Exam 3 ppt 2 Movement Disorders Flashcards

1
Q

What are three parts of the CNS that influence voluntary movement?

A
  1. Corticospinal Tract
  2. Basal Ganglia
  3. Cerebellum
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2
Q

what is the center of motor cordination?

A

the cerebellum

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3
Q

In general, what does the cerebellum do in regards to voluntary movement?

A

Cerebellum- center of motor coordination

  • Complex interaction to ensure smooth, purposeful movement without extraneous muscular contractions
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4
Q

Describe the system that are usually involved in movement disorders (because they are part of motor control)?

A
  • •Pyramidal tracts- pass through the medullary pyramids
    • –Connect cerebral cortex to brain stem and SC lower motor centers
  • •Extrapyramidal system- Basal ganglia
    • –Caudate nucleus, putamen, globus pallidus, subthalamic nucleus and substantia nigra
    • –Deep to the forebrain, direct output rostrally through thalamus to cerebral cortex
    • –Movement disorders typically occur in this system

Dr. Shappy basically skipped over this slide. She said When we have Disordered movement, we are looking at movement disorders that are cause by problems in this system (didn’t specify if she meant both or one or the other)

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5
Q

Describe Pyramidal tracts and what they do

A

•Pyramidal tracts- pass through the medullary pyramids

  • –Connect cerebral cortex to brain stem and SC lower motor centers

More from wikipedia:

The pyramidal tracts (pyramides)[citation needed] include both the corticospinal and corticobulbar tracts. These are aggregations of upper motor neuron nerve fibres that travel from the cerebral cortex and terminate either in the brainstem (corticobulbar) or spinal cord (corticospinal) and are involved in control of motor functions of the body.

The corticobulbar tract conducts impulses from the brain to the cranial nerves.[1] These nerves control the muscles of the face and neck and are involved in facial expression, mastication, swallowing, and other functions.

The corticospinal tract conducts impulses from the brain to the spinal cord. It is made up of a lateral and anterior tract. The corticospinal tract is involved in voluntary movement. The majority fibres of the corticospinal tract cross over in the medulla, resulting in muscles being controlled by the opposite side of the brain. The corticospinal tract also contains Betz cells (the largest pyramidal cells), which are not found in any other region of the body.

The pyramidal tracts are named because they pass through the pyramids of the medulla.

http://en.wikipedia.org/wiki/Pyramidal_tracts

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6
Q

Describe extrapyramidal system and what it does

A

•Extrapyramidal system- Basal ganglia

  • –Caudate nucleus, putamen, globus pallidus, subthalamic nucleus and substantia nigra
  • –Deep to the forebrain, direct output rostrally through thalamus to cerebral cortex
  • –Movement disorders typically occur in this system

I found this confusing without explanation, so below is a helpful section from wikipedia:

In anatomy, the extrapyramidal system is a neural network that is part of the motor system that causes involuntary reflexes and movement, and modulation of movement (i.e. coordination). The system is called “extrapyramidal” to distinguish it from the tracts of the motor cortex that reach their targets by traveling through the “pyramids” of the medulla. The pyramidal pathways (corticospinal and some corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers on the modulation and regulation (indirect control) of anterior (ventral) horn cells.

Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target neurons in the spinal cord involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.

The extrapyramidal system is very old and three of the four tracts of the human extrapyramidal system are clearly present in salamanders.[1][2]

The extrapyramidal tracts include parts of the following:[3]

rubrospinal tract
pontine reticulospinal tract
medullary reticulospinal tract
lateral vestibulospinal tract
tectospinal tract

http://en.wikipedia.org/wiki/Extrapyramidal_system

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7
Q

What are three classifications of movement disorders?

and some examples

A
  1. •Hypokinetic disorders- Decreased or slow movement
    • –Parkinson’s disease
  2. •Hyperkinetic disorders- Increased movement
    • –Tremors, myoclonus, dystonia, chorea, hemiballismus, athetosis, tics
  3. •Overlap
    • like tremors in Parkinson’s disease

Shappy said all of these terms were defined in last class.

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8
Q

what is dystionia?

symptoms?

A

Dystonia: Sustained involuntary muscle contractions of antagonistic muscle groups

Symptoms: Abnormal posturing or jerky, twisting, intermittent spasms

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9
Q

Dystonia: diagnosis

A

Diagnosis by Exclusion of other diseases, such as:

  • •Tardive dyskinesia
  • •Basal ganglia and other CNS infections
  • •Neck infections or tumors
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10
Q

what is Tardive dyskinesia?

A

Wikipedia:

Tardive dyskinesia /ˈtɑrdɨv ˌdɪskɨˈniːʒə/ is a difficult-to-treat and often incurable form of dyskinesia, a disorder resulting in involuntary, repetitive body movements. In this form of dyskinesia, the involuntary movements are tardive, meaning they have a slow or belated onset.[1] This neurological disorder most frequently occurs as the result of long-term or high-dose use of antipsychotic drugs,[Note 1] or in children and infants as a side effect from usage of drugs for gastrointestinal disorders.[Note 2][2]

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11
Q

Three Treatments for Dystonias

A
  • –Physical measures
  • –Botulinum toxin injections or medication
  • –Surgery to release (like in dorsal rhizotomy)
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12
Q

will most movement disorders show up on scans?

Can we treat them if they dont?

A

A lot of these conditions will not show up on scans until they are very severe.

Too hard to test in the basal nuclei down to the neuron level (to see it degenerating). Most of these disorders are identified post mortem.

So we may not have a specific diagnosis, but we can treat the symptoms

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13
Q

Dystonia Pathophysiology

A

Progressive neuron degeneration of the basal nuclei and cerebellum

What does degeneration of the neuron mean?

  • •Something wrong with the synapse
    • •She listed several things that could go wrong at the synapse (I think it is from previous lectures)
  • •Not in the synapse
    • •Demyelination
      • •Progressive degenerative process that causes abnormal responses
    • •Death of neuron
      • •Louie bodies
        • •Build up of protein and eosinophil
        • •Common in Alzheimer’s and Parkinson’s
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14
Q

What two ways the neuron can degenerate?

A
  1. Something wrong in the synapse
  2. Problem not in the synapse
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15
Q

What are ways neurons can degenerate at the synapse?

why is it important to know what is wrong?

A

Problems with:

  1. receptors,
  2. reuptake,
  3. neurotransmitter production (amount of neurotransmitters)

if you know what is wrong, then you can give the correct meds to help with the synapse

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16
Q

Neuron degeneration: what are some problems that can occur outside of the synapse?

A

•Demyelination is the main one

  • •Progressive degenerative process that causes abnormal responses
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17
Q

what can both demyelination and synaptic degeneration lead to?

A

•Death of neuron

  • •Louie bodies
    • •Build up of protein and eosinophil
    • •Common in Alzheimer’s and Parkinson’s
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18
Q

what are Lewy Bodies?

A

Wikipedia:

Lewy bodies are abnormal aggregates of protein that develop inside nerve cells in Parkinson’s disease (PD), Lewy body dementia, and some other disorders. They are identified under the microscope when histology is performed on the brain.

Lewy bodies appear as spherical masses that displace other cell components. The two morphological types are classical (brain stem) Lewy bodies and cortical Lewy bodies. A classical Lewy body is an eosinophilic cytoplasmic inclusion consisting of a dense core surrounded by a halo of 10-nm-wide radiating fibrils, the primary structural component of which is alpha-synuclein. In contrast, a cortical Lewy body is less well defined and lacks the halo. Nonetheless, it is still made up of alpha-synuclein fibrils. Cortical Lewy bodies are a distinguishing feature of dementia with Lewy bodies (DLB), but may occasionally be seen in ballooned neurons characteristic of Pick’s disease and corticobasal degeneration,[1] as well as in patients with other tauopathies.[2] They are also seen in cases of multiple system atrophy, particularly the Parkinsonian variant.[3]

http://en.wikipedia.org/wiki/Lewy_body

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19
Q

what is Fragile X?

Who and what structures it affects

Transmission
Signs and symptoms
Diagnostic testing
Treatment

A

It is a genetic Disorder (involves the X chromosome), and the most common intellectual disability in males. Affects cerebellar peduncles, but may impact other areas- need more research. May occur before school age, so IEP (individualized education plan) are developed for education in the school setting.

Carrier is the female (daughters of males who have the disease) . dad can be symptomless, but pass it on to the daughter who will then give to her sons who will show the symptoms

s/s: Progressive neural dysfunctional diseases: tremors, dystonia, mood issues (impatience, hostility), autonomic nervous system issues (sweating, bowel, bladder, ect), Parkinson like, and eventually dementia

Diagnostic testing: Genetic testing can identify it, MRI, EKG can show the deficiencies in the brain.

Treatment: There are some med that can help, but only slow the progression/ does not fix (behavioral, speech, balance, etc). IEPs fdeveloped for education at school

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20
Q

Fragile X:

Who and what structures it affects

A

It is a genetic Disorder (involves the X chromosome), and the most common intellectual disability in males. Affects cerebellar peduncles, but may impact other areas- need more research. May occur before school age, so IEP (individualized education plan) are developed for education in the school setting.

Carrier is the female (daughters of males who have the disease) . dad can be symptomless, but pass it on to the daughter who will then give to her sons who will show the symptoms

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21
Q

Fragile X:

Transmission

A

Transmission:

Carrier is the female (daughters of males who have the disease) . dad can be symptomless, but pass it on to the daughter who will then give to her sons who will show the symptoms

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22
Q

Fragile X:

Signs and symptoms

A

Signs and symptoms:

s/s: Progressive neural dysfunctional diseases: tremors, dystonia, mood issues (impatience, hostility), autonomic nervous system issues (sweating, bowel, bladder, ect), Parkinson like, and eventually dementia

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23
Q

Fragile X:

Diagnostic testing

A

Diagnostic testing:

Diagnostic testing: Genetic testing can identify it, MRI, EKG can show the deficiencies in the brain.

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24
Q

Fragile X:

Treatment

A

Treatment:

There are some med that can help, but only slow the progression/ does not fix (behavioral, speech, balance, etc). IEPs fdeveloped for education at school

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25
Q

Huntington’s Disease (everything):

Type of Disorder:

Pathophysiology:

Cause:

S/S:

Progression/Prognosis:

Diagnostics:

Non PT treatment options:

PT role in Treatment:

A

Type of Disorder:

  • Autosomal dominant disorder

•Pathophysiology:

  • Caudate nucleus from a pathophysiologic standpoint
    • Spiny neurons in corpus striatum degenerate and there is a
    • decrease in neurotransmitters,
      • substance P and GABA neurotransmitters specifically

Cause:

  • gene mutations

•Signs and symptoms:

  • List of s/s is large. There are similarities to schizophrenia, bipolar, antisocial, dementia, depression, apathy, irritability, and then obvious movement disorders (Chorea, gross movement disorders – see video): puppet like gait, huntington’s dance, tongue protrusion, mouth movements, head thrusting, quick eye movements,

•Progression/Prognosis:

  • –Very severe – ends in long term care and maybe psych ward.
  • – Usually live 13-15 years from onset of symptoms.

•Diagnostics

  • –Some CT MRI imaging on caudate nucleus and frontal lobe.
    • Usually starts to show up at 40-50 years old on a CT scan.
      • must have a certain number of neurons degenerate in order to pick up dz on scan
  • –Can be genetically tested for
  • Often diagnosed by presence of symptoms

Non PT treatment options:

  • there are some medications that can help with symptoms a bit

PT role in Treatment

  • we might be the first medical professional to recognize symptoms
  • We can teach adaptations
  • We can try to slow progression
26
Q

Huntington’s Disease

Type of Disorder:

A

Type of Disorder:

Autosomal dominant disorder

27
Q

Huntington’s Disease

Pathophysiology:

A

Pathophysiology:

  • Caudate nucleus from a pathophysiologic standpoint
    • Spiny neurons in corpus striatum degenerate and there is a
    • decrease in neurotransmitters,
      • substance P and GABA neurotransmitters specifically
28
Q

Huntington’s Disease

Cause:

A

Cause:

gene mutations

29
Q

Huntington’s Disease

S/S: (6 movement examples, 7 other examples)

A

Signs and symptoms:

List of s/s is large.

  • There are similarities to
    1. schizophrenia,
    2. bipolar,
    3. antisocial,
    4. dementia,
    5. depression,
    6. apathy,
    7. irritability, and then
  • obvious movement disorders (Chorea, gross movement disorders – see video):
    1. puppet like gait,
    2. huntington’s dance,
    3. tongue protrusion,
    4. mouth movements,
    5. head thrusting,
    6. quick eye movements,
30
Q

Huntington’s Disease

Progression/Prognosis:

A

Progression/Prognosis:

  • –Very severe – ends in long term care and maybe psych ward.
  • – Usually live 13-15 years from onset of symptoms.
31
Q

Huntington’s Disease

Diagnostics:

A

Diagnostics

  • –Some CT MRI imaging on caudate nucleus and frontal lobe.
    • Usually starts to show up at 40-50 years old on a CT scan.
    • must have a certain number of neurons degenerate in order to pick up dz on scan
  • –Can be genetically tested for
  • Often diagnosed by presence of symptoms
32
Q

Huntington’s Disease

Non PT treatment options

A

Non PT treatment options:

there are some medications that can help with symptoms a bit

33
Q

Huntington’s Disease

PT role in Treatment:

A

PT role in Treatment

  1. we might be the first medical professional to recognize symptoms
  2. We can teach adaptations
  3. We can try to slow progression
34
Q

What are two diseases that Progressive Supranuclear Palsy is easily confused with?

A

Easily confused with Parkinson’s and Alzheimer’s

35
Q

what is something that distigueshis Progressive Supranuclear Palsy from Parkinson’s?

A

Progressive Supranuclear Palsy doesn’t respond to dopamine replacement therapy

36
Q

Progressive Supranuclear Palsy (everything):

What is it/what does it damage?

Transmission:

S/S:

Diagnosis:

Prognosis:

Treatment:

A

What is it/what does it damage?

  • Rare degenerative CNS disorder
  • Affects Basal ganglia and brainstem
  • Has protein depositis like other similar diseases

Transmission:

  • seems to have a genetic component

S/S:

  • bradykinesia,
  • rigidity,
  • eye movement,
    • Cant look down (can look side to side but the eyes can not go down; if the head is moved up and down, the eyes stay forward- compared pt to a doll’s eyes
  • progressive,
  • pseudo-bulbar palsy (facial),
  • dementia,
  • From Video: gait is wide and staggering (not like parkinson’s with the shuffling)
    • I think they lean backwards too (not forwards like parkinson’s)
    • pt seems apethetic to their unsteadyness and “plunges ahead”
  • From Video: Characteristic speech pattern: spastic speech in combo with ataxic speech
    • strained and slow
    • syllables grouped into unnatural groups with unnatural pauses
    • this speech pattern occurs in almost no other condition
  • The video of the guy in his underwear had Progressive Supranuclear Palsy (“don’t worry about his underwear!”)

Diagnostic Testing:

  • MRI will not show until severe atrophy.
    • so diagnosis must be by symptoms before it is severe
  • Has protein depositis like other similar diseases, possibly part of scar tissue while body is trying to heal (so it doesn’t show until that point)

Prognosis:

  • degenerative,
  • most live 6-8 years (according to video Dr. Shappy posted)
    • death is usually from related problems, not the actual condition

Treatment:

  • does not respond to dopamine replacement like parkinson’s dz
  • a fact sheet I found discussed treatment for symptoms (like difficulty swallowing), but said there was no treatment for the actual disease.
  • PT’s treat symptoms
37
Q

Progressive Supranuclear Palsy:

What is it/what does it damage? (3)

A

What is it/what does it damage?

  1. Rare degenerative CNS disorder
  2. Affects Basal ganglia and brainstem
  3. Has protein depositis like other similar diseases
38
Q

Progressive Supranuclear Palsy:

Transmission:

A

Transmission:

seems to have a genetic component

39
Q

Progressive Supranuclear Palsy:

S/S: (8 examples)

A

S/S:

  1. bradykinesia,
  2. rigidity,
  3. eye movement,
    • Cant look down (can look side to side but the eyes can not go down; if the head is moved up and down, the eyes stay forward- compared pt to a doll’s eyes
  4. progressive,
  5. pseudo-bulbar palsy (facial),
  6. dementia,
  7. From Video: gait is wide and staggering (not like parkinson’s with the shuffling)
    • I think they lean backwards too (not forwards like parkinson’s)
    • pt seems apethetic to their unsteadyness and “plunges ahead”
  8. From Video: Characteristic speech pattern: spastic speech in combo with ataxic speech
    • strained and slow
    • syllables grouped into unnatural groups with unnatural pauses
    • this speech pattern occurs in almost no other condition
  • The video of the guy in his underwear had Progressive Supranuclear Palsy (“don’t worry about his underwear!”)
40
Q

Progressive Supranuclear Palsy:

Diagnosis: (3)

A

Diagnosis:

  1. MRI will not show until severe atrophy.
  2. so diagnosis must be by symptoms before it is severe
  3. Has protein depositis like other similar diseases, possibly part of scar tissue while body is trying to heal (so it doesn’t show until that point)
41
Q

Progressive Supranuclear Palsy:

Prognosis: (2)

A

Prognosis:

  1. degenerative,
  2. most live 6-8 years (according to video Dr. Shappy posted)
    • death is usually from related problems, not the actual condition
42
Q

Progressive Supranuclear Palsy:

Treatment: (3)

A

Treatment:

  1. does not respond to dopamine replacement like parkinson’s dz
  2. a fact sheet I found discussed treatment for symptoms (like difficulty swallowing), but said there was no treatment for the actual disease.
  3. PT’s treat symptoms (I surmise)
43
Q

Parkinson’s Disease (everything):

What is it?/Cause/Progression:

Pathophysiology:

S/S:

Diagnosis, Non PT:

DIagnosis, PT:

Treatment:

A

What is it?/Cause/Progression:

  • Idiopathic, slow progressive, degenerative disorder
  • Can be caused by drugs, trauma, strokes, lots of stuff. May be a familial connection

Pathophysiology:

  • Degeneration of Substantia Nigra, Locus Ceruleus, and brainstem,
    • dorsal aspect of putamen is also involved
  • –Neuroglial cells issues
  • –Lewy bodies ultimately get formed (IMPORTANT to KNOW!
    • •Synuclein Filled
      • a chemical marker (an inflametory protein)

S/S (but not a check-list; pt may not have all symptoms):

  1. –Festinating gait
  2. –Resting tremor
  3. –Pill rolling
  4. –Stooped posture
  5. –Bradykinesia
  6. –No arm swing
  7. –Rigidity
  8. –Dementia
  9. –Akinesia
  10. –Sleep disorder issues (typically)
  11. –Flat affect

Diagnosis, Non PT:

  • –Looking for levels of dopamine, L-dopa, and markers that is Synuclein in lewy bodies
  • –Ultimately, we can see degeneration on CT scan and MRI
    • •Degeneration of Substantia Nigra, Locus Ceruleus, brainstem, and dorsal aspect of putamen
    • •Results in the motor deficits we define as Parkinsons
  • Try treating like parkinsons (L-dopa or other dopamine replacement therapy) to see if it responds

DIagnosis, PT:

  • PT tests
    • reflexes - positive babinski (so hyperreflexive)
    • Speed dependent tone
    • •Finger to nose,
    • tone and rigidity
    • diadodyskenisia
    • •Postural reflexes
    • •Analyze gait
    • balance
    • facial expressions (flat affect)
    • lack of blinking
    • Try treating like parkinson’s to see if it improves condition

Treatment:

  • Treat even if MRI is negative
    • Dopamine replacement therapy (L-dopa is common)
    • PT:
      1. shappy told us about BIG therapy; DO NOT CALL IT “BIG” therapy in your notes unless certified!!!
      2. Walker with laser beam that can help break akinesia in pt
      3. Treat symptoms
      4. Don’t give up, our brains are the limit on treatment options!
44
Q

Parkinson’s Disease

What is it?/Cause/Progression:

A

What is it?/Cause/Progression:

  1. Idiopathic, slow progressive, degenerative disorder
  2. Can be caused by drugs, trauma, strokes, lots of stuff. May be a familial connection
45
Q

Parkinson’s Disease

Pathophysiology:

A

Pathophysiology:

  • Degeneration of Substantia Nigra, Locus Ceruleus, dorsal aspect of putamen, and brainstem.
    • –Neuroglial cells issues
      • –Lewy bodies ultimately get formed (IMPORTANT to KNOW!)
        • •Synuclein Filled
          • a chemical marker (an inflametory protein)
46
Q

Parkinson’s Disease

S/S: (11 examples)

A

S/S (but not a check-list; pt may not have all symptoms):

  1. –Festinating gait
  2. –Resting tremor
  3. –Pill rolling
  4. –Stooped posture
  5. –Bradykinesia
  6. –No arm swing
  7. –Rigidity
  8. –Dementia
  9. –Akinesia
  10. –Sleep disorder issues (typically)
  11. –Flat affect
47
Q

Parkinson’s Disease

Diagnosis, Non PT: (3)

A

Diagnosis, Non PT:

  1. –Looking for levels of dopamine, L-dopa, and markers that is Synuclein in lewy bodies
  2. –Ultimately, we can see degeneration on CT scan and MRI
    • •Degeneration of Substantia Nigra, Locus Ceruleus, brainstem, and dorsal aspect of putamen
    • •Results in the motor deficits we define as Parkinsons
  3. Try treating like parkinsons (L-dopa or other dopamine replacement therapy) to see if it responds
48
Q

Parkinson’s Disease

DIagnosis, PT: (11 examples of things to test)

A

DIagnosis, PT:

PT tests

  1. reflexes - positive babinski (so hyperreflexive)
  2. Speed dependent tone
  3. •Finger to nose,
  4. tone and rigidity
  5. diadodyskenisia
  6. •Postural reflexes
  7. •Analyze gait
  8. balance
  9. facial expressions (flat affect)
  10. lack of blinking
  11. Try treating like parkinson’s to see if it improves condition
49
Q

Parkinson’s Disease

Treatment: (Non PT and PT)

A

Treatment:

  • Treat even if MRI is negative
    1. Dopamine replacement therapy (L-dopa is common)
    2. PT:
      • shappy told us about BIG therapy; DO NOT CALL IT “BIG” therapy in your notes unless certified!!!
      • Walker with laser beam that can help break akinesia in pt
      • Treat symptoms
      • Don’t give up, our brains are the limit on treatment options!
50
Q

9 sysmptoms to evaluate for differential diagnosis

A
  1. •Chorea: non-rhythmic jerky rapid movements. Non-suppressible, involuntary. Distal muscles, facial muscles are commonly involved.
  2. •Athetosis: like slow chorea. Impaired inhibition of thalamocortical neurons by the basal ganglia. Excess dopamine activity?
  3. •Hemiballismus: severe chorea. Unilateral rapid, non-rhythmic, wild flinging movements. Lesion in or around the contralateral subthalamic nucleus.
    • –Tx: antipsychotic medications.
  4. •Ballismus: bilateral version of hemiballisums, but less common.
  5. •Myoclonus: restless leg syndrome falls into this category. Brief shock-like muscle contractions.
  6. •Tics: the urge to do it and the relief felt afterwards. “it” is whatever.
  7. •Ataxia: really wide based gait.
  8. •Tremors; rhythmic, non-rithmic, oscilating, regular
  9. •Dystonias: sustained abnormal posturing movements. Or jerky, twisting movements.
51
Q

what is chorea?

A

•Chorea: non-rhythmic jerky rapid movements. Non-suppressible, involuntary. Distal muscles, facial muscles are commonly involved.

52
Q

what is athetosis?

A

•Athetosis: like slow chorea. Impaired inhibition of thalamocortical neurons by the basal ganglia. Excess dopamine activity?

(this is the one Dr. Lake showed as part of CP)

53
Q

what is hemiballisums?

what is a non-pt treatment?

A
  • •Hemiballismus: severe chorea. Unilateral rapid, non-rhythmic, wild flinging movements. Lesion in or around the contralateral subthalamic nucleus.
    • –Tx: antipsychotic medications.
54
Q

what is ballismus?

treatment?

A

•Ballismus: bilateral version of hemiballisums, but less common.

probably has same treatment ast hemiballisums: antipsychotic meds

55
Q

what is myclonus?

A

•Myoclonus: restless leg syndrome falls into this category. Brief shock-like muscle contractions.

(I think it is just one symptom of restless leg - shock-like symptoms are not always present, but go with what shappy said)

56
Q

What are tics?

A

•Tics: the urge to do it and the relief felt afterwards. “it” is whatever.

57
Q

what is ataxia?

A

•Ataxia: really wide based gait.

(I think it is broader than just gait, but go with what shappy said)

58
Q

what are tremors? (what are some variables of tremors?)

A

•Tremors; rhythmic, non-rithmic, oscilating, regular

59
Q

what is dystonia

A

•Dystonias: sustained abnormal posturing movements. Or jerky, twisting movements.

(spasmotic torticolis was an example she gave)

60
Q

how will we determine the difference between dementia and alzheimer’s?

A

The pathophysiology will help us know.