Neuromuscular Units 1-7 Finals Review Flashcards
What are potential impairments with Perceptual and Cognitive Impairments?
- Perceptual: Agnosia, Neglect, Apraxia
- Cognitive: Orientation, Memory, Arousal
What are potential impairments with Speech and Language Impairments?
- Aphasia
- Dysarthria
- Dysphagia
What are potential impairments with Composite Impairments?
This is both Motor and Sensory Impairments
- Postural control/balance (equilibrium coordination)
If a patient has a Upper Motor Neuron pathology, where would the patient be affected?
- The clinical presentation will be contralateral to the side of the deficit
If a patient has a Lower Motor Neuron pathology, where would the patient be affected?
- The clinical presentation will be on the ipsilateral side of the deficit
In terms of muscle weakness associated with UMN lesions, what is the def. of paralysis?
Complete absence of muscle strength or the inability to voluntarily recruit motor units.
In terms of muscle weakness associated with UMN lesions, what is the def. of Plegia?
The same as Paralysis:
- Complete absence of muscle strength or the inability to voluntarily recruit motor units.
In terms of muscle weakness associated with UMN lesions, what is the def. of Hemiplegia/Hemiparesis?
Hemiplegia: One-sided paralysis
Hemiparesis: One-sided Weakness
In terms of muscle weakness associated with UMN lesions, what is the def. of Paraplegia?
Lower Extremity Paralysis
In terms of muscle weakness associated with UMN lesions, what is the def. of Tetraplegia?
Both upper and lower extremity paralysis to include the trunk
Hypertonia in the form of muscle stiffness is an example of a Direct or Indirect impairment?
This will be an indirect impairment
A lot of times muscle stiffness will occur the longer the patient becomes chronic with their condition, ideally because they’ve become more sedentary
With involuntary movements, what is Dystonia?
Excessive twisting and bizarre repetitive movements caused by axial and proximal limb musculature, typical with basal ganglion lesions (Parkinson’s). Often exhibited in patients that have been using long term parkinson’s medications as a side effect.
With involuntary movements, what is Chorea?
Rapid and jerky movements, associated with basal ganglion lesions, hence the term Huntington’s Chorea
With involuntary movements , what is Athetosis?
Slow twisting, snakelike movements, often associated with Cerebral Palsy
With involuntary movements, what are Resting Tremors?
The tremor that occurs when the muscles and the patients body are at rest. Very common in patients with parkinson’s, especially with the upper extremity. Sometimes referred to as the “Pill Rolling Tremor”
With Visual defects, what are terms associated with UMN lesions?
- Blurred vision: loss of visual acuity
- Diplopia: double vision
- Strabismus: Eyes aren’t parallel, have altered visual axis
- Nystagmus: Rapid, rhythmic, repetitive involuntary eye movements
- Homonymous Hemianopsia: Partial blindness resulting in loss of vision in the same visual fields of both eyes
- Occipital Blindness: Legally blind, loss or absence of the ability to perceive images
What are the subcategories of Aphasia?
- Expressive Aphasia: (aka Broca’s or non-fluent/motor aphasia, occur when there is damage to broca’s area (Frontal lobe on left or dominant hemisphere) Have intact auditory comprehension. They have a hard time expressing what they want to say.
- Receptive Aphasia: (aka Wernicke’s or Fluent/Sensory Aphasia, occurs when there’s damage to Wernicke’s area (Association cortex in Temporal Lobe on left or dominate hemisphere). They have auditory comprehension that is impaired, they dont understand whats being said to them
- Global Aphasia: When patients have elements of both Expressive and Receptive Aphasia, there is going to be widespread, significant damage to the left or dominant hemisphere
With Composite Impairments, what are the main systems for Posture Control/Balance?
Somatosensory System (Dorsal Column-Median Lemniscal tract), Vestibular System (Peripheral sensory apparatus in inner ear), and Visual system
- All these systems will bring information to the CNS where both the brain, brainstem and cerebellum are going to integrate and understand for an appropriate motor plan
What are the 2 main types of stroke?
Type 1 - Ischemic Stroke (occlusive)
Type 2 - Hemorrhagic Stroke (Abnormal bleeding)
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
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.
What are the risk factors and early signs for stroke? What are the 5 “sudden” warnings?
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
What are common problems with ACA Strokes?
Common Problems with ACA stroke are:
- Contralateral Hemiparesis or Hemiplegia
- Contralateral Sensory loss (mostly in LE)
- Mental confusion because of frontal lobe involvement
What are common problems with MCA Strokes?
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
What are common problems with PCA Strokes?
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)
What happens if there is Vertebrobasilar Artery insufficiency?
What are common problems with is artery?
- 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
What is a specific syndrome related to Vertebrobasilar Artery? How does this syndrome occur?
“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
What are the characteristics of Right Sided CVA /Left sided Hemiplegia/paresis Post Stroke?
- 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
What are the characteristics of Left Sided CVA /Right sided Hemiplegia/paresis Post Stroke?
- 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
What is Parkinson’s Disease?
A slowly progressive neuro-degenerative disorder of the CNS
What is Idiopathic PD?
The most common kind of PD, and its referred to as “True Parkinson’s Disease”.
- It has no known cause
What is the Etiology of Secondary Parkinsonism?
- 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 does
What is the Etiology of Parkinsonism-plus syndromes?
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)
What is the Pathophysiology of Parkinson’s?
- 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.
With Motor impairments, what are abnormal synergy patterns?
When joint movement cannot be isolated, due to an inability to activate or coordinate muscle contractions, an abnormal mass pattern of movement occurs
What are the Cardinal Features for PD?
- 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)
What are Secondary Motor Symptoms for PD?
- 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)
What are Secondary Motor Symptoms of PD, for GAIT?
- 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
How do patients get Clinically diagnosed with PD?
- 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
With the Hoehn and Yahr Classification of Disability, what is Stage 1?
Minimal disability, unilateral symptoms
With the Hoehn and Yahr Classification of Disability, what is Stage 2?
Bilateral, or midline involvement (no balance impairment)
With the Hoehn and Yahr Classification of Disability, what is Stage 3?
Postural instability present but can still live independently
With the Hoehn and Yahr Classification of Disability, what is Stage 4?
All symptoms present, standing/walking only possible with assistance
With the Hoehn and Yahr Classification of Disability, what is Stage 5?
Wheelchair or bed bound
What happens if you were to give Levodopa by itself?
The stomach and small intestines, they would digest most of it and very little would actually get to the brain
What are potential side effects of taking Levodopa and Carbidopa?
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
What is the Pathophysiology of TBI?
Primary Brain injury-damage occurs at the moment of impact, they may exhibit:
- Focal Brain Injury
–Coup-contrecoup injury
–Polar Brain Injury - Blast Injury
- Diffuse Axonal Injury (DAI)
With TBI, what is a Focal Brain Injury?
Coup-Contrecoup Vs Polar Brain injuries.
These injuries occur at the site of impact. Damage may take the form of a contusion or laceration or both.
- Coup-contrecoup: If the brain is hit hard enough, the brain will bounce and make contact with the skull at the opposite site of the local brain damage. (Coup=the injury that occurs within the first point of contact. Contrecoup= the injury on the opposite side)
- Polar Brain injury: Occurs in response to an acceleration, deceleration as well as rotational forces (Common in head on collisions), the frontal and temporal lobes are most susceptible to injury
With TBI, what are Blast Injuries?
Defined as an explosive device that may detonate and a transient shockwave is produced and causes the brain damage.
- Result from the direct effect of blast overpressure on the brain
- Secondary injury results from the shrapnel and other objects being hurled at the individual
- Tertiary injury the patient is being pushed or flung backwards and hitting an object
With TBI, What is Diffuse Axonal Injury (DAI)?
These occur in response to acceleration, deceleration as well as rotation and occur in conjunction with focal and polar brain injuries
With Diffuse Axonal Injury, What is the affect of rapid movement of the brain within the skull? What happens if the damage is severe?
This causes widespread stretching and tearing of the neuronal axons within the myelin sheath. This is labeled as the patient having subcortical white matter shearing.
- If the injury is severe, damage will extend to the brainstem and lead to coma and abnormal posturing
- Not usually evident on CT or MRI, if the pt. is exhibiting DAI, this is found during the neurological exam
One of the medical management for TBI is the monitoring of ICP. What is normal ICP and when is it a red flag or a danger?
- Normal ICP is 4-15 mmHG
- After TBI, 15-20 mmHG is expected
- > 25mmHG is a Red Flag and measures will be taken to reduce the pressure
- Danger >40mmHG because impaired blood flow to the brain can cause secondary injury
If ICP goes above 20mmHG notify the nurses &/or doctor and modify intervention
If ICP goes above 30mmHG immediately STOP all interventions and notify nurses and doctors
What is the Sequlae of TBI?
Neuromuscular Impairments
Cognitive Impairments
Neurobehavioral Impairments
With the Sequlae, what are common impairments with Neuromuscular Impairments?
- Paresis
- Abnormal Tone
- Motor Function
- Postural Control
With the Sequlae, what are common impairments with Cognitive Impairments?
- Arousal Level
- Attention
- Concentration
- Memory
- Learning
- Executive functions
What are specific cognitive impairments that are unique to TBI?
They deal with the altered levels of consciousness:
- Coma: Arousal state not functioning,No sleep/wake cycle, Not usually permanent
- Vegetative State: Disassociation between wakefulness and awareness, Sleep/wake cycles are present, patient will demo reflexive, non-purposeful responses
- Minimally conscious state (MCS): The patient will now exhibit localization to stimuli and may inconsistently reach for objects
With perceptual and Cognitive Impairments with TBI, What is Lethargy, Obtunded, Stuper, and Coma?
- Lethargy: Altered consciousness in which a person’s level of arousal is diminished; drowsy but able to answer
- Obtunded: Diminished arousal and awareness; difficult to arouse and when aroused is confused
- Stuper: Altered mental status and responsiveness to one’s environment; can only be aroused with vigorous stimuli
- Coma: Unconscious patient, can not be aroused, eyes remain closed, no sleep wake cycles
With Rancho Los Amigos (RLA), what are the Levels Of Cognitive Functioning (LOCF)?
I. No response
II. Generalized Response
III. Localized Response
IV. Confused-Agitated
V. Confused-Inappropriate
VI. Confused-Appropriate
VII. Automatic-Appropriate
VIII. Purposeful-Appropriate
The first 3 are severe disorder of consciousness on the Coma Recovery Scale (coma, vegetative, MCS)
With the RLA of Cognitive Function, what are the Characteristics of Level 1: No Response?
Complete absence of observable change in behavior
With the RLA of Cognitive Function, what are the Characteristics of Level 2: Generalized Response?
Demonstrates generalized reflex response to painful stimuli
- Responds to repeated auditory stimuli with increased or decreased activity
With the RLA of Cognitive Function, what are the Characteristics of Level 3: Localized Response?
Demonstrates withdrawal or vocalization to painful stimuli
- Turns toward or away from auditory stimuli
- Blinks when strong light crosses visual field
- Follows moving object passing within visual field
With the RLA of Cognitive Function, what are the Characteristics of Level 4: Confused/Agitated?
Alert and heighted state of activty
- Purposful attempts to remove restraints or tubes or crawl out of bed
- Absent ST memory
- May cry out or scream out of proportion to stimulus even after its removal
- May exhibit aggressive or flight behavior
With the RLA of Cognitive Function, what are the Characteristics of Level 5: Confused, Inappropriate Non-Agitated?
Alert, not agitated but may wander randomly or with a vague intention of going home
- May become aggitated in response to exernal stimulation, and/or lack of environmental structure
- Not oriented to person, place, or time
- Unable to learn new information
With the RLA of Cognitive Function, what are the Characteristics of Level 6: Confused, Appropriate?
Inconsistently oriented to person, time and place
- Able to attend to highly familiar task in non-distracting environment for 30 min with moderate redirection
- Max assist for new learning with little or no carry over
With the Pathophysiology of Blast-Related Concussion, what are the Primary, Secondary, and Tertiary injuries?
- Primary Injury
–Shock waves from a blast disrupts brain tissue
–Similar to diffuse axonal injury
–More widespread injury - Secondary injury
–Fragments cause penetrating injury - Tertiary Injury
–Blunt trauma from striking solid surface
Using the Pic, what system is the patient dependent on if they have increased sway or LOB on conditions 2, 3, 5, and 6 during the Sensory Organization Test and Foam and Dome?
This will indicate that the patient is dependent on Vision for Postural Control
Using the Pic, what system is the patient dependent on if they have increased sway or LOB on conditions 4, 5 and 6 during the Sensory Organization Test and Foam and Dome?
This may indicate that the patient is dependent on Somatosensation for Postural Control
Using the Pic, what system did the patient loss if they have increased sway or LOB on conditions 5 and 6 during the Sensory Organization Test and Foam and Dome?
This may indicate that the patient is has Vestibular Loss
