Movement disorder
Mohamed rizk
khodair
Lecturer of neurology
October 6 university
Classification of movement disorder
Movement disorder manifestations are characterized as either: hyperkinetic (increased movement) or hypokinetic
(decreased movement).
Hypokinetic (mainly Parkinsonism) includes Bradykinesia, Freezing, Rigidity
Hyperkinetic movement disorders include:
Tremor, Chorea, Ballismus, Athetosis, Myoclonus, Tics, and Dyskinesias.
Parkinsonism
Parkinson disease (PD) is the most common cause of parkinsonism, a syndrome manifested by rest tremor, rigidity,
bradykinesia, and postural instability.
Epidemiology:
Parkinson disease is recognized as one of the most common neurologic disorders, affecting approximately 1% of
individuals older than 60 years. Onset in persons younger than 40 years is relatively uncommon.
Parkinson disease is about 1.5 times more common in men than in women.
Pathophysiology:
Dopamine depletion from the basal ganglia results in major disruptions in the connections to the thalamus and motor
cortex and leads to parkinsonian signs such as bradykinesia
Cardinal Manifestations:
The cardinal features of PD are tremor, bradykinesia, and rigidity. A fourth feature, postural instability, is commonly
mentioned
A) Tremor:
The tremor in PD, typically described as "pill-rolling," is a rest tremor, usually begins in one upper extremity and initially
may be intermittent.
Upper extremity tremor generally begins in the fingers or thumb, but it can also start in the forearm or wrist. After
several months or years, the tremor may spread to the ipsilateral lower extremity or the contralateral upper extremity
before becoming more generalized; however, asymmetry is usually maintained. Tremor can vary considerably, emerging
only with stress, anxiety, or fatigue.
B) Bradykinesia:
Bradykinesia is a generalized slowness of movement and is present at onset of PD in approximately 80 percent of patients
in the legs, common complaints related to bradykinesia when walking include dragging the legs, shorter (shuffling) steps.
Patients may also have difficulty standing up from a chair or getting out of a car. As the disease progresses, gait freezing,
and festination may develop. James Parkinson defined festination as "an irresistible impulse to take much quicker and
shorter steps, and thereby to adopt unwillingly a running pace"
C) Rigidity:
Occurs in approximately 75 to 90 percent of patients with PD. Rigidity, often begins unilaterally, and eventually progresses
to the contralateral side, and remains asymmetric throughout the disease.
Two types of rigidity occur:
1) Cogwheel rigidity (refers to a ratchety pattern of resistance and relaxation as the examiner moves the limb through
its full range of motion; occurs when the rigidity is interrupted by tremors).
2) Lead-pipe rigidity, a tonic resistance that is smooth throughout the entire range of passive movement. Rigidity can
affect any part of the body and may contribute to complaints of stiffness and pain.
Features, such as the striatal hand (extension of the proximal and distal interphalangeal joints with flexion at the
metacarpophalangeal joints), decreased arm swing with walking, and the typical stooped posture, result, at least in part,
from rigidity.
D) Postural Instability:
Postural instability is an impairment of centrally mediated postural reflexes that cause a feeling of imbalance and a
tendency to fall with a significant risk of injury.
E) Non-Motor Symptoms:
These features include the following:
● Cognitive dysfunction and dementia
● Psychosis and hallucinations
● Mood disorders including depression, anxiety, and apathy/abulia
● Sleep disturbances
● Fatigue
● Autonomic dysfunction
● Olfactory dysfunction
● Gastrointestinal dysfunction
● Pain and sensory disturbances
● Dermatologic findings (seborrhea)
● Rhinorrhea
Investigation:
Parkinson disease is a clinical diagnosis.
No laboratory biomarkers exist for the condition, and findings on routine magnetic resonance imaging (MRI) and
computed tomography (CT)scan are unremarkable.
No laboratory or imaging study is required in patients with a typical presentation.
Treatment:
Treatment can be divided into pharmacologic, non-pharmacologic, and surgical therapy.
A) pharmacologic management of Parkinson disease
The major drugs available for the treatment of PD motor symptoms include:
1.Levodopa remains the gold standard of treatment. Starting dose is Madopar or Sinemet with meals tds.
2. Dopamine agonists as Pergolide, Ropinirole, Pramipexole, Rotigotine (patch),.
3. Monoamine oxidase (MAO) B inhibitors
4. Anticholinergic agents5. amantadine
6. Catechol-O-methyl transferase (COMT) inhibitors
B) Non-pharmacologic management of Parkinson disease
 A high fiber diet and adequate hydration help manage the constipation of PD.
 Large, high-fat meals that slow gastric emptying and interfere with medication absorption should be avoided.
 Device-assisted and surgical treatments for Parkinson disease
-Approach to Device Assisted Treatment:
For patients with levodopa-responsive PD who develop motor complications that compromise quality of life with
noninvasive medical therapies, device-assisted treatment options include Deep brain stimulation (DBS). Other
Procedures: Several other surgical procedures have been studied in advanced PD, including:
 Thalamotomy
 Pallidotomy
 Sub-thalamotomy
Chorea and athetosis
Chorea: continuous flow of irregular, brief, jerky, semi-purposive or purposeless, flowing movements.
Athetosis: a slow continuous stream of slow, writhing or snake-like movements.
Causes
1) Hereditary: Huntington ‘s disease; Wilson ‘s disease; ataxia telangiectasia.
2) Infection: Sydenham ‘s chorea (poststreptococcal); HIV.
3) Vascular (often hemichorea): infarction.
4) Metabolic: hyper- and hypoglycemia; hyperthyroidism.
5) Immunological: SLE; anti-phospholipid syndrome; pregnancy (chorea gravidarum).
6) Drug-induced: anti-Parkinsonian drugs; dopamine antagonists’ drugs, e.g., phenothiazines; amphetamines, cocaine.
Tremor
Defined as a rhythmical involuntary oscillatory movement of a body part.
• Physiological tremor: 5–12 Hz (↑ anxiety, caffeine, T4↑).
Phenomenological classification
• Rest tremor as parkinsonian tremors
• Action tremor: produced by voluntary contraction of muscle.
•Postural tremor: present while maintaining posture against gravity.
•Kinetic tremor—occurs during voluntary movement.
•Intention tremor—occurs with target-directed movement with increase in amplitude at termination of movement (cerebellar tremors).
•Task-specific tremor, e.g., writing tremor, dystonic tremors
•Isometric tremor, e.g., orthostatic tremor.
 Essential tremors
Tics
• Rapid stereotypic involuntary movements.
• Can be voluntarily suppressed but suppression leads to build-up of internal tension.
• Triggered by stress or boredom.
• Male preponderance (3:1).
• Peak age of onset around 7 years.
Causes :
Gilles de la Tourette syndrome ; neuroleptics ; Head trauma.
Patients present with the following:
• Motor tics: eye winks; eye blinks; grimaces; head tosses; sniffs; throat clearing.
• Vocal tics: foul utterances (coprolalia); repeating sounds or words (echolalia). Resolution usually occurs at the end of adolescence.
Thank you
Mohamedrizk.med@o6u.edu.eg

movement disorder for physiotherapy .pptx

  • 1.
    Movement disorder Mohamed rizk khodair Lecturerof neurology October 6 university
  • 2.
    Classification of movementdisorder Movement disorder manifestations are characterized as either: hyperkinetic (increased movement) or hypokinetic (decreased movement). Hypokinetic (mainly Parkinsonism) includes Bradykinesia, Freezing, Rigidity Hyperkinetic movement disorders include: Tremor, Chorea, Ballismus, Athetosis, Myoclonus, Tics, and Dyskinesias.
  • 3.
    Parkinsonism Parkinson disease (PD)is the most common cause of parkinsonism, a syndrome manifested by rest tremor, rigidity, bradykinesia, and postural instability.
  • 4.
    Epidemiology: Parkinson disease isrecognized as one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years. Onset in persons younger than 40 years is relatively uncommon. Parkinson disease is about 1.5 times more common in men than in women.
  • 6.
    Pathophysiology: Dopamine depletion fromthe basal ganglia results in major disruptions in the connections to the thalamus and motor cortex and leads to parkinsonian signs such as bradykinesia
  • 7.
    Cardinal Manifestations: The cardinalfeatures of PD are tremor, bradykinesia, and rigidity. A fourth feature, postural instability, is commonly mentioned
  • 8.
    A) Tremor: The tremorin PD, typically described as "pill-rolling," is a rest tremor, usually begins in one upper extremity and initially may be intermittent. Upper extremity tremor generally begins in the fingers or thumb, but it can also start in the forearm or wrist. After several months or years, the tremor may spread to the ipsilateral lower extremity or the contralateral upper extremity before becoming more generalized; however, asymmetry is usually maintained. Tremor can vary considerably, emerging only with stress, anxiety, or fatigue.
  • 9.
    B) Bradykinesia: Bradykinesia isa generalized slowness of movement and is present at onset of PD in approximately 80 percent of patients in the legs, common complaints related to bradykinesia when walking include dragging the legs, shorter (shuffling) steps. Patients may also have difficulty standing up from a chair or getting out of a car. As the disease progresses, gait freezing, and festination may develop. James Parkinson defined festination as "an irresistible impulse to take much quicker and shorter steps, and thereby to adopt unwillingly a running pace"
  • 10.
    C) Rigidity: Occurs inapproximately 75 to 90 percent of patients with PD. Rigidity, often begins unilaterally, and eventually progresses to the contralateral side, and remains asymmetric throughout the disease. Two types of rigidity occur: 1) Cogwheel rigidity (refers to a ratchety pattern of resistance and relaxation as the examiner moves the limb through its full range of motion; occurs when the rigidity is interrupted by tremors). 2) Lead-pipe rigidity, a tonic resistance that is smooth throughout the entire range of passive movement. Rigidity can affect any part of the body and may contribute to complaints of stiffness and pain. Features, such as the striatal hand (extension of the proximal and distal interphalangeal joints with flexion at the metacarpophalangeal joints), decreased arm swing with walking, and the typical stooped posture, result, at least in part, from rigidity.
  • 11.
    D) Postural Instability: Posturalinstability is an impairment of centrally mediated postural reflexes that cause a feeling of imbalance and a tendency to fall with a significant risk of injury.
  • 12.
    E) Non-Motor Symptoms: Thesefeatures include the following: ● Cognitive dysfunction and dementia ● Psychosis and hallucinations ● Mood disorders including depression, anxiety, and apathy/abulia ● Sleep disturbances ● Fatigue ● Autonomic dysfunction ● Olfactory dysfunction ● Gastrointestinal dysfunction ● Pain and sensory disturbances ● Dermatologic findings (seborrhea) ● Rhinorrhea
  • 13.
    Investigation: Parkinson disease isa clinical diagnosis. No laboratory biomarkers exist for the condition, and findings on routine magnetic resonance imaging (MRI) and computed tomography (CT)scan are unremarkable. No laboratory or imaging study is required in patients with a typical presentation.
  • 14.
    Treatment: Treatment can bedivided into pharmacologic, non-pharmacologic, and surgical therapy. A) pharmacologic management of Parkinson disease The major drugs available for the treatment of PD motor symptoms include: 1.Levodopa remains the gold standard of treatment. Starting dose is Madopar or Sinemet with meals tds. 2. Dopamine agonists as Pergolide, Ropinirole, Pramipexole, Rotigotine (patch),. 3. Monoamine oxidase (MAO) B inhibitors 4. Anticholinergic agents5. amantadine 6. Catechol-O-methyl transferase (COMT) inhibitors
  • 15.
    B) Non-pharmacologic managementof Parkinson disease  A high fiber diet and adequate hydration help manage the constipation of PD.  Large, high-fat meals that slow gastric emptying and interfere with medication absorption should be avoided.  Device-assisted and surgical treatments for Parkinson disease -Approach to Device Assisted Treatment: For patients with levodopa-responsive PD who develop motor complications that compromise quality of life with noninvasive medical therapies, device-assisted treatment options include Deep brain stimulation (DBS). Other Procedures: Several other surgical procedures have been studied in advanced PD, including:  Thalamotomy  Pallidotomy  Sub-thalamotomy
  • 16.
    Chorea and athetosis Chorea:continuous flow of irregular, brief, jerky, semi-purposive or purposeless, flowing movements. Athetosis: a slow continuous stream of slow, writhing or snake-like movements.
  • 17.
    Causes 1) Hereditary: Huntington‘s disease; Wilson ‘s disease; ataxia telangiectasia. 2) Infection: Sydenham ‘s chorea (poststreptococcal); HIV. 3) Vascular (often hemichorea): infarction. 4) Metabolic: hyper- and hypoglycemia; hyperthyroidism. 5) Immunological: SLE; anti-phospholipid syndrome; pregnancy (chorea gravidarum). 6) Drug-induced: anti-Parkinsonian drugs; dopamine antagonists’ drugs, e.g., phenothiazines; amphetamines, cocaine.
  • 18.
    Tremor Defined as arhythmical involuntary oscillatory movement of a body part. • Physiological tremor: 5–12 Hz (↑ anxiety, caffeine, T4↑). Phenomenological classification • Rest tremor as parkinsonian tremors • Action tremor: produced by voluntary contraction of muscle. •Postural tremor: present while maintaining posture against gravity. •Kinetic tremor—occurs during voluntary movement. •Intention tremor—occurs with target-directed movement with increase in amplitude at termination of movement (cerebellar tremors). •Task-specific tremor, e.g., writing tremor, dystonic tremors •Isometric tremor, e.g., orthostatic tremor.  Essential tremors
  • 19.
    Tics • Rapid stereotypicinvoluntary movements. • Can be voluntarily suppressed but suppression leads to build-up of internal tension. • Triggered by stress or boredom. • Male preponderance (3:1). • Peak age of onset around 7 years. Causes : Gilles de la Tourette syndrome ; neuroleptics ; Head trauma. Patients present with the following: • Motor tics: eye winks; eye blinks; grimaces; head tosses; sniffs; throat clearing. • Vocal tics: foul utterances (coprolalia); repeating sounds or words (echolalia). Resolution usually occurs at the end of adolescence.
  • 20.