Neuro Flashcards
Please describe how the nervous systems works for sensory and motor function
See image in sensory and motor function section
What are the two goals of neuro physio treatment?
Restorative function / impairments
Compensatory approach
*not mutually exclusive
What is sensory function and what does it look like for different areas to be impacted?
Help with differential diagnosis by identifying pattern of sensory involvement
Peripheral nerve - pattern of innervation of affected nerve
Nerve root - dermatomal pattern
Spinal cord - diffuse pattern of sensory involvement below the level of the lesion (bilaterally usually) (depends on spinal tracts affected)
Brainstem - ipsilateral facial impairments, contralateral trunk and limb impairments
Brain involvement - cortical: dependent on area of somatosensory cortex (homunculus) or deeper lesion involving thalamas and adjacent structures - diffuse unilateral dysfunction. Contralateral side affected (crossing of tracts)
What happens with sensation and movement?
As more motor - anticipate, correct and modify movement based on sensory inputs organized and integrated by CNS
Feedback: sensory input received and adjusted for motor output
Feedforward:sensory input from past used as anticipatory adjustments
How do you do sensation testing?
*prior to motor and coordination testing
Eyes closed, test at random, give reference for normal
What do you record for sensation testing
Modality tested
Surface areas affected
Degree or severity of involvement
Subjective feelings about altered sensation
Potential impact of sensory impairment on function
What is the order of testing for sensation
Superficial sensations
Pain
Temperature
Light touch
Pressure
Deep sensations
Proprioception
Kinesthesia
Vibration
Combined cortical sensation
Stereognosis
Tactile localization
Two point discrimination
Double simultaneous stimulation
Graphesthesia
Recognition of texture
Barognosis
What are the superficial sensations and how do you test them?
Pain
sharp/dull
Indicates function of protective sensation
Temperature
Hot (warm) / cold
Light touch
Assess perception of tactile touch
Lighty stroke and ask if they feel it
Can quantify using monofilaments
Pressure
Assess perception of pressure by deep receptors (firm pressure to indent skin)
What are the deep sensations and how do you test them?
Proprioception
Determine joint position and awareness at rest
Grasp joint at sides, get patient to describe or mirror the joint position
Kinesthesia
Determine awareness of movement - same as above but just throughout the range of movement
Vibration
Ability to perceive vibratory stimuli
Strikes tuning fork, place on bony prominences - random applications of it (*strike for auditory though every time)
What are the combined corticol sensations and how do you test them?
Stereognosis
Assess tactile object recognition
Tactile localization
Assess ability to localize touch sensation
Point exact location where therapist touches (distance between is senstiviity)
Two point discrimination
Ability to perceive two separate points - measure between the last point before it becomes one - this is minimum detectable distance
Double simultaneous stimulation
Assess ability to perceive touch on
Identical locations on opposite sides
Proximal and distal on similar extremity
Proximal and distal on one side of body
Extinction - only proximal stimulus is perceived
Graphesthesia
Ability to identify numbers, letters or designs (with orientation first)
Recognition of texture
Assess and differentiate between various textures
Barognosis
Assess recognition of weight (if no han then do in series)
What are terms for sensory impairment?
Allodynia - non-noxious stimulus that produces pain
Analgesia - loss of pain sensitivity (inability to feel pain)
Causalgia - burning painful sensation, often along nerve distribution
Dysesthesia: touch sensation produces pain
Hyperalgesia: heightened sensitivity to pain
Hyperesthesia: heightened sensitivity to sensory stimulus
Hypoalgesia - decreased sensitivity to pain
Paresthesia: abnormal sensation with no apartment cause (numbness, tingling)
What are interventions for sensory impairments?
Compensatory approach
Make accommodations to accomplish tasks (alternate strategies or environmental adaptations)
Sensory integration approach
Achieve functional skill through guided practice with controlled sensory intake - activate sensory receptors and higher brain centers
Presented through meaningful activities
Goal enhances sensory input (e.g., sensory avoidance for autism - gradual introduction, sensory seeking - giving tactile feedback)
What is a UMN vs. LMN
UMN - originate in brain, SC, brainstem
Inform to LMN
Originate before anterior horn cell of SC
LMN - originate in cranial nerves nuclei and motor neurons
Originate after anterior horn cell of SC
Receives information and take toward muscle
Comparison - UMN vs. LMN
Weakness - Yes(Spastic), No (flaccid)
Atrophy - No, Yes
Fasciculations - No, Yes
Reflexes - Hyperreflexia, Hyporeflexia/Areflexia
Tone - Increased, decreased
What are the S + S of UMNL and LMNL
UMN
Hyperactive stretch reflex
Involuntary flexor and extensor spasm
Clonus
Babinski’s sign
Exaggerated cutaneous reflexes
Loss of precise autonomic control
Dyssynergic movement patterns
E.g., ALS, brain injury, CP, MS, SCI, stroke, tumour in brain or SC
LMN
Decreased or absent tone
Decreased or absent reflexes
Paresis
Muscle fasciculations and fibrillations with denervation
Neurogenic atrophy
E.g., ALS, bell’s palsy, CES, GBS, peripheral nerve injuries, poliomyelitis, post-polio syndrome
What is tone and the types of tone?
Resistance to passive elongation
Hypertonia - increased
1. Spasticity
Velocity dependent (increased speed= increased resistance)
Clasp-knife - spastic catch, follwed by sudden inhibition
Associated with abnormal posturing, contractures, functional limitations and disabiltiy
2. Rigidity
Velocity independent
Leadpipe - constant through entire range
Cogwheel - ratchet-like jerkiness
Associated with contractures, stiffness, inflexibility, functional limitations and disabiltiy
Hypotonia - decreased
Decreased or absent muscle tone, decrease resistance to passive elongation, decrease or absent stretch reflex, difficulty with anti-gravity positions, difficulty moving against gravity, associated with hyperextensibility of joints, floppy limbs, LMN syndrome
*temporary states may be seen in UMNL during spinal shock ro cerebral shock - duration is variable
Dystonia - disorder tonicity
Characterized by involuntary twisting and repetitive movements, abnormal fixed postures and disordered tone
Dystonic posturing - co-contraction causing sustained abnormal posturing
Types - generalized, focal (only one body part), segmental (2 or more adjacent areas)
What are the two different types of posturing (e.g., for those in comas)
Decorticate
Corticospinal tract lesion at diencephalon (thalamus and hypothalamus)
Abnormal flexor response
UE - shoulder adduction, elbow flexion, wrist flexion, finger flexion
LE - legs extended and internal rotation*, ankle PF
Decerbrate
Corticospinal tract lesion at brainstem
Abnormal extensor response
UE - shoulder adduction, elbow extension, forearm pronation, wrist/ finger flexion
LE - leg extension, ankle PF
What is the examination of tone?
Observation (resting)
Abnormal posturing or limbs, trunk, head
Palpation
Hypertonia (hard and taut), hypotonia (soft and flabby)
PROM/AROM
Response to stretch
Modified ashworth
* see chart
0 is normal
1 - slight increase with catch and release and minimal resistance at end
1+ - minimal resistance less than half of ROM, slight increase, manifested by a catch
2 - more marked increase through ROM, easily moved
3 - increased tone, passive movement difficult
4 - rigid
Modified tardieu scale
Moving at different speeds (V2 = normal, gravity)
If happens at different speeds - spacitiy, if constant - rigidity
Asymmetry vs. symmetry
Hypertonia - stiff and resistance
Hypotonia - heavy and unresponsive
*if can fix posture = not neurological
What are the interventions for abnormal tone, hypotonia and hypertonia?
Abnormal tone
-Stretching, casting, splinting, orthoses
-Sensory stimulation techniques
Hypotonia
-Decreased support
-Increased resistance
-Joint compression (axial - reflex for extensors) - not for down syndrome
-Manual facilitation techniques - tactile input
Hypertonia
-Increase support
-Modify tasks
-Positioning in lengthened position
-Heat (not for MS or sensory deficits)
What are the UMN reflexes?
-Babinski
-Clonus
-Hoffman sign - middle finger - flick DIP of index or middle into flexion
Abnormal - reflex flexion of DIP of thumb and DIP of index or middle (whichever not flicked)
See hyperreflexia of DTR - used for UMNL
What is postural control made up of?
Postural orientation and postural balance (need to maintain stability and orientation (CoM over BoS))
Please define the following terminology:
-postural orientation
-balace
-center of mass
-Bass of support
-Limits of stability
Postural orientation - control of body segments in relation to each other
Balance: ability to maintain CoM within BoS- forces acting on body must be balanced
CoM: imaginary balancing point - average position of all part of system according to masses
-Changes based on weight, amputation- moves forward as you move forward
Bos: area of body or extension in contact with support surface
LoS: max distance that one can lean to without losing balance or having to change BoS (step, grab something)
-Or else you fall
What system interactions are required for postural control?
Sensory (afferent) input
Visual
Vestibular
Somatosensory
CNS integration
Processes afferent input and determines appropriate output
Motor (efferent) output
Execution of motor response (muscle synergies, timing and force)
feedback system
What is the clinical test for sensory interaction in balance (CTSIB)
Tests the sensory input
See book for image - hold for 20 sec, if arms or feet change, or open eyes = fails
Eyes closed fails - too much visual reliance
Dome fails - vestibular issue
Foam - somatosensory problem
What are the postural control strategies?
Maintain when internal (from self) or external (from external source) perturbations occur
Strategies
1.Reactive - external pertubations - feedback (dependent on sensory feedback)
2.Proactive (anticipatory) - internal perturbations - feedforward (predict what is going to happen)
What are the motor strategies for postural control?
Ankle
Distal to proximal
Fixed support
Ankle joint is axis, fixed pendulum for shifting - small displacements
Forward - gastroc, hamstring, paraspinals
Back - tib ant, quads and abs
Hip
Proximal to distal
Fixed support
Head and hips move in opposite direction
Larger and faster which exceeds the limit of support
Use when task (not big enough for stepping) or environment (pool, balance beam)
In elderly
Forward sway - abs, quads
Backward sway - paraspinals, hamstring
Stepping
Re-establish new BoS to a new contact support surface
Change in support strategy
Large, fast displacements
Rapid steps or hops in direction of CoM
Lateral step - towards side falling
Crossover - other foot goes to step because of the weight shifting - easier to move but gets caught on feet and can cause falls especially in elderly
Please describe the functional balance tests for balance
Functional balance grades
0-4 - see chart (used for charting)
The romberg test
Static
Eyes open / eye closed - fails on eyes open (cerebellar or vestibular), on eyes closed = proprioceptive (+ve test)
Functional reach tests
Measure from 3rd MCP and get them to lean forward without moving feet or touching wall - measure
The berg balance scale
Static and dynamic balance and determind risk of falls
0 to 4 (good), total 56
41-56 = low risk, 21-40 = medium risk (walking with assistance), 0-20 high fall risks (w/c)
Decreased sore = increased risk of falls
Performance-orientated mobility assessment (Tinetti)
Static and dynamic balance
<19 = high risk, 19-24 = moderate, total is 28
Get up and go test
Dynamic balance and mobilty
Measure at normal speed the look of how they do it from 1-5 (severely abnormal)
Use an assistive device if this is what they normally use
Timed up and go test
Assess mobility, balance, walking ability, and falls
Time how long is takes to walk 3 m and back down
<10 sec = normal, >12sec = falls, 11-20 = normal limits of frail elderly or individuals with disability
>30 sec impaired functional mobility
What are the general principles for balance training and what are ways balance can be further challenged?
General principles - clear obstacles, proper footwear, guard appropriately (weaker side), monitor for for signs of fear/unsteadiness, start with most to least stable then challenge from least to most difficult movements, regress if needed
-External harder than internal (but actually CoG displacement closed to LoS makes it harder)
Challenges - altered BoS, internal perturbations, reactive balance strategies (expected vs. unexpected), altered vision, speed, moving CoM higher, include cognitive demanding tasks
What is a cerebrovascular accident?
CVA - disruption in cerebral circulation causing sudden loss of neurons and neurological function - problem with blood flow causing tissue/cell death
What is the etiology of a stroke?
-Ischemic (80%)
-Hemorrhagic (20%)
What are the types of ischemic stroke?
Thrombus
Forms within the vessel wall and interrupts cerebral blood flow
Embolus
Forms elsewhere and dislodges and travels through circulatory system to lodge in cerebral arteries’ vessels interrupting cerebral blood flow
SUDDEN
Low systemic perfusion
Cardiac failure or significant blood loss (decrease blood circulating, decrease BP, decrease perfusion, systemic hypotension, decrease cerebral blood flow
What is a hemorrhagic stroke and what are the types?
From aneurysm, artery, arteriovenous malformation (AVM)
Weakening of artery wall causes an abnormal localized dilation of an artery - can burst and create bleeding
Types
1.Intracerebral
-Due to rupture or leak of weak blood vessels in brain
2.Subarachnoid
-Due to AVM or ruptured aneurysm causing bleeding in subarachnoid space
-Edema also goes into space causing compressive load and increased ICP
-Need rapid intervention (decompression and clip hemorrhage do doesn’t continue to bleed)
What is an arteriovascular malformation ?
AVM - congenital defect resulting in tangle of abnormal arteries and veins which bypass the capillary system
Progressive dilation with age
Eventual bleeding in ~50% of AVM cases
What is a TIA?
Ischemic stroke without tissue death - symptoms resolve in 24 hours or less “mini-stroke or “warning stroke)
What is ischemic penumbra?
Area surrounding ischemic event
Remain viable or several hours due to supply of collateral arteries
Need thrombolytic agents (NOT HEMORRHAGIC STROKE) within 4.5 hours to decrease ICP from cerebral edema (compressive load on brain)
What are the risk factors for stroke (modifiable and non-modifiable)
Hypertension
Heart disease
Disorders of heart rhythm
Diabetes mellitus
Hypercholesterolemia
High levels of LDL
Low levels of HDL
Elevated hematocrit
End stage renal disease and chronic kidney disease
Sleep apnea
Female
Early menopause
Estrogen supplementation
Pregnancy, birth, first 6 weeks post -partum
Preeclampsia - increased BP during pregnancy
Modifiable
Smoking
Physical inactivity
Obesity
Diet
Excessive alcohol use
Non-modifiable
Family history
Age
Gender (M>F)
Race (african american)
What are the warning signs of a stroke?
Face dropping
Arms - can you raise both
Speech - slurred/jumbled
Time - call 911
Describe anterior cerebral artery (ACA) syndrome. Including supply and characteristics
SUPPLIES -
medial aspect of cerebral hemisphere (frontal and parietal lobes)
subcortical structures (basal ganglia, anterior fornix, corpus callosum)
Anterior communicating artery allows perfusion to proximal ACA
If proximal to artery - minimal deficits
If distal to artery - greater deficits
Characteristics
Contralateral hemiparesis and hemi-sensory loss
LE affected > UE
Because of homunculus and the LE sits more towards medial aspect
Urinary incontinence
Abulia - absence of will power and can’t act decisively
Akinetic mutism - don’t move/speak much
Apraxia - difficulty with motor planning
Broca’s aphasia (frontal lobe) - trouble with speech production
Describe middle cerebral artery (MCA) syndrome. Including supply and characteristics
*more common, extensive damage
SUPPLIES
Lateral aspect of cerebral hemispheres (frontal, temporal and parietal lobes)
Subcortical structures - internal capsule, corona radiata, globus pallidus, caudate and putamen
Common characteristics
Contralateral hemiparesis and hemi-senosry loss of face, UE and LE
UE affected > LE - due to homunculus again
Contralateral homonymous hemianopia
Wernicke aphasia (temporal lobe) - trouble with comprehension/ receptive speech
Broca’s (frontal) - trouble with speech production
Global aphasia - both broca’s and wernicke’s - nonfluent speech and poor comprehension
Perceptual deficits - unilateral neglect, anosognosia, apraxia, spatial disorganization/depth perception
Typically lesion in non-dominant hemisphere (e.g., usually right)
Describe internal cerebral artery (ICA) syndrome. Including supply and characteristics
SUPPLIED
Both the MCA and ACA
Results in large obstruction of area supplied by MCA
ACA has collateral circulation from circle of willis, but if absent - area supplied by ACA will also be affected
Significant edema - increased ICP - leading to uncal herniation (inner part of temporal lobe has so much pressure - herniates down and pressure on brain stem), coma or death
Describe posterior cerebral artery (PCA) syndrome. Including supply and characteristics
SUPPLIES
Occipital lobe, medial and inferior temporal lobe, upper brainstem (midbrain), posterior diencephalon (includes most of thalamus)
Posterior communicating artery - allows for perfusion of proximal PCA
Proximal to artery - minimal
Distal to artery - greater deficits
Common characteristics
Peripheral territory - amnesia, homonymous hemianopia, visual agnosia (difficult recognizing objects/ people), prosopagnosia (difficulty naming people), dyslexia, colour naming and discrimination
Central territory - central post-stroke (thalamic pain) - burning, intermittent shooting, severe, hemianesthesia, sensory impairments (all modalities), contralateral hemiplegia, oculomotor nerve palsy (helps control movement of eye)
Describe vertebrobasilar artery syndrome
Vertebral artery - supplied cerebellum and medulla
Basilar artery - supplies pons, internal ear and cerebellum
*injury occurs after forced Cx motion (WAD, manipulation)
Produced ipsilateral (cerebellum) or contralateral S + S
Common characteristics
Ataxia (ipsilateral), impaired sensation over face, impaired pain and thermal sensation (contralateral), vertigo, diplopia, dysarthria, dysphagia
Describe lacunar stroke
Occlusion of small penetrating arteries supplying brain and deep structures
Associated with hypertension and diabetes
Symptomatic or silent
Consistent with specific anatomical sites
Pure motor lacunar stroke
Pure sensory lacunar stroke
Other lacunar syndromes: dysarthria/ clumsy hand syndrome, ataxic hemiparesis, sensory / motor stroke, dystonia / involuntary movements
Higher cortical areas are perceived (consciousness, language, visual fields)
What do impairments depend on for stroke?
*dependent on what area of brain affected, size of lesion, hemisphere involved, blood vessel involved, collateral blood flow availability, neural redundancies, individual anatomical differences
What is homonymous hemianopia and what is the difference between this and neglect
Hemianopia - loss of visual field on one side of midline
Homonymous - loss on the same side of both eyes
can’t see the area but know it is there so can turn head
Where as neglect - can’t perceive the side so doesn’t know it exists
What is locked in syndrome
Patient is aware and awake - complete paralysis of all voluntary muscles except for eyes but otherwise cognitively intact - communication through blinking/ vertical eye movement
Sudden onset
Preserved consciousness and sensation
Eye paralyzed too = total locked - in syndrome
What are the associated conditions from stroke
Disorder and speech
Dysphagia
Difficulty swallowing - aspiration can occur
Cognitive dysfunction
Altered emotional status
Pseudobulbar
Hemispheric behavioral differences **
Perceptual dysfunction
Seizures
Bladder and bowel dysfunction
CV and pulmonary dysfunction
DVT and PE
OP and fracture risk
*above 3 are more a consequence of inactivity
Describe the two types of disorder and speech impairments for stroke
Dysarthria - motor speech disorder affecting muscles that produce speech (may be slow/slurred/ difficult to understand)
Aphasia - impairment of language affecting comprehension / productive
-Receptive aphasia - Wernike’s aphasia (instructions simple, one by one)
Difficulty with comprehension of language
Speech flows smoothly and melody of speech is preserved
-Expressive aphasia - Broca’s aphasia (instructions with hand signals)
Difficulty with speech production
Flow of speech is slow, hesitant, limited vocab and impaired syntax (agrammatism)-mostly content words
Comprehension is not affected
-Global aphasia (instructions are simple and with hand signal)
Difficulty with language comprehension and productive
Indicative of extension brain damage
Limits ability to learn, therefore affects outcomes of rehab
What is dysphagia?
Difficulty swallowing - aspiration can occur
Lead to respiratory distress, aspiration pneumonia or death
If severe - nothing-per-oral precautions are given
Even water
Through tube feeding - NG or G tube
Associated with dehydration and poor nutritional status
What is cognitive dysfunction (memory and perseveration) that is affected by stroke
Impairs alertness, orientation, attention, memory or executive function
Memory
Short term - affected, long - not
Memory gaps - made up stories or inappropriate words
Perseveration
Repetition of words, thoughts or gestures without appropraite context- gets “Stuck”
What are the altered emotional status that may be affected by stroke?
Pseudobulbar
Sudden and unpredictable outbursts of crying, laughing or other emotional displays not consistent with mood
Quickly changes from one extreme to another
Apathy
Blunted emotional response - mislabelled as depressed or poor motivation
Euphoria
Exaggerated feelings of well being and happiness
Depression
Persistence feeling of sadness
Psychomotor slowing - motor changes due to depressed state
Patients with left hemisphere lesions may experiences more frequent and severe depression
What are the hemispheric behavioural differences between left and right
Left
Slow, cautious, anxious, unorganized
Hesitant to try new tasks - requires more feedback, support and encouragement
Aware of deficits
Difficulties with communication, processing information in sequential linear order
Right
Quick, impulsive, poor judgment
Overestimate abilities, unaware of deficits
Increased safety risk - focus on slowing down, recognize risks and consequences
Difficulties with spatial-perceptual tasks and grasping whole idea of an activity or task
What are the components of perceptual dysfunction
Body schema/body image
Body scheme: internal awareness of relationship of body parts to each other and the environment
Body image: the mental image and feelings of one’s own body
Impairments
-Unilateral neglect
—Visual, auditory and somatosensory - no reaction when presented on the affected side
—Lack of awareness of one’s own body or of external environment
—Limited use on more affect limb, could lead to injury
—Seen in right hemisphere
——–L side can perceive just the R
——–R side can see both
——–So R hemisphere lesion = just see the R side now
——–Also assocaited with L sided hemi-paresis and then can’t see the L so big bag of no fun
——–Increased falls risk and injury
-Anosognosia - lack of insight
-Somatagnosia - disordered body awareness - can’t recognize spatial awareness
-Right left discrimination
-Finger agnosia - loss in ability to recognize and distinguish own fingers
Spatial relations
Difficulty perceiving relationships between self and objects in space - can’t recognize vertical, horizontal, depth and distance
Agnosia
Inability to interpret sensory information (despite intact sensations) - impairment in recognition
Visual / auditory / tactile - if impaired use cues that don’t involve this
Nothing actually wrong with it, just can’t perceive it
What are the components of a stroke exam?
Patient history
Systems review
Tests and measures
What does a stroke examination consist of?
Cranial nerve integrity
Sensation - previous tests
Flexibility and joint integrity
-Contractures, ROM (wrist and shoulder specifically)
-Wrist edema - carpal bones malaligned = more prone to impingement in wrist
Motor function
Muscle strength
-ACA - affects LE, MCA - affects UE
-If you can’t isolate the muscle, MMT would be invalid
Postural control and Balance
-Balance impairments following a stroke - weakness, poor reactive/anticipatory, sensory loss, even weight distribution, delayed/abnormal contracture
-Fall towards hemiplegic side
-Assess static and dynamic in sitting and standing
-Use performance based or stroke specific tests (PASS, FIST)
Gait and locomotion
Integumentary integrity (Skin)
Aerobic capacity and endurance
Functional status
Stroke - specific intrsument
FMA
STREAM
Chedoke-McMaster
SIS
How to assess motor function for stroke patients
Stages of motor recovery
Twitchell and Brunnstrom
*through different stages - see chart - not everyone goes through, can plateau at one of the stages
Tone
Initial flaccidity (cerebral shock) - days to weeks then spascity
UE - scapular retraction, shoulder adduction, depression and internal rotation, elbow flexor and forearm pronator, wrist and finger flexors
LE - pelvic retractors, hip adductors, extensors, and internal rotators, knee extensors, plantarflexion and supinators, toe flexors
In neck and trunk, strong spascitiy - cause increased lateral flexion to hemiplegic side (pusher syndrome - lean towards weak side)
Reflexes
Initial hyporeflexia (cerebral shock) then hypereflexia comes when spasticity and synergies emerge
DTR: hyperreflexia, clonus, babinkski, clasp knife response
Associated reaction - all or none - strong obligatory synergies occur (can be both sides) (can be in response to a stimuli - e.g., cough/sneeze)
Volunatry movements
Obligatory synergies - unable to perform isolated movements - interfere with functional mobility and normal ADLs
May vary from one limb to another
*see book for UE and LE synergy patterns
Coordination
Sensory ataxia (proprioceptive losses)
Cerebellar ataxia
Bradykinesia. Choreoarthetosis (involuntary, twisting movements), hamiballismus (basal ganglion affected) - sudden uncontrolled movements
Use unilateral and bilateral movement - may vary depending on position - due to postural demand and degrees of freedom
Could go into spasm or synergies if more postural demand
Motor programming
-Apraxia - difficulty planning and performing tasks or purposeful movements
No primary motor impairments
More evident with L side hemisphere impairment
-Ideational apraxia
Inability to produce purposeful movement on command or automatically
No idea how to do the movement
-Ideomotor apraxia
Inability to produce purposeful movement on command but is able to perform movement automatically
Often perseverates
What are common gait abnormalities with stroke
Circumduction - Leg is in extension synergy - can’t clear limb - PF (tone, contracture, weak DF)
Decrease time on stance for affected - weakness, decrease confidence, pain
Hyperextension at knee - poor quad control, weak quads, in PF at ankle
In PF at ankle - poor motor control, weakness at DF, contracture/spasticity in PF
What is pusher’s syndrome? Including the Ax tool and implications
Contraversive pushing or ipsilateral pushing
Disorder of postural control - lead to loss of balance
Push weight from strong side to hemiparetic side with resistance to passive correction
Fall towards hemiparetic side
Altered sense of verticality
Occurs in 10% with posterolateral thalamus involvement (either side)
Clinical assessment scale for contraversive pushing (SCP)
Tilting towards paretic side often
Abduction and extension of unaffected limbs
Resistance to passive correction
*done in sitting and standing - if all three = pushers
Implications
Avoid transfers to paretic side
Avoid gait aids - help push to side since in opposite hand (can give short one so they lean more)
Be aware of where and how you position patient (push off objects, falls, block abduction so they can’t do it)
How do you classify interventions for stroke?
*based on stage of recovery, degree of disability, and patient goals
Preventative - minimizing complications and secondary impairments
Restorative - improving impairments and limitations
Compensatory - aimed at modifying the task, activity, or environment to improve function and participation
How do you improve sensory function in someone with a stroke? Including hemianopia and unilateral neglect
Sensory retraining / stimulation approach
Mirror therapy
Sensory discrimination activities
Compression techniques - weight bearing, pneumatic compression
Electrical stimulation
Thermal stimulation
Safety education - improve awareness and protect
Hemianopia and unilateral neglect
Encourage awareness and use of environment on hemiparetic side
Active visual scanning movements
Cueing to direct attention
UE exercises crossing midline towards hemiparetic side
Functional activities involving bilateral interaction
Prism glasses (unilateral neglect)
How do you improve flexibility and joint integrity in someone with a stroke? Including positioning and the benefits
PROM / AROM daily
Scapula - emphasis on protraction / upward rotation to prevent impingement with overhead activities
Overhead pulley CONTRAINDICATED if haven’t achieved proper scapula-humeral movements
Weight bearing with open hands and extended wrist - work on tightness - given proprioception through shoulder
Positioning to maintain ST length and encourage joint alignment - always opposite of spasticity
Use of protective devices resting splints
Positions (see book for more details)
-Sidelying on affected shoulder -Allows more awareness, regulates abnormal muscle tone, inhibits abnormal postures
-Side lying on unaffected side -Inhibits extension synergy in LE, allows control for abnormal movement patterns
-Supine-Prevents knee flexion contractures, allows symmetry of trunk and limbs
How do you improve strength in someone with a stroke? Including precautions
Progressive strengthening resistance - no evidence of negative effects on spasticity and ROM
Combined with functional activities - assists with ADLs (GO WITH MOST FUNCTIONAL ONE ON PCE)
Precautions
Specially designed gloves or wrist weights - with poor hand function
Impairment sensation = increase injury risk
Postural deficit = increased falls risk
High incidence of hypertension and cardiac disease in patient with stroke (monitor S + S- might have caused it too)
How do you improve motor control and UE function in someone with a stroke
Focus on dissociation of segments and selective out-of-synergy movements
As close to normal as possible
Help to guide movement and use facilitation techniques - active control ASAP
Task-orientated practice - using affected limb
-Modified plantagrade - weight bearing through arms over table - LE does movement
Constraint induced movement therapy (CIMT) - increased use of affected UE (other is tied)
What is a hemiplegic shoulder and what are the interventions?
- Flaccid stage
Proprioceptive impairment, lack of tone, muscle paralysis = decreased support and positioning from RC (supra, deltoid, biceps and some coracobrachilais)
Get shoulder abduction, flexion; or scapular depression and downward rotation = instability of GH = inferior subluxation
Pain does not equal subluxation
Predictor of pain = decrease external rotation (subscap and pec major - tight into internal rotation)
Shoulder impingement syndrome may develop - pain with flexion or abduction - Spastic stage
Abnormal muscle tone - poor positioning (scapula retraction, depression and downward rotation) = movement restrictions and subluxation
Adhesive capsulitis
CRPS- type 1
Interventions
Support at all times (e.g., transfers, education)
-Proper position / handling
-Tray for w/c
-Arm sling
—Only when transferring or need hands to keep out of way
-Strapping / tapping
Gentle guided exercises
PROM - for upward rotation and protraction
FES/NMES
Don’t pull arm or leave unsupported
How do you improve postural control and balance in someone with pusher’s syndrome?
Train active movement shift towards strong side
Encourage to problem solve
Visual, verbal and tactile cues (e.g., on quad on strong side)
How do you improve gait and location in someone is a stroke
Body weight support and motorized treadmill training
Controls upright posture when postural stability is poor
Decrease fear of falling
Not much difference between that and regular PT
FES
DF
Quads (prevent buckling)
Orthosis and assistive devices
Temporary vs. permanent
AFO - in DF, prevent hyperextension
Post leaf spring - common, control foot drop
Solid AFO - max stability at subtalar and talocrural
Wheelchairs
Hemi height (foot propulsion)
One arm drive wheelchair - rare - needs strength and coordination
Power wheelchair
*watch for PPT and pressure sores
What is a TBI and what is the etiology?
Injury caused by an external force
All info applies to a non-TBI as well (infection, tumor, stroke)
Etiology
1. Primary injury
Immediate trauma to brain parenchyma at moment of insult or injury
2. Secondary injury
Result of secondary effects of initial injury
hypoxia/ischemia, edema and increased ICP - evolves over time after initial insult or injury
MOI
Contact - open vs. closed penetration
Acceleration - deceleration - compression, tension, shearing
Rotation - angular acceleration
What is the pathophysiology of a TBI?
Focal injury - non-penetrating (coup/contracoup) vs. penetrating
-Can have diffuse effects on focal injury
Diffuse axonal injury - widespread - shearing of axons - damage brain structures
Hypoxic - ischemic injury: due to constriction, disruption of blood vessels - also from systemic hypotension
Increased ICP
What are the normal and elevated values for ICP?
Normal: 5-20 cm H20
Severe elevated ICP - results in brain herniation and needs medical emergency treatment ASAP
Icp >20 cm H20 = elevated, ICP >25 cm H20 = critical
*older adults may take longer for ICP to rise - senile atrophy - brain smaller from aging
What are the sign of elevated ICP
Altered vital signs
Decreased consciousness (stupor or coma)
Non-reacting pupils (CNIII)
Papilledema (optic disc or nerve swelling)
Widened pulse pressure
Irregular (Cheyne-Stokes) breathing
-Breathing increased in depth then decrease and have a period of apnea
Vomiting
Headache
Seizures
Progressive impairment of motor function
What is the treatment for elevated ICP?
Elevated HOB to 30 degrees
-Promotes venous drainage
-Time to onset of effect: immediate
-*lowering this may be C/I for treatment - especially flat or trendelenburg, also for suctioning - monitor especially for hypoventilation (as someone will vasodilate as they feel they need O2)
Intubate and hyperventilation - vasoconstriction
IV mannitol (osmotic agent) - promotes removal of fluid from CNS while maintain perfusion to brain
Ventricular drainage - CSF removed to decrease ICP
If above fails
-Barbiturate induced coma - gets vasoconstriction and decreased metabolic demands
-Surgical decompression (hemicraniectomy - remove skull to reduce pressure)
-Steroids
What are the possible impairments for TBI?
Neuromuscular
Cognitive
Neurobehavioural
Communication
Swallowing
Dysautonomia
Visio-perceptual
post-traumatic seizures
secondary impairments and complications
