BY : ABBAS ALAM

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Abbas Alam

Anatomy of BG
Grey matter masses located within cerebral hemisphere 3 nuclei located at base of cerebral cortex: Caudate nucleus Putamen Globus pallidus 2 brainstem nuclei: Substantia nigra Subthalamic nucleus of Luys.
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Substantia Nigra:
A component of midbrain Extends from level of Subthalamus to upper Pons

Subdivisions:

Pars Compacta: containing pigmented neurons

Pars Reticulata: contains nonpigmented neurons

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 Dopaminergic neurons in substantia nigra

Pigmentation due to neuromelanin in cytoplasm Neuromelanin: combined product of autooxidation of DOPAMINE(DA) & LIPOFUSCIN

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Function :1. Inhibition of muscle tone. 2. Co-ordination of slow, sustained movements. 3. Supression of useless patterns of movement. 4. Works as internal cues system.

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HEAD

TAIL

It is an elongated arched gray matter mass, with head, tail and amygdaloid nucleus at its tip. Function:1. Learning and memory. 2. Language comprehension. 3. It has some cognitive funtions also..
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Is also a botanical name for the stone in a fruit such as peach. Function: 1. Regulate movements & influence various types of learning. 2. It employes dopamine to perform its function. 3. It has role in automatic performance of previously learned movements.(as in parkinsons). 4. In a study it was found that the putamen controls limb movement and is a part of Brains HATE circuit.
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Is situated below red nucleus. Made up of small unpigmented cells and large pigmented cells and the pigment contains high quality of iron.

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Also known as paleostritum. Is a subcortical structure of brain. Function: 1. Is involved in the planning and inhibition of movements from the dorsal striatopallidal complex.

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The basal ganglia are found lateral and inferior to the lateral ventricles.

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The caudate nucleus lies alongside the lateral ventricle.

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The caudate nucleus forms a long thin tube curving around the side of the lateral ventricle.

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The caudate nucleus forms a long thin tube curving around the side of the lateral ventricle.

It is attached by spokes of grey matter to the putamen, a bean-shaped nucleus inferior and lateral to the caudate 11/26/2010 AbbasAlam

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The caudate and putamen are functionally closely related. The globus pallidus has a separate function. In old text books, the putamen and globus pallidus are sometimes referred to as the lenticular nucleus.
Caudate Internal capsule (anterior limb)

Putamen

Lenticular nucleus

The caudate is incompletely separated from the putamen & globus pallidus by the bundle of fibres known as the internal capsule
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Globus pallidus

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The caudate, internal capsule and putamen are often referred to together as the striatum. Striatum means striped and the two regions of grey matter with a white matter sandwich between them always has a striped appearance.
Caudate Internal capsule (anterior limb)

striatum Neostraitum
Putamen

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Globus pallidus AbbasAlam

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The basal ganglia and internal capsule are all supplied by the first part (m1) of the middle cerebral artery Caudate Blood Supply
Internal capsule (anterior limb) lenticulostriate arteries

Putamen

Small arteries branch off the mca and supply the basal ganglia; these are the lenticulo-striate arteries
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Globus pallidus

middle cerebral artery

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Afferent pathways: Structures: Caudate & Putamen

Input from: Entire cerebral cortex Intralaminar thalamic nucei Centromedian-parafascicular complex of thalamus

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CORTEX

THALAMUS

INPUT SIGNALS

CENTROMEDIANPARAFASCICULAR COMPLEX

CAUDATE/PUTAMEN

SUBSTANTIA NIGRA

GLOBUS PALLIDUS

THALAMUS & MOTOR CORTEX

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SUBTHALAMIC NUCEI

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EFFERENT PATHWAYS: Structures:

External
Globus pallidus

Internal Dorsal pars compacta

Substantia nigra

Ventral pars reticulata

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PATHWAYS:
No direct pathway to spinal cord or periphery from BG Direct pathway Indirect pathway

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Direct Pathway
Direct connection between striatum (striosomes) and globus pallidus internal

PPN

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CORTEX ACTIVATES STRIATAL NEURONS

INHIBIT
MEDIAL GLOBUS PALLIDUS & SN pars reticulata

INHIBIT

THALAMIC NUCEI

Supplementary motor area & Prefrontal cortex

WHEN a specific motor behavior is selected : cortical activation of striatum : disinhibition or excitation of thalamic nuclei : activate supplementary motor area & prefrontal cortex( concerned with generation of motor programs)
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CORTICAL ACTIVATION OF BG results in a facilitation of selected motor programmes

Striatal neurons also receive excitatory dopaminergic

input from SN pars compacta.

In PD: LOSS OF DOPAMINERGIC NEURONS:

reduction in activity of DIRECT PATHWAY

REDUCED FACILITATION & SUSTENANCE OF

MOTOR PROGRAMMES & DESIRED MOVEMENTS

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Indirect Pathway
Indirect connection between the striatum (matrix) and globus pallidus internal via globus pallidus external and subthalamic nucleus
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PPN

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CORTEX EXCITES STRIATAL NEURONS

INHIBIT
LATERAL GLOBUS PALLIDUS INHIBIT SUBTHALAMIC NUCLEUS EXCITES MEDIAL GLOBUS PALLIDUS & SN pars reticulata INHIBIT
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THALAMIC NEURONS
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 CORTICAL ACTIVATION OF STRIATUM VIA

DISINHIBITION OF SUBTHALAMIC NUCLEUS SERVES TO INHIBIT THALAMUS

THUS, indirect pathway is responsible for suppression of

unwanted motor behavior

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 Striatal neurons receive inhibitory input from SN pars

compacta
In PD: loss of indirect pathway leads to increased

subthalamic nuclear activity resulting in an excessive suppression of unwanted movts & inability to switch to new motor programmes

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In PD:
INDIRECT PATHWAY FOR SUPPRESSION OF

MOVEMENTS IS OVERACTIVE
DIRECT PATHWAY THAT FACILITATES &

MAINTAINS MOTOR BEHAVIOR IS UNDERACTIVE

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 BG ACTIVATE ONLY THE MOST NECESSARY

PATHWAYS & INHIBIT UNNECESSARY PATHWAYS

UNDERACTIVE DIRECT PATHWAY &/or OVERACTIVE

INDIRECT PATHWAY: DECREASED ACTIVATION OF CORTEX & HENCE BRADYKINESIA & AKINESIA
OVERACTIVE DIRECT PATHWAY &/or UNDERACTIVE

INDIRECT PATHWAY: PRESENCE OF EXTRANEOUS MOVEMENTS

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NEUROTRANSMITTERS
Dopamin (DA)
Acetylcholine (Ach) Gama aminobutyric acid(GABA) Substance P Enkephalins & Endorphins
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DOPAMINE:
Major neurotransmitter of nigrostriatal pathway Produced in SN pars compacta Excitatory to neurons in direct pathway &

inhibitory to neurons indirect pathway

Thus, loss of DA : loss of excitation of direct

pathway & excess of excitation of indirect pathway: powerful decrease in activation of THALAMOCORTICAL pathway
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ACh:
Neurotransmitter of small interneurons of caudate &

putamen
Inhibit action of DA Must be IN BALANCE with DA

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General Clinical Characteristics of Degenerative Diseases

Two outstanding characteristics:

(1) Tend to affect specific parts or functional systems of the nervous system (2) Begin insidiously, after a long period of normal nervous system function, and pursue a gradually progressive course that continues for many years, often a decade or longer
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3 characteristics motor disturbances in BG disease:

Tremor & other involuntary movts

Changes in posture & muscle tone

Poverty & slowness of movt WITHOUT paralysis

Disorders of BG may result in either diminished movt( PD) or excessive movt (Huntingtons disease)
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Parkinsonism
Clinical syndrome characterized by a disorder of movement which consists of

Resting tremor Rigidity Bradykinesia Postural abnormalities

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 6 CARDINAL FEATURES:
1. 2.

3.
4. 5.

6.

Tremor at rest Rigidity Bradykinesia-hypokinesia Flexed posture Loss of postural reflexes Freezing phenomenon

Atleast 2 of cardinal features, with atleast one being either tremor at rest or bradykinesia, must be present for a diagnosis of definite Parkinsonism
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CLASSIFICATION
A. Primary Parkinsonism

1. Parkinsons disease (Shaking Palsy)

2. Juvenile Parkinsonism

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B. Secondary Parkinsonism
1. Infections

Encephalitis lethargica

2. Drugs

Phenothiaxines Tetrabenzine Dopamine receptor blockers(antipsychotics/neuroleptics, antoemetics)

3. Toxins

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MPTP(1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine) Manganese, CS2, CO, Cyanide etc

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4. Vascular

Multiinfarct disease (Atherosclerotic Parkinsonism)

5. Metabolic

Abnormal calcium metabolism, Hypo/ Parathyroidism Chronic hepatocerebral degeneration

6. Traumatic

Multiple brain damage- Punch boxers syndrome

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C. Parkinson Plus Syndromes

1. Progressive Supranuclear palsy (PSP)
2. Multiple System Atrophy (MSA) 3. Hereditary disorders

Huntingtons Chorea Hallevorden-Spatz disease

4. Dementia Syndromes

Alzheimers disease Cortico-Basal-Ganglionic Degeneration (CBGD) Diffuse Lewy body disease

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D. Other Extrapyramidal Syndromes

Olivo-Ponto-Cerebellar Atrophy (OPCA)
Shy Drager syndrome Striato-nigral degeneration Wilsons disease

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Parkinsons Disease

James Parkinson in 1817 Paralysis agitans

Shaking Palsy
> 60 Years Insidious onset Slow Progression Males > Females
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 First described by : James Parkinson (1817)

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 a running pace, the senses and intellect being uninjured.
An essay on THE SHAKING PALSY
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 1867: Troursear : noted muscular rigidity &

cogwheeling
1877: Charcot: named it Parkinsons Disease 1913: Lewy: described concentric hyaline cytoplasmic

inclusion
1919: Tretiakoff: first to observe characterstic lesions of

substantia nigra
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 PD was the first disease of nervous system to be

identified as a molecular disease caused by a specific defect in transmitter metabolism

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Definition
Parkinson disease (PD) is a chronic progressive

neurodegenerative disorder associated with a loss of dopaminergic nigrostriatal neurons; characterized by cardinal features of rigidity, akinesia, bradykinesia, tremor & postural instability
It is named after James Parkinson, the English physician

who described the shaking palsy in 1817.

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Natural history of disease:

As a rule: begins between 40 and 70 years of age, with

the peak age of onset in the sixth decade. It is infrequent before 30 years of age

M>F

Predisposing factors: Trauma, emotional upset,

overwork, exposure to cold, rigid personality, and so on countries, all ethnic groups, and all socioeconomic classes

Idiopathic Parkinson disease is observed in all

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Pathology
Loss of atleast 60% of dopaminergic neurons in pars compacta of substantia nigra Presence of Lewy bodies in surviving neurons of substantia nigra Striatonigral degeneration

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 Degeneration of nerve cells & fibers in Pallidum: basis

of postural dysequilibrium, bradykinesia & other negative symptoms

Degeneration of Putamen: rigidity

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 APOPTOSIS:

PROGRAMMED CELL DEATH

NECROSIS:

ACCIDENTAL CELL DEATH

Sequential process initiated by cell itself in which genetic material of cell is enzymatically degraded
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Neuronal Loss
Substantia nigra Focal loss of

Non-ngro-striatal system 30-90% cases Neurons involved: Tegmental area of

dopaminergic neurons in substantia nigra pars compacta

Cell loss more in rigid-

akinetic than in tremor dominant form

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midbrain Nor-adrenergic locus in pons

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LEWY BODY:
Described by Lewy in 1913 Major pathological feature in PD Intracytoplasmic circular or oval structures, approx

5-25 micrometer in diameter

Consists of a characteristic dense central core & a

clear peripheral halo

Located in cell body of affected neurons
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Possible mech. of formation of lewy bodies: Abnormal processing of neurfilaments & subsequent failure of their transport into axons
A diagnosis of PD is rarely confirmed without presence

of Lewy bodies in substantia nigra

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Coronal section of the brain, showing nigrostriatal pathways and location of selective dopaminergic degeneration in patients with Parkinson's 11/26/2010 AbbasAlam 58 disease

CORTICAL

ATROPHY???????????

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 Dopamine Activation of nigro-striatal pathway

Inhibition of Direct Pathway

Facilitation of Indirect pathway

Rigidity

Bradykinesia
Akinesia

Tremors

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ETIOLOGY
Unknown

Recent discoveries: several factors involved, operating simultaneously or sequentially

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 Environmental factors:

Exogenous neurotoxins
Infectious agents: viruses
Endogenous neurotoxins(oxidative stress)

hypothesis
Mitochondrial hypothesis

enzyme complex in mitochondria

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 Genetic hypothesis

Controversial Gene defect: PARK2 on chromosome 6q25.2-q27

Other factors:

Aging ?????????? (PD IS NOT JUST AN EXAGGERATION OF NORMAL AGING) IN AGING: LOSS OF NEURONS OCCUR IN DORSAL TIER OF SN pars compacta IN PD: NEURONS OF VENTRAL TIER ARE MOST AFFECTED
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SMOKING:
NON-SMOKING is an established

risk factor for PD

POSSIBLE EXPLANATION: 1. Nicotine is a pyridine derivative & may

compete with uptake of MPTP like toxins 2. Toxin activity is 25% lower in smokers as compared to non-smokers 3. CO as a reducing agent diminishes some of the oxidative stress

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 SMOKING DOES NOT AMELIORATE

PATHOGENETIC PROCESS

SMOKING IS INJURIOUS TO HEALTH

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 PERSONALITY:

Relatively quiet, uncreative, rule abiding features

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CLINICAL FEATURES

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 Overactive indirect pathway:

AKINESIA, RIGIDITY Underactive indirect pathway: CHOREA, HEMIBALLISMUS

Overactive direct pathway:

DYSTONIA, ATHETOSIS Underactive direct pathway: BRADYKINESIA

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Initial Symptoms in Patients with PD

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CARDINAL FEATURES
TREMOR

RIGIDITY
BRADYKINESIA/AKINESIA POSTURAL PROBLEMS

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Rigidity
Resistance to passive movements which in NOT velocity dependent; ROM

Increase in tone in agonists and antagonists

Unequal in distribution Sensation of heaviness or stiffness of limbs

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2 types:
Lead pipe: constant, uniform resistance to passive movt with no fluctuations Cogwheel: a jerky, rachetlike resistance to passive movt as muscles alternately tense &

relax

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 Involves axial & limb girdle musculature before

peripheral segment
Affects proximal muscles first esp. shoulders & neck Progresses to face & extremities

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SIGNPOST PHENOMENON:
Depends upon rigidity of wrist extensor muscles Pt. asked to rest his elbow on a table with forearm

in vertical position & to let his arms & wrist joint relax
Healthy people: wrist joint assumes a flexed

posture of about 90 degrees in relation to forearm

Parkinsonian patients: wrist more or less extended

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 No direct relationship between degree of rigidity &

postural deformities of head & trunk

Severe degree of rigidity can cause a relative

REDUCTION OF TENDON REFLEXES REFLEXES ARE NOT OTHERWISE ALTERED IN PD

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 Loss of bed mobility

Loss of arm swing

Muscle ache and stiffness

Energy expenditure

Secondary complications

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Contractures Deformities
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Pathophysiological basis of Rigidity:

Conflicting opinions 2 opposing schools of thought:

Hyperactive gamma-efferent system 2. Release of alpha motor neurons from supraspinal control
1. RIGIDITY IS DUE TO AN ALTERATION OF

NORMAL BALANCE BETWEEN ALPHA & GAMMA MOTOR SYSTEM

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Bradykinesia
Slowness or poverty of movements Bradyphrenia Reaction time ADL difficulties

Bathing
Dressing

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Getting up & turning in bed

Loss of dexterity (buttoning)
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 Mask like Face( HYPOMIMIA)

Blinking Continuous starring expression Constant frowning

Loss of expressive gesture

Mi

crogr

aphia

( terminal)

Sialorreah(excessive salivation): due to immobility of

mouth,tongue & palatal muscles. NO INCREASED

PRODUCTION OF SALIVA
Dysphagia
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 AKINESIA
HYPOKINESIA BRADYKINESIA

HYPOKINESIA IS INDEPENDENT OF RIGIDITY

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Tremor
Involuntary oscillation of a body part Excitation of cholinergic pathway

Resting type

with stress
With goal directed movements

Absent in sleep PILL ROLLING TREMOR

4 6 Hz
Absent during sleep
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 Cogwheel phenomenon, or Negros sign: Even the

least degree of tremor is felt during passive movement of a rigid part

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Origin of Parkinsonian tremors:

Posterior part of lateral ventral nucleus of thalamus

is a relay station of complex neural pathway concerned with tremor mechanism

Corticopallidal fibres: important link

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 Affects distal segments of limbs first

Upper limbs more than lower Greater amplitude & constancy in arm than in leg

Spread from arm to leg of same side is THE RULE

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Postural abnormalities
Stooped posture Flexion of head, trunk & extremities Loss of postural reflexes Loss of protective mechanisms

Fear of fall and injury

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 Extensor muscles of trunk more weak than

flexors

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Quality of postural movements

The patient is slow and ineffective in attempts to deliver a

quick hard blow

Cannot complete a quick (ballistic) movement

Alternating movements, at first successful, if repeated

become progressively impeded and finally are blocked completely or adopt the rhythm of the patients alternating tremor
Also, the patient has difficulty in executing two motor acts

simultaneously (BIMANUAL TASKS)

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 The difficulty is not one of rigidity but one of

bradykinesia (slowness in both the initiation and execution of movement in contrast to the reduced frequency and amplitude of movement, hypokinesia), the extreme degree of bradykinesia being akinesia, in which the patient is motionless

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 Despite a perception of muscle weakness, the patient

is able to generate normal or near-normal power, especially in the large muscles; however, in the small ones, strength is slightly diminished.

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KINESIS PARADOXICA: In the excitement of some unusual circumstance (as escaping from a fire, for example), the patient with all but the most advanced disease is capable of brief but remarkably effective movement

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Gait abnormalities
Festinating gait

Shuffling gait

Hurrying gait

Freezing phenomenon

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Characteristics of gait
Stooped

posture length

Short step

Cadence

Loss of

arm swing

Propulsive/Retropulsive Tries

to catch up his COG

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Visual disturbances Decreased blinking

The usual blink rate (12 to 20 per

minute) is reduced to 5 to 10 per minute

Blurring of vision
Diplopia

Impaired color-contrast sensitivity

+ ve Glabellar tap
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Asthenia

Generalized weakness

Deconditioning and rigidity

Sensory Involvement

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Generalized body pain and cramps Inactivity & stiffness

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Psychological Impairment

Dementia

Depression

Perceptual defects

Body scheme Body image Topographical disorientation

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Autonomic Dysfunction

Orthostatic hypotension

Sweating disorders

Bladder & Bowel disturbance

Urinary urgency and frequency Constipation

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Sleep disturbances

Insomnia Fragmented nocturnal sleep Excessive daytime drowsiness Rapid eye movement sleep behavior disorder

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Other features
Weight loss Limb paresthesias Restless legs syndrome

Sexual dysfunction
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Elicitable Neurologic Signs

Myerson sign: an inability to inhibit blinking in

response to a tap over the bridge of the nose or glabella (Glabellar tap)
Grasp and Suck reflexes are not present
Buccal and Jaw jerks are rarely enhanced Impairment of upward gaze and convergence

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 Stellwag sign: a slight widening of the palpebral

fissures, creating a stare Limitation of upward gaze, with sparing of downward gaze

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 The bradykinesia may extend to eye movements, in that there is a delay in the initiation of gaze to one side, slowing of conjugate movements Drooling is troublesome; an excess flow of saliva has been assumed, but actually the problem is one of failure to swallow with normal frequency

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 Exceptionally, the reflexes on the affected side are

slightly brisker, which raises the question of corticospinal involvement BUT

The plantar reflex remains flexor

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Secondary complications
Contractures & Deformities (Kyphotic) Muscle atrophy & Weakness Deconditioning of cardiopulmonary system Osteoporosis Edema Skin infections
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Hoehn & Yahr scale

STAGE I
STAGE II

Unilateral Involvement
Bilateral involvement No Postural abnormality

STAGE III

Bilateral involvement Mild Postural abnormality

Independent
STAGE IV Bilateral, moderate postural abnormality Substantial help STAGE V Severe postural abnormality Bedridden/ Wheelchair bound
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DIAGNOSIS
DEFINITE DIAGNOSIS: Neuropathological

examination at autopsy
Presence of CARDINAL FEATURES PD should be excluded if there is no response to

LEVADOPA & if there are cerebellar or pyramidal signs, early dementia, early postural imbalance or falls, early autonomic findings or a significant abnormality of eye movements
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 3 diagnostic categories: 1.

Clinically possible PD: Presence of any 1 of 3 salient features of PD- tremor, rigidity, or bradykinesia. Tremor must be recent onset Clinically probable PD: Combination of any 2 cardinal features- resting tremor, rigidity bradykinesia or impaired postural reflexes Clinically definite PD: A combination of 3 of the features- resting tremor, rigidity, bradykinesia, or impairment of postural reflexes

2.

3.

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PROGNOSIS
PD: a progressive disorder

Rate of progression: variable

Exact prognosis for an individual patient is difficult to

predict
Signs, symptoms & disability: increase with time
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ASSESSMENT
History Observation Examination CT / MRI EMG

EEG
Neuropsychological testing
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Medical Management

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Levodopa

Precursor of dopamine

Crosses BBB & gets converted into dopamine

Carbidopa

Dopa-decarboxylase inhibitor

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Dopamine agonists
Mimic

the action of dopamine

( Dyskinesia)

Bromocriptine

Anticholinergics
Re-balance

Ach levels with dopamine. ( Tremors)

Benztropine

Amantadine

Has anticholinergic properties and

enhances dopamine transmission.

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Symmetrel ( Dyskinesia)
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Side effects

Nausea Vomiting Postural hypotension Dyskinesia Dystonia Response fluctuations

Wearing

off phenomenon

ON & OFF Phenomenon

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Increased diurnal fluctuations (ON-OFF phenomenon):

Presence of periods during the day when patient does not

respond as adequately as he/she normally does to Levadopa. Periods of poor response: OFF periods Persists from 30 min to 3-4 hrs
Once a day to 10 or more times daily Develops within about 5 yrs of start of Levadopa therapy

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WEARING OFF phenomenon :

End of dose deterioration Gradual fading of benefits, occuring usually between 1-

3 hrs after taking Levadopa

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SUDDEN-OFF phenomenon:
Occurs within few seconds More random & unpredictable Patient can improve just suddenly

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Other phenomenon:
Episodic failure to respond Delayed ON

Yo-yo-ing: a combination of dyskinesia &

fluctuation

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Behavioral adverse effects with LEVADOPA: Drowsiness Reverse sleep-wake cycle Vivid dreams Confusion Hallucinations Dementia

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Surgical Management
Stereotaxic surgeries

Pallidotomy
Thalamotomy

Deep brain stimulation

Radiosurgery

Brain cell transplant

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Physiotherapy Evaluation
Chief complaints Onset Past medical history Associated problems Vital signs

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Observation
Mode of ambulation Stooped posture Festinating gait External appliances Hypo mimetic face Smooth and shiny skin Pill rolling tremor Wounds
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Examination
Higher Mental functions

MMSE (Dementia)

Emotional status

Depression

Cranial nerves

II III IV VI VII IX X

(Acuity, colour contrast sensitivity) (EOM, nystagmus, diplopia) (Facial expression) (Dysphagia, Dysarthria, Dysphonia)

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Sensory assessment

Pain and cramps

Muscle tone

Rigidity Time of drug and assessment Due to rigidity

ROM

Muscle power Isometric strength

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Tremor
Location

Frequency
Duration Amplitude Relation to dosage and timing of drug

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Reflexes

or Absent or NORMAL

Rigidity

Posture

Plumbline
Still photography

Video analysis

Posturography
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Pictorial grading system

1) Normal

2)
3)

Head protruding
Head protruding

Marked kyphosis of thoracic spine

Slight flexion at knees & elbow

4)

Marked flexion of trunk, elbows, hips &

knees

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Balance
Static balance
Sit unsupported for 1 minute
Stand without aid for 5 seconds
Perturbations

Dynamic Balance

Forward reach

Stand on one leg without aid for 5

seconds

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Gait assessment
10 meter walkway

Type Assistive aid used Posture Step & stride length Cadence Trunk rotation Arm swing Propulsion / Retropulsion Freezing

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Autonomic function
Drooling
Sweating Skin changes Hypotension
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Cardio-respiratory evaluation
Type Pattern Chest expansion Pulmonary function testing

Six minute walking test

RPE
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Functional evaluation
FIM
Quantity

Quality
Time taken

Fine movements
Buttoning Time taken No of

buttons done

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Evaluation scales
Berg Balance Scale

Timed up and go test

Unified Parkinsons Disability Rating Scale

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Principles of Physiotherapy Management

Early referral to encourage participation in regular

physical activities to prevent muscle weakness, restricted ROM, reduced exercise capacity & social isolation
Ongoing assessment & review, incorporating

patient centered goals & meaningful outcome measures to monitor progress

Targeted intervention for movt difficulties, base on

current knowledge of BG pathology, in context of functional tasks of everyday living

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 Training in home & community

Modification of treatment & home exercise regime to

take account of level of cognitive impairment, medication, aging & multiple pathology
Regular group sessions Multidisciplinary management
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Models of Physiotherapy Management of PD

A. CURE Paradigm/Model

Acute Event

REHABILITATION
Diagnosis

Discharge /Cure

INAPPROPRIATE FOR LONG TERM CONDITIONS

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B. CURRENT Paradigm/Model

Diagnosis Onset of subclinical symptoms

MEDICATIONNO PT

DISABILIT Y

Learning of Coping Strategies, Maintenance of Vital functions

REFERRAL TAKING PLACE ONLY WHEN PHARMACOLOGICAL APPROACH BEGINS TO FAIL

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C. PROGRESSIVE paradigm/model
Diagnos Onset of is Subclini cal Prevention of sympto Complications ms & Maintenance of Function

Learning of Coping Strategies

Maintenan ce of Vital Functions

AIMS TO MAINTAIN OPTIMAL FUNCTION OVER TIME BY EARLY & CONTINUING TARGETTED PHYSIOTHERAPY
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WHEN SHOULD PD pts. BE REFERRED FOR PHYSIOTHERAPY???

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 CLINICAL STAGE:

Diagnosis- Maintenance
Reason for referral for physiotherapy: To address concerns about differential diagnosis, e.g.

early onset of postural instability For assessment & monitoring to allow early identification of movt problems Encourage general fitness(CVS, Musculoskeletal, Neuro) Preventive management of secondary complications such as learned non-use To introduce movt strategies Education to pt & family Monitoring drug efficacy
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 CLINICAL STAGE:

Maintenance- early complex

Reasons for PT referral: Specific PT intervention for: Musculskeletal impairment Gait, falls & transfer difficulties Environmental assessment Provision for aids & equipments Advice

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 CLINICAL STAGE:

Late complex- Palliative

Reasons for PT referral:
Fall prevention strategies Promote nutrition, skin care, chest care etc

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Aims of PT Management
To improve / maintain flexibility To prevent secondary complications To prevent / manage falls Posture and balance training Gait retraining To maintain / improve independence in ADL

To improve physical fitness

To improve psychological wellbeing
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METERS
Movement Enablement Through

Exercise Regime & Strategies

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THOSE WHO EXERCISE HAVE LOWER MORTALITY RATES

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ONE OF STRIKING FEATURE OF PD

ABILITY TO MOVE IS NOT LOST RATHER THERE IS AN ACTIVATION PROBLEM

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PRIMARY MOTOR CORTEX, BRAINSTEM & SPINAL CORD ARE MAJOR ANATOMICAL REGIONS INVOLVED IN CONTROL OF SIMPLE, REFLEXIVE MOVTS WHEREAS MORE COMPLEX ACTIONS ARE REGULATED BY CEREBELLAR CIRCUITS & CORTEX-BGCORTEX FEEDBACK LOOP

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TRAIN PEOPLE WITH PD TO BREAK DOWN LONG OR COMPLEX SEQUENCES INTO COMPONENT PARTS &
TO FOCUS THEIR ATTENTION ON PERFORMING EACH PART SEPARATELY

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ALSO, FOCUS ATTENTION ON PERFORMING ONE TASK AT A TIME & AVOIDING DUAL TASK
SIMPLE TASKS SINGLE TASK AT A TIME

COMPLEX TASK
DUAL TASK
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 When 2 activities are performed at the same time, 1 activity is controlled by faulty BG while attention is focused on other activity & task that runs through BG reduces in speed & size

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TASK SPECIFIC/TASK ORIENTED APPROACH

Training within context of functional tasks of everyday living such as walking, standing up from sitting, turning around, moving around in bed, writing, dressing etc

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Treatment of Rigidity
Relaxation techniques

Jacobson Yoga

Transdental meditation
Biofeedback Audio tapes Vestibular ball Rocking Chair

Slow rocking- vestibular stimulation

Cradle

Rhythmic initiation

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 Relaxation better achieved in sitting

Follow a distal to proximal progression

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Tremors
Relaxation techniques

Directing attention towards minimizing tremors Weighted cuffs

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Maintain / Improve Flexibility

Passive movements & Stretching
Therapist Caregiver

Emphasis

on improving extension

Spinal flexibility
Trunk
Upper
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rotation
& lower trunk dissociation
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 Movt throughout a full ROM is crucial, especially early in disease process to prevent changes in properties of muscles
In PD: contractile elements of flexors shortened & of extensors lengthened

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 PNF techniques
D2

Flexion in upper limb

D1

Extension in lower limb

relax

Hold

Contract relax

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Active movements

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Posture re-education
Positioning

PHANTOM PILLOW POSTURE

Pillow

under upper thorax

Stretching Feedback
Visual Verbal

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Mirror/ tape

Command Alert
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BASAL GANGLI CALCIFICATION (PD)

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Balance retraining
Low COG to High COG With support to without support

Static to Dynamic
DO NOT cross the stability limits
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 POSTUROGRAPHY

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SITTING
Maintain sitting (progress with time) Weight shifts Reach outs (Progress with distance) Perturbations (Progress with amplitude)

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 Vestibular ball
Positioning Slow

rocking

Bouncing Reaching

out activities

Trunk

rotations
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SIT to STAND

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SIT to STAND
High stool to Low stool

Teach proper and safe technique

Emphasize on timing

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STANDING
Normal base of support

Weight shifts
Trunk rotations PNF patterns Reaching out activities Perturbations
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Gait Retraining
Use of external cues

Cognitive strategies

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CUES:
VISUAL: floor markers
AUDITORY: music

commands TACTILE: shoulder taps

CONBINATION OF VISUAL & AUDITORY CUES:

BEST

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Parallel bar

Visual feedback

Mirror

(Posture)

Foot prints (Step length and BOS)

Verbal feedback

Command Music

(Heel toe pattern) (Speed of walking)

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Gait Initiation

Pelvic rotation in swing leg Weight transference to stance leg

Assistive aid (Walker)

Not low / high

No rollator

Toe wedge

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Body weight support treadmill training

30%

to 45 %

Reduction

in freezing

Freezing
Marching Step

in place

back before starting side to side

176

Rocking
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Doorways Threshold Narrow spaces WITH VISUAL CUES

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TURNING AROUND:
Most problematic for people with freezing Normal elderly: take 6 steps to complete 360 degree

turn PD: 20 steps

Training: turning in large arc of movt

use full body movt

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IMPROVING ADAPTATION:

Various walking surfaces Obstacles Starting & stopping Turning head while walking

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Prevent / Manage Falls

Improve reaction time Train balance strategies

Improve confidence
Shoe modification Modify home environment Teach techniques

To fall safely

To get off from the floor

To call for help

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Compensatory strategies
Break down complex sequence into simple parts

Arrange the objects in order or sequence

Single task at a time

Use mental rehearsal before any activity

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Improve independence
Aids and adaptations

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 Ambulation

Walker / Stick

Clothing

Loose fitting with velcro straps

Getting up from bed

Elevated head end using blocks Knotted rope to climb up

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 Chair

High Arm rest

Shoe

Propulsion

- Toe wedge

Retropulsion - Heel raise

Reaching

Reachers
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Reaching, grasping, manipulating objects & writing:

Mental rehearsal Visual cueing

Break task into components

Verbal cues Avoid dual task

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Cardio-respiratory exercises
Breathing exercises Chest mobility exercises Clearance of secretions
Postural

drainage

Chest percussion FET

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Improve Physical fitness

General mobility exercises
Calisthenics Walking Cycling Swimming

Individualized exercise program

Group therapy
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Improve Psychological wellbeing

Functional independence

Confidence

Depression

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Group exercises Home exercises Caregiver training Speech therapy Occupational therapy

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ADVANCED NEUROLOGICAL TREATMENT METHODS FOR PARKINSONS PATIENTS

VIRTUAL REALITY

MENTAL IMAGERY
POSTUROGRAPHY BWSTT

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WILSONS DISEASE

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PARKINSONISM-PLUS SYNDROMES

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Hemiparkinsonism-Hemiatrophy Syndrome
Relatively benign Hemiparkinsonism with ipsilateral body

hemiatrophy or contralateral brain hemiatrophy

Usually begins in young adults Tends to be non-progressive Result of brain injury early in life, sometimes even

perinatally
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Multiple System Atrophy

Term introduced in 1969 by Graham & Oppenheimer
A group of disorders characterized clinically by any

combination of autnomic, cerebellar, parkinsonian or pyramidal signs

Parkinsons + Ataxia + Autonomic Dysfunction + CST Neuronal loss of substantia nigra, globus pallidus,

cerebellum, pons, AHC & CST

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Progressive Supranuclear Palsy (PSP) (Steele-Richardson-Olszewski Syndrome)

Most common Parkinsonism-plus syndrome A progressive disorder with onset after age of 40 yrs Diagnostic clinical feature:

Inability to move the eyes voluntarily (Supranuclear Gaze Palsy) Impairment of DOWNWARD & LATERAL gaze Other features: akinesia, rigidity, gait ataxia, pyramidal tract dysfunction, dysarthria & dysphagia
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Thanks for your patience and support

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