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Introduction
1. Cardiopulmonary system
2. Pulmonary system
3. Neuromuscular system
3.1 Central nervous system
3.2 Anatomy and function of spinal cord
3.3 Peripheral nervous system
3.4 Stroke deficits and recovery
3.5 Traumatic brain injury
3.6 Spinal cord injury
3.7 Neurodegenerative disorders and epilepsy
3.8 Peripheral nervous system conditions
3.9 Other neurological conditions
3.10 Interventions for neurological conditions
3.11 Vestibular system
4. Pediatrics
5. Musculoskeletal system
6. Other system
7. Non systems
Wrapping up
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3.4 Stroke deficits and recovery
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3. Neuromuscular system
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Stroke deficits and recovery

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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.

Definitions
Transient ischemic attack (TIA)
A brief episode in which a temporary loss of blood flow causes stroke symptoms such as vision deficits, weakness, and numbness. Symptoms resolve on their own, within a variable timeframe of less than 24 hours. A TIA is still a medical emergency and a warning sign of a future stroke: while symptoms are present there is no way to tell a TIA from a stroke, so emergency medical services are called right away, even if the symptoms go away.

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.

Definitions
Craniotomy
A surgical procedure in which a section of the skull (bone flap) is temporarily removed to access the brain, e.g., to evacuate a hemorrhage or repair the bleeding vessel.
Arterial clipping
A procedure in which a clamp is placed on the hemorrhaging brain artery to reduce blood flow and stop bleeding.

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

PTA scope of practice: The PTA carries out the plan of care established by the supervising PT, including any stroke-recovery or rehabilitation program. If a patient shows a change in neurological status or an adverse response during treatment (e.g., sudden confusion or escalating agitation), the PTA’s role is to stop, document, and report the finding to the supervising PT rather than re-evaluate or modify the plan. New F.A.S.T. signs are a medical emergency: call 911 immediately, as the list above says, then notify the supervising PT.

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
  • 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)
  • 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)

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

Definitions
Homonymous hemianopsia
A type of visual field loss that affects the same side of the visual field in both eyes.

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

Definitions
Apraxia
A motor planning disorder characterized by the inability to execute purposeful, learned movements, even when the individual has the physical capacity and desire to perform the movement. It is commonly caused by lesions in the left hemisphere of the brain, particularly the parietal and frontal lobes, and can significantly impair functional independence.

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

Cerebral vascular accidents (CVA, stroke)

  • Caused by ischemia (clot) or hemorrhage (rupture); ischemic more common
  • TIA: temporary stroke symptoms resolving <24 hrs; still a medical emergency, call EMS immediately
  • Risk factors: hypertension, arteriosclerosis, diabetes, cardiac disease, hyperlipidemia, smoking, sedentary lifestyle, prior TIA
  • Ischemic stroke: tPA within 3 hrs (up to 4.5 hrs select patients); otherwise anticoagulants/antihypertensives
  • Hemorrhagic stroke: craniotomy or arterial clipping; plus antihypertensive/antiepileptic meds

Cardinal symptoms & F.A.S.T.

  • Sudden weakness/numbness, speech difficulty, gait trouble, confusion, visual changes, facial drooping
  • F.A.S.T.: Face drooping, Arm weakness, Speech difficulty, Time to call 911
  • PTA scope: stop, document, report new neuro changes/F.A.S.T. signs to PT; call 911 if emergency; do not modify plan of care

Neurological deficits by hemisphere

  • Left hemisphere injury: right hemiplegia/hemisensory, speech-language deficits, planning/sequencing difficulty
  • Right hemisphere injury: left hemiplegia/hemisensory, visual-perceptual deficits, poor judgment/impulsivity, difficulty with abstract concepts/emotions

Deficits by arterial territory

  • MCA: contralateral UE>LE weakness/paresthesia, homonymous hemianopsia, Broca’s (motor) and Wernicke’s (receptive) aphasia, gaze deviation
  • ACA: contralateral LE>UE weakness/paresthesia, urinary incontinence, apraxia, mutism, akinesia
  • PCA: contralateral sensory loss, homonymous hemianopsia, involuntary movements (intention tremor, chorea, hemiballismus), visual agnosia, dyslexia, thalamic pain, oculomotor palsy
  • Vertebral-basilar artery: locked-in syndrome (paralysis except eye movement, cognition intact)
  • Millard-Gubler syndrome (ventral pons): ipsilateral facial/abducens CN deficits, contralateral hemiplegia
  • Wallenberg/PICA syndrome (lateral medulla): ipsilateral CN V/X deficits, Horner’s syndrome, ataxia; contralateral pain/temp loss; no hemiparesis

Brunnstrom stages of recovery

  • Stage 1: flaccidity, no voluntary movement
  • Stage 2–3: spasticity develops/increases, synergy patterns emerge and become voluntary
  • Stage 4–5: spasticity decreases, non-synergy and complex movements possible
  • Stage 6–7: spasticity resolves, return to normal function
  • No fixed timetable; progression varies per patient

Synergy patterns

  • Flexion synergy: scapular retraction/elevation, shoulder abduction/ER, elbow flexion, forearm supination; hip flexion/abduction/ER, knee flexion, ankle dorsiflexion
  • Extension synergy: scapular protraction/depression, shoulder adduction/IR, elbow extension, forearm pronation; hip extension/adduction/IR, knee extension, ankle plantarflexion

Homonymous hemianopsia

  • Visual field loss on same side in both eyes
  • Caused by lesions in optic tract/radiation/occipital lobe contralateral to vision loss
  • Common causes: stroke (PCA), TBI, tumors
  • Symptoms: bumping into objects, reading difficulty, navigation/driving issues
  • Diagnosed via perimetry
  • Rehab: visual scanning training, head-turning compensation, environmental modification

Apraxia

  • Motor planning disorder; purposeful movement impaired despite intact physical ability/desire
  • Linked to left hemisphere (parietal/frontal) lesions
  • Ideomotor apraxia: understands task but can’t perform on command/imitation; may improve with automatic actions
  • Ideational apraxia: loses concept of task sequence; misuses objects, skips/misorders steps
  • Common causes: stroke (ideomotor), dementia/widespread cortical damage (ideational)

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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.

Definitions
Transient ischemic attack (TIA)
A brief episode in which a temporary loss of blood flow causes stroke symptoms such as vision deficits, weakness, and numbness. Symptoms resolve on their own, within a variable timeframe of less than 24 hours. A TIA is still a medical emergency and a warning sign of a future stroke: while symptoms are present there is no way to tell a TIA from a stroke, so emergency medical services are called right away, even if the symptoms go away.

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.

Definitions
Craniotomy
A surgical procedure in which a section of the skull (bone flap) is temporarily removed to access the brain, e.g., to evacuate a hemorrhage or repair the bleeding vessel.
Arterial clipping
A procedure in which a clamp is placed on the hemorrhaging brain artery to reduce blood flow and stop bleeding.

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

PTA scope of practice: The PTA carries out the plan of care established by the supervising PT, including any stroke-recovery or rehabilitation program. If a patient shows a change in neurological status or an adverse response during treatment (e.g., sudden confusion or escalating agitation), the PTA’s role is to stop, document, and report the finding to the supervising PT rather than re-evaluate or modify the plan. New F.A.S.T. signs are a medical emergency: call 911 immediately, as the list above says, then notify the supervising PT.

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
  • 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)
  • 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)

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

Definitions
Homonymous hemianopsia
A type of visual field loss that affects the same side of the visual field in both eyes.

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

Definitions
Apraxia
A motor planning disorder characterized by the inability to execute purposeful, learned movements, even when the individual has the physical capacity and desire to perform the movement. It is commonly caused by lesions in the left hemisphere of the brain, particularly the parietal and frontal lobes, and can significantly impair functional independence.

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
Key points

Cerebral vascular accidents (CVA, stroke)

  • Caused by ischemia (clot) or hemorrhage (rupture); ischemic more common
  • TIA: temporary stroke symptoms resolving <24 hrs; still a medical emergency, call EMS immediately
  • Risk factors: hypertension, arteriosclerosis, diabetes, cardiac disease, hyperlipidemia, smoking, sedentary lifestyle, prior TIA
  • Ischemic stroke: tPA within 3 hrs (up to 4.5 hrs select patients); otherwise anticoagulants/antihypertensives
  • Hemorrhagic stroke: craniotomy or arterial clipping; plus antihypertensive/antiepileptic meds

Cardinal symptoms & F.A.S.T.

  • Sudden weakness/numbness, speech difficulty, gait trouble, confusion, visual changes, facial drooping
  • F.A.S.T.: Face drooping, Arm weakness, Speech difficulty, Time to call 911
  • PTA scope: stop, document, report new neuro changes/F.A.S.T. signs to PT; call 911 if emergency; do not modify plan of care

Neurological deficits by hemisphere

  • Left hemisphere injury: right hemiplegia/hemisensory, speech-language deficits, planning/sequencing difficulty
  • Right hemisphere injury: left hemiplegia/hemisensory, visual-perceptual deficits, poor judgment/impulsivity, difficulty with abstract concepts/emotions

Deficits by arterial territory

  • MCA: contralateral UE>LE weakness/paresthesia, homonymous hemianopsia, Broca’s (motor) and Wernicke’s (receptive) aphasia, gaze deviation
  • ACA: contralateral LE>UE weakness/paresthesia, urinary incontinence, apraxia, mutism, akinesia
  • PCA: contralateral sensory loss, homonymous hemianopsia, involuntary movements (intention tremor, chorea, hemiballismus), visual agnosia, dyslexia, thalamic pain, oculomotor palsy
  • Vertebral-basilar artery: locked-in syndrome (paralysis except eye movement, cognition intact)
  • Millard-Gubler syndrome (ventral pons): ipsilateral facial/abducens CN deficits, contralateral hemiplegia
  • Wallenberg/PICA syndrome (lateral medulla): ipsilateral CN V/X deficits, Horner’s syndrome, ataxia; contralateral pain/temp loss; no hemiparesis

Brunnstrom stages of recovery

  • Stage 1: flaccidity, no voluntary movement
  • Stage 2–3: spasticity develops/increases, synergy patterns emerge and become voluntary
  • Stage 4–5: spasticity decreases, non-synergy and complex movements possible
  • Stage 6–7: spasticity resolves, return to normal function
  • No fixed timetable; progression varies per patient

Synergy patterns

  • Flexion synergy: scapular retraction/elevation, shoulder abduction/ER, elbow flexion, forearm supination; hip flexion/abduction/ER, knee flexion, ankle dorsiflexion
  • Extension synergy: scapular protraction/depression, shoulder adduction/IR, elbow extension, forearm pronation; hip extension/adduction/IR, knee extension, ankle plantarflexion

Homonymous hemianopsia

  • Visual field loss on same side in both eyes
  • Caused by lesions in optic tract/radiation/occipital lobe contralateral to vision loss
  • Common causes: stroke (PCA), TBI, tumors
  • Symptoms: bumping into objects, reading difficulty, navigation/driving issues
  • Diagnosed via perimetry
  • Rehab: visual scanning training, head-turning compensation, environmental modification

Apraxia

  • Motor planning disorder; purposeful movement impaired despite intact physical ability/desire
  • Linked to left hemisphere (parietal/frontal) lesions
  • Ideomotor apraxia: understands task but can’t perform on command/imitation; may improve with automatic actions
  • Ideational apraxia: loses concept of task sequence; misuses objects, skips/misorders steps
  • Common causes: stroke (ideomotor), dementia/widespread cortical damage (ideational)

More from Neuromuscular system

  • Central nervous system
  • Anatomy and function of spinal cord
  • Traumatic brain injury
  • Spinal cord injury
  • Neurodegenerative disorders and epilepsy