Parkinson's disease is a progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra. Its main symptoms include bradykinesia, tremors, rigidity, and postural instability. Diagnosis is based on the presence of two or more of these cardinal symptoms. Treatment involves pharmacological management using levodopa and dopamine agonists as well as physiotherapy focusing on exercises to improve flexibility, strength, balance, gait, and pulmonary function. Surgery such as deep brain stimulation may also be used in advanced cases.

1. PARKINSON’S
DISEASE
Khairul Nizam bin Abdul Rahman
4262143008
Neurology
BPY 1
Sir Jibi

2. INTRODUCTION
• Parkinson’s disease (PD) is a chronic progressive neurodegenerative disorder and is
the second most common cause of chronic neurological disability. Although PD is
usually classified as a movement disorder, it also causes disorders of cognitive
function.

3. ETIOLOGY
• The term parkinsonism is a generic term used to describe a group of disorders with
primary disturbances in a dopamine systems of basal ganglia.
• Parkinson’s disease or idiopathic parkinsonism is the most common form.
• Secondary parkinsonism results from a number of different identifiable causes
including viruses, toxins, drugs, and tumors.
• Parkinsonism-plus syndromes refers to those condition that mimic PD in some
respects, but the symptoms are caused by other neurodegenerative disorders.

4. PATHOPHYSIOLOGY
• Parkinson’s disease is defined by (1) degeneration of dopaminergic neurons in the
BG in the pars compactus of the substania nigra that produce dopamine and (2) as
the disease progresses and neurons degenerate, the presence of cytoplasmic
inclusion bodies called, Lewy bodies.

5. PATHOPHYSIOLOGY
• Loss of dopaminergic pigmented neurons in the substania nigra (SN) pars compacta
with dopaminergic deficiency in the putamen and caudate nucleus.
• Dopamine loss in other brain areas including the brainstem, thalamus and cortex
also occurs.
• Degeneration of the dopaminergic nigrostriatal pathway to the basal ganglia results
in underactivity of the direct motor pathway (normally facillates movement) and
overactivity of the indirect motor loop (normally inhibits movement).
• This results in inhibition of the motor cortex manifested with bradykinesia and
rigidity.

6. PATHOPYSHIOLOGY
• Lewy bodies, fibrillary intracellualar eosinophilic inclusions, and high concentrations of
alpha-synuclein, ubiquitin, tauprotein, tuberculin, and other proteins are found in the
SN, LC and other areas of the brain and are a marker for neuronal degeneration.
• Degeneration of the locus coeruleus LC, which contains noradrenergic neurons, also
occurs in PD. Norepinephrine is thought to be neuroprotective and loss of LC neurons
may be associated with a worsening of disease progression and the behavioural
symptoms of PD.
• Molecular events thought to be associated with the neurodegeneration of PD include
mitochondrial dysfunction, oxidative stress, abnormal folding and accumulation of
alpha-synuclein, abnormal phosphorylation and dysfunction of the ubiquitin proteasome
system.

7. 1)The cortex will increase the inhibitory action of
neostriatum.
2)Due to increased inhibitory action,the globus pallidus
internus inhibitory action is decreased or inhibit by
neostriatum.
3)When inhibitory action of the globus pallidus
decreased,the excitatory action of thalamus is increased.
4)The thalamus excites the cortex,thus movement initiated.
5)The substantia niagra compacta will receive a cortical
input from the motor cortex that a movement will occur.The
dopamine neurotransmitter will activate the cortical input.
6)Once receive the cortical input,the substantia niagra
compacta will stimulate the direct pathway and inhibit the
direct pathway.
7)In Parkinson disease,there will be decreased in dopamine
that will cause inactivation of the cortical input.
8)Inactivation in cortical input will make the complication
in substantia niagra to stimulate direct pathway and
inhibit direct pathway.
9)Thus,Parkinson disease associated with the decrease of
dopamine cause substantia niagra cannot receive a cortical
input from cortex to stimulate movement.

8. STAGES OF PARKINSON’S DISEASE
Stages 1
• Lesions are found in the medulla oblongata
Stages 2
• Pathology is expanded to involve lesions of the caudal raphe nuclei, the gigantocellular reticular nucleus, and
coeruleus-subcoeruleus complex.
Stages 3
• Involvement of the nigrostriatal system is apparent
Stages 4
• Lesions are also found in the cortex
Stages 5
• Pathology is extended to involve the sensory association areas of the neocortex and prefrontal neocortex.
Stages 6
• Pathology is extended to involve the sensory association areas of the neocortex and premotor areas.

9. CLINICAL FEATURES
Major symptoms:
• Bradykinesia
• Tremor
• Rigidity
• Postural Instability
Other motor symptoms:
• Gait
• Loss muscle performance
• Loss motor function
• Sensory problem
• Dysphagia
• Speech disorder
• Cognitive dysfunction
• Autonomic dysfunction
• Sleep disorders
• Depression and anxiety

10. BRADYKINESIA
• Bradykinesia is a poverty of voluntary movement with a slower initiation of
movement.
• And a progressive reduction in the speed and amplitude of repetitive actions.
• Weakness, tremor and rigidity may contribute to bradykinesia.
• Bradykinesia is a mandatory sign; no bradykinesia means no PD.

11. TREMOR
• Tremor involves involuntary shaking or oscillating movement of a part or parts of
the body resulting from contractions of opposing muscles.
• In early stages, most patient experience a slight tremor of the hand or foot on one
side of the body, or less commonly in the jaw or tounge.
• Tremor is known as resting tremor because it is present at rest, suppressed briefly
by voluntary movement and disappears with sleep.
• Tremor in lower limbs is most apparent while the patient is supine.
• Tremor of the head and trunk can be seen when muscles are used to maintain an
upright posture against gravity.

12. RIGIDITY
• Rigidity is experienced as stiffness and muscular pain.
• Increase resistance to passive motion.
• Patients frequently complain of heaviness and stiffness of their limbs.
• It is felt uniformly in both agonist and antagonist muscles.
• Spinal stretch reflexes are normal.
• Rigidity is fairly constant regardless of the task, amplitude, or speed of movement.
• Prolonged rigidity results in contracture and postural deformity.

13. POSTURAL INSTABILITY
• Abnormalities of posture and balance.
• Abnormal and inflexible postural responses controlling their centre of mass within
their base of support.
• Experience increased difficulty during dynamic destabilizing activities such as self-
initiated movements.
• And perform poorly under conditions of perturbed balance.
• Difficulty in regulating feed-forward, anticipatory adjustments of postural muscles
during voluntary movements.

14. GAIT
• Involuntary flexion of the trunk limbs and the neck.
• Hesitation in starting to walk.
• Steps are short and the feet barely clears the ground as patient shuffles
along.
• Once walking started patient takes increasingly short and rapid steps as
though trying to catch up to his centre of gravity.
• Freezing briefly when encountering doorways or other obstacles.
• Diminished or reduced arm swing.
• Inability to make appropriate postural adjustments to tilting and falling.
• Anticipatory and compensatory righting reflexes are impaired.

15. MUSCLE PERFORMANCE
• A reduction in strength is evident in patients in PD.
• Torque production is decreased at all speeds resulting in activity limitations and
muscle weakness.
• Once initiated, contraction is characterized by multiple bursts and
asynchronization, that is pauses and an inability to smoothly increase firing rate as
contraction continues.
• These difficulties are compound during production of complex movements.

16. MOTOR FUNCTION
• In PD, motor planning deficits are evident, involving a loss regulatory control of
both automatic and voluntary movement responses.
• Paucity of movements occurs with less accurate movements over all.
• This deficit in accuracy becomes more pronounced as the patient attempts to
increase the speed of movement.
• Patients experience difficulty performing complex, sequential, or simultaneous
movements.

17. SENSORY SYMPTOMS
• Patients with PD do not suffer from primary sensory loss.
• However, 50% experience paresthesias and pain including sensations of numbness,
tingling cold, aching pain, and burning.
• Most patients with PD loss sense of smell (anosmia)

18. DYSPHAGIA
• Impaired swallowing is present.
• Is the result of rigidity, reduced mobility and restricted range of movement.
• Demonstrates abnormal tongue control and problems with chewing, bolus formation,
delayed swallow response, and peristalsis.
• Dysphagia can lead to choking or aspiration pneumonia and impaired nutrition with
significant weight loss.

19. SPEECH DISORDER
• Patients with PD experience hypokinetic dysarthria, which is characterized by
decreased voice volume, monotone speech, imprecise or distorted articulation and
uncontrolled speech rate.
• Patient experience timing difficulty of vocal onsets and offsets.
• Voice becoming monotonous, exhibiting reduced volume and lack of rhythm and
variety of emphasis.
• Often associated with problem of swallowing leading to drooling.

20. COGNITIVE DYSFUNCTION
• Impairments in cognitive function can be mild or severe.
• PD dementia occurs in approximately 20%-40% of patients.
• Dementia associated with PD is characterized by loss of executive functions
(planning, reasoning, abstract thinking, judgment) and changes in visuospatial
skills, memory and verbal fluency.
• Bradyphrenia, slowed thinking is seen in patients with PD.

21. DEPRESSION AND ANXIETY
• Demonstrate a variety of symptoms including feeling of guilt, hoplessness and
worthlessness, loss of energy , poor concentration, deficits in short term memory,
loss of ambition, and disturbances in appetite and sleep.
• Suicidal thoughts may also be present.
• Hypomimia, a reduction in facial expressiveness, can give the appearance of
depression.

22. SLEEP DISORDERS
• Patients can experience excessive daytime somnolence (sleepiness).
• At night, insomnia (disturbed sleep pattern).
• This includes problems in falling asleep, staying asleep, and goof quality of sleep.
• Dream-enacting behaviours include agitation and physical activity during sleep (e.g
talking, yelling, punching, kicking and grabbing).

23. AUTONOMIC DYSFUNCTION
• Gastrointestinal disorder
• Constipation
• Urinary incontinence
• Erectile dysfunction
• Airway obstruction
• Restrictive lung dysfunction

24. DIAGNOSIS
• Diagnosis at onset of PD is difficult with accurate diagnosis possible only with
continued observation of evolving clinical signs and symptoms.
• There is no single definitive test or group test used to diagnose the disease.
• The diagnosis is made on the basis of history and clinical examination.
• A diagnosis of PD is typically made if at least two of the four cardinal features are
present.

25. HOEHN-YAHR CLASSIFICATION OF
DISABILITY
Stage Character of Disability
I Minimal or absent; unilateral if present
II Minimal bilateral or midline involvement. Balance not impaired
III Impaired righting reflexes.
Unsteadiness when turning or rising from chair.
Some activites are restricted, but patient can live independently and continue
some forms of employment.
IV All symptoms present and severe.
Standing and walking possible only with assistance
V Confined to bed or wheelchair
An estimate of the stage and sverity of the disease

26. PHARMACOLOGICAL MANAGEMENT
• Levodopa (L-dopa).
Nerve cells use l-dopa to make and replenish the brain’s supply of dopamine. L-dopa is often given along with carbidopa. Carbidopa
delays the conversion of levdopa into dopamine until it reaches the brain. This prevents, or diminishes some of the side effects of L-
dopa and reduces the amount of L-dopa needed. L-dopa delays the onset of debilitating symptoms and allows many patients to
extend the period of time they are able to live “normal” lives. Bradykinesia and rigidity respond best and tremor may be only slightly
reduced.
• Bromocriptine, pergolide, pramipexole, and ropinirole.
These drugs all mimic the role of dopamine in the brain.
• Selegiline (deprenyl).
This drug may delay the need of l-dopa therapy. When given with l-dopa, it seems to enhance and prolong the response of l-dopa.
• Anticholinergics.
These may help control tremor and rigidity. They appear to act by blocking the action of acetylcholine.
• Amantadine.
This is an antiviral drug. It is effective at reducing many symptoms, but its efficacy wears off after several months. Effectiveness
may return after a brief withdrawal.

27. SURGICAL APPROACHES
• Implantation
Transplanted fetal mesencephalic cells harvested from aborted foetuses, grown in cell
culture and injected into the brain in a form of cell suspension, have been shown to survive
in the brain and replace the production of dopamine. This surgery disabling dyskinetic
movements.
• Stereotatic surgery and implantation of stimulators
The target for the surgery is thalamus. This has this has been replaced by targeting either
globus pallidus or more recently the STN. The target area of the brain may be lesioned to
reduce its output to benefit the movement disorder or it may be stimulated in order to
inhibit output with similar effect.

28. PHYSIOTHERAPY MANAGEMENT
• Physical activities to prevent muscle weakness, restricted ROM, reduced exercise
capacity and social isolation.
• Assessment to monitor progress and jointly identify management priorities.
• HEP training in the home and community setting
• Modification of treatment and HEP to take account of levels of cognitive impairment,
medication, ageing and multiple pathology.
• Provision of a forum such as regular group session to share information and identify
continuing needs of both individuals and carers.
• Physical management to ensure co-ordination and integration of professional input
around patient centred goals.

29. RELAXATION EXERCISES
• Hook-lying, lower trunk rotation or side lying rolling can be used to promote
relaxation.
• During therapy, slow, rhythmic, rotational movements of the extremities and trunk
can precede interventions such as ROM, stretching and functional training.

30. FLEXIBILITY EXERCISE
• The purpose of flexibility exercise (stretching) is to improve ROM and physical
function.
• A combination of PROM, AROM and PNF exercise is used to achieve maximum
ROM.
• Flexibility exercise should be performed a minimum 2 to 3 days per week and a
minimum of 4 repetitions per stretch for 15 to 60 seconds.

31. RESISTANCE TRAINING
• Resistance training (strengthening) is indicated for muscle weakness.
• Weakness of muscles associated poor posture and functional deficits.
• Strengthening has been show to improve muscle force, bradykinesia
and quality of life in PD.
• Starting with lower intensity than load can be applied using
resistance machines, free weights elastic resistance bands or
manually.
• Strengthening can be performed 2days per week.

32. FUNCTIONAL TRAINING
• The exercise program should be based on focused practice of functional skills.
• Progression to more difficult motor activities should be gradual.
• Bed mobility skills
• Sitting
• Sit-to-stand
• Standing

33. BALANCE TRAINING
• Important focus of balance training is on COG centre of gravity and BOS base of
support.
• Patients should be instructed how COG influences balance and how to improve
posture in sitting and standing.
• Patient should also explore their BOS and practice working toward expanding
them in sitting and standing.
• Balance training should emphasize practice of dynamic stability task (eg. Weight
shifts, alternating unilateral weight-bearing, reaching and axial rotation of head
and trunk)
• Seated activities can include sitting on a compliant surface (inflatable disc).

34. LOCOMOTOR TRAINING
• Locomotor training goals focus on reducing primary gait
impairments, which typically include slowed speed, and shuffling gait
pattern.
• Goals also focus on increasing patient’s ability to safely perform
functional mobility activities and prevent falls.
• Large step and arm swing were more effective instructional
strategies than the command to walk fast.
• Sidestepping and crossed-step walking also can be practiced.

35. SPINAL ORTHOTICS
• Spinal bracing may be an appropriate adjunct to therapy for patients
with postural deformities.
• Thoracolumbar orthosis is not only corrects faulty posture but also
has been shown to increase trunk stability and also increase
respiratory vital capacity.
• When brace was use for 6month, 73%increase in back extensor
strength and 58% increase in abdominal flexor strength.

36. PULMONARY REHABILITATION
• Diaphragmatic breathing exercises, air shifting techniques, exercise that recruit
neck, shoulder and trunk muscles.
• Manual techniques such as vibration and shaking can be used to ensure complete
exhalation, distal alveoli opening, and to assist with secretion clearance.

37. SPEECH THERAPY
• Lee Silverman Voice Treatment was designed specifically for PD patient.
• It focus on intensive high-effort exercise with a single functionally relevant target
(loudness) and a recalibration of self-perception of vocal loudness.
• This technique effectively increases vocal loudness and improves facial expressions.

38. HOME EXERCISES PROGRAM
• HEP include exercises designed to improve relaxation, flexibility, strength and
cardiopulmonary function.
• Early morning warm-up often helpful in reducing stiffness.
• Stretching and strengthening exercises.
• ROM exercises.
• Balance activities.
• HEP should be realistic and of moderate duration and intensity.