4.1 Stroke Vascular Syndromes & Acute Assessment

ABPMR Physical Medicine and Rehabilitation Board Exam Study Guide Exam

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1 Chapter 1: Introduction & Exam Overview

1.1 ABPMR Part I Exam Overview & Format 1.2 Board Review Strategy & Content Blueprint Breakdown

2 Chapter 2: Musculoskeletal Medicine

2.1 Shoulder & Upper Extremity Diagnostics 2.2 Knee, Hip & Lower Extremity Conditions 2.3 Spine Pathology, Radiculopathy & Myelopathy 2.4 Inflammatory Arthritis, Tendinopathies & Concussion 2.5 Bone Health, Osteoporosis & Metabolic Bone Disease 2.6 Thoracic Outlet Syndrome & Peripheral Nerve Entrapment 2.7 Fracture Rehabilitation & Immobilization Complications 2.8 Overuse Tendinopathies & Regenerative Medicine 2.9 Gait Analysis & Abnormal Gait Patterns

3 Chapter 3: Spinal Cord Injury Rehabilitation

3.1 ASIA Examination & Impairment Scale 3.2 Spinal Cord Injury Syndromes 3.3 Autonomic Dysreflexia & Acute Complications 3.4 Neurogenic Bladder, Bowel & Secondary Complications

4 Chapter 4: Stroke & Neuromuscular Rehabilitation

4.1 Stroke Vascular Syndromes & Acute Assessment 4.2 Stroke Motor Recovery & Hemiplegic Complications 4.3 Spasticity Assessment & Multimodal Management 4.4 ALS, GBS, CIDP & Neuromuscular Disease Rehab 4.5 Multiple Sclerosis & Demyelinating Disease Rehabilitation 4.6 Parkinsonism, Movement Disorders & Functional Neurologic Disorder

5 Chapter 5: Electrodiagnostics (EMG/NCS)

5.1 Nerve Conduction Studies Principles & Physics 5.2 Needle Electromyography & MUAP Analysis 5.3 Mononeuropathies & Radiculopathy Patterns 5.4 Neuromuscular Junction Disorders & Myopathies

6 Chapter 6: Traumatic Brain Injury

6.1 TBI Severity Classification, Glasgow Coma Scale, and Pathophysiology 6.2 Rancho Los Amigos Levels of Cognitive Functioning and Disability Rating Scale 6.3 Neurobehavioral Sequelae and Agitation Management 6.4 Concussion Evaluation, Vestibular-Ocular Dysfunction, and Return-to-Play/Work Protocols

7 Chapter 7: Chronic Pain & Interventional Spine

7.1 Fluoroscopic Spine Interventions 7.2 Opioid Stewardship & Controlled Substance Compliance 7.3 Complex Regional Pain Syndrome, Fibromyalgia & Myofascial Pain 7.4 Spinal Cord Stimulation & Intrathecal Therapy

8 Chapter 8: Amputee Rehabilitation & Prosthetics

8.1 Amputation Surgical Levels & Medicare K-Levels 8.2 Socket Designs & Suspension Systems 8.3 Prosthetic Feet & Microprocessor Knee Mechanisms 8.4 Post-Amputation Care, Residual Limb & Phantom Pain

9 Chapter 9: Pediatric Rehabilitation

9.1 Cerebral Palsy Classification & GMFCS 9.2 Spina Bifida & Myelomeningocele Management 9.3 Muscular Dystrophies & Neuromuscular Disease in Children 9.4 Pediatric Brachial Plexopathy & Congenital Disorders

10 Chapter 10: Prosthetics, Orthotics & Assistive Technology

10.1 Lower Limb Orthoses — AFOs & KAFOs 10.2 Spinal & Upper Extremity Orthoses 10.3 Upper Limb Prosthetics — Body-Powered vs Myoelectric 10.4 Wheelchairs, Seating Systems & Pressure Mapping

11 Chapter 11: Medical Rehabilitation & Outcomes

11.1 Dysphagia Assessment & Management 11.2 Neurogenic Bladder & Bowel Management 11.3 Pressure Injuries & Wound Management 11.4 Outcome Measures & Medical Complications 11.5 Cancer Rehabilitation & Oncologic Rehabilitation 11.6 Burns, Endocrine/Metabolic & Medical Complications Rehabilitation

12 Chapter 12: Cardiopulmonary Rehabilitation

12.1 Cardiac Rehabilitation Phases & Metabolic Equivalents 12.2 Pulmonary Rehabilitation & COPD Management

13 Chapter 13: Foundational Rehabilitation Concepts

13.1 Kinesiology, Biomechanics & Functional Anatomy 13.2 Rehabilitation Pharmacology & Medication Management 13.3 Research Methodology, Biostatistics & Evidence-Based Practice 13.4 Nutrition, Metabolism & Energy Expenditure in Rehabilitation 13.5 Diagnostic Procedures: Imaging, MSK Ultrasound, Urodynamics & Neuropsych Assessment

4.1 Stroke Vascular Syndromes & Acute Assessment

Key Takeaways Explain This Topic AI

Middle Cerebral Artery (MCA) strokes classically present with contralateral face and arm weakness greater than leg weakness, combined with Broca aphasia (expressive, inferior frontal gyrus), Wernicke aphasia (receptive, superior temporal gyrus), or hemispatial neglect (right parietal lobe).

Anterior Cerebral Artery (ACA) strokes characteristically affect the medial frontal and parietal cortices, producing contralateral leg weakness greater than arm/face weakness, urinary incontinence, gait apraxia, and abulia (lack of initiation).

Posterior Cerebral Artery (PCA) strokes affect the occipital cortex and medial temporal lobe, resulting in contralateral homonymous hemianopia with macular sparing, alexia without agraphia (left PCA/splenium of corpus callosum), and memory deficits.

Lacunar syndromes arise from small vessel lipohyalinosis of penetrating arteries; classic types include pure motor hemiparesis (posterior limb of internal capsule), pure sensory stroke (ventral posterolateral thalamus), clumsy hand-dysarthria (paramedian pons), and ataxic hemiparesis (corona radiata or pons).

The National Institutes of Health Stroke Scale (NIHSS) quantifies acute neurological deficit severity (0-42 score), while functional independence measure tools (FIM / IRF-PAI Section GG) evaluate post-stroke functional mobility, self-care, and cognitive burden for inpatient rehabilitation admission and goal setting.

Last updated: July 2026

Stroke Vascular Syndromes & Acute Assessment

Acute ischemic stroke remains one of the primary diagnoses managed by physical medicine and rehabilitation (PM&R) specialists. Precise neuroanatomical localization based on clinical presentation allows physiatrists to anticipate functional deficits, formulate targeted rehabilitation plans, and direct secondary prevention strategies. Ischemic stroke syndromes are broadly divided into anterior circulation territories ( Middle Cerebral Artery and Anterior Cerebral Artery ) and posterior circulation territories ( Posterior Cerebral Artery , vertebrobasilar branches, and penetrating brainstem perforators), alongside small-vessel lacunar syndromes .

Anterior Circulation Syndromes
Middle Cerebral Artery (MCA) Territory

The Middle Cerebral Artery (MCA) is the largest branch of the internal carotid artery and the most common site of ischemic stroke. It supplies the lateral surface of the frontal, parietal, and temporal lobes, as well as deep subcortical structures (via lenticulostriate branches).

Motor and Sensory Manifestations : MCA territory strokes produce contralateral hemiparesis and hemisensory loss affecting the face and upper extremity significantly more than the lower extremity (arm/face > leg) . This classic pattern reflects the cortical homunculus, where motor and sensory representations of the face and arm lie on the lateral cerebral convexity (supplied by the MCA), while the lower extremity representation lies medially (supplied by the ACA).

Dominant Hemisphere (Left MCA) Deficits : Occlusion of the dominant MCA (typically left hemisphere) disrupts cortical language networks:

Broca Aphasia (Expressive / Non-Fluent Aphasia) : Results from damage to the left inferior frontal gyrus ( Brodmann areas 44 and 45 ). Patients exhibit non-fluent, labored, telegraphic speech with impaired repetition, but speech comprehension remains remarkably intact. Patients are typically aware of their deficit, leading to significant frustration.

Wernicke Aphasia (Receptive / Fluent Aphasia) : Results from damage to the left posterior superior temporal gyrus ( Brodmann area 22 ). Patients present with fluent, voluminous, but paraphasic and nonsensical speech ("word salad"), accompanied by severely impaired auditory and reading comprehension and impaired repetition. Patients are typically unaware of their comprehension deficit (anosognosia).

Global Aphasia : Stem occlusion of the proximal M1 segment causes extensive frontotemporal infarction, producing a severe combination of non-fluent speech, absent comprehension, and complete right hemiplegia.

Nondominant Hemisphere (Right MCA) Deficits : Occlusion of the nondominant MCA affects parietal spatial processing networks:

Hemispatial Neglect (Visuospatial / Personal Neglect) : Patients fail to perceive, respond to, or attend to stimuli presented in the extrapersonal or personal space contralateral to the lesion (most commonly left-sided spatial neglect following a right parietal lesion).

Anosognosia : Lack of awareness of one's own neurological deficits (e.g., denying hemiplegia).

Constructional and Dressing Apraxia : Inability to draw, block-design, or align clothing with body parts.

Anterior Cerebral Artery (ACA) Territory

The Anterior Cerebral Artery (ACA) supplies the medial aspect of the frontal and parietal lobes, including the primary motor and sensory strips representing the lower extremity, as well as the anterior corpus callosum and supplementary motor area.

Motor and Sensory Deficits : ACA strokes characteristically present with contralateral hemiparesis and hemisensory loss affecting the lower extremity significantly more than the upper extremity and face (leg > arm/face) .

Frontal Lobe and Cognitive Features : ACA infarction produces distinct behavioral and executive alterations:

Abulia : A profound state of apathy, lack of initiative, motor impersistence, and poverty of spontaneous speech, stemming from frontostriatal disruption.

Urinary Incontinence : Caused by infarction of the medial frontal micturition center, leading to loss of voluntary bowel/bladder inhibition.

Frontal Release Signs : Re-emergence of primitive reflexes including grasp, snout, and sucking reflexes.

Gait Apraxia : Magnetic or apraxic gait where the patient struggles to initiate walking despite preserved leg strength when lying supine.

Posterior Circulation Syndromes
Posterior Cerebral Artery (PCA) Territory

The Posterior Cerebral Artery (PCA) supplies the occipital cortex, inferior and medial temporal lobes, thalamus, and splenium of the corpus callosum.

Visual Field Deficits : The hallmark of PCA stroke is contralateral homonymous hemianopia . Crucially, this hemianopia typically exhibits macular sparing because the extreme occipital pole representing macular vision receives dual collateral blood supply from terminal branches of the MCA.

Higher Cortical Visual Syndromes :

Alexia Without Agraphia (Pure Alexia) : Patients lose the ability to read written language but retain the full ability to write spontaneously and to dictation. This classic disconnection syndrome occurs when a left PCA stroke destroys the left primary visual cortex and the splenium of the corpus callosum . Visual information received by the intact right occipital cortex cannot cross the splenium to reach the left language areas (Wernicke area).

Visual Agnosia and Prosopagnosia : Inability to recognize familiar objects or faces, stemming from bilateral ventral occipitotemporal (fusiform gyrus) lesions.

Thalamic Syndromes : PCA perforating branches supply the ventral posterolateral (VPL) and ventral posteromedial (VPM) thalamic nuclei. Dejerine-Roussy Syndrome (Post-Stroke Thalamic Pain) begins with transient contralateral sensory loss, followed weeks to months later by severe, agonizing, burning neuropathic pain provoked by light tactile stimuli (allodynia).

Lacunar Syndromes

Lacunar strokes result from lipohyalinosis and microatheroma occlusion of small penetrating arteries (100–400 μm diameter) such as lenticulostriate, thalamoperforating, and pontine perforator vessels. They produce small (<15 mm) subcortical focal infarcts.

Pure Motor Hemiparesis : The most frequent lacunar syndrome (~33–50%), caused by an infarct in the posterior limb of the internal capsule or basis pontis. It presents with proportional weakness of the contralateral face, arm, and leg without sensory loss or cortical signs (no aphasia, no neglect).

Pure Sensory Stroke : Infarction of the ventral posterolateral (VPL) nucleus of the thalamus . Presents with numbness, tingling, or sensory loss involving the contralateral face, arm, trunk, and leg without motor weakness.

Clumsy Hand-Dysarthria Syndrome : Infarction of the paramedian pontine base or anterior limb/genu of the internal capsule. Characterized by severe dysarthria, facial weakness, dysphagia, and prominent upper extremity motor clumsiness out of proportion to weakness.

Ataxic Hemiparesis : Infarction of the corona radiata, posterior limb of the internal capsule, or basis pontis. Characterized by a combination of cerebellar ataxia and weakness on the same side of the body.

Vascular Territory / Syndrome Key Anatomical Structures Primary Clinical Features Pathognomonic / Distinguishing Signs

MCA (Dominant) Lateral frontoparietal cortex, left inferior frontal / superior temporal Contralateral face/arm > leg weakness & sensory loss Broca (non-fluent) or Wernicke (fluent) aphasia

MCA (Nondominant) Lateral frontoparietal cortex, right parietal lobe Contralateral face/arm > leg weakness & sensory loss Left hemispatial neglect, anosognosia, dressing apraxia

ACA Medial frontal & parietal cortex, micturition center Contralateral leg > arm/face weakness & sensory loss Abulia, urinary incontinence, gait apraxia, grasp reflex

PCA Occipital cortex, splenium of corpus callosum, VPL thalamus Contralateral homonymous hemianopia Macular sparing; Alexia without agraphia (left PCA)

Lacunar (Pure Motor) Posterior limb of internal capsule or basis pontis Equal face, arm, leg motor weakness Complete absence of cortical signs (no aphasia/neglect)

Lacunar (Pure Sensory) Ventral posterolateral (VPL) nucleus of thalamus Contralateral hemisensory loss (face, arm, leg) Pure sensory loss; no motor weakness

Acute Stroke Assessment Tools
National Institutes of Health Stroke Scale (NIHSS)

The National Institutes of Health Stroke Scale (NIHSS) is a standardized 15-item quantitative assessment tool used to measure neurological deficit severity in acute stroke (score range 0–42).

Key Categories : Evaluates level of consciousness, horizontal eye movement, visual fields, facial palsy, upper and lower extremity motor function, limb ataxia, sensory loss, best language (aphasia), dysarthria, and extinction/inattention (neglect).

Severity Stratification :

0 : No stroke symptoms
1–4 : Mild stroke
5–15 : Moderate stroke
16–20 : Moderate-to-severe stroke

21–42 : Severe stroke (NIHSS ≥21 predicts high mortality and severe functional dependency).

Functional Independence Measure (FIM) & IRF-PAI Section GG

Functional recovery assessment guides inpatient rehabilitation facility (IRF) admission, goal setting, and discharge planning.

Functional Independence Measure (FIM) : Historically comprised 18 items (13 motor, 5 cognitive), rated on a 7-point ordinal scale ranging from 1 (Total Assistance - patient performs <25%) to 7 (Complete Independence) . Total FIM scores range from 18 to 126.

Inpatient Rehabilitation Facility Patient Assessment Instrument (IRF-PAI) Section GG : Modern CMS-mandated assessment tool replacing FIM. Measures functional performance across self-care and mobility items using a 6-point Function Scale :

6 : Independent
5 : Setup or clean-up assistance
4 : Supervision or touching assistance
3 : Partial/moderate assistance (helper does <50% of effort)
2 : Substantial/maximal assistance (helper does 50–99% of effort)
1 : Dependent (helper does 100% of effort)