A CVA is a result of ischemia (blood clot) or hemorrhage (rupture in blood vessels) in the brain, causing sudden, focal neurological deficits. Ischemic strokes are more likely to occur in contrast to hemorrhagic strokes.
The risk factors contributing to the likelihood of developing a stroke are due to hypertension, arteriosclerosis, diabetes, cardiac disease, hyperlipidemia, smoking, sedentary lifestyle, and a previous history of TIA.
Ischemic strokes can be medically managed with tissue plasminogen activator (tPA) if given within the first 12 hours after the onset of symptoms. Post-12-hour management is management via anticoagulant and antihypertensive medications.
Hemorrhagic strokes are medically managed via craniotomy or arterial clipping of bleeding arteries. Management also involves antihypertensive and epileptic medications.
Cardinal symptoms of stroke
Sudden weakness and/or numbness
Difficulty speaking
Difficulty walking
Confusion
Visual changes
Facial drooping
Be able to spot the signs of stroke using the F.A.S.T. Acronym
F: face Drooping: Does one side of the face droop or feel numb
A: arm Weakness: Is one arm weak or numb? Does one arm drift downward when raised
S: speech Difficulty: Is speech slurred, or are they unable to speak
T: time to call 911: If any of these signs appear
Neurological deficits associated with stroke
Left hemisphere injury
Right side hemiplegia
Right side hemisensory
Speech-language deficits
Trouble planning/sequencing movement
Difficulty processing
Right hemisphere injury
Left side hemiplegia
Left side hemisensory
Visual-perceptual deficits
Poor judgement
Impulsive
Abstract concepts are difficult to comprehend
Difficulty perceiving emotions
Middle cerebral artery stroke
Contralateral hemiplegia with upper extremity involvement greater than lower extremity weakness
Contralateral paresthesia with upper extremity weakness greater than lower extremity weakness
Homonymous hemianopsia
Motor speech deficits
Broca’s aphasia
Receptive speech deficits
Wernicke’s aphasia
Loss of gaze to the opposite side
Anterior cerebral artery stroke
Contralateral hemiplegia with lower extremity weakness greater than upper extremity weakness
Contralateral paresthesia with lower extremity weakness greater than upper extremity weakness
Urinary incontinence
Apraxia
Mutism (less verbal)
Akinetic (less mobile)
Posterior cerebral artery stroke
Contralateral sensory loss
Homonymous Hemianopia- a loss of half the visual field in both eyes
Involuntary movements
Intention tremors- unintentional movement of an extremity when performing a task
Chorea- irregular, involuntary movements that can be chorea or writhing
Thalamic pain: chronic, burning, or constrictive pain all over the body
Oculomotor nerve palsy
Generalized brainstem deficits
Vertebral-basilar artery injured- occlusion of a large portion of the vertebral-basilar artery
Locked-in syndrome develops
Paralysis of all muscles except eye movement
Cognition remains intact
Ventral pons area deficits
Millard-Gilbert syndrome
Basilar artery injured- small branch of occlusion
Impacts the facial and abducens cranial nerves, as well as the corticospinal tract
Facial muscles and the lateral rectus are impacted on the ipsilateral side
Inability to abduct the eye on the ipsilateral side
Weakness of the upper and lower extremities contralateral side (hemiplegia)
Lateral medulla deficits
Lateral medullary syndrome (Wallenburg syndrome or PICA syndrome)
Impacts the posterior inferior cerebellar artery
Deficits in cranial nerves- trigeminal and vagus on the ipsilateral side
Deficits in pain and temperature
Decreased gag reflex
Nystagmus on the ipsilateral side
Horner’s syndrome on the ipsilateral side
Diplopia (double vision), anhidrosis (inability to sweat), ptosis (drooping of eyelid)
Pain and temperature of the contralateral body
Hemiparesis contralateral to the body
Brunnstrom stages for recovery
The Brunnstrom stages of recovery are a guide to describe the motor recovery status post-stroke. Individuals post-stroke may progress through all stages or remain at a certain level for an extended period of time. There is no timetable for recovery.
Stage 1: Flaccidity, with little or no voluntary movement
Stage 2: Spasticity appears, and voluntary movement is possible
Stage 3: Spasticity increases, and patients can voluntarily perform limb synergies
Stage 4: Spasticity decreases, and patients can perform movement combinations that are not synergies
Stage 5: Patients can perform complex movement combinations
Stage 6: Spasticity disappears
Stage 7: Patients return to normal function
Synergy patterns
Synergy patterns are abnormal muscle patterns developing status-post stroke. The two synergy patterns that exist are flexion and extension synergy patterns. Below are descriptions of muscle activation during the synergy patterns.
Flexion synergy
Upper limb
Scapula: retraction and/or elevation
Shoulder: abduction and external rotation
Elbow: flexion
Forearm: supination
Lower limb
Hip: flexion, abduction, and external rotation
Knee: flexion
Foot and ankle: dorsiflexion
Extension synergy
Upper limb
Scapula: protraction and/or depression
Shoulder: adduction and internal rotation
Elbow: extension
Forearm: pronation
Lower limb
Hip: extension, adduction, and internal rotation
Knee: extension
Foot and ankle: plantarflexion
Homonymous hemianopia
Key features
Cause: Most commonly due to lesions in the optic tract, optic radiation, or occipital lobe on the opposite side of the vision loss (e.g., a left-sided brain lesion causes right homonymous hemianopsia).
Common causes: Stroke (especially affecting the posterior cerebral artery), traumatic brain injury, and brain tumors.
Symptoms:
Bumping into objects on the affected side
Reading difficulties (especially when vision loss is on the right)
Difficulty with driving or navigating environments
Diagnosis: Confirmed with visual field testing (perimetry).
Rehabilitation focus:
Visual scanning training
Compensatory strategies (e.g., turning the head to scan the blind side)
Environmental modifications
Apraxia
Ideomotor apraxia
Clinical presentation:
A patient can describe a movement but cannot perform it when asked.
May improve with automatic or habitual actions.
Common errors include awkward or incorrect limb positioning during tasks like waving or brushing teeth.
Common causes:
Left parietal lobe lesions
Stroke, particularly in the dominant hemisphere
Ideational apraxia
Clinical presentation
Misuse of objects (e.g., attempting to write with a fork)
Skipping essential steps in a task (e.g., putting on shoes before socks)
Incoherent task sequencing (e.g., pouring juice after trying to drink from the empty cup)
Common causes:
Extensive damage to the left hemisphere
Dementia or widespread cortical disease
Traumatic brain injury (TBI)
Types of injury:
Open head injury: skull fracture that results in brain exposure
Increased risk of the development of infection
Closed head injury: no skull fracture or exposed brain
Increased risk for intracranial pressure
Pathophysiology:
Local brain injury
Damage to a specific region of the brain due to bruising, bleeding, laceration, or swelling
Coup-countercoup injury
Injury in which the brain is damaged due to the point of impact and the opposite side due to rebound forces
Diffuse axonal injury
Tearing of axons and small vessels due to the acceleration of the brain in the skull, leading to neuronal death
Edema
Increased swelling due to increased intracranial pressure, typically from increased volume of cerebrospinal fluid in ventricles
Hypoxic-ischemic injury
Loss of cerebral circulation due to compromise, typically from deficits in the cardiovascular and respiratory systems
Stratification of brain injury
Brain injuries can be stratified into three (3) categories: mild, moderate, and severe based on symptomatology present. Stratification can be done with the use of the Glasgow Coma Scale (GCS):
Mild TBI (i.e., concussion)
GCS score: 13-15
Loss of consciousness: 0-30 minutes
Alteration of consciousness: brief; >24 hours
Post-traumatic amnesia: <1 day
Imaging: normal
Recovery: full recovery of physical and cognitive function, with the patient seen in an outpatient setting
Moderate TBI
GCS score: 9-12
Loss of consciousness: >30 minutes; less than 24 hours
Alteration of consciousness: >24 hours
Post-traumatic amnesia: 1-7 days
Imaging: normal or abnormal
Recovery: potential to have full recovery of physical and cognitive function with intense rehabilitation in an inpatient rehabilitation or skilled nursing facility
Severe TBI
GCS score: 8 or less
Loss of consciousness: >24 hours
Alteration of consciousness: >24 hours
Post-traumatic amnesia: >7 days
Imaging: normal or abnormal
Recovery: permanent physical and cognitive impairment; typically in a nursing home setting or home setting with total care
Behavioral stratification of traumatic brain injury
Ranchos los amigos cognitive scale is utilized to classify behaviors through a predictable sequence. Individuals progress through levels in sequence but can plateau at any point. Level of behavior:
Level I- No response
Cognitive assistance needed: total assistance with all cognitive functions
Response to stimuli: inconsistent responses to stimuli
*Single-step commands: unable to follow single-step commands
Characteristics of level: individuals are typically in a comatose state
Level II- Generalized response
Cognitive assistance needed: total assistance with all cognitive functions
Response to stimuli: consistent, generalized response to stimuli
Single-step commands: unable to follow single-step commands
Characteristics of level: individuals in a vegetative state
Level III- Localized response
Cognitive assistance needed: total assistance with all cognitive functions
Response to stimuli: localized response to stimuli
Single-step commands: unable to follow single-step commands
Characteristics of level: individuals within a minimally conscious state; able to inconsistently track objects and respond to their name
Level IV- Confused, agitated
Cognitive assistance needed: maximal assistance for cognitive function
Response to stimuli: localized response
Single-step commands: unable to follow single-step commands
Characteristics of level: confused, combative, easily agitated, hypersexual behavior
Level V- Confused, inappropriate
Cognitive assistance needed: maximal assistance for cognitive function
Response to stimuli: localized response
*Single-step commands: unable to follow single-step commands
Characteristics of level: confused, inappropriate behaviors (combative and hypersexual behaviors have subsided), severely impaired memory
Level VI- Confused, appropriate
Cognitive assistance needed: moderate assistance for cognitive function
Response to stimuli: localized response
*Single-step commands: able to follow single-step commands
Characteristics of level: remote memory is more consistent than recent memory, requires assistance with problem solving, minimal carry-over with new tasks
Level VII- Automatic, appropriate
Cognitive assistance needed: minimal assistance for cognitive function
Response to stimuli: localized response
Single-step commands: able to follow single-step commands
Characteristics of level: improve carry over with activity, minimal assistance for learning new tasks, increased awareness of deficits
Level VIII- Purposeful and appropriate
Cognitive assistance needed: stand-by assistance for cognitive function
Response to stimuli: localized response
Single-step commands: able to follow single-step commands
Characteristics of level: able to integrate new and old memory into making decisions, able to make adjustments to behavior in social interaction with minimal assistance
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