Exam 3 ppt 2 Movement Disorders Flashcards Preview

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Flashcards in Exam 3 ppt 2 Movement Disorders Deck (60)
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1

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

  1. Corticospinal Tract
  2. Basal Ganglia
  3. Cerebellum

2

what is the center of motor cordination?

 

the cerebellum

3

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

 

Cerebellum- center of motor coordination

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

4

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

  • •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)

5

Describe Pyramidal tracts and what they do


•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

6

Describe extrapyramidal system and what it does

 


•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

7

What are three classifications of movement disorders?

and some examples

 

  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.

8

what is dystionia?

symptoms?


Dystonia: Sustained involuntary muscle contractions of antagonistic muscle groups

Symptoms: Abnormal posturing or jerky, twisting, intermittent spasms
 

9

Dystonia: diagnosis

 


Diagnosis by Exclusion of other diseases, such as:

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

10

what is Tardive dyskinesia?

 

 

 

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]

11

Three Treatments for Dystonias

 

 

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

12

will most movement disorders show up on scans?

Can we treat them if they dont?

 

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

 

 

13

Dystonia Pathophysiology

 

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

14

What two ways the neuron can degenerate?

 

  1. Something wrong in the synapse
  2. Problem not in the synapse

15

What are ways neurons can degenerate at the synapse?

 

why is it important to know what is wrong?

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

16

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

 


•Demyelination is the main one

  • •Progressive degenerative process that causes abnormal responses



 

17

what can both demyelination and synaptic degeneration lead to?

 

 

•Death of neuron

  • •Louie bodies
    • •Build up of protein and eosinophil
    • •Common in Alzheimer's and Parkinson's

18

what are Lewy Bodies?

 

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

19

what is Fragile X?

Who and what structures it affects

Transmission
Signs and symptoms
Diagnostic testing
Treatment
 

 

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

20

Fragile X:

Who and what structures it affects

 

 

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

21

Fragile X:

Transmission
 

 

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

22

Fragile X:

Signs and symptoms
 

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

23

Fragile X:

Diagnostic testing
 

 

Diagnostic testing:

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

 

24

Fragile X:

Treatment

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

25

Huntington's Disease (everything):

Type of Disorder:

Pathophysiology:

Cause:

S/S:

Progression/Prognosis:

Diagnostics:

Non PT treatment options:

PT role in Treatment:

 

 


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

Huntington's Disease

Type of Disorder:


Type of Disorder:

Autosomal dominant disorder

 

27

Huntington's Disease

Pathophysiology:

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

Huntington's Disease

Cause:

 

 

Cause:

gene mutations

 

29

Huntington's Disease

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

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

Huntington's Disease

Progression/Prognosis:

 

 

Progression/Prognosis:

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