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Term 3 > Neuromuscular Stroke and PD > Flashcards

Neuromuscular Stroke and PD Flashcards

1
Q

What is the Epidemiology of Stoke?

A
  • Stroke is the leading cause of long-term disability and the leading preventable cause of disability
  • More women than men have strokes
  • Majority >65 y.o; 28% <65 y.o
  • African Americans are more impacted by stoke than any other racial group within the American population
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2
Q

What are the 2 main types of stroke?

A

Type 1 - Ischemic Stroke (occlusive)

Type 2 - Hemorrhagic Stroke (Abnormal bleeding)

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3
Q

Describe Type - Ischemic Stroke.

A
  • Account for approx. 80% of all strokes, and associated with a higher survival rate
  • Commonly linked to atherosclerosis of the cerebral arteries, which can lead to the formation of a Thrombus (Platelet aggregation within vessel wall) or an embolus.
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4
Q

What are Types of Ischemic Strokes?

A
  • Thrombus: This is platelet aggregation within vessel wall. This clot disrupts or blocks distal blood flow to the brain and it causes neuronal cell death and injury due to lack of O2 and glucose, this can break off and become a traveling embolism.
  • Embolus is a traveling clot or a bit of matter the forms elsewhere in the body and finds itself in the cerebral circulation, which then gets lodged in the vessel and blocks distal blood flow to the brain causing cell death and injury lack of O2 and glucose; Emboli are thrown from the heart and are related to types of Cardiovascular disease, can be caused by trauma
  • Atherosclerosis is that paste or plaque buildup that occurs in the arteries and the hardening of the BV wall, these plaque consist of fatty substances of calcium and cellular waste as well as cholesterol, over time these plaque can build up and can rupture the body then uses platelet aggregation and blood clot formation resulting in a thrombus
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5
Q

Describe Type 2 - Hemorrhagic Stroke. What happens if the bleeding is sudden and severe?

A
  • Referred to as Abnormal bleeding
  • Hemorrhagic stroke accounts for approximately 20% of all strokes, and is associated with a much higher mortality rate
  • A hemorrhagic stroke is bleeding in the brain due to a ruptured blood vessel, most often due to an aneurysm or trauma. The blood leaks into or around the brain and the loose blood clot is an irritant to the nervous system tissue and it leads to neuronal death.
  • In addition, when a hemorrhagic stroke is occurring there is lack of blood flow or ischemia distal to the ruptured vessel which further causes neuronal cell death
  • If the bleeding is sudden and severe it can cause a rise in intracranial pressure, and cortical tissue will shift or become compressed, or your brain matter can herniate resulting in secondary brain damage
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6
Q

What are 2 types of Hemorrhagic Stroke?

A
  • Intracerebral Hemorrhage: Bleeding within the brain that occurs from smaller ruptured arteries that penetrate the brain, usually from small aneurysms related to things like chronic hypertension and atherosclerosis. This is also the more deadly type of stroke and those that survive often have very significant impairments and activity limitations.
  • Subarachnoid Hemorrhage: Bleeding occurs from much larger vessels that travel in the subarachnoid space. This is usually due to a berry aneurysm, which is defined as a congenital defect of an artery which causes weakness of the arterial wall and ballooning at bifurcation. This hemorrhage is typically easier in terms of medical treatment.
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7
Q

What is the Pathophysiology of Stoke? What is the area around the core area? What is the cascade of events that occurs in terms of deprivation of O2 to the cerebral tissue?

MUST KNOW

A

Complete occlusion of blood flow leads to a core area of neuronal cell death
- Around the core area is what’s referred to as the ischemic penumbra (area where neurons are lethargic, but remain viable)
- Firstly we have ischemia causing the neurons to release excessive glutamate, then we have altered Ca ion channels causing influx of Ca into neuron, because of this you have high levels of intracellular Ca it then activates a series of destructive Ca sensitive enzymes leading further neuronal cell death in ischemic penumbra area.

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8
Q

What are the risk factors and early signs for stroke?

A

Balance
Eyes
Face
Arm
Speech
Time: Huge in terms of getting medical intervention

Warning signs:
- Sudden numbness or weakness of the face, arm or leg especially one side of the body.
- Sudden confusion, trouble speaking or understanding
- Sudden trouble seeing in one or both eyes
- Sudden trouble walking, dizziness, loss of balance or coordination
- Sudden sever headache with no known cause

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9
Q

What are Stoke Vasculature Syndromes?

A

Typically involve the large cerebral vessels, which are:
- Anterior Cerebral
- Middle Cerebral
- Posterior Cerebral
- Vertebrobasilar Artery

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10
Q

What is the role of the Anterior Cerebral Artery? What are common problems with this artery?

A
  • Supports the medial aspect of the Frontal and Parietal lobes, the anterior limb of the internal capsule, the caudate nucleus, the putamen and the Corpus callosum.

Common Problems with ACA stroke are:
- Contralateral Hemiparesis or Hemiplegia
- Contralateral Sensory loss (mostly in LE)
- Mental confusion because of frontal lobe involvement

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11
Q

What is the role of the Middle Cerebral Artery? What are some common problems with this artery?

A
  • Supplies the lateral aspect of the Frontal Temporoparietal and Occipital lobes, as well as the head of the caudate nucleus and putamen, or basal ganglia structures, the external capsule, colostrum and the anterior internal capsule

Common Problems with MCA stroke are:
- Contralateral hemiparesis or Hemiplegia
- Contralateral Sensory loss (mostly in UE)
Can include:
- Homonymous Hemianopia or other visual and spatial perceptual deficits, that being neglect if its the non-dominant hemisphere and apraxia if its the dominant hemisphere

The MCA is the most common site for Infarct

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12
Q

What is the role of the Posterior Cerebral Artery? What are some common problems with this artery?

A
  • Supports the medial aspect of the occipital lobe and the medial and inferior aspects of the temporal lobe, as well as the corpus callosum, the posterior diencephalon (involving both thalamus and hypothalamus) as well as midbrain

Common problems with PCA Stoke are:
- Visual Changes (Pt. may exhibit homonymous hemianopsia
- May have very transient contralateral hemiparesis or hemiplegia
- Transient contralateral sensory loss (mainly because of thalamus and diencephalon involvement)

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13
Q

What is the role of the Vertebrobasilar Artery? What happens if there is Vertebrobasilar Artery insufficiency?
What are common problems with is artery?

A
  • Supports the medulla, the pons, the midbrain, the cerebellum as well as the labyrinth
  • If there is Vertebrobasilar Artery insufficiency death may occur because of the life function that are housed in within the brainstem

Common problems with Vertebrobasilar Artery are:
- Ipsilesional or ipsilaterally taction coordination. Pt. could be in a coma, have diplopia, tetraplegia and bulbar paralysis

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14
Q

What is a specific syndrome related to Vertebrobasilar Artery? How does this syndrome occur?

A

“Locked-In” Syndrome
- Tetraplegia with preserved consciousness, preserved sensation and vertical gaze

This occurs with a basilar artery occlusion and typically with bilateral infarction of the ventral aspect of the pons

*This can be very devastating because an individual is completely dependent and the only type of communication and/or mobility that they have would be to blink their eyes

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15
Q

With Motor impairments, what are abnormal synergy patterns?

A

When joint movement cannot be isolated, due to an inability to activate or coordinate muscle contractions, an abnormal mass pattern of movement occurs

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16
Q

What is the Medical Management of stoke in the acute setting?

A

Neuroimaging
- CT scan: used to figure out whether the patient has had a Hemorrhagic stroke. Its not available to delineate in acute setting an ischemic stroke or cerebral edema until three to five days after the neurological event.

  • MRI:
  • Angiography: (Invasive test where dye is injected to give specific info about the BVs prior to injury; dye allows vasculature to be shown on x-ray or CT)
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17
Q

What are different Interventions for Stoke?

A

Pharmacological
- tPA
- Glutamate and Ca antagonists:

Surgical
- Clot evacuation

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18
Q

With Pharmacological management of stroke, What is tPA? When is this drug most optimal? When should it not be used?

A
  • Tissue Plasminogen Activase: A clot busting drug, with optimal effectiveness when the drug is administered within a 3hr window of the onset of symptoms
  • This can dramatically improve recovery and decrease the long-term participation restrictions.
  • Should not be used with Pt. that have hemorrhagic stroke, this would cause more bleeding and a worsening of symptoms
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19
Q

With Pharmacological management of stroke, How can Glutamate and Ca antagonist be beneficial for a patient?

A

This drug is given as Neuroprotectant-type agents, may be administered to help prevent further neuronal cell death in the area of the ischemic penumbra

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20
Q

With Surgical Management of stoke, why would clot evacuation be important?

A

For example, after a hemorrhagic stoke, it may be necessary to remove the blood to prevent secondary damage and an unfortunate rise in intracranial pressure

21
Q

What is the Preventative Medical Management of Stroke?

A
  • Pharmacological
  • Anticoagulants and anti-platelets: these help prevent recurrent thrombi/blood clot formation
  • Surgical
    –Internal Carotid Endartectomy: removal of plaque formation
    –Ballon Angioplasty with stents: ballon catheter is fed through the vasculature until it reaches the blocked artery, ballon then inflated to expand BVs wall, wire/mesh is then implanted to prevent BV collapsing
    –Aneurysm clipping: Helps block blood flow and preventing the aneurysm from getting larger and further expanding
22
Q

What are the characteristics of Right Sided CVA /Left sided Hemiplegia/paresis Post Stroke?

A
  • Unilateral neglect as a perceptual impairment.
  • Agnosia, also a perceptual impairment
  • Quick and impulsive behavior and many times poor judgement
  • Unaware of their deficits
  • May exhibit emotional lability, cant manage their emotions

Your initial encounter with the patient, your initial assessment of the medical record should be safety concerns

23
Q

What are the characteristics of Left Sided CVA /Right sided Hemiplegia/paresis Post Stroke?

A
  • More likely to have aphasia (Expressive or Receptive)
  • Apraxia
  • Slow, cautious and hesitant in their behavior
  • They are aware of their deficits
  • May be very depressed and have negative attitudes
    (These Pt. are more susceptible of being clinically depressed, especially has they move into more chronic disease states)
  • PT need to provide a lot of motivation, external support and cueing
24
Q

What is Parkinson’s Disease?

A

A slowly progressive neuro-degenerative disorder of the CNS

25
Q

What is Idiopathic PD?

A

The most common kind of PD, and its referred to as “True Parkinson’s Disease”.
- It has no known cause

26
Q

What is the incidence of Idiopathic PD?

A

2% of the population > 65yrs of age have PD
- Incidence dramatically increases with age
- Average onset is 50-60 yrs, young onset is 21-40 yrs (Juvenile onset is <21 yrs)
- Men are more affected than women (1.2-1.5x more men than women)

27
Q

What is the Etiology of Parkinson’s Disease?

A
  • Idiopathic (No known cause)
  • 10% genetically caused
28
Q

What is the Etiology of Secondary Parkinsonism?

A
  • Virus
  • Toxins, or medication side effects
  • Multi infarct vascular disease (small stokes that can cause symptoms that mimic parkinson’s)
  • Normal pressure hydrocephalus (causes an increase in the amount of cerebral spinal fluid in the brain, however pressure doesn’t get elevated, their ventricles become enlarged. The increase of CSF compresses regions of the brain, causes shuffling gait, incontinence, confusion and cognitive decline.) In order to DD NPH with PD is that NPH does not have tremors and parkinson’s doe
29
Q

What is the Etiology of Parkinsonism-plus syndromes?

A

This is super rare

  • Progressive Supranucular Palsy
  • Multi-system atrophy
  • Lew body disease
  • Alzheimer’s disease with Parkinsonism

(All of these present similar with slowness of movement and rigidity, however other symptoms later present themselves and are not characteristics of PD and the diagnosis changes)

30
Q

What is the Pathophysiology of Parkinson’s?

A
  • Degeneration of Dopamine (DA) producing neurons in the Basal Ganglia.
    –Its the Pars compactus of the Substantia Nigra
  • Net effect is a reduction of DA acting on the striatum that affects:
    –Direct loop (initiated voluntary movement)
    –Indirect loo (inhibits voluntary movement)
  • Lewy Body inclusions, protein accumulations that build up inside of neurons causing further damage.
31
Q

What are the Cardinal Features for PD?

A
  • Tremor (resting, but progresses to action), starts asymmetrical.
  • Rigidity, is hypertonia (Increased resistance to passive movement)
    –Leadpipe: uniform increase in resistance in both FLX and EXT
    –Cogwheel: is leadpipe with a tremor superimposed
    –Masked Face: Rigidity in the face
  • Akinesia (no movement; freezing)/Bradykinesia (slow movement) PD pts. may also have hypokinesia (small movements) Narrow spaces, turns and obstacles may cause freezing
  • Postural Instability (Occurs later in disease, ~5 years post diagnosis), determined through the Pull test.
    –Postural deformity (stooped posture)
32
Q

What are Secondary Motor Symptoms for PD?

A
  • Stooped kyphotic posture, FHP (forward head posture)
  • Reduced extensor strength: may start strong but with repetitions movement weakness and amplitude is reduced.
  • Increased flexor tightness:
    –neck, hip, elbow flx, ADD of shoulder, IR of shoulder, PF
    –fatigue, comes from the rigidity
    –joint hypomobility: spine, shoulders, hips, ankles
  • Start hesitation
  • Difficulty with dual tasking (ex. walking and talking)
33
Q

What are Secondary Motor Symptoms of PD, for GAIT?

A
  • Shuffling: gait pattern with reduced step length (feet are”glued” to floor (typical pattern)
  • Asymmetrical: arm swing and reduced trunk rotation
  • Festinating (sudden increase in cadence and reduction in step length, COM is also affecting them so their falling and they cant catch themselves)
    –Anteropulsive: when the COM is in forward direction
    –Retropulsive: when the COM is in backward direction
  • Freezing of gait (triggers can be narrow spaces, changes in flooring, difficulty with turning may also cause a freeze)
  • Bradykinetic
34
Q

What are non-motor symptoms of PD? (11)

A
  • Depression, anxiety
  • Sleep disturbances
  • Psychosis
  • Dementia
  • Lack of smell
  • Excessive sweating, saliva production, oily skin
  • Constipation
  • Orthostatic Hypotension/Low BP
    –Drop of 20mmHg systolic or 10mmHg diastolic w/
    increased HR
  • Proprioception is altered with consistent under scaling
  • Dysphagia (issues swallowing, can lead to death)
  • Dysarthria (Hypophonia, reduced volume and/or Hypokinetic, problems with rate of speech)
35
Q

How do patients get Clinically diagnosed with PD?

A
  • There is no definitive test to diagnose PD

Based on signs and symptoms:
- History: lack of smell, constipation, sleep disturbances, postural hypotension

  • Clinical Exam: hand writing, speech, 2/4 cardinal signs with asymmetry
  • Rule out: other neurodegenerative diseases
  • Response to dopamine to replacement therapy
  • Observation over time
36
Q

Once a pt. is diagnosed with PD, what are the 2 clinical sub-groups they can be placed in?

A
  • Postural Instability Gait Disturbed (PIGD) (~13-33% of pt.)
  • Tremor (~67-87% of pt., more common)
37
Q

When a pt. is diagnosed with PD and they are place in the PIGD subgroup, what does this mean for the patient?

A
  • Postural instability, gait disturbances at onset (freezing)
  • Bradykinesia (akinesia)
  • More debilitating
  • Rapid progression compared to tremor
  • More likely to have impaired cognition/dementia (late onset; 65yrs)
38
Q

When a pt. is diagnosed with PD and they are place in the Tremor subgroup, what does this mean for the patient?

A
  • They will have less bradykinesia and postural instability
  • Less debilitating compared to PIGD
  • Slower progression
  • Earlier onset (<65yrs)

Eventually the pt. will develop PIGD

39
Q

With the Hoehn and Yahr Classification of Disability, what is Stage 1?

A

Minimal disability, unilateral symptoms

40
Q

With the Hoehn and Yahr Classification of Disability, what is Stage 2?

A

Bilateral, or midline involvement (no balance impairment)

41
Q

With the Hoehn and Yahr Classification of Disability, what is Stage 3?

A

Postural instability present but can still live independently

42
Q

With the Hoehn and Yahr Classification of Disability, what is Stage 4?

A

All symptoms present, standing/walking only possible with assistance

43
Q

With the Hoehn and Yahr Classification of Disability, what is Stage 5?

A

Wheelchair or bed bound

44
Q

What is the Medical Management of PD? What do these drugs do?

A

Its important of trailing dopamine replacement therapy to make PD diagnosis and to start treatment, the medication used is Sinemet
- Sinemet is made of two drugs:
–Levodopa/Carbidopa

  • Levodopa is a dopamine precursor allows dopamine to cross Blood-brain-barrier, its combined with Carbidopa
  • Carbidopa inhibits the metabolism of levodopa and allows more of it to reach the brain
    The dopamine acts on the striatum within the Basal Ganglia
45
Q

What happens if you were to give Levodopa by itself?

A

The stomach and small intestines, they would digest most of it and very little would actually get to the brain

46
Q

What are potential side effects of taking Levodopa and Carbidopa?

A

Important
- Pt. will experience End-of Dose deterioration (wearing off); predictable worsening of symptoms toward the end of the expected time frame of medication dose
- After 4-6 yrs: the patient may develop Dyskinesia (abnormal movement) and Dystonia (Severe muscle posturing). They may also experience “On-Off” Phenomenon which is unpredictable worsening of symptoms

47
Q

With medical management of PD, what is Deep Brain Stimulation (DBS)?

A
  • Electrical stimulation delivered deep into the brain, a battery pack is surgically inserted under the skin in the chest, then a wire goes under the scalp to the brain to stimulate the Subthalamic nucleus or the Globus Pallidus Internus.
  • This is best for patient who are experiencing unpredictable fluctuations in their motor symptoms (On-Off Phenomenon), or complications with dyskinesia.
  • Can dramatically reduce the amount of meds. required (up to 30%)
  • Very effective in reducing or eliminating tremors
  • However this may worsen balance, speech impairment and depression
    This therapy is reversible if it doesn’t work
48
Q

What is the Frame Work for Rehabilitation for PD?

A
  • Interdisciplinary Team (Movement specialist, PT, OT, SLP, etc.)
  • Preventative (PT should NOT be delayed), restorative, and compensatory
  • Consider timing of meds.
  • Outpatient (on-going) most common setting, PT’s should be treating their pt once or twice a year (4-6 episodes of care)
  • Inpatient
  • Homecare (another common setting), here you can eval. the patient in their environment, this can improve QOL

Term 3 (13 decks)

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