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DYSKINESIA
OVERVIEW
 Dyskinesias are abnormal, involuntary muscle
movements that can be mild or severe, and
can even be painful in nature.
 Movement disorders characterized as
dyskinesias can be caused by certain
medications, by changes to the chemistry of
the brain, or by brain injury or damage.
Defining Dyskinesia
 Dyskinesia is characterized by involuntary or
uncontrolled muscle movements that are
abnormal in character and may make it
difficult to coordinate normal movements.
 There are several forms of dyskinesia that are
associated with different symptoms and
causes.
 Dyskinesia is most commonly caused by
medications, such as long term use of
levodopa in Parkinson's disease and use of
antipsychotic medications.
 Dyskinesia caused by brain injury such as
vascular event ( stroke) or other brain
damage is less common.
 Movement symptoms typically start as minor
shakes, tics, or tremors.
 They can occur in just one body part like a
person’s head or leg, or movements can
affect the entire body.
 These symptoms can range from mild to
severe, and some may be painful.
There are different types of
dyskinesias which lead to
different symptoms as well as
treatments.
Common types of dyskinesias
include:
 Athetosis: A form of dyskinesia associated
with brain damage, mainly cerebral palsy.
 Movements in athetosis are slow and
writhing
 Chorea: A form of dyskinesia often seen in
Huntington's disease, structural damage of
the brain, and caused by medications.
 Chorea refers to quick movements of the
limbs and can resemble dancing.
 Levodopa-induced or Parkinson’s
dyskinesia:
A form of dyskinesia that may occur due to the
long-term use of levodopa, a medication used
to treat Parkinson’s disease.
 Tardive or delayed dyskinesia: A form of
dyskinesia associated with the use of
antipsychotic medications, often used to treat
schizophrenia.
 Myoclonus dyskinesias: A form of dyskinesia
seen in progressive myoclonic encephalopathy.
Movements are severe and very disabling.
Symptoms
 Symptoms can vary from person to person
and might appear differently depending on
the type of dyskinesia diagnosed.
 They may begin as fine movements called
tremors, or even as tics, and then develop
into the common symptoms characteristic of
dyskinesia like:
 Body swaying
 Fidgeting
 Head bobbing
 Restlessness
 Twitching
 Wriggling
 It is notable that restlessness and twitching
occur less often in levodopa-induced
dyskinesia.
 Symptoms can worsen over time gradually or
develop suddenly and intensify after a serious
brain injury.
 Patients with tardive dyskinesia have
symptoms characterized by abnormal
movements of the jaw, lips, and tongue.
Rapid blinking and waving of the arms and
hands, and in severe cases, symptoms of hip or
waist swaying and difficulty breathing may also
appear.
 In myoclonus dyskinesias, movements are
characterized by being sudden and repetitive
muscle spasms and jerks.
These movements can be so severe that they
become painful and debilitating.
 Chorea movements may be continuous, last a
few seconds, or involve sudden, jerking
behaviors.
 These movements most commonly affect the
limbs, face, and head.
 In cases of athetosis, movements may be
slow turning, bending, or writhing and affect
fingers, hands, and toes.
 Athetosis may affect the arms, legs, neck,
and tongue of someone diagnosed with the
disorder.
Causes
 Dyskinesias are often related to medications,
secondary to other diagnoses, or due to
structural changes in the brain.
 There are times that dyskinesias can appear
with no particular cause or known risk factor.
BY MEDICATION
 Dyskinesia is a complication of long-
term levodopa use in people who have had
Parkinson's for several years.
 Other risk factors include being younger at
diagnosis and using higher amounts of
levodopa for longer periods of time.
 Researchers don't know exactly why
dyskinesia develops, but they believe a
number of brain chemicals, including
serotonin, glutamate and dopamine, play a
role.
 Dopamine is particularly important.
 In Parkinson's, the brain cells that make
dopamine are lost, so dopamine levels decrease.
 Levodopa temporarily restores dopamine, but
because the medication has to be taken several
times per day, dopamine levels rise and fall.
 These fluctuating levels, and the continued loss
of dopamine-producing brain cells, make it
impossible to keep a steady level of dopamine,
which contributes to dyskinesia.
 Tardive dyskinesia is caused by the long-term
use of neuroleptic drugs that treat
neurological, gastrointestinal, and mental
disorders like schizophrenia or bipolar
disorder.
 These medications are dopamine-receptor
blocking agents, and they impact the ability
of cells to communicate.
 Gender, age, genetics, and mental and
medical disorders, like diabetes, can be
important risk factors for the development of
tardive dyskinesia.
 Tardive dyskinesia tends to happen earlier in
women than in men.
 Chorea can also be caused by the use of
certain medications, like antipsychotic
medications, antiepileptic medications, and
other medications used to treat Parkinson’s
disease.
 This specific dyskinesia can also develop
through a variety of diseases, conditions, and
deficiencies, from Lyme disease
to Huntington's disease to hormone
replacement therapy
 Generally, changes in the levels of specific
brain chemicals—like dopamine, serotonin,
and glutamate—are associated with the
development of dyskinesia.
Brain Injury and Damage
 Altering chemistry through damage or injury
to the brain’s tissues is another common
cause of dyskinesia.
 People may develop athetosis due to a loss of
blood supply or oxygen within the brain.
 Ballism, a form of chorea characterized by a
wild and sometimes violent flinging of the
arms and legs, may develop after
cerebrovascular events, like after a stroke or
suffocation.
 Generally, if there is an injury to the basal
ganglia, an area of the brain responsible for
controlling voluntary movements and learned
habits, dyskinesia could possibly develop.
Diagnosis
 The different abnormal movements that
characterize the distinct types of dyskinesia
will generally require the careful observation
and clinical judgment of a neurologist or
movement disorders specialist.
 It will be important to note the type of
movements, and areas of the body affected
when determining the proper diagnosis.
TREATMENT
 Treatment can vary depending on the type of
dyskinesia diagnosed and the individual and
may include:
 Medication Changes
For levodopa-induced dyskinesia, controlling
the dose and the timing of taking levodopa
may balance the levels of dopamine and
decrease symptoms.
Different forms of the medication, such as
extended-release Rytary or the gel-infusion
Duopa, may also be helpful.
An extended-release form of amantadine,
called Gocovri, may also help control levels of
glutamate in the brain and reduce symptoms.2
 People with tardive dyskinesia may be
prescribed Ingrezza or Austedo, which are
both neuroleptic drugs approved by the FDA
as treatment in 2017
Treatment of dyskinesias
 stopping the antipsychotic
 Change from typical to atypical
 Use clozapine and quetiapine
 Other medications: valproic acid,
anticholinergics, or botulinum toxin injections
Refractory cases: reserprine or
tetrabenazine.
 Other approaches include baclofen (40–80
mg/d), clonazepam (1–8 mg/d), or valproic
acid (750–3000 mg/d).
DEEP BRAIN STIMULATION
 To control symptoms, deep brain stimulation
(DBS) is a surgical procedure that is another
treatment option, but it is not right for
everyone.
 Minimum requirements include a diagnosis of
Parkinson’s for at least four years, recurrent
episodes of dyskinesia, and ongoing
responsiveness to and benefit from the use of
levodopa in most cases.
 The DBS surgical procedure involves the
placement of electrodes by a neurosurgeon
into areas of the brain that control movement
and posture, most commonly the subthalamic
nucleus (STN) and globus pallidus interna (GPI).
 A wire travels from the electrodes to a
pacemaker-like device that is implanted in the
chest wall.
 After implantation, the clinician will set
parameters that will determine the amount of
electrical stimulation delivered.
 DBS is approved by the FDA as a form of
treatment for patients with Parkinson’s disease,
dystonia, and essential tremor
OTHER THERAPIES
 For dyskinesias that impact the facial, neck,
and limb region, some patients try injections
of botox, or botulinum toxin, to reduce
movement.
 There are several additional therapies that
are currently undergoing clinical trials for the
treatment of dyskinesias.
 Potential treatments for tardive dyskinesia
include melatonin and estrogen, which
modulate dopamine-controlled behavior and
protect against cell damage from the long-
term use of antipsychotic medications.
 For the treatment of levodopa-induced
dyskinesia, drugs that target different brain
chemicals are being studied.
 In addition, under-the-skin levodopa pumps are
also being studied to test if they can effectively
maintain consistent dopamine levels.
 Finally, researchers are investigating ways to
best optimize deep brain stimulation and are
testing a technique called focused ultrasound, a
non-invasive, irreversible procedure to treat
dyskinesia.
 .
 Coping
 Dealing with dyskinesias can be stressful and
impact daily activities and social interactions.
 Exercise, like walking or swimming, may be
recommended.
 Managing stress may also be crucial to
control symptoms, as stress tends to
exacerbate the uncontrolled movements.
AIMS OF PHYSIOTHERAPY
 Maintain and improve levels of function and
independence, which will help to improve a person’s
quality of life
 Use exercise and movement strategies to improve
mobility
 Correct and improve abnormal movement patterns
and posture, where possible
 Maximize muscle strength and joint flexibility
 Correct and improve posture and balance, and
minimise risks of falls
 Maintain a good breathing pattern and effective cough
 Educate the person with Parkinson’s and their carer or
family members
 Enhance the effects of drug therapy
PHYSIOTHERAPY
 Passive movements
 Ex.; co-ordination
 Movement control
 Functional training
 Auditory and visual cuing
 Strengthening
 Rom
 Endurance
 Cardiopulmonary fitness
By
VINEESHA CHANDRAN

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Dyskinesia

  • 2. OVERVIEW  Dyskinesias are abnormal, involuntary muscle movements that can be mild or severe, and can even be painful in nature.  Movement disorders characterized as dyskinesias can be caused by certain medications, by changes to the chemistry of the brain, or by brain injury or damage.
  • 3. Defining Dyskinesia  Dyskinesia is characterized by involuntary or uncontrolled muscle movements that are abnormal in character and may make it difficult to coordinate normal movements.  There are several forms of dyskinesia that are associated with different symptoms and causes.
  • 4.  Dyskinesia is most commonly caused by medications, such as long term use of levodopa in Parkinson's disease and use of antipsychotic medications.  Dyskinesia caused by brain injury such as vascular event ( stroke) or other brain damage is less common.
  • 5.  Movement symptoms typically start as minor shakes, tics, or tremors.  They can occur in just one body part like a person’s head or leg, or movements can affect the entire body.  These symptoms can range from mild to severe, and some may be painful.
  • 6. There are different types of dyskinesias which lead to different symptoms as well as treatments. Common types of dyskinesias include:
  • 7.  Athetosis: A form of dyskinesia associated with brain damage, mainly cerebral palsy.  Movements in athetosis are slow and writhing
  • 8.  Chorea: A form of dyskinesia often seen in Huntington's disease, structural damage of the brain, and caused by medications.  Chorea refers to quick movements of the limbs and can resemble dancing.
  • 9.  Levodopa-induced or Parkinson’s dyskinesia: A form of dyskinesia that may occur due to the long-term use of levodopa, a medication used to treat Parkinson’s disease.
  • 10.  Tardive or delayed dyskinesia: A form of dyskinesia associated with the use of antipsychotic medications, often used to treat schizophrenia.  Myoclonus dyskinesias: A form of dyskinesia seen in progressive myoclonic encephalopathy. Movements are severe and very disabling.
  • 11. Symptoms  Symptoms can vary from person to person and might appear differently depending on the type of dyskinesia diagnosed.
  • 12.  They may begin as fine movements called tremors, or even as tics, and then develop into the common symptoms characteristic of dyskinesia like:  Body swaying  Fidgeting  Head bobbing  Restlessness  Twitching  Wriggling
  • 13.  It is notable that restlessness and twitching occur less often in levodopa-induced dyskinesia.  Symptoms can worsen over time gradually or develop suddenly and intensify after a serious brain injury.
  • 14.  Patients with tardive dyskinesia have symptoms characterized by abnormal movements of the jaw, lips, and tongue. Rapid blinking and waving of the arms and hands, and in severe cases, symptoms of hip or waist swaying and difficulty breathing may also appear.
  • 15.  In myoclonus dyskinesias, movements are characterized by being sudden and repetitive muscle spasms and jerks. These movements can be so severe that they become painful and debilitating.
  • 16.  Chorea movements may be continuous, last a few seconds, or involve sudden, jerking behaviors.  These movements most commonly affect the limbs, face, and head.
  • 17.  In cases of athetosis, movements may be slow turning, bending, or writhing and affect fingers, hands, and toes.  Athetosis may affect the arms, legs, neck, and tongue of someone diagnosed with the disorder.
  • 18. Causes  Dyskinesias are often related to medications, secondary to other diagnoses, or due to structural changes in the brain.  There are times that dyskinesias can appear with no particular cause or known risk factor.
  • 19. BY MEDICATION  Dyskinesia is a complication of long- term levodopa use in people who have had Parkinson's for several years.  Other risk factors include being younger at diagnosis and using higher amounts of levodopa for longer periods of time.
  • 20.  Researchers don't know exactly why dyskinesia develops, but they believe a number of brain chemicals, including serotonin, glutamate and dopamine, play a role.  Dopamine is particularly important.
  • 21.  In Parkinson's, the brain cells that make dopamine are lost, so dopamine levels decrease.  Levodopa temporarily restores dopamine, but because the medication has to be taken several times per day, dopamine levels rise and fall.  These fluctuating levels, and the continued loss of dopamine-producing brain cells, make it impossible to keep a steady level of dopamine, which contributes to dyskinesia.
  • 22.  Tardive dyskinesia is caused by the long-term use of neuroleptic drugs that treat neurological, gastrointestinal, and mental disorders like schizophrenia or bipolar disorder.  These medications are dopamine-receptor blocking agents, and they impact the ability of cells to communicate.
  • 23.  Gender, age, genetics, and mental and medical disorders, like diabetes, can be important risk factors for the development of tardive dyskinesia.  Tardive dyskinesia tends to happen earlier in women than in men.
  • 24.  Chorea can also be caused by the use of certain medications, like antipsychotic medications, antiepileptic medications, and other medications used to treat Parkinson’s disease.  This specific dyskinesia can also develop through a variety of diseases, conditions, and deficiencies, from Lyme disease to Huntington's disease to hormone replacement therapy
  • 25.  Generally, changes in the levels of specific brain chemicals—like dopamine, serotonin, and glutamate—are associated with the development of dyskinesia.
  • 26. Brain Injury and Damage  Altering chemistry through damage or injury to the brain’s tissues is another common cause of dyskinesia.  People may develop athetosis due to a loss of blood supply or oxygen within the brain.  Ballism, a form of chorea characterized by a wild and sometimes violent flinging of the arms and legs, may develop after cerebrovascular events, like after a stroke or suffocation.
  • 27.  Generally, if there is an injury to the basal ganglia, an area of the brain responsible for controlling voluntary movements and learned habits, dyskinesia could possibly develop.
  • 28. Diagnosis  The different abnormal movements that characterize the distinct types of dyskinesia will generally require the careful observation and clinical judgment of a neurologist or movement disorders specialist.  It will be important to note the type of movements, and areas of the body affected when determining the proper diagnosis.
  • 29. TREATMENT  Treatment can vary depending on the type of dyskinesia diagnosed and the individual and may include:
  • 30.  Medication Changes For levodopa-induced dyskinesia, controlling the dose and the timing of taking levodopa may balance the levels of dopamine and decrease symptoms. Different forms of the medication, such as extended-release Rytary or the gel-infusion Duopa, may also be helpful. An extended-release form of amantadine, called Gocovri, may also help control levels of glutamate in the brain and reduce symptoms.2
  • 31.  People with tardive dyskinesia may be prescribed Ingrezza or Austedo, which are both neuroleptic drugs approved by the FDA as treatment in 2017
  • 32. Treatment of dyskinesias  stopping the antipsychotic  Change from typical to atypical  Use clozapine and quetiapine
  • 33.  Other medications: valproic acid, anticholinergics, or botulinum toxin injections Refractory cases: reserprine or tetrabenazine.  Other approaches include baclofen (40–80 mg/d), clonazepam (1–8 mg/d), or valproic acid (750–3000 mg/d).
  • 34. DEEP BRAIN STIMULATION  To control symptoms, deep brain stimulation (DBS) is a surgical procedure that is another treatment option, but it is not right for everyone.  Minimum requirements include a diagnosis of Parkinson’s for at least four years, recurrent episodes of dyskinesia, and ongoing responsiveness to and benefit from the use of levodopa in most cases.
  • 35.  The DBS surgical procedure involves the placement of electrodes by a neurosurgeon into areas of the brain that control movement and posture, most commonly the subthalamic nucleus (STN) and globus pallidus interna (GPI).  A wire travels from the electrodes to a pacemaker-like device that is implanted in the chest wall.  After implantation, the clinician will set parameters that will determine the amount of electrical stimulation delivered.  DBS is approved by the FDA as a form of treatment for patients with Parkinson’s disease, dystonia, and essential tremor
  • 36. OTHER THERAPIES  For dyskinesias that impact the facial, neck, and limb region, some patients try injections of botox, or botulinum toxin, to reduce movement.
  • 37.  There are several additional therapies that are currently undergoing clinical trials for the treatment of dyskinesias.  Potential treatments for tardive dyskinesia include melatonin and estrogen, which modulate dopamine-controlled behavior and protect against cell damage from the long- term use of antipsychotic medications.
  • 38.  For the treatment of levodopa-induced dyskinesia, drugs that target different brain chemicals are being studied.  In addition, under-the-skin levodopa pumps are also being studied to test if they can effectively maintain consistent dopamine levels.  Finally, researchers are investigating ways to best optimize deep brain stimulation and are testing a technique called focused ultrasound, a non-invasive, irreversible procedure to treat dyskinesia.  .
  • 39.  Coping  Dealing with dyskinesias can be stressful and impact daily activities and social interactions.  Exercise, like walking or swimming, may be recommended.  Managing stress may also be crucial to control symptoms, as stress tends to exacerbate the uncontrolled movements.
  • 40. AIMS OF PHYSIOTHERAPY  Maintain and improve levels of function and independence, which will help to improve a person’s quality of life  Use exercise and movement strategies to improve mobility  Correct and improve abnormal movement patterns and posture, where possible  Maximize muscle strength and joint flexibility  Correct and improve posture and balance, and minimise risks of falls  Maintain a good breathing pattern and effective cough  Educate the person with Parkinson’s and their carer or family members  Enhance the effects of drug therapy
  • 41. PHYSIOTHERAPY  Passive movements  Ex.; co-ordination  Movement control  Functional training  Auditory and visual cuing  Strengthening  Rom  Endurance  Cardiopulmonary fitness