Visual Analogue (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).
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Assessment instrument : Tinettis Performance Oriented Mobility Assessment (POMA) (13) POSTURE ::
Flexed or stooped. Kyphosis & cervical lordosis. lordosis.
Assessment instrument : Postural grids or Plumb lines. Still photography. Videotapes.

(14) GAIT:GAIT:
Freezing episodes. Shuffling gait pattern. Stride length, step width decreases. Cadence increased.
(Gait should be examined during all movement directions; forward, backward, sideward).
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE (15) AUTONOMIC CHANGES:
Excessive drooling (salivation). Excessive sweating. Greasy skin.
CARDIORESPIRATORY EXAMINATION
Cardio respiratory endurance may be reduced from impaired respiratory functions & long standing inactivity. (1)ABNORMAL BREATHING PATTERNS: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.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE (3) ALTERED VITAL SIGNS:
HRmax reduced. Respiratory rate increased. PaO2 is decreased. BP decreased (orthostatic hypotension).
Assessment instrument : 6 Minute walking test. Exercise tolerance test. Sphygmomanometer.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE FUNCTIONAL STATUS:STATUS:
Difficulty in performing ADL. Activities having a rotational component are reduced or absent.
Assessment instrument : The functional independence measure Katz index of independence in activities of daily life.

GENERAL HEALTH MEASURES:MEASURES:
Decrease in physical & social function. Decrease in emotional well being.
Assessment instrument: Rand 36 item health survey SF 36 Sickness impact profile. SKIN INTEGRITY & CONDITION:CONDITION:
Bruising & skin breakdown. Pressure sore may be present in patient confined to bed.
FINGER DEXTERITY:
Pt. May unable to button up three shirt buttons up to 3 minutes.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE OUTCOME MEASURES

Outcome measure serves as an aid in charting and objectively assessing health problems, to evaluate preliminary treatment effectiveness and make inventory of the patient problems for possible intervention. The KNGF development group Guidelines 2004, recommends the following outcome for PD measurement:

The Retropulsion test; For general impression of problems with balance
The MODIFIED Parkinsons Activity scale(PAS)-for quality of scale(PAS)movement during certain ADL;functional mobility
OUTCOME MEASURES

Time up and go test(TUG)-for functional mobility and balance test(TUG)The six minute walk test- for physical capacity in the absence testof freezing.
The Ten-meter walk test- To evaluate comfortable walking Tentestspeed.
GRADING OF PARKINSONs DISEASE

(1) (2)
HOEHN & YAHR SCALE (1967). HE UNIFIED PARKINSONS DISEASE RATING SCALE UPDRS (1987).
(3)
THE PARKINSONS DISEASE QUESTIONNAIRE (PDQ-39). (PDQ-
OUTCOME MEASURES
HOEHN AND YAHR SCALE

STAGE 1 Disability or functional impairment 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 patient can
live. - Disability is mild to moderate.
OUTCOME MEASURES STAGE 4 All symptoms present & severally disabled. - Standing & walking possible only with assistance. STAGE 5 Confined to wheelchair or bed. MODIFIED HOEHN AND YAHR STAGING STAGE 0 = No signs of disease. STAGE 1 = Unilateral disease. STAGE 1.5 = Unilateral plus axial involvement. involvement. STAGE 2 = Bilateral disease, without impairment of balance. STAGE 2.5 = Mild bilateral disease, with recovery on pull test.
OUTCOME MEASURES MODIFIED HOEHN AND YAHR STAGING STAGE 3 = Mild to moderate bilateral disease; some postural instability; physically independent. STAGE 4 = Severe disability; still able to walk or stand unassisted. STAGE 5 = Wheelchair bound or bedridden unless aided.
UNIFIED PARKINSONS DISEASE RATING SCALE It is a rating tool to follow the longitudinal course of PD.

It is made up of ::(a) (b) (c)
Mentation, Mentation, Behavior & Mood. ADL. Motor sections.

These are evaluated by interviewing the patient A total of 199 points are possible. 199 points represents the worst (total disability) & 0 point represents no disability.
THE PARKINSONS DISEASE QUESTIONNAIRE (PDQ 39)

The PDQ is a 39 items questionnaire. It focuses on the subjective reports of the impact of PD on daily life.

These are interviewed with patients. Scored are given & summarized as Parkinsons disease Summary Index (PDSI).
ANALYSIS OF FINDINGS

Is physiotherapy indicated? Can the guidelines be applied to this individual patient?
Physiotherapy will be indicated if the patient;

1. Is limited in one or more activities (transfers, posture, reaching and grasping, balance and gait); 2. Has (or has the risk of) a decreased physical capacity caused by inactivity; 3. has an increased risk of falling or has fear to fall; 4. Has an increased chance of pressure sores; or 5. has the need for information or advice on the disorder, natural course and prognosis
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE AIMS OF PHYSIOTHERAPY TREATMENT According to Disease Progression
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE PLAN OF TREATMENT 1. To increase safety and independence in the performance of activities, with the emphasis on:

Transfers; Posture; Reaching and grasping; Balance; Gait;
2. To preserve or improve physical capacity;
PLAN OF TREATMENT 3. To prevent falling; 4. To prevent pressure sores; 5. To stimulate insight into impairments in functions and limitations in activities, especially in the area of posture and movement.
THERAPEUTIC PROCESS:
GENERAL TREATMENT PRINCIPLES
i.
Location of the treatment: to improve functional

activity, it is recommended it preferably takes place at the patient home. This can also improve physical capacity
ii. iii.
Involvement of care giver Avoidance of dual tasking

iv. v.
Multidisciplinary agreement Frequency and duration of treatment: there are

indications that a period of AT LEAST FOUR WEEKS is needed to decrease limitations in functional activities (disability) while a period of AT LEAST EIGHT WEEKS of aerobic exercises and other exercises is necessary to improve physical capacity, in which period of a low frequency of treatment is sufficient for example once a week to adjust exercise program. (Kamsma et al., 1995; Comelle et al,. 1994; Dam et al., 1996; Patti, 1996; Thaut et al., 1996)

vi.

Time of treatment:
Exercises in PD patients can be performed in the On- as well as in the Off- period (including cognitive movement strategies and cueing strategies)

It is advisable also to train physical capacity (including strength) in patient with PD during the On- period, because at this time, neurological problems have less influence on the level of performance.

vii.
Tempo of exercising: in cognitive impairment and

fatigue. Tempo and schedule of treatment need to be adjusted.
viii.
Recognising a response of fluctuation: physical

therapist should draw the patient attention to response fluctuation.
ix.

Contraindications:
Deep brain stimulation (SWD, MWD, electromagnetic pulses, electromagnetic fields)

ix.
Contraindications:

Freezing hydrotherapy is contraindicated in freezing. Mental impairment: Impairment in cognition (e.g.

poor memory, dementia and severe hallucinations), personality and attention are relative contraindications for the treatment of health problems related to PD.
EvidenceEvidence-Based Analysis of Physical Therapy in Parkinsons Disease with Recommendations for Practice and
Research. Research. (keus et al., 2006) al. 2006)
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE TREATMENT STRATEGIES OR MEANS

For PD patients with sufficient understanding, insight, and memory

Cognitive movement strategies Cueing strategies Modifying coping strategies. Are recommended treatment means based on Hoehn and Yahr classification of PD into three phases as related to treatment goal.
Cognitive movement strategies strategies

Cognitive movement strategies can be applied by physical therapist to improve TRANSFERS. (Morris, 2000; Kamsma et al., 1995; Iansek, 1999; Nieuwboer, 2001; Muller et al., 1997) In Cognitive movement strategies, complex (automatic) activities are transformed to a number of separate elements which are executed in a defined sequence and which consist of relatively simple movement elements. This will prevent dual tasking during complex (automatic) activities in daily life. Performance is consciously controlled and can be guided by using CUES in initiation.
Cognitive movement strategies

Example; Rising from a chair.

place your hands on the arms or the side of the seat; move your feet towards the chair (just in front of the chair legs, two fists apart); shift your hips to the edge of the chair; bend your trunk (not too far, nose above the knees); rise gently, from your legs, let your hands lean on the arms of the chair, the seat or your thighs, and then extend your trunk completely (if necessary, make use of a visual cue). In case of starting problems rock back and forth a few times and rise at the third count.

Cueing strategies
Cues are used to complete or replace the fundamental problems of internal control in PD patient as in performance of automatic and repetitive movements. Cues are stimuli from the environment or stimuli generated by the patient which increase attention and facilitate (automatic) movements.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Cueing Strategies Rhythmical

recurring cues
CUES
OneOne-off cues Internal cue e.g. bow, stretch, wave. External Cue NonNon-moving stimuli e.g. sound of metronome, Stripes on the floor, A grip of a walking stick.
Moving stimuli e.g. light of laser pen, A moving foot, A falling bunch of keys
Example of cueing strategy to improve gait Freezing at the Doorway
Example of cueing strategy to improve gait Freezing at the Doorway` arrow show red light for correction
Solution a red line is added

RHYTHMICAL RECURRING CUES are given as a continuous rhythmical stimulus, which can serve as a control mechanism for walking. walking. The distance between (frequency of) rhythmic cues during walking will be based on the number of steps needed to perform the Ten-meter walk test at comfortable pace. Tenpace.
ONEONE-OFF CUES are used to keep balance, for example when performing transfer and for initiating ADL or when getting started again after a period of freezing. freezing.
Rhythmic recurring cues

Auditory Visual
the patient moves on music of a walkman the patient moves on rhythmical ticking of a metronome the patient or someone else sings or counts the patient follows another person the patient walks over stripes on the floor or over stripes he projects to himself with a laser pen the patient walks with an inverted walkingwalkingstick and has to step over the grip
Rhythmic recurring cues

Tactile
the patient taps his hip or leg
OneOne-off cues
Auditory Visual
initiation of movement, for example, stepping out at the third count initiation of movement, for example, by stepping over some elses foot, an object on the floor or an inverted walking-stick walking maintenance of posture, for example, by using a mirror or by focusing on an object (clock, painting) in the environment
OneOne-off cues Cognitive

initiation of movement (and continuation of walking), for example, by focusing on the spot he wants to go to, and not on the doorway he has to go through

RECOMMENDATIONS FROM EVIDENCE BASED RESEARCH
EARLY OR MAINTENANCE PHASE

Stimulate balance
Goal: to optimize balance and training strength. Strategy : Exercises for balance and training strength. e.g. Taichi (two group sessions a week for fifteen weeks) - walking outside three times a week, completed with a home exercise program (30 minutes, 3 times a week).
Taichi for balance training ,perception of posture and coordination of arms and legs and backward and lateral large step.
Walking on toes
strengthening exercises to the legs
Stepping over an object

These decreases the number of falls (b) Exercise to increase the mobility of among others, neck, knees and hips.
- Referral to occupational therapy to identify and alter any changes present in the home environment.

PREVENTION OF INACTIVITY OR MAINTENANCE OF PHYSICAL CAPACITY.
Goal: Maintenance or improvement of physical capacity. Strategy: providing information on the importance of exercising or playing sports, training of aerobics capacity, muscle strength (with emphasis on the muscles of the trunk and legs), joint mobility (among others axial) and muscle length (among others, muscles of the calf and hamstrings)
A THERA CYCLE: to improve physical capacity
PROGRESSIVE RESISTANCE STRENGTHENING EXERCISES

Joint mobility training Exercise programs focused on improving joint mobility, combined with training of gait and balance, improve motor skills. (Comelle et al., 1994; Patti et al., 1996; Pachetti et al., 2000; Marchese et al., 2000).

Improves ADL (Comelle et al., 1994; Patti et al., 1996; (Comelle Pachetti et al., 2000; Formisano et al., 1992; Palmer et al., 1986)
Improves mental functioning (Comelle et al., 1994; Patti et (Comelle al., 1996).
Shenkman et al., 1998 shows that exercise program focused at improving joint mobility and coordinated movement incorporated in ADL improves functional axial rotation and reach (balance).
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Training of strength

Exercise program which are among others, focused on improving muscle strength (of the lower extremities and trunk)
ANKLE JOINT MOBILITY
Trunk rotation exercises
SQUATTING EXERCISES
LUNGES

May also improve muscle strength in patients with PD (in early to middle phase). (Reuter et al., 1999; Scandalis et al., 2001).
Training aerobic Capacity

Aerobic exercise that improves aerobic capacity also improve motor skills of patient with PD in the early phase (Reuter et al., 1999; Baatile et al., 2000; Bergen et al., 2002).
Training aerobic capacity
Group therapy

Fall Prevention
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Mid or Complex Phase

Cognitive movement strategies improve transfers

CUEING STRATEGIES TO IMPROVE GAIT: As disease progresses and medication is not as effective, some people present freezing of gait. One common problem is to freeze when trying to go through a doorway. It is possible to overcome this problem with a simple visual cue, such as a line on the floor. This cue attracts attention to the task, and the person can step over it. Another strategy to overcome freezing of gait is the use of auditory cues, such as a metronome, that can be adjusted to the persons walking rhythm.
Solution a red line is added
Improving gait using modified footwear
Photoboards providing insight to stance phase function. In both photoboards, a photoboards, physiotherapist can be seen walking alongside the patient and a walking stick is being used. The top strip shows the unmodified footwear position and the bottom strip shows the modified footwear position.
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Normalizing body posture and upper limb function:
Cueing and cognitive movement strategies are creatively used in physiotherapy to design exercises to improve posture, such as straightening the back an maintaining posture by looking at a target at eye level, or training functional arm movements, such as drinking from a cup by dividing the complex sequence into different steps and practicing each step separately. Balance training could include stepping on the spot while lifting the knees up high, following the sound of a metronome.
Boxing: Anticipatory postural adjustments, postural corrections, fast arm and foot motions, backward walking, timing, sequencing actions
PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE Late (Palliative) Phase

Aim Prevention of Complications
DYSKINESIAS: One of the complications in the late stage of

PD is severe unpredictable fluctuations and dyskinesias. Relaxation techniques, which include breathing exercises and correct posture, are effective in some patients. They have only a short-term effect of about five to 10 minutes, but despite this, patients should be allowed to enjoy a few minutes of rest or a nap, which will make a difference to their overall quality of life.
WALKING AIDS: Stimulating mobility as much as

possible is a goal in physiotherapy. Walking is encouraged, sometimes with the help of walking aids. Not every walking aid is appropriate and some are potentially dangerous if given to the wrong person. Sometimes using a walking aid at certain periods of the day under close supervision could maintain a certain level of mobility, with all of the attendant benefits.
Walking Aids
WALKING AID
WALKING AIDS
TREATMENT TECHNIQUES

Keep Moving Exercise Program METERS(Movement Enablement T hrough Exercise Regimes) (Plant et al. ,2001) Task specific approach (Morris,2000) Systematic approach(schenkman et al.,1989 and 1996) approach(schenkman
Sensorimotor Agility Exercise Program

Tiachi Kayaking Agility Boxing Lunges Prepilate
(king and Horak,2009)
TREATMENT TECHNIQUES Relaxation techniques

Autogenic Progressive muscle Visualization Tiachi Music Light stoking massage Hartha yoga Exercise Alexander technique(stallibrass,1997) Deep Breathing technique Vestibular rehabilitation Therapy
CONCLUSION
EVALUATION

PATIENTS SPECIFIC COMPLAINTS QUESTIONNAIRE, MEASUREMENT OF THE GLOBAL PERCEIVED EFFECT SHOULD ALSO BE USED
AFTERCARE

Preservation of improved activities in daily living CheckCheck-up Final evaluation Reporting
REFERENCES

Baatile J, Langbein WE, Weaver F, Maloney C, Jost MB. Effect of exercise on perceived quality of life of . individuals with Parkinsons disease. J Rehabil Res Dev 2000 Sep;37(5):529-34 Sep;37(5):529Bergen JL, Toole T, Elliott III RG, Wallace B, Robinson K, Maitland CG. Aerobic exercise intervention improves aerobic Bloem BR, Beckley DJ, van Dijk JG, Zwinderman AH, Remler MP, Roos RA. Influence of dopaminergic medication on automatic postural responses and balance impairment in Parkinsons disease. Mov Disord 1996 Sep;11(5):509-21. Sep;11(5):509-
REFERENCE Bloem BR, van Vugt JP, Beckley DJ. Postural instability and falls in Parkinsons disease. Adv Neurol 2001;87:209 223. Bloem BR, Beckley DJ, van Dijk JG, Zwinderman AH, Remler MP, Roos RA. Influence of dopaminergic medication on automatic postural responses and balance impairment in Parkinsons disease. Mov Disord 1996 Sep;11(5):509-21. Sep;11(5):509Bloem BR, Grimbergen YA, Cramer M, Willemsen M,Zwinderman AH. Prospective assessment of falls in Parkinsons disease. J Neurol 2001 Nov;248(11):950-8 Nov;248(11):950-
REFERENCE Chartered Society of Physiotherapy (2001) Effectiveness bulletin: Neurology: Parkinsons disease, Multiple Sclerosis and severe traumatic brain injury Effectiveness Bulletin Evidence-based EvidencePractice Vol 3, Issue 2, pp13 pp1 Chesson R. Psychosocial aspects of measurement. Physiotherapy 1998;84(9):435-8. 1998;84(9):435Comella CL, Stebbins GT, Brown-Toms N, Goetz BrownCG. Physical therapy and Parkinsons disease: a controlled clinical trial. Neurology 1994 Mar;44(3 Pt 1):376-8 1):376-
REFERENCE Dam M, Tonin P, Casson S, Bracco F, Piron L, Pizzolato G, etal. Effects of conventional and etal. sensorysensory-enhanced physiotherapyon disability of Parkinsons disease patients. Adv Neurol 1996;69:551-5. 1996;69:551Formisano R, Pratesi L, Modarelli FT, Bonifati V, Meco G.Rehabilitation and Parkinsonsdisease. Parkinsonsdisease. Scand J Rehabil Med1992 Sep;24(3):157-60. Sep;24(3):157Garrett NA, Brasure M, Schmitz KH, Schultz MM, Huber MR.Physical inactivity: direct cost to a health plan. Am J Prev Med2004;27:304 309.
REFERENCE

Global Parkinsons Disease Survey Steering Committee. Factors impacting on quality of life in Parkinsons disease: results from an international survey. Mov Disord 2002;17(1):60-7. 2002;17(1):60Grimbergen Y, Munneke M, Bloem BR. Falls in Parkinsons disease. Review. Curr Opin Neurol 2004;17:40515. 2004;17:405 Guttman M,Kish JS and Furukawa Y(2003);Current concept in the diagnosis and management of parkinsons disease CMAJ 2003,168:3 Heuvel CMF van den, Vogels EMHM, Mellink M, Dijkstra ZM,Pieters HM. Handreiking verslaggeving. verslaggeving. http://www.paramedisch.org.
REFERENCE

Iansek R. Interdisciplinary rehabilitation inParkinsons disease. In: Stern GM, editor. Advances in Neurology. Parkinsons disease. 80 ed. Philidelphia: Lippincot Williams & Philidelphia: Wilkins;1999. p. 555-9 555Jankovic J, McDermott M, Carter J, Gauthier S, Goetz C, GolbeL, GolbeL, et al. Variable expression of Parkinsons disease: a base-line analysis of the DATATOP cohort. The baseParkinson Study Group.Neurology 1990 Oct;40(10):1529Oct;40(10):152934. Kamsma YPT, Brouwer WH, Lakke JPWF. Training of compensation strategies for impaired gross motor skills in Parkinsons disease. Physiother Theory Pract 1995;11:2091995;11:20929.
REFERENCE

Keus SHJ, Bloem BR, Verbaan D, et al. Physiotherapy in Parkinson's disease: utilisation and patient satisfaction. J Neurol 2004;251:680687. 2004;251:680 King LA, Horak FB. Delaying mobility disability in people with Parkinson disease using a sensorimotor agility exercise program. program. PhysTher. 2009;89:384 PhysTher. 2009;89:384393. KNGF Guidelines for Physical Therapy in Parkinsons disease, Supplement to the Dutch Journal of Physiotherapy, 2004;11 Physiotherapy, Laar Tv, Wolters ECMJ. Cognitieve stoornissen en psychose bijde Tv, ziekte van Parkinson. Dimensies in dementie 2002;2:3-7. 2002;2:3Mathieson I,Curran S,Hallam S,Corne J: Improving gait performance in Parkinsons disease:a case report suggesting a role for footwear modifications. physiotherapy 94(2008)85-88 94(2008)85-
REFERENCE Marchese R, Diverio M, Zucchi F, Lentino C, Abbruzzese G. The role of sensory cues in the rehabilitation of parkinsonian patients: a comparison of two physical therapy protocols. Mov Disord 2000 Sep;15(5):879-83. Sep;15(5):879MclnerneyMclnerney-Leo AMS,Gwinn-Hardy; and Nussbaum AMS,GwinnB(2004):Prevalence of parkinsons Disease in populations of Africa Ancestry ;A Review J Natl Med Assoc 2004;96:974-979 2004;96:974Management of Parkinsons disease: an evidenceevidencebased review .Mov Disord 2002;17(Suppl. 4):S1 .Mov 4):S1 S166.4.
REFERENCE Morris M et al (1998) The role of the physiotherapist in quantifying movement fluctuations in Parkinsons disease Australian Physiotherapy 44,105 44,105 114 Morris ME. Movement disorders in people with Parkinson disease: a model for physical therapy. Phys Ther 2000 Jun;80(6):578-97. Jun;80(6):578Morris M, Iansek R, Smithson F, Huxham F. Postural instability in Parkinsons disease: a comparison with and without a concurrent task. Gait Posture 2000 Dec;12(3):205-16. Dec;12(3):205-
REFERENCE

Muller V, Mohr B, Rosin R, Pulvermuller F, Muller F, BirbaumerN. BirbaumerN. ShortShort-term effects of behavioral treatment on movement initiation and postural control in Parkinsons disease: a controlled clinical study. Mov Disord 1997 May;12(3):306-14 May;12(3):306Muller J, Wenning GK, Jellinger K, McKee A, Poewe W, Litvan Progression of Hoehn and Yahr stages in Parkinsoniandisorders: a Parkinsoniandisorders: clinic pathologic study. Neurology 2000 Sep 26;55(6):888-91 26;55(6):888Nieuwboer A, de Weerdt W, Dom R, Truyen M, Janssens L,Kamsma Y. The effect of a home physiotherapy programfor persons with Parkinsons disease. J Rehabil Med 2001Nov;33(6):266-72. 2001Nov;33(6):266Olanow CW, Watts RL, Koller WC. An algorithm (decision treefor the management of Parkinsons disease (2001): treatmentguidelines. treatmentguidelines. Neurology 2001 Jun;56(11 Suppl 5):S1-S8 8 5):S1Okubadejo UN,Ojo OO,and Oshinaike OO(2010): clinical profile of Parkinsonism and parkinsons disease in lagos, south western lagos, Nigeria.BMC Neurology 10;1
REFERENCE

Osuntokun BO, Bademosi O: Parkinsonism in the Nigerian African:a prospective study of 217 patients. East Afr Med J 1979, 56:59756:597-607 Pacchetti C, Mancini F, Aglieri R, Fundaro C, Martignoni E,Nappi G. Active music therapy in Parkinsons disease: anintegrative method for motor and emotional rehabilitation.Psychosom Med 2000;62(3):386-93. 2000;62(3):386Patti F. Effects of rehabilitation therapy on Parkinsons disability and Parkinsons functional independence . J Neurol Rehabil 1996;14(4):223-31. 1996;14(4):223Plant R, Jones D, Hutchinson A, Thomson J, Ashburn A,Loader S, et al. Physiotherapy in Parkinsons disease - referral,contact and discharge patterns. MovDisord 2000;15 (Suppl3):171
REFERENCE

Plant R & Jones D (2001) Guidelines for physiotherapy with Parkinsons disease. London: Institute of Rehabilitation, University of Northumbria Plant R (2000) Physiotherapy for people with Parkinsons disease: UK best practice short report, Institute of Rehabilitiation, University of Northumbria, Newcastle Rehabilitiation, upon Tyne. Rescue Project www.rescueproject.org/overview/welcome.htm Poewe WH, Wenning GK. The natural history of Parkinsons disease. Ann Neurol 1998 Sep;44(3 Suppl 1):S1-S9. 1):S1Pressley JC, Louis ED, Tang MX, et al. The impact of comorbidity disease and injuries on resource use and expenditures in parkinsonism.Neurology 2003;60:87 2003;60:8793. 93 Reuter I, Engelhardt M, Stecker K, Baas H. Therapeutic value of exercise training in Parkinsons disease. Med Sci Sports Exerc1999 Nov;31:1544-9 patients. Nov;31:1544NeuroRehabilitation 2002;17(2):161-8. 2002;17(2):161-
REFERENCES

Scandalis TA, Bosak A, Berliner JC, Helman LL, Wells MR.Resistance training and gait function in patients withParkinsons disease. Am J Phys Med Rehabil 2001 Jan;80(1):38-43. Jan;80(1):38Schenkman M et al (1989) Management of individuals with Parkinsons disease: Rationale and case study Physical Therapy 69(11),944955 69(11),944 Stallibrass C (1997) An evaluation of the Alexander technique for the management of disability in Parkinsons disease a preliminary Rehabilitation 11,8 11,812
REFERENCE

Schenkman M, Cutson TM, Kuchibhatla M, Chandler JM,Pieper CF, Ray L, et al. Exercise to improve spinal flexibility and function for people with Parkinsons disease: a randomized,controlled trial. J Am Geriatr Soc 1998;46:1207-16. 1998;46:1207Schrag A, Jahanshahi M, Quinn N. How does Parkinsons diseaseaffect quality of life? A comparison with quality of life in the general population. Mov Disord 2000;15:11121118 2000;15:1112 Schrag A, Jahanshahi M, Quinn N. What contributes t oquality of life in patients with Parkinsons disease? J NeurolNeurosurg Psychiatry 2000;69(308):312.
REFERENCE

Schultz JH, Luthe W. Autogenic therapy methods. New York:Gruen and Stratton. New York: Gruen and Stratton; 1969. Stolze H, Klebe S, Baecker C, et al. Prevalence of gait disorders in hospitalized neurological patients. Mov Disord 2005;20:8994. 2005;20:89 Thaut MH, McIntosh GC, Rice RR, Miller RA, Rathbun J,Brault JM. Rhythmic auditory stimulation in gait training forParkinsons disease patients. Mov Disord 1996 Mar;11(2):193-200 Mar;11(2):193Wenning GK, Ebersbach G, Verny M, Chaudhuri KR,Jellinger K, McKee A, et al. Progression of falls in postmortem-Confirmed postmortemparkinsonian disorders. Mov Disord 1999Nov;14(6):947-50. 1999Nov;14(6):947World Health Organisation (1980) The international classification of impairments,disabilities and handicaps A manual of classification relating to the consequences of disease. Geneva; WHO
THANK YOU VERY MUCH FOR YOUR ATTENTION
QUESTIONS AND COMMENT. COMMENT.

Irogue Seminar Presentation October 2010

Caricato da

Informazioni sul documento

Copyright

Formati disponibili

Condividi questo documento

Condividi o incorpora il documento

Opzioni di condivisione

Hai trovato utile questo documento?

Questo contenuto è inappropriato?

Copyright:

Formati disponibili

Irogue Seminar Presentation October 2010

Caricato da

Copyright:

Formati disponibili

PHYSIOTHERAPY IN THE MANAGEMENT OF PARKINSONS PARKINSONS DISEASE

To inform our knowledge of current evidenceevidencebased recommendations of physiotherapy in Parkinson's disease.

Overview of Parkinsons disease

Why Parkinsons disease ?

In 1880, Charcot listed PD as the 5th most common disease.

CLASSIFICATION BASED ON AETIOLOGY

Primary or idiopathic Parkinsons disease Secondary or acquired or symptomatic Parkinsons disease

PRIMARY OR IDIOPATHIC PARKINSONS DISEASE

Rest tremor Rigidity Bradykinesia Postural instability

(The first three are together called the classical triad)

SECONDARY OR SYMPTOMATIC OR ACQUIRED PARKINSONISM

parkinsonia features, with various combinations of pyramidal, cerebella, and autonomic

Examples of Parkinson-plus syndrome are: Parkinson1) PROGRESSIVE SUPRANUCLEAR PALSY:

Examples of Parkinson-plus syndrome: Parkinson2) MULTIPLE SYSTEMIC ATROPHY

3) LEWY BODY DEMENTIA 4) VASCULAR PARKINSONISM 5) PUGILISTIC ENCEPHALOPATHY (TRAUMA)

Examples of Parkinson-plus syndrome: Parkinson6) POST ENCEPHALOPATHY

The diagnosis of PD is based on the clinical symptoms & signs.

Single Photon Emission Computerised Tomography (SPECT).

Guttman, M. et al. CMAJ 2003;168:293-301

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

It is a rhythmic involuntary movement normally affecting the limbs.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Rigidity is defined as resistance to passive motion that is not velocity dependent.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Present in almost all cases of PD

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Patient feels hesitation on initiation of movements & early fatigue.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Parkinsonian gait / Freezing / Festinating / Shuffling / Toe heel / Hurrying gait.

Loss of arm swing & pelvic rotation.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

There is an overall decrease in total number of movements. movements.

Movement impoverishment can lead to mental fatigue & loss of motivation.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Patient shows the effects of generalized musculoskeletal deconditioning.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Scoliosis generally results from unequal distribution of rigidity in the trunk.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Dysphagia is the result of rigidity,reduced mobility& restricted range of movement.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

7) VISUAL & SENSORIMOTOR DISTURBANCES

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Postural stress syndrome.

Dementia occurs in approximately 1/3rd of the patients with PD.

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

CLINICAL PRESENTATION OF PARKINSONS DISEASE

Drug related psychoses can occur.

10) AUTONOMIC DYSFUNCTION

Dysautonomia ; autonomic nervous system dysfunction occurs in patient.

Sleep: Bowels Bladder Pain Postural hypotension * Sexual dysfunction Sweating

Assessment instrument: Goniometer (9) TREMORS ::

PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE (10) SENSORY INTEGRITY:

PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE (15) AUTONOMIC CHANGES:

(2) ALTERED LUNG VOLUMES & CAPACITIES:

PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE (3) ALTERED VITAL SIGNS:

PHYSIOTHERAPY MANAGEMENT OF PARKINSONS DISEASE FUNCTIONAL STATUS:STATUS: