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PARKINSON
DISEASES
INTRODUCTION
? Parkinson's disease is a progressive nervous system
disorder that affects movement. Symptoms start
gradually, sometimes starting with a barely
noticeable tremor in just one hand. Tremors are
common, but the disorder also commonly causes
stiffness or slowing of movement.
Parkinson’s disease (PD)
? Parkinson’s disease (PD) is a
chronic, progressive
neurodegenerative disorder
characterized by slowness in
the initiation and execution
of movement (bradykinesia),
increased muscle tone
(rigidity), tremor at rest, and
gait changes.
ETIOLOGY
? Exact cause is unknown
? Heredity
? Family History: Having one or more
close relatives with the disease
increase the rise of getting.
? Advancing age : Above 60 years
mostly seen
? Sex: male are more likely to get
than female.
? Low Estrogen Level: most
menopausal women who don’t use
hormone replacement therapy are
more risk of getting the disease.
like
reserpine,
lithium,
and
? Medications
metoclopramide,
methyldopa,
haloperidol,
chlorpromazine
? Agricultural work: exposure to
such as
environmental toxin
pesticide, herbicides
? Head injury.
PATHOPHYSIOLOGY
Tremor, rigidity and Akinesia
Degeneration of the Dopamine-producing neurons in
the substantia nigra of the midbrain
Disrupts the normal balance between Dopamine (DA)
and acetylcholine (ACh) in the basal ganglia.
Impaired extra pyramidal tract controlling
Loss of motor control
CLINICAL MANIFESTATIONS
? Rigidity:- Defined as increased
resistance to passive motion.
– Cogwheel rigidity: jerky, ratchet
like resistance to
movement and
passive
muscles
alternately tense and relax.
? Tremor:- It is an involuntary
oscillation of body part.
– Parkinsonian tremor is described
as resting tremor, as it is typically
present at rest and disappears
with voluntary movement.
Manifests as pill-rolling tremor
of hand.
? Akinesia:- absence of movement.
– Moments of freezing may occur and are
block in
characterized by a sudden break or
movement.
– Hypokinesia: reduced amplitude of the movement
? Postural Instability
– Postural instability is common. Patients may
describe being unable to stop themselves from
going forward (propulsion) or backward
(retropulsion).
? Hypomimia
? Drooling of saliva
? Low volume speech.
? Dysarthria .
? Problem with swallowing
and Involuntary flow of
saliva .
? Longer time to complete a
task.
? Stiff face in advanced PD.
? Altered cognitive function
– Dementia .
? Disorder of intellectual
function.
COMPLICATIONS
? These include motor symptoms
– Dyskinesia
– Dementia
– Depression, hallucinations, psychosis
– Dysphagia
– Malnutrition
– Aspiration – pneumonia
– Orthostatic hypotension
– Risk for fall
ANTI-PARKINSONISM MEDICATIONS
? LEVEDOPA (L-Dopa): it is the most effective
agents and the mainstay of treatment, for
controlling the symptoms.
? SINEMET: it is made up
carbidopa. Levodopa enters
of Levodopa and
the brain and is
converted to Dopamine while carbidopa increase
its effectiveness and prevents the side effects of
levodopa such as nausea, vomiting.
? DOPAMINE RECEPTOR AGONISTS:
– This are the drugs that activate or stimulate the
dopamine receptors
– Ergot derivatives : bromocriptine or pergolite.
– Non-ergot derivatives: ropinirole, pramipexole
? MONOAMINE OXIDIZED INHIBITORS:
– It blocks the breakdown of dopamine , and are used
primarily to treat motors fluctuation associated with
levodopa treatment most commonly drugs used are
Seligiline and Rosagiline.
Surgery
Surgery is optional only when medicine doesn't
make the symptoms better.
? Thalatomy - is a surgical procedure in which an
opening is made into the thalamus to improve the
overall brain function.
? Deep brain stimulation – pulse generator, high
frequency electrical impulses to the thalamus and
block the nerve pathway to control tremors
Deep Brain Stimulation
? Deep brain stimulation
(DBS) can be used to
treat tremors and
uncontrolled
movements of
Parkinson’s disease.
Electrodes are surgically
placed in thebrain and
connected to a
neurostimulator
(pacemaker device) in
the chest.
Physiotherapy
? A combined approach of physical therapy and
in
pharmacological intervention plays a key role
management of the patient.
? Physical therapist should be fully aware of the medications
the patient is taking and its potential adverse effects.
? Optimal performance can be expected at peak dosage (on-
state) whereas worsening performance is associated with
end of dose cycle.
– Exercise training
– Strength training
– Balance training
– Correcting eating impairments.
– Verbal skills practiced with breath control.
DIAGNOSIS
General
? Blank (masked) facial expression, slow and monotonous speech, infrequent
blinking
Integumentary
? Seborrhea, dandruff; ankle Oedema
Cardiovascular
? Postural hypotension
Gastrointestinal
? Drooling
Neurologic
? Tremor at rest, first in hands (pill rolling), later in legs, arms, face, and tongue.
Aggravation of tremor with anxiety, absence in sleep. Poor coordination,
cognitiveimpairment and dementia, impaired postural reflexes
Musculoskeletal
? Cogwheel rigidity, dysarthria, bradykinesia, contractures, stooped posture,
shuffling gait
Possible Diagnostic Findings
? No specific tests. Diagnosis based on history and physical findings and ruling
out of other diseases
DIAGNOSIS
to physical limitation and loss of
? Impaired physical mobility related to Bradykinesia, rigidity and
tremors
? Imbalance nutrition less than body requirement related to motor
difficulties with feeding, chewing and swallowing
? Impaired verbal communication related to decreased speech volume
? Constipation related to diminished motor function and inactivity
? Ineffective coping related
independence.
? Risk for fall-related injury
? Impaired sleep pattern
THANK YOU

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527751381-Parkinson-Disease-狠狠撸s (1).pdf

  • 2. INTRODUCTION ? Parkinson's disease is a progressive nervous system disorder that affects movement. Symptoms start gradually, sometimes starting with a barely noticeable tremor in just one hand. Tremors are common, but the disorder also commonly causes stiffness or slowing of movement.
  • 3. Parkinson’s disease (PD) ? Parkinson’s disease (PD) is a chronic, progressive neurodegenerative disorder characterized by slowness in the initiation and execution of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and gait changes.
  • 4. ETIOLOGY ? Exact cause is unknown ? Heredity ? Family History: Having one or more close relatives with the disease increase the rise of getting. ? Advancing age : Above 60 years mostly seen ? Sex: male are more likely to get than female. ? Low Estrogen Level: most menopausal women who don’t use hormone replacement therapy are more risk of getting the disease. like reserpine, lithium, and ? Medications metoclopramide, methyldopa, haloperidol, chlorpromazine ? Agricultural work: exposure to such as environmental toxin pesticide, herbicides ? Head injury.
  • 5. PATHOPHYSIOLOGY Tremor, rigidity and Akinesia Degeneration of the Dopamine-producing neurons in the substantia nigra of the midbrain Disrupts the normal balance between Dopamine (DA) and acetylcholine (ACh) in the basal ganglia. Impaired extra pyramidal tract controlling Loss of motor control
  • 6. CLINICAL MANIFESTATIONS ? Rigidity:- Defined as increased resistance to passive motion. – Cogwheel rigidity: jerky, ratchet like resistance to movement and passive muscles alternately tense and relax. ? Tremor:- It is an involuntary oscillation of body part. – Parkinsonian tremor is described as resting tremor, as it is typically present at rest and disappears with voluntary movement. Manifests as pill-rolling tremor of hand.
  • 7. ? Akinesia:- absence of movement. – Moments of freezing may occur and are block in characterized by a sudden break or movement. – Hypokinesia: reduced amplitude of the movement ? Postural Instability – Postural instability is common. Patients may describe being unable to stop themselves from going forward (propulsion) or backward (retropulsion).
  • 8. ? Hypomimia ? Drooling of saliva ? Low volume speech. ? Dysarthria . ? Problem with swallowing and Involuntary flow of saliva . ? Longer time to complete a task. ? Stiff face in advanced PD. ? Altered cognitive function – Dementia . ? Disorder of intellectual function.
  • 9. COMPLICATIONS ? These include motor symptoms – Dyskinesia – Dementia – Depression, hallucinations, psychosis – Dysphagia – Malnutrition – Aspiration – pneumonia – Orthostatic hypotension – Risk for fall
  • 10. ANTI-PARKINSONISM MEDICATIONS ? LEVEDOPA (L-Dopa): it is the most effective agents and the mainstay of treatment, for controlling the symptoms. ? SINEMET: it is made up carbidopa. Levodopa enters of Levodopa and the brain and is converted to Dopamine while carbidopa increase its effectiveness and prevents the side effects of levodopa such as nausea, vomiting.
  • 11. ? DOPAMINE RECEPTOR AGONISTS: – This are the drugs that activate or stimulate the dopamine receptors – Ergot derivatives : bromocriptine or pergolite. – Non-ergot derivatives: ropinirole, pramipexole ? MONOAMINE OXIDIZED INHIBITORS: – It blocks the breakdown of dopamine , and are used primarily to treat motors fluctuation associated with levodopa treatment most commonly drugs used are Seligiline and Rosagiline.
  • 12. Surgery Surgery is optional only when medicine doesn't make the symptoms better. ? Thalatomy - is a surgical procedure in which an opening is made into the thalamus to improve the overall brain function. ? Deep brain stimulation – pulse generator, high frequency electrical impulses to the thalamus and block the nerve pathway to control tremors
  • 13. Deep Brain Stimulation ? Deep brain stimulation (DBS) can be used to treat tremors and uncontrolled movements of Parkinson’s disease. Electrodes are surgically placed in thebrain and connected to a neurostimulator (pacemaker device) in the chest.
  • 14. Physiotherapy ? A combined approach of physical therapy and in pharmacological intervention plays a key role management of the patient. ? Physical therapist should be fully aware of the medications the patient is taking and its potential adverse effects. ? Optimal performance can be expected at peak dosage (on- state) whereas worsening performance is associated with end of dose cycle. – Exercise training – Strength training – Balance training – Correcting eating impairments. – Verbal skills practiced with breath control.
  • 15. DIAGNOSIS General ? Blank (masked) facial expression, slow and monotonous speech, infrequent blinking Integumentary ? Seborrhea, dandruff; ankle Oedema Cardiovascular ? Postural hypotension Gastrointestinal ? Drooling Neurologic ? Tremor at rest, first in hands (pill rolling), later in legs, arms, face, and tongue. Aggravation of tremor with anxiety, absence in sleep. Poor coordination, cognitiveimpairment and dementia, impaired postural reflexes Musculoskeletal ? Cogwheel rigidity, dysarthria, bradykinesia, contractures, stooped posture, shuffling gait Possible Diagnostic Findings ? No specific tests. Diagnosis based on history and physical findings and ruling out of other diseases
  • 16. DIAGNOSIS to physical limitation and loss of ? Impaired physical mobility related to Bradykinesia, rigidity and tremors ? Imbalance nutrition less than body requirement related to motor difficulties with feeding, chewing and swallowing ? Impaired verbal communication related to decreased speech volume ? Constipation related to diminished motor function and inactivity ? Ineffective coping related independence. ? Risk for fall-related injury ? Impaired sleep pattern