Stroke deficits and recovery
Cerebral vascular accidents (CVA, stroke)
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 than hemorrhagic strokes.
Risk factors that contribute to the likelihood of developing a stroke include hypertension, arteriosclerosis, diabetes, cardiac disease, hyperlipidemia, smoking, a sedentary lifestyle, and a previous history of TIA.
Ischemic strokes can be medically managed with tissue plasminogen activator (tPA) if given within 3 hours of symptom onset (up to 4.5 hours in select patients). Management beyond that window involves anticoagulant and antihypertensive medications.
Hemorrhagic strokes are medically managed via craniotomy or arterial clipping of bleeding arteries. Management also involves antihypertensive and antiepileptic 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 - call immediately if any of these signs appear
Neurological deficits associated with stroke
| Left hemisphere injury | Right hemisphere injury |
|---|---|
| Right side hemiplegia | Left side hemiplegia |
| Right side hemisensory | Left side hemisensory |
| Speech-language deficits | Visual-perceptual deficits |
| Trouble planning/sequencing movement | Poor judgment, impulsive |
| Difficulty processing | Abstract concepts are difficult to comprehend; difficulty perceiving emotions |
- Middle cerebral artery stroke
- Contralateral hemiplegia with upper extremity weakness 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 hemianopsia: 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
- Hemiballismus: forceful throwing of body segments
- Visual agnosia: difficulty recognizing objects, people, places
- Dyslexia
- Thalamic pain: chronic, burning, or constrictive pain on the contralateral side of the body
- Oculomotor nerve palsy
- Generalized brainstem deficits
- Vertebral-basilar artery injury: occlusion of a large portion of the vertebral-basilar artery
- Locked-in syndrome develops
- Paralysis of all muscles except eye movement
- Cognition remains intact
- Locked-in syndrome develops
- Vertebral-basilar artery injury: occlusion of a large portion of the vertebral-basilar artery
- Ventral pons area deficits
- Millard-Gubler syndrome
- Basilar artery injury: occlusion of a small branch
- 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 on the contralateral side (hemiplegia)
- Millard-Gubler syndrome
- Lateral medulla deficits
- Lateral medullary syndrome (Wallenberg 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
- Ptosis (drooping of eyelid), miosis (pupil constriction), and anhidrosis (inability to sweat)
- Loss of pain and temperature sensation on the contralateral body
- Ipsilateral limb and gait ataxia (no hemiparesis, because the corticospinal tract is spared)
- Deficits in cranial nerves: trigeminal and vagus on the ipsilateral side
- Impacts the posterior inferior cerebellar artery
- Lateral medullary syndrome (Wallenberg syndrome or PICA syndrome)
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 begins to develop, and basic limb synergies begin to appear, with minimal voluntary movement
- 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 hemianopsia
Key features
- Anatomical basis: Most commonly, 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
Understanding the various forms of apraxia is essential for physical therapists working in neurological rehabilitation. The table below contrasts the two forms so their overlapping presentations are easier to distinguish.
| Feature | Ideomotor apraxia | Ideational apraxia |
|---|---|---|
| Definition | Inability to perform purposeful motor acts on command or imitation, even though the idea of the task is understood and motor function is intact | Inability to carry out a sequence of actions to achieve a goal, due to loss of the concept of the task |
| Clinical presentation | Can describe a movement but can’t perform it when asked; may improve with automatic/habitual actions; awkward or incorrect limb positioning (e.g., waving, brushing teeth) | Misuse of objects (e.g., writing with a fork); skipping essential steps (e.g., shoes before socks); incoherent task sequencing (e.g., pouring juice after trying to drink from an empty cup) |
| Common causes | Left parietal lobe lesions; stroke, particularly in the dominant hemisphere | Extensive damage to the left hemisphere; dementia or widespread cortical disease |