Stroke Flashcards
(67 cards)
1
Q
What is CVA
A
Cerebrovascular accident - it is a disruption in cerebral circulation causing a sudden loss of neurons and neurological function
2
Q
What is the etiology of stroke
A
- Ischemic:
a) Thrombus blocking an artery (clot formed at the vessel and stays there)
b) Embolus blocking an artery: Clot that is dislodged and blocks blood flow
c) low systemic perfusion: may be due to cardiac failure or significant blood loss leading to systemic hypotension (bleeding out) –> decreased perfusion in the brain - Hemorrhage:
- from and aneurysm: weaking of the artery wall –> dilation –> burst and cause bleeding.
- from an artery
- from an arteriovenous malformation (AVM)
3
Q
What is a TIA
A
Transient ischemic attack
- ischemia WITHOUT tissue damage
- causing a transient episode of neurological dysfunction - Warning stroke
- symptoms resolve in 24hrs
- people who have had strokes have ad one or more TIAs before their storke
4
Q
Describe the Ischemic Penumbra
A
- area surrounding ischemic event
- PENUMBRA is the area that may stay viable for several hours after ischemic attack due to collateral blood flwo
NEED TO SAVE ISCHEMIC PENUMBRA - Thrombolytic agents (NOT APPROPRIATE FOR HEMMORHAGIC STROKE***) are administered for ischemic within 4.5hrs following ONSET of symptoms in attempts decrease ICP from cerebral edema
In ISCHEMIC cerebral vessels can dilate and compress.
5
Q
What are the types of Hemorrhagic stroke
A
- Intracerebral: Due to rupture or leak of a weak blood vessel in the brain
- Subarachnoid: Due to arteriovenous malformation (AVM) or a ruptured aneurysm which causes bleeding in the subarachnoid space
6
Q
Describe atriovenous malformation
A
- CONGENITAL DEFECT resulting in tangled abnormal arteries and veins, which bypass the capillary system
- progressive DILATION WITH AGE
- eventual bleeding in 50% of AVM cases
7
Q
What are the warning signs of STROKE
A
FAST
Facial - is it drooping
A: arms can you raise both arms
S: speech, is it slurred?
T: time: call 911
8
Q
What are the 6 Vascular syndromes
A
-1. Anterior cerebral artery syndrome (ACA)
2. MIddle cerebral artery syndrome (MCA)
3. Internal carotid artery syndrome (ICA)
4. Posterior Cerebral Artery syndrome (PCA)
5. vertebobasilar Artery Syndrome
6. Lacunar Strokes
9
Q
Describe the ACA and its syndrome
A
- ACA supplies medial aspect of the cerebral hemisphere (FRONTAL AND PARIETAL), and subcortical structures (basa ganglia, anterior fornix, corpus callosum)
- Anterior communicating artery allows for perfusion of the proximal ACA from either side
–> if proximal occlusion to ACA - minimal deficits
–> distal to ACA: greater deficits (bc it will occlude both pathways
10
Q
What are common characteristics of ACA syndrome
A
- CONTRALATERAL (tracts cross) hemiparesis and hemi-sensory loss
2. LE affected> UE (hommonculus)
3. Urinary incontinece
- Abulia - Absence of Will power (sounds like Abuela “grandma” don’t want to do much)
- Akinetic mutism - does not move or speak much
- Apraxia - difficulty with MOTOR planning
- BROCAS Aphasia - no issue with comprehension - difficulty producing speech
11
Q
Describe MCA and MCA syndrome
A
MOST COMMON site of occulsion in stroke
MCA supplies LATERAL aspect of cerebral hemisphere
- FRONTAL, Temporal, and parietal lobes
- subcortical: internal capsule, corona radiata, globus pallidus, caudate, and the putamen
- Occlusion of the proximal MCA results in extensive neurological damage
12
Q
What are common characteristics of MCA
A
- contralateral hemiparesis and hemisensory loss of Face, UE and LE
-2.UE>LE
3. Contralateral homonymous HEMIANOPIA
- WERNICKEs Aphasia (temporal lobe)
- Brocas Aphasia (frontal)
- Global Aphasia (non-fluent speech + poor comprehension)
- Perceptual deficits (unilateral neglect, anosognosia, apraxia, spatial disorganization/depth perception) - TYPICALLY IF LESION IS IN NON-DOMINANT HEMISPHERE (usually right)
13
Q
What is Homonymous Hemianopia
A
- Hemianopia = loss of visual field on one side of midline
- Homonymous = loss on the same side of both eyes
Ex: can’t see left visual field of both eyes
14
Q
What is ICA and ICA syndrome
A
- ICA supplies both the MCA and ACA* (Internal carotid)
- Occlusion of ICA - large obstruction of area supplied by MCA
- ACA has collateral curculation from CIRCLE OF WILLIS - but if absent then area supplied by ACA will also be affected
- Significant edema is common which may increase ICP possibly leading to UNCAL herniation (occurs when rising intracranial pressure causes portions of the brain to flow from one intracranial compartment to another)
Coma, even death
15
Q
What is PCA and PCA syndrome
A
- Spplies the OCCIPITAL lobe, medial and inferior Temporal lobe, UPPER BRAINSTEM (midbrain), Posterior diencephalon (includes most of thalamus)
- the posterior communicating artery allows for perfusion og the proximal PCA from wither side \- if occlusion proximal: minimal deficit
Distal = greater deficits
16
Q
What are Common characteristics of PCA (peripheral vs central territory)
A
- Peripheral Territory: Amnesia, Homonymous Hemianopia, Visual agnosia (difficulty recognizing objects and people), Prosopagnosia (Naming people on sight), dyslexia (leanring diorder), color naming and discrimination problem
Central: Central-Post stroke (thalamic) pain, Hemianesthesia, sensory impairments (all modalities: visual, smell, touch), contralateral hemiplegia, oculomotor nerve palsy (movement of eye)
16
Q
Describe Vertebrobasilar Syndrome
A
- Vertebral artery supplies CEREBELLUM and MEDULLA
- Basilar artery supplies: pons, internal ear and cerebellum
may porduce ipsilateral and contra s+s bc some tracts have crossed and some have not at site affected.
17
Q
What are the common characteristics of vertebrobasilar syndrome
A
ATAXIA (ipsilateral), impaired sensation over face, impaired pain and thermal sensation
MOI: forceful neck motions - agressive neck rotations
MVA
18
Q
Define LOCKED-IN Syndrome (LIS)
A
- patient is aware and awake, but complete paralysis of nearly all voluntary muscles of the body except for the eye - cognitively intact
- some able to communicate through blinking or vertical eye movements
- LIS sudden oset
- Preserved conciousness and sensation
TOTAL Locked-in syndrome - when eye muscles also paralysed
19
Q
Describe Lacunar Syndrome
A
- occlusion of sall penetrating arteries supplying the brain deep structures
- STRONG ASSOCIATION WITH HTN and DM
- symptomatic or silent
20
Q
What are other lacunar syndromes
A
dysarthria/clumsy hand syndrome, ataxic hemiparesis, sensory/motor stroke, dystonia/involuntary movements
21
Q
What are Associated conditions of Stroke
A
- Disorders of Speech and Language
- Dysphagia
- Cognitive dysfunction
- Altered Emotion status
- Hemispheric Behavioral differences
- Perceptual dysfunction
- Seizures
- Bladder and Bowel dysfunction
- Cv and pulmonary dysfunction (bed ridden)
- DVT and Pulmonary Embolus (bed ridden)
- Osteoporosis and # risk (Bed ridden)
22
Q
What are Disorders of speech and language (2)
A
- Dysarthria
- Aphasia
23
Q
What is dysarthria
A
- motor speech disorder affecting muscles used to produce speech (lips, tongue and vocal cord)
- pseech may be slow, slurred and difficult to understand
24
What is Aphasia
3 types
Impairment of language (speech or written) affecting COMPREHENSION and /or PRODUTION
a) receptive aphasia (Wernickes): Difficulty with comprehension
- speech flows smoothly and melody of speech is preserved (but what they say makes no sense)
FLUENT APHASIA
Expressive Aphasia (BROCAs)
- difficulty with speech production
- flow of speech is slow and hesitant, limited vocab and imapired syntax (agrammatism) - struggles to get the words out
- fully comprehends
GLOBAL aphasia
- difficulty with language comprehension and production
- extensive brain damage
- limits patients ability to learn, therefore affects outcomes of rehab
--> for them make instrutions more simple (one thing at a time) - use hand signals
25
What is Dysphagia
- Difficulty swallowing
- Aspiration occurs in 1/3 of patients
- lead to resp distress, aspiration pneumonia and possibly even death
IF SEVERE --> NPO (nothing-per-oral)
- Dysphagia associated with dehydration and poor nutritional status
26
What are the 2 cognitive dysfucntions
- impairments in alertness, orientation, attention, memory or executive functions
Memory
* short term memory may be affected, long-term memory unaffected
* memory gaps may be filled with "made-up" stories or inappropriate wirds (confabulation) (fable)
Perseveration
- persistent repition of words, thoughts or gestures without contex
- gets "stuck: and repeats words or acts
--> thought to be related to OCD
27
Describe the 4 altered emotional status
1. Pseudobulbar affect: sudden and unpredictable outbursts of crying, laughing or other emotional displays - not consistent with mood --> AKA emotional lability or emotional dysregulation syndrome
2. Apathy: Blunted emotional repsonse (can misdiagnose with depression)
3. Euphoria: exaggerated feelings of Well-being and hapiness
4. Depression: perssitent feeling of sadness
-psychomotor slowing - motor changes due to dperessed state (not due to stroke)
- patient LEFT hemisphere lesions may experience more frequent depression
28
What are behavioural changes you may see in the left hemisphere
- slow, cautious, anxious and disorganized
- Hesitant to try new tasks: require more feedback, support and encouragement
-aware of deficits
- hard processing sequential information - so break it down
29
What are behavioural changes you may see in the right hemisphere
Quick, impulsive, poor judgement
- over-estimate abilities
- unaware of their deficits** Anosognosia
- Increasing saftey risk
Feedback: slow down, and recognizing risks and concequences of actions
Difficulty: spatial-perceptual tasks and in grasping the whole idea of an activity or task
30
Describe Perceptual Dysfunction
- Lesion of right parietal cortex**
include
- body scheme/body image
- spatial relations
- Agnosia --> Inability to process sensory info: smell, sight, sound
31
Describe body scheme (perceptual Dysfucntion)
Internal awareness of the relationship of the body parts to eachother and to the environemnt
32
Describe body image (perceptual Dysfucntion)
The mental image and feelings of ones own body
33
What are specific impairments of body scheme/image
* unilateral neglect
* Anosognosia - unaware of their deficits
* Somatagnosia - unable to recognize body part and spatial relationship (Test take dolls that is taken apart and ask to put them back - wont be able to put correct body part in place)
* Right-left discrimination
* Finger agnosia
34
Describe Unilateral neglect
1. Lack of awareness of part of ones own bosy or external environment
2. limited use of affected limb
3. No reaction to sensory (visual, auditory or somatosensory) stimuli presented on the more affected side
4. lead to injury of affected limbs
5. almost always seen in RIGHT EMISPHERE LESION
AKA hemi-neglect
35
What is Agnosia
inability to interpret sensory information (despite intact sensations) - results in an impairment in recognition
3 types
1. visual: nothing wrong with vision but cannot understand what they are looking at - use less visual cues - more auditory and tactile
2. Auditory
3. tactile (astereognosis): cannot recognize things through touch
36
What is included in Stroke examination
1. Cranial Nerve integrity
2. Sesnation (thermal sensation)
3. Flexibility and joint integrity
Motor fucntion
- stages of motor recovery (brunnstrom)
- tone
- reflexes
- voluntary moevemnts
- coordination
- Motor programing
Muscle strength
* postural control and baalnce
* Gait and locomotion (circumduction, short stance on affected leg, knee hyper ext due to quad weakness, stuck in PF
* Integumentary integrity
* Aerobic capcity and Endurance
* Funcitonal status
Stroke-specific instruments
FMA
STREAM
Chedoke-McMaster
SIS
37
What are the 6 stages of Brunnstrom stages of Motor recovery
Stage 1: Flaccid paralysis
Stage 2: Recovery begins. Spasticity begins. Development of min movement in synergies
Stage 3: Voluntary motor control of movement in synergies. Spasticity increased
Stage 4: spasticity begins to decrease. Some movement out of synergies
Stage 5: Further decrease in spasticity. Movement almost independent of synergies
Stage 6: No spasticity. Patterns of movement almost normal
38
Describe TONE
Immediately following stroke: Flaccidity (cerebral shock)
- spasticity emerges in 90% of cases
-
39
Describe spasticity in UE
Strong in scapular retractors; shoulder adductors, depressors, and internal rotators; elbow flexors and forearm pronators; and wrist and finger flexors
40
Describe spasticity in LE
strong in Pelvic Retractors; Hip adductors, extensors, and internal rotators; knee extensors; PF and supinator's and flexors of the toe
in neck and trunk strong spasticity may cause increased lateral flexion TO HEMIPLEGIC SIDE (pusher syndrome)
41
Descirbe Reflexes in Stroke patients
- Initial hyporeflexia (cerebral shock)
- Hyperreflexia when spasticity and synergies emerge (think of it like UMN lesion)
- may demonstrate UMN syndrome responses
+ clonus
+babinski
DTR:hyperreflexia
Clasp knife response
Associated reactions may be seen and may affect function (trying to do one movement but another occurs)
42
Describe Voluntary Movements in Stroke
Obligatory synergies with spasticity following stroke
- patient UNABLE to perform an isolated movement of an isolated movement of a single segment without producing movement in other segments of the same limb
- interferes with functional mobility and ADLs
- synergistic influence and voluntary control may vary from one limb to the other
43
What are the Obligatory synergy patterns of the UE (Flexion Synergy)
Bicep pose**
Scapula: Retraction and Elevation
Shoulder: Abd and ER
Elbow: FLEXION
Forearm: Suppination
Wrist: Flexion
Finger: flexion
44
What are the Obligatory synergy patterns of the UE (Extensor Synergy)
Tricep pose**
Scapular: Protraction
Shoulder: Adduciton and IR
elbow: extension
Forearm: pronation
wrist: flexion
Finger: FLexion
45
Describe Obligatory Synergy in LE (Flexion)
Hip: Flexion*, abd, ER
Knee: flexion
Ankle: DF
Toe: Ext
46
Describe Obligatory Synergy in LE (extension synergy)
Hip: Extension, adduction*, IR
knee: Extension
Ankle: PF (if PF ankle think that it slingshots knee into HE)
Toes: flexion
47
Describe Coordination in Stroke (3)
Sensory ataxia (proprioceptive losses):
Cerebellar ataxia
Bradykinesia, choreo (involuntary movement) athetosis (twisting movement)
hemiballismus (fast invluntary moevemnts) (basal ganglia affected)
examine coordination in unilateral and bilateral
performance may vary based on position (supine, sitting, standing) due to postural demands and degrees of freedom
48
Describe postural demand in stroke
The more postural demand (for example doing tasks in standing vs sitting) - requires more energy and coordination - due to more energy being required they are likely to go into obligatory synergy
49
What are the 3 types of Apraxia (Motor programming)
1. Apraxia: motor disorder causing difficulty in PLANNING and PERFORMIN|G tasks or purposeful moveemnts
- MORE EVIDENT IN LEFT HEMI**
2. Ideational apraxia
- inability to produce purposeful movement on COMMAND OR AUTOMATICALLY (no idea how to do a movement)
3. Ideomotor apraxia:
- Inability to produce purposeful moveemnt ONLY ON COMMAND, but able to perform automatically
- can perform habitual tasks when not asked to do so
- often perseverates (involuntary repetition of a previous movement or gesture, even when the task or command has changed)
50
Describe Postural Control and Balance in Stroke patients
- balance imapirments --> hemiparesis --> poor reactive anticipatory rxn --> poor sensation (poor somatosensory feedback)
--> Uneven weight distribution -> spasticity --> mm contraction delay
- pts with hemiplegia fall towards side of hemiplegia
- assess both static and dynamic balance control in sitting and standing
use: BBS, POMA, TUG
stroke-specific tests for postural control and balance may be used to assess postural control and balance
51
What is Pusher syndrome
AKA contraversive pushing or ipsilateral pushing
- unusual tendency to push weight from non-hemiparetic side to hemiparetic
- resistance to passive correction (will push against therapist)
- ALTERED SENSE OF VERTICALITY (distorted position of midline - therefore pushes to try to be in their midline)
52
What is the clinical assessment Scale Contraversive pushing (SCP)
1. Tilting toward the paretic side
2. Abduction and extension of unaffected limbs
3. Resitive to passive correction
Done in sittign and standing - need all 3 criteria
53
What are PT implications for Stroke patients with Pushers syndrome (Contraversive pushing)
- Avoid transfers to paretic side (might pus themselves over) - Transfer towards strong side**
- Avoid gait aids (will often use to assist to pushing over) - Can use short cane on good side - therfore has to lean to good side to for cane to touch and support
- Beware of positioning - position them where it blocks leg from going into abd - but in a way they cannot push off - against wall
54
What are the interventions for pushers syndrome (based on stage of recovery, degree of diability and patient goals)
Preventative: aimed at minimizing potential complications and secondary impairments (mobilizing)
Restorative: aimed at improving impairments and limitations - help someone to walk or STS
Compensatory
- aimed at modifying the task, activity, or environment to improve function and participation
55
What are the 8 goals in PT intervention
1. improve sensory fucntion
2. improve flexibility and joint integrity
3. improve strnegth
4. imporve movement control and UE function
5. improve fucntional status
6. improve postural control and balance
7. improve Gait and Locomotion
8. Improve aerobic Capacity and Endurance
56
How do we improve Sensory function?
- sensory retraining/stim approach
- Mirror therapy
- Sensory discrimination acitvities (touching diffferent textures)
- Compression techniques (weight-beauring, pneumatic compression (sleeves))
- Electrical stim
- Thermal Stim
** Think of Class Mark ran - used warm water, different textured material, weiaght shifting, self stretching, TENS
57
How do you improve sensory function for those with Hemianopia and Unilateral Neglect
- encourage awareness and use of environemnt on hemiparetic side (easier with hemianopia)
- active visual scanning movements (head, trunk rotation to affected side) --> follow tape on ground
- Cueing (visual, verbal, tactile)
- UE exercises involving crossing midline towards hemipartetic side (reaching) (UNILATERAL NEGLECT)
- Functional activities involving bilateral interaction (pouring drink) (LATE STAGE)
- prism glasses (unilateral neglect)
58
How do we improve Flexibility and Joint Integrity
* PROM and AROM performed daily
- scapula should be mobilized on thoracic wall with EMPHASIS on PROTRACTION and UPWARD ROTATION (prevent shoulder impingement) with overhead activities and prepare for reaching activities***
- Overhead pulley self-movements is CONTRAINDICATED if proper scapula-humeral movement is not achieved
- weightbearing with open hand and extended wrist is often prescribed to work on wrist and finger flexor tightness
- positioning to maintain soft tissue length and encourage proper joint alignment
- use of protective devices (splints)
59
How doe we imporve strength?
- progressive resistive strnegth training
- resistance training with functional activities in order to enhance carry over to assist with daily functional tasks
60
What are exercise precautions?
- Specifically designed gloves (gloves with velcro) or wrist weights may be used for patients demonstrating poor hand fucntions
* impaired sensation= increased injury risk
* postural deficit = increased falls risk
= high incidence of HTN and CVD in patients with stroke
61
How do we imporve MOvement Control and upper extremity fucntion
- focus on DISSOCIATION of segments and selective out-of-synergy movement patterns (isolate segments and stabilize others)
- practice movements as "close to normal"
- PT help guide or use facilitation techniques but should shift to active control ASAP
- Meaningful task oriented practice
- Contrained induced moveemnt therapy - 90% of waking hours
62
What is the management for a Hemiplegic shoulder (2 stages)
Stage 1: Flaccid
- Proprioceptive impairment, lack of tone, and muscle paralysis = decreased support and positioning of shoulder from RC (especially supraspinatus)
- in absence of supporting muscles: shoulder abd, flexion, or scapular depression, and downward rotation reduces stability of GH - can lead to inferior subluxation
- SUBLUXATION DOES NOT EQUAL PAIN
- significant predictor of pain: decreased ER of shoulder(if subscap and pecs get tight - prevent ER)
- shoulder impingement pain due to lack of scapulohumeral rhythm
Stage 2: SPASTIC
- abnormal muscle tone may lead to poor positiong of scapula (retracted, depressed and downward rotation) - lead to moevemnt restrictions and sublux
- AC
- CRPS type-1 AKA RSD may develop
63
What are the interventions for hemiplegic shoulder
- Arm shoudl be supported at all times
- proper positioning and handling - esp with transfers
- tray or arm trough for wheelchair
- ARM SLING ONLY IN TRANSFER (if prolonged can cause contractures)
- Gentle guided exercises (get upward rotation + protraction)
FES, NMES
dont let arm hang unsuppported or pull down
64
How do we improve postural control and Balance for Pusher syndrome
- traina ctive moevemnt shift towards strong side
- Encourage patient to problem solve (ask questions - what direction are you tilted)
- Visual cues (mirror)
- Verbal cues or stim
- Tactile cues
65
How do we improve Gait and Locomotion
- body weight supported treadmill
- controls upright posture
- decreases fear of falling
- can gradually decrease % of support
FMES
- Dorsiflexion (drop foot)
- Quads (prevent knee buckling)
Orthosis and Assitive devices
- temp vs permanent
- AFO
Wheelchairs
1. hemi-heigh (foot propulsion)
2. one-arm drive (rarely used and requires alot of coordination )
3. power-wheelchair (expensive)
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