Neuroimaging in Hemiplegia: A Comprehensive Review of Anatomical Variants and Clinical Correlates

Dr Neeraj Manikath , claude.ai

Abstract

Hemiplegia represents a cardinal manifestation of central nervous system pathology, with diverse etiologies and anatomical presentations that challenge clinicians in diagnosis and management. While classic contralateral hemiplegia following supratentorial lesions is well-recognized, variant presentations including alternating hemiplegia, hemiplegia cruciata, double hemiplegia, and crural variants require sophisticated neuroimaging interpretation. This review synthesizes current understanding of imaging approaches across the spectrum of hemiplegic syndromes, emphasizing anatomical correlates, diagnostic pearls, and practical approaches for the practicing internist.

Introduction

Hemiplegia, defined as complete paralysis affecting one side of the body, serves as a neurological localizing sign par excellence. The advent of modern neuroimaging has revolutionized our ability to correlate clinical presentations with precise anatomical lesions. Understanding the neuroimaging patterns of various hemiplegic subtypes is essential for accurate diagnosis, prognostication, and therapeutic decision-making. This review addresses imaging strategies for recognizing both common and rare hemiplegic presentations that internists encounter in clinical practice.

Neuroanatomical Foundation

The corticospinal tract originates from the primary motor cortex (Brodmann area 4), premotor cortex, and supplementary motor area. Fibers descend through the corona radiata, posterior limb of the internal capsule (with somatotopic organization: face anterior, arm middle, leg posterior), cerebral peduncles, pons, and medullary pyramids before decussating at the cervicomedullary junction. Approximately 85-90% of fibers cross at the pyramidal decussation, forming the lateral corticospinal tract, while 10-15% continue ipsilaterally as the anterior corticospinal tract.

Pearl #1: The internal capsule's posterior limb is extraordinarily compact—a lesion measuring just 15-20mm can produce complete contralateral hemiplegia. This explains why small lacunar infarcts in this region cause disproportionate deficits compared to much larger cortical strokes.

Imaging Modalities: Strategic Selection

Computed Tomography

Non-contrast CT remains the first-line imaging in acute settings, primarily to exclude hemorrhage before thrombolytic therapy. Modern multidetector CT provides excellent sensitivity for hemorrhage but limited sensitivity for acute ischemia in the first 6-8 hours.

Hack #1: The insular ribbon sign (loss of gray-white differentiation in the insula) is one of the earliest CT signs of middle cerebral artery (MCA) territory infarction, appearing within 3-4 hours. Always scrutinize the insula in patients presenting with acute hemiplegia.

Magnetic Resonance Imaging

MRI with diffusion-weighted imaging (DWI) represents the gold standard for acute ischemic stroke detection, with sensitivity exceeding 95% within minutes of symptom onset. The combination of DWI, apparent diffusion coefficient (ADC) maps, FLAIR, T2, gradient echo (GRE) or susceptibility-weighted imaging (SWI), and vascular imaging provides comprehensive assessment.

Pearl #2: DWI-FLAIR mismatch (DWI positive, FLAIR negative) suggests stroke onset within 4.5 hours, helping determine thrombolysis eligibility in patients with unknown symptom onset, including wake-up strokes.

Classic Hemiplegia: Imaging Patterns

Cortical Hemiplegia

Lesions of the motor cortex produce contralateral weakness following a homuncular distribution. MCA territory infarctions commonly cause face-arm predominant hemiplegia, while anterior cerebral artery (ACA) infarctions produce leg-predominant weakness.

Imaging approach:

DWI/ADC sequences identify acute infarction
FLAIR hyperintensity appears after 6-8 hours
Vascular imaging (MR angiography or CT angiography) identifies proximal occlusions
Perfusion imaging (CT perfusion or MR perfusion) delineates penumbra in candidates for thrombectomy beyond conventional time windows

Oyster #1: Watershed infarctions at the border zones between ACA-MCA or MCA-posterior cerebral artery (PCA) territories produce distinctive patterns on imaging. The "man-in-a-barrel" syndrome (bilateral proximal arm weakness) results from bilateral watershed infarctions following severe hypotension, appearing as bilateral parasagittal hyperintensities on FLAIR/DWI.

Subcortical Hemiplegia

Lacunar infarctions in the internal capsule, corona radiata, or basis pontis produce pure motor hemiplegia without cortical signs (aphasia, neglect, visual field defects).

Imaging characteristics:

Small (<15mm) lesions in typical locations
T2/FLAIR hyperintense
DWI hyperintense in acute phase
May be associated with chronic small vessel disease (white matter hyperintensities, old lacunes, microbleeds)

Pearl #3: The absence of cortical signs with complete hemiplegia strongly suggests a subcortical lesion. If MRI shows a negative DWI in this context, consider repeat imaging at 24-48 hours—small brainstem infarcts occasionally show delayed appearance on DWI.

Brainstem Hemiplegia: Crossed Syndromes

Brainstem lesions produce alternating or crossed hemiplegia—ipsilateral cranial nerve palsies with contralateral motor deficits. These clinicoanatomical syndromes require precise imaging localization.

Medial Medullary Syndrome

Occlusion of the anterior spinal artery or vertebral artery branches affects the medullary pyramid, medial lemniscus, and hypoglossal nucleus, causing contralateral hemiplegia, contralateral proprioceptive loss, and ipsilateral tongue deviation.

Imaging: DWI shows hyperintensity in the medial medulla, often triangular in axial sections. Vascular imaging may demonstrate vertebral artery dissection or occlusion.

Weber Syndrome (Medial Midbrain)

Infarction of the cerebral peduncle and oculomotor nerve fascicles produces contralateral hemiplegia with ipsilateral oculomotor palsy.

Imaging: DWI hyperintensity in the ventral midbrain, involving cerebral peduncle. Consider basilar artery branch occlusion or top-of-the-basilar embolism.

Hack #2: When evaluating brainstem stroke, always obtain both axial and sagittal T2/FLAIR sequences. The serpentine course of vertebrobasilar arteries means that axial-only imaging may miss critical vascular pathology.

Hemiplegia Cruciata

This rare syndrome involves ipsilateral arm and contralateral leg weakness (or vice versa), resulting from lesions at the cervicomedullary junction affecting decussating pyramidal tract fibers.

Pathophysiology: Arm fibers decussate rostral to leg fibers in the lower medulla. A strategically placed lesion can interrupt crossed arm fibers while sparing ipsilateral descending leg fibers, or vice versa.

Imaging findings:

DWI hyperintensity at the cervicomedullary junction
Often small (<1cm) lesions
May involve the pyramidal decussation specifically
Etiologies include demyelination, small vessel disease, or vertebral artery dissection

Oyster #2: Hemiplegia cruciata is frequently misdiagnosed initially due to its counterintuitive presentation. The imaging clue is finding a lesion exactly at the pyramidal decussation level—if the clinical presentation doesn't match a single-level lesion elsewhere, think cruciata.

Double Hemiplegia

Bilateral hemiplegia (quadriplegia or tetraplegia) indicates bilateral involvement of motor pathways and suggests severe, often catastrophic pathology.

Supratentorial Causes

Parasagittal bilateral lesions: Falx meningiomas, parasagittal venous thrombosis, or bilateral ACA infarctions produce bilateral leg-predominant weakness.

Imaging approach:

Venography (MRV or CTV) for superior sagittal sinus thrombosis
FLAIR sequences show parasagittal hyperintensities
Contrast enhancement may reveal dural-based masses

Bilateral internal capsule lesions: Uncommon but seen in top-of-the-basilar syndrome, central pontine myelinolysis, or bilateral small vessel disease.

Brainstem Causes

Basilar artery occlusion: Bilateral pontine infarction produces quadriplegia, pseudobulbar palsy, and locked-in syndrome.

Imaging characteristics:

Extensive bilateral pontine DWI hyperintensity
Basilar artery occlusion on vascular imaging
"Owl's eyes" appearance in axial sections with bilateral tegmental involvement

Central pontine myelinolysis: Subacute quadriplegia following rapid sodium correction shows characteristic T2/FLAIR hyperintensity in the central pons, sparing the periphery ("trident sign" on axial images).

Pearl #4: In suspected basilar thrombosis, perform immediate vascular imaging. Posterior circulation strokes are frequently missed on initial CT—if clinical suspicion is high, proceed directly to MRI/MRA or CT angiography.

Spinal Cord Causes

High cervical cord lesions (above C5) produce quadriplegia. Distinguishing spinal from cerebral pathology relies on associated findings:

Sensory level
Bladder/bowel dysfunction
Absence of cortical or cranial nerve signs
Preserved consciousness

Imaging protocol: Sagittal T2, T1, STIR (short tau inversion recovery), and post-contrast T1 sequences of the cervical spine.

Common pathologies:

Acute transverse myelitis: T2 hyperintensity extending over multiple segments, often with enhancement
Spinal cord infarction: "Owl's eyes" or "snake eyes" appearance (bilateral anterior horn hyperintensity) on axial T2
Epidural abscess or hematoma: Extra-axial fluid collection with cord compression
Demyelinating disease: Focal T2 hyperintensity, typically <2 vertebral segments

Hack #3: Spinal cord stroke is often misdiagnosed as Guillain-Barré syndrome. Key distinguishing feature: upper motor neuron signs (spasticity, hyperreflexia, Babinski sign) indicate cord pathology, while areflexia suggests peripheral nerve pathology. MRI clinches the diagnosis.

Crural Hemiplegia

Isolated leg weakness (crural monoplegia or predominant leg involvement) localizes to the paracentral lobule (medial motor cortex) supplied by the ACA.

Imaging findings:

Medial frontal lobe infarction on DWI
May extend into supplementary motor area
ACA territory involvement on vascular imaging
Consider cardiac source of embolism (ACA territory strokes are more commonly embolic)

Pearl #5: Pure crural monoplegia without arm involvement is rare and should prompt consideration of focal cortical pathology. If imaging is negative for infarction, consider focal seizures (Todd's paralysis), cortical dysplasia, or low-grade gliomas.

Pediatric Considerations

Hemiplegic cerebral palsy in children requires different imaging approaches:

Term neonates: Hypoxic-ischemic injury, MCA stroke, venous thrombosis
Preterm infants: Periventricular leukomalacia, germinal matrix hemorrhage
Chronic imaging: Volume loss, gliosis, ex vacuo ventricular dilatation

Imaging protocol: T1, T2, FLAIR, DWI, and SWI sequences. Consider MR spectroscopy in metabolic disorders.

Advanced Imaging Techniques

Diffusion Tensor Imaging (DTI)

Tractography visualizes white matter tracts, assessing corticospinal tract integrity. Fractional anisotropy (FA) values decrease in damaged tracts, correlating with motor recovery potential.

Clinical application: Predicting motor recovery after stroke. Preserved FA values in the affected hemisphere predict better outcomes.

Functional MRI (fMRI)

Blood oxygen level-dependent (BOLD) imaging identifies motor cortex reorganization following injury. Task-based or resting-state fMRI maps functional connectivity.

Pearl #6: Cortical reorganization following stroke can involve ipsilateral motor areas, contralesional hemisphere recruitment, or unmasking of latent pathways. This plasticity underlies rehabilitation potential.

Perfusion Imaging

CT perfusion or MR perfusion (dynamic susceptibility contrast or arterial spin labeling) quantifies cerebral blood flow, helping identify salvageable tissue.

Parameters:

Cerebral blood flow (CBF): Reduced in ischemia
Cerebral blood volume (CBV): May be preserved by collaterals
Mean transit time (MTT): Prolonged in hypoperfusion
Time to peak (TTP): Delayed in ischemia

Penumbra = Diffusion-perfusion mismatch (normal DWI, abnormal perfusion)

Mimics and Diagnostic Pitfalls

Stroke Mimics Producing Hemiplegia

Todd's paralysis: Post-ictal weakness following focal seizures. Imaging may show transient cortical edema/FLAIR hyperintensity, gyral enhancement, and restricted diffusion that reverses.
Hemiplegic migraine: Transient hemiplegia during migraine attacks. Diagnosis of exclusion; imaging typically normal.
Hypoglycemia: Can produce focal deficits. Check glucose; may show posterior circulation FLAIR hyperintensities.
Conversion disorder: Inconsistent examination findings, absence of upper motor neuron signs, normal imaging.

Oyster #3: Always check glucose in acute hemiplegia before assuming stroke. Hypoglycemia produces focal deficits in 20% of cases and is immediately reversible with treatment.

Prognostic Imaging Markers

Several imaging features predict functional outcomes:

Lesion volume: Larger infarcts predict worse outcomes
Corticospinal tract involvement: Complete disruption portends poor motor recovery
Hemorrhagic transformation: Associated with worse outcomes; detected on GRE/SWI
Collateral circulation: Robust leptomeningeal collaterals predict smaller final infarct volumes
White matter disease burden: Extensive leukoaraiosis predicts poor functional outcomes independent of acute stroke size

Practical Imaging Algorithms

Acute Setting (<6 hours)

Non-contrast CT (exclude hemorrhage)
CT angiography (identify large vessel occlusion)
CT perfusion (optional, assess penumbra)
If CT negative and high suspicion: Emergency MRI with DWI

Subacute Evaluation

MRI brain with DWI, FLAIR, T2, GRE/SWI, T1 post-contrast
MR angiography (circle of Willis, neck vessels)
Consider echocardiography, Holter monitoring for embolic sources

Atypical Presentations

Cervical spine MRI (suspected myelopathy)
Venography (suspected thrombosis)
Contrast-enhanced imaging (inflammatory, infectious, neoplastic etiologies)
Advanced sequences (MR spectroscopy for metabolic disorders, PET for vasculitis)

Conclusion

Neuroimaging has transformed the evaluation of hemiplegia from purely clinical localization to precise anatomical correlation. Understanding the imaging patterns of various hemiplegic subtypes—from classic presentations to rare variants like hemiplegia cruciata—enables accurate diagnosis and guides management. The modern internist must be fluent in selecting appropriate imaging modalities, recognizing characteristic patterns, avoiding mimics, and integrating imaging findings with clinical context. As imaging technology advances, our ability to predict outcomes, tailor rehabilitation, and understand neuroplasticity will continue to evolve, ultimately improving patient care.

Key Takeaways

DWI-MRI is the gold standard for acute stroke detection
Internal capsule lesions produce disproportionate deficits relative to size
Brainstem lesions cause crossed syndromes requiring precise localization
Hemiplegia cruciata results from cervicomedullary junction pathology
Bilateral hemiplegia suggests catastrophic pathology requiring urgent vascular imaging
Always exclude stroke mimics, particularly hypoglycemia
Multimodal imaging improves diagnostic accuracy and guides therapy

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Final Pearl: The best imaging test is the one that answers your clinical question. Don't order an MRI when CT will suffice, but don't rely on CT when MRI is necessary. Clinical judgment guides imaging selection, and imaging findings must always be interpreted in clinical context.