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Introduction
1. Cardiovascular 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 systems
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. Carotid endarterectomy is a surgery in which the surgeon removes the plaque inside a narrowed carotid artery to restore blood flow to the brain, which may help lower the chance of having a stroke.

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). Beyond that window, selected patients with a large-vessel clot may have mechanical thrombectomy (up to 24 hours after last known well); medical management includes antiplatelet medication such as aspirin and blood pressure control, while urgent anticoagulation is generally not recommended.

Hemorrhagic strokes are medically managed via craniotomy or arterial clipping of bleeding arteries. Management also involves antihypertensive and antiepileptic medications. Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space; the most common cause of spontaneous bleeding is a ruptured aneurysm, and the symptoms include a sudden, severe headache.

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, done through a craniotomy, in which a small metal clip is placed across the neck of a ruptured aneurysm to seal it off from the circulation and prevent rebleeding.

Cardinal symptoms of stroke

Stroke also commonly causes sudden confusion, visual changes, and difficulty walking, in addition to the deficits captured by the F.A.S.T. acronym below.

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, left unilateral neglect
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 sensory loss, upper extremity greater than lower extremity
    • Homonymous hemianopsia
    • Aphasia (dominant/left MCA): Broca’s aphasia (expressive) or Wernicke’s aphasia (receptive)
      • Communicating with a person who has aphasia: use short, uncomplicated sentences, repeat or write down key words, and encourage any type of communication, including speech, gesture, pointing, or drawing
    • Right (nondominant) MCA: unilateral neglect and visual-perceptual deficits
    • Loss of gaze to the opposite side
  • Anterior cerebral artery stroke
    • Contralateral hemiplegia with lower extremity weakness greater than upper extremity weakness
    • Contralateral sensory loss, lower extremity greater than upper extremity
    • Urinary incontinence
    • Apraxia
    • Mutism (less verbal)
    • Akinetic (less mobile)
  • Posterior cerebral artery stroke
    • Contralateral sensory loss
    • Homonymous hemianopsia
    • Involuntary movements
      • Intention tremor: a tremor that appears or worsens during purposeful movement toward a target
      • Chorea: rapid, irregular, jerky involuntary movements (called choreoathetosis when combined with slow 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 paralysis and inability to abduct the eye on the ipsilateral side (lateral rectus impacted)
        • 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)
  • Lateral pontine syndrome (AICA)
    • Ipsilateral facial palsy, facial sensory loss, hearing loss, vertigo and limb ataxia, with contralateral loss of pain and temperature sensation in the body
  • Medial medullary syndrome (vertebral and anterior spinal artery branches)
    • Ipsilateral tongue weakness with contralateral hemiparesis
  • Weber syndrome (paramedian branches of the posterior cerebral artery)
    • Ipsilateral oculomotor palsy with contralateral hemiplegia

PTA safety considerations: Protect the hemiplegic shoulder from subluxation and traction injury during transfers and exercise - use supportive positioning and proper handling, and avoid pulling on the involved arm. A patient with pusher syndrome (often seen with neglect) actively pushes toward the weaker side and resists correction toward midline; guard from the weaker (hemiplegic) side, where the patient is likely to fall; avoid forcing them back to midline, and use visual cues of vertical (a mirror or doorframe) while having the patient shift weight or reach toward the stronger side. Monitor vital signs during activity and stop the session if blood pressure exceeds safe limits or new neurological signs appear (e.g., sudden confusion, facial drooping, slurred speech) - report these findings to the supervising PT immediately, and call 911 if F.A.S.T. signs are new.

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

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 to its peak, 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

Homonymous hemianopsia

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

Unlike unilateral neglect (a right parietal lesion), a patient with hemianopsia is usually aware of the field loss and can learn to compensate by turning the head; a patient with neglect is unaware of the affected side, so they need cueing and need to have their attention drawn toward that side.

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).
  • Bitemporal hemianopsia is loss of the outer (temporal) half of the visual field in each eye, typically from a tumor or lesion affecting the optic chiasm, unlike homonymous hemianopsia, which is caused by damage behind the chiasm.
  • 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
  • Rehabilitation focus:
    • Visual scanning training
    • Compensatory strategies (e.g., turning the head to scan the blind side)
    • Environmental modifications
    • Fresnel prism glasses shift the view toward the blind side to expand the visible field, but the patient must still turn the head to look toward the blind side, and visual search (scanning) training gives the greatest functional improvement

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.

As a PTA, you’ll observe these presentations during treatment and report them to the supervising PT. 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

Stroke overview & types

  • CVA = sudden focal neuro deficits from ischemia (clot, more common) or hemorrhage (vessel rupture)
  • TIA: temporary stroke symptoms resolving <24 hrs; still a medical emergency since it’s indistinguishable from stroke while symptoms present
  • Risk factors: hypertension, arteriosclerosis, diabetes, cardiac disease, hyperlipidemia, smoking, sedentary lifestyle, prior TIA

Medical management

  • Ischemic: tPA within 3 hrs (up to 4.5 in select cases); mechanical thrombectomy up to 24 hrs for large-vessel clot; antiplatelets (aspirin) + BP control; urgent anticoagulation generally avoided
  • Hemorrhagic: craniotomy (temporary skull removal) or arterial clipping (seals aneurysm); antihypertensives/antiepileptics

F.A.S.T. & PTA role

  • Face drooping, Arm weakness/drift, Speech slurred, Time to call 911
  • PTA scope: stop, document, report neuro changes to PT; never re-evaluate/modify plan; new F.A.S.T. signs = call 911 then notify PT

Hemisphere & artery-specific deficits

  • Left hemisphere injury → right hemiplegia, speech-language deficits, trouble sequencing movement
  • Right hemisphere injury → left hemiplegia, visual-perceptual deficits/neglect, impulsivity, poor emotion perception
  • MCA stroke: contralateral UE>LE weakness/sensory loss, homonymous hemianopsia, aphasia (Broca’s/Wernicke’s) if dominant side, neglect if nondominant
  • ACA stroke: contralateral LE>UE weakness, incontinence, apraxia, mutism, akinesia
  • PCA stroke: contralateral sensory loss, hemianopsia, involuntary movements (intention tremor, chorea, hemiballismus), visual agnosia, thalamic pain
  • Brainstem syndromes: locked-in syndrome (vertebral-basilar, paralysis except eyes, cognition intact); Millard-Gubler (ipsilateral facial/abducens palsy + contralateral hemiplegia); Wallenberg/PICA syndrome (ipsilateral CN deficits, Horner’s, ataxia; contralateral pain/temp loss; no hemiparesis)

PTA safety considerations

  • Protect hemiplegic shoulder from subluxation/traction during transfers
  • Pusher syndrome: guard from weak side, don’t force to midline, use visual vertical cues, encourage weight shift toward strong side
  • Monitor vitals; stop session and report any new neuro signs immediately; call 911 for new F.A.S.T. signs

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

Brunnstrom stages of recovery

  • Progression: flaccidity (1) → synergies emerge (2-3, spasticity peaks) → movement out of synergy (4-5) → spasticity resolves (6) → normal function (7)
  • No fixed timetable; patients may plateau at any stage

Visual/perceptual deficits

  • Homonymous hemianopsia: same-side visual field loss both eyes; patient usually aware, can learn to compensate by turning head (unlike neglect, where patient is unaware and needs cueing)
  • Caused by lesions opposite the vision loss (optic tract/radiation/occipital lobe); common after stroke (PCA), TBI, tumor
  • Rehab: visual scanning training, head-turning compensation, environmental modification

Apraxia

  • Motor planning disorder: can’t perform purposeful movements despite intact strength/desire; left hemisphere (parietal/frontal) lesions
  • Ideomotor apraxia: understands task, can’t execute on command (awkward limb positioning); may improve with automatic actions
  • Ideational apraxia: loses concept of task sequence, misuses objects, skips steps; linked to extensive left hemisphere damage/dementia

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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. Carotid endarterectomy is a surgery in which the surgeon removes the plaque inside a narrowed carotid artery to restore blood flow to the brain, which may help lower the chance of having a stroke.

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). Beyond that window, selected patients with a large-vessel clot may have mechanical thrombectomy (up to 24 hours after last known well); medical management includes antiplatelet medication such as aspirin and blood pressure control, while urgent anticoagulation is generally not recommended.

Hemorrhagic strokes are medically managed via craniotomy or arterial clipping of bleeding arteries. Management also involves antihypertensive and antiepileptic medications. Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space; the most common cause of spontaneous bleeding is a ruptured aneurysm, and the symptoms include a sudden, severe headache.

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, done through a craniotomy, in which a small metal clip is placed across the neck of a ruptured aneurysm to seal it off from the circulation and prevent rebleeding.

Cardinal symptoms of stroke

Stroke also commonly causes sudden confusion, visual changes, and difficulty walking, in addition to the deficits captured by the F.A.S.T. acronym below.

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, left unilateral neglect
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 sensory loss, upper extremity greater than lower extremity
    • Homonymous hemianopsia
    • Aphasia (dominant/left MCA): Broca’s aphasia (expressive) or Wernicke’s aphasia (receptive)
      • Communicating with a person who has aphasia: use short, uncomplicated sentences, repeat or write down key words, and encourage any type of communication, including speech, gesture, pointing, or drawing
    • Right (nondominant) MCA: unilateral neglect and visual-perceptual deficits
    • Loss of gaze to the opposite side
  • Anterior cerebral artery stroke
    • Contralateral hemiplegia with lower extremity weakness greater than upper extremity weakness
    • Contralateral sensory loss, lower extremity greater than upper extremity
    • Urinary incontinence
    • Apraxia
    • Mutism (less verbal)
    • Akinetic (less mobile)
  • Posterior cerebral artery stroke
    • Contralateral sensory loss
    • Homonymous hemianopsia
    • Involuntary movements
      • Intention tremor: a tremor that appears or worsens during purposeful movement toward a target
      • Chorea: rapid, irregular, jerky involuntary movements (called choreoathetosis when combined with slow 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 paralysis and inability to abduct the eye on the ipsilateral side (lateral rectus impacted)
        • 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)
  • Lateral pontine syndrome (AICA)
    • Ipsilateral facial palsy, facial sensory loss, hearing loss, vertigo and limb ataxia, with contralateral loss of pain and temperature sensation in the body
  • Medial medullary syndrome (vertebral and anterior spinal artery branches)
    • Ipsilateral tongue weakness with contralateral hemiparesis
  • Weber syndrome (paramedian branches of the posterior cerebral artery)
    • Ipsilateral oculomotor palsy with contralateral hemiplegia

PTA safety considerations: Protect the hemiplegic shoulder from subluxation and traction injury during transfers and exercise - use supportive positioning and proper handling, and avoid pulling on the involved arm. A patient with pusher syndrome (often seen with neglect) actively pushes toward the weaker side and resists correction toward midline; guard from the weaker (hemiplegic) side, where the patient is likely to fall; avoid forcing them back to midline, and use visual cues of vertical (a mirror or doorframe) while having the patient shift weight or reach toward the stronger side. Monitor vital signs during activity and stop the session if blood pressure exceeds safe limits or new neurological signs appear (e.g., sudden confusion, facial drooping, slurred speech) - report these findings to the supervising PT immediately, and call 911 if F.A.S.T. signs are new.

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

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 to its peak, 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

Homonymous hemianopsia

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

Unlike unilateral neglect (a right parietal lesion), a patient with hemianopsia is usually aware of the field loss and can learn to compensate by turning the head; a patient with neglect is unaware of the affected side, so they need cueing and need to have their attention drawn toward that side.

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).
  • Bitemporal hemianopsia is loss of the outer (temporal) half of the visual field in each eye, typically from a tumor or lesion affecting the optic chiasm, unlike homonymous hemianopsia, which is caused by damage behind the chiasm.
  • 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
  • Rehabilitation focus:
    • Visual scanning training
    • Compensatory strategies (e.g., turning the head to scan the blind side)
    • Environmental modifications
    • Fresnel prism glasses shift the view toward the blind side to expand the visible field, but the patient must still turn the head to look toward the blind side, and visual search (scanning) training gives the greatest functional improvement

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.

As a PTA, you’ll observe these presentations during treatment and report them to the supervising PT. 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

Stroke overview & types

  • CVA = sudden focal neuro deficits from ischemia (clot, more common) or hemorrhage (vessel rupture)
  • TIA: temporary stroke symptoms resolving <24 hrs; still a medical emergency since it’s indistinguishable from stroke while symptoms present
  • Risk factors: hypertension, arteriosclerosis, diabetes, cardiac disease, hyperlipidemia, smoking, sedentary lifestyle, prior TIA

Medical management

  • Ischemic: tPA within 3 hrs (up to 4.5 in select cases); mechanical thrombectomy up to 24 hrs for large-vessel clot; antiplatelets (aspirin) + BP control; urgent anticoagulation generally avoided
  • Hemorrhagic: craniotomy (temporary skull removal) or arterial clipping (seals aneurysm); antihypertensives/antiepileptics

F.A.S.T. & PTA role

  • Face drooping, Arm weakness/drift, Speech slurred, Time to call 911
  • PTA scope: stop, document, report neuro changes to PT; never re-evaluate/modify plan; new F.A.S.T. signs = call 911 then notify PT

Hemisphere & artery-specific deficits

  • Left hemisphere injury → right hemiplegia, speech-language deficits, trouble sequencing movement
  • Right hemisphere injury → left hemiplegia, visual-perceptual deficits/neglect, impulsivity, poor emotion perception
  • MCA stroke: contralateral UE>LE weakness/sensory loss, homonymous hemianopsia, aphasia (Broca’s/Wernicke’s) if dominant side, neglect if nondominant
  • ACA stroke: contralateral LE>UE weakness, incontinence, apraxia, mutism, akinesia
  • PCA stroke: contralateral sensory loss, hemianopsia, involuntary movements (intention tremor, chorea, hemiballismus), visual agnosia, thalamic pain
  • Brainstem syndromes: locked-in syndrome (vertebral-basilar, paralysis except eyes, cognition intact); Millard-Gubler (ipsilateral facial/abducens palsy + contralateral hemiplegia); Wallenberg/PICA syndrome (ipsilateral CN deficits, Horner’s, ataxia; contralateral pain/temp loss; no hemiparesis)

PTA safety considerations

  • Protect hemiplegic shoulder from subluxation/traction during transfers
  • Pusher syndrome: guard from weak side, don’t force to midline, use visual vertical cues, encourage weight shift toward strong side
  • Monitor vitals; stop session and report any new neuro signs immediately; call 911 for new F.A.S.T. signs

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

Brunnstrom stages of recovery

  • Progression: flaccidity (1) → synergies emerge (2-3, spasticity peaks) → movement out of synergy (4-5) → spasticity resolves (6) → normal function (7)
  • No fixed timetable; patients may plateau at any stage

Visual/perceptual deficits

  • Homonymous hemianopsia: same-side visual field loss both eyes; patient usually aware, can learn to compensate by turning head (unlike neglect, where patient is unaware and needs cueing)
  • Caused by lesions opposite the vision loss (optic tract/radiation/occipital lobe); common after stroke (PCA), TBI, tumor
  • Rehab: visual scanning training, head-turning compensation, environmental modification

Apraxia

  • Motor planning disorder: can’t perform purposeful movements despite intact strength/desire; left hemisphere (parietal/frontal) lesions
  • Ideomotor apraxia: understands task, can’t execute on command (awkward limb positioning); may improve with automatic actions
  • Ideational apraxia: loses concept of task sequence, misuses objects, skips steps; linked to extensive left hemisphere damage/dementia

More from Neuromuscular system

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