Sunday, July 13, 2025

Hemiparesis With Normal Brain Imaging

 

Hemiparesis With Normal Brain Imaging: Think Spinal, Think Functional

Dr Neeraj Mnaikath ,claude.ai

Abstract

Hemiparesis with normal brain imaging presents a diagnostic challenge that frequently perplexes clinicians in critical care settings. While cerebral pathology remains the most common cause of acute hemiparesis, a subset of patients presents with convincing neurological deficits despite normal brain computed tomography (CT) and magnetic resonance imaging (MRI). This review explores the differential diagnosis of hemiparesis with normal brain imaging, emphasizing spinal cord pathology, functional neurological disorders, and evolving cerebrovascular events. We provide practical clinical pearls and diagnostic approaches to guide post-graduate trainees in critical care medicine through this challenging clinical scenario.

Keywords: Hemiparesis, spinal cord, functional neurological disorder, cervical myelopathy, cord infarct, conversion disorder

Introduction

The presentation of acute hemiparesis typically triggers an immediate neurological workup focused on cerebral pathology. However, approximately 5-10% of patients presenting with acute hemiparesis demonstrate normal brain imaging, creating a diagnostic dilemma that requires systematic clinical reasoning and expanded differential diagnosis consideration.¹ This clinical scenario demands a paradigm shift from the traditional "brain-first" approach to a more comprehensive evaluation encompassing spinal cord pathology and functional neurological disorders.

The critical care physician must navigate between the urgency of potential treatable conditions and the recognition that not all neurological presentations have structural correlates. This review provides a structured approach to evaluating hemiparesis with normal brain imaging, emphasizing time-sensitive spinal pathology and the increasingly recognized spectrum of functional neurological disorders.

Spinal Cord Pathology: The Hidden Culprit

Cervical Myelopathy

Cervical myelopathy represents one of the most important causes of hemiparesis with normal brain imaging, particularly in elderly patients or those with degenerative cervical spine disease. The pathophysiology involves compression of the cervical spinal cord, most commonly at the C3-C6 levels, leading to upper motor neuron signs that can present as apparent hemiparesis.²

Clinical Presentation Pearls:

  • Asymmetric presentation: Cervical myelopathy often presents with asymmetric weakness, mimicking stroke-like hemiparesis
  • Nurick's sign: Loss of finger dexterity and fine motor control, often preceding gross motor weakness
  • Inverted radial reflex: Flexion of fingers when testing brachioradialis reflex (C5-C6 pathology)
  • Hoffmann's sign: Positive in 80% of cases with cervical myelopathy
  • Spurling's test: Neck extension with lateral flexion reproducing symptoms

Diagnostic Hack:

The "10-second test" - asking patients to rapidly open and close their hands for 10 seconds. Inability to perform this task smoothly suggests cervical myelopathy, even in the absence of obvious weakness.³

Spinal Cord Infarction

Spinal cord infarction, while rare (incidence 1.2 per 100,000), can present as acute hemiparesis, particularly when involving the cervical anterior spinal artery territory. The watershed areas at C1-C3 and T1-T4 are most vulnerable.⁴

Clinical Patterns:

  • Anterior spinal artery syndrome: Bilateral motor weakness with preserved posterior column sensation
  • Unilateral presentation: Can occur with partial anterior spinal artery occlusion
  • Associated features: Neurogenic bladder/bowel dysfunction, sensory level

Oyster Warning:

Unlike cerebral infarction, spinal cord infarction may not show acute changes on MRI for 24-48 hours. Diffusion-weighted imaging (DWI) has limited sensitivity for acute spinal cord ischemia compared to cerebral stroke.⁵

Brown-Séquard Syndrome

Brown-Séquard syndrome results from hemisection of the spinal cord and presents with ipsilateral motor weakness and proprioceptive loss with contralateral pain and temperature sensation loss. Common causes include trauma, tumors, multiple sclerosis, and vascular malformations.

Clinical Recognition:

  • Ipsilateral hemiparesis: Upper motor neuron pattern
  • Ipsilateral loss of vibration and proprioception
  • Contralateral loss of pain and temperature sensation
  • Sensory level: Usually 2-3 dermatomes below the lesion

Functional Neurological Disorders

Functional Hemiparesis

Functional neurological disorders (FND), previously termed conversion disorders, account for approximately 16% of neurological consultations and represent the second most common cause of neurological disability after stroke.⁶ Functional hemiparesis can present convincingly and requires careful clinical assessment.

Positive Clinical Signs:

  • Hoover's sign: Absence of involuntary hip extension when testing contralateral hip flexion
  • Collapsing weakness: Give-way weakness with inconsistent effort
  • Dragging gait: Affected leg dragged behind rather than circumducted
  • Tremor entrainment: Functional tremor changes frequency with voluntary movement of unaffected limb

Diagnostic Pearls:

  • Incongruent examination: Weakness that doesn't follow anatomical patterns
  • Distractibility: Improvement in function when attention is diverted
  • Inconsistency: Variability in weakness during the same examination

Conversion Disorder vs. Malingering

Distinguishing between conversion disorder and malingering requires careful clinical assessment. Conversion disorder involves unconscious symptom production without intentional deception, while malingering involves conscious symptom fabrication for external gain.

Clinical Differentiators:

  • Onset: Conversion disorder often follows psychological stressors
  • La belle indifférence: Inappropriate lack of concern about symptoms (present in only 20% of cases)
  • Consistency: Functional symptoms may be inconsistent but not deliberately varied
  • Response to suggestion: Functional symptoms may improve with therapeutic suggestion

Evolving Cerebrovascular Events

Transient Ischemic Attacks (TIA)

TIA can present as fluctuating hemiparesis with normal brain imaging, particularly in the hyperacute phase. The ABCD² score helps stratify stroke risk, but normal imaging doesn't exclude high-risk TIA.⁷

Clinical Considerations:

  • Timing: Symptoms may resolve before imaging
  • Microemboli: Small emboli may not be visible on standard imaging
  • Perfusion deficits: May exist without structural changes
  • Recurrence risk: High in first 48 hours despite normal imaging

Migraine with Aura

Hemiplegic migraine can present as acute hemiparesis and may be difficult to distinguish from stroke. The International Headache Society criteria require complete reversibility of motor symptoms.⁸

Clinical Features:

  • Familial vs. sporadic: Genetic forms (CACNA1A, ATP1A2, SCN1A mutations)
  • Aura progression: Symptoms typically develop over 5-20 minutes
  • Recovery: Complete resolution within 24 hours
  • Associated symptoms: Visual aura, sensory symptoms, aphasia

Urgent Spinal Imaging Indications

When to Image the Spine Urgently

The decision to obtain urgent spinal imaging in patients with hemiparesis requires careful clinical judgment. The following clinical scenarios warrant urgent spinal MRI:

Absolute Indications:

  1. Sensory level: Clear dermatomal sensory loss
  2. Neurogenic bladder/bowel: Urinary retention or incontinence
  3. Bilateral motor signs: Even if asymmetric
  4. Neck pain with neurological deficit: Especially in trauma or cancer patients
  5. Progressive weakness: Despite normal brain imaging

Relative Indications:

  1. Isolated hemiparesis: In elderly patients with cervical spondylosis
  2. Atypical presentation: Symptoms not fitting vascular territories
  3. Risk factors: History of malignancy, anticoagulation, or recent spinal procedures
  4. Clinical deterioration: Worsening despite normal brain imaging

Imaging Protocols

Spinal MRI Sequences:

  • T1-weighted: Anatomical detail, hemorrhage detection
  • T2-weighted: Edema, myelomalacia, CSF evaluation
  • STIR (Short-TI Inversion Recovery): Sensitive for cord edema
  • DWI: Limited utility for spinal cord ischemia but may show acute changes

Timing Considerations:

  • Acute presentation: Within 6 hours if suspecting cord compression
  • Subacute: Within 24 hours for progressive symptoms
  • Chronic: Elective imaging for stable symptoms

Clinical Approach and Decision-Making

Systematic Evaluation Framework

Initial Assessment:

  1. Detailed history: Onset, progression, associated symptoms
  2. Neurological examination: Pattern recognition, inconsistencies
  3. Risk factor assessment: Vascular, traumatic, malignancy, psychological
  4. Medication review: Anticoagulation, recent procedures

Diagnostic Workup:

  1. Brain imaging: CT/MRI with DWI and perfusion if indicated
  2. Vascular imaging: CTA/MRA if vascular cause suspected
  3. Spinal imaging: Based on clinical indications outlined above
  4. Laboratory studies: Inflammatory markers, vitamin B12, syphilis serology

Treatment Considerations

Acute Management:

  • Airway protection: If bulbar involvement suspected
  • Hemodynamic monitoring: Spinal shock in cord injury
  • Corticosteroids: Controversial in acute spinal cord injury
  • Anticoagulation: Contraindicated in hemorrhagic cord lesions

Specific Interventions:

  • Surgical decompression: Emergent for cord compression
  • Thrombolysis: Not indicated for spinal cord infarction
  • Multidisciplinary approach: Neurology, neurosurgery, psychiatry for FND

Pearls and Oysters

Clinical Pearls:

  1. Pattern recognition: Functional hemiparesis often violates anatomical boundaries
  2. Timing: Spinal cord symptoms may fluctuate with position or activity
  3. Associated symptoms: Bowel/bladder dysfunction strongly suggests spinal pathology
  4. Examination consistency: Repeat examinations may reveal inconsistencies in functional disorders

Oysters (Pitfalls):

  1. Normal MRI: Doesn't exclude spinal cord pathology in hyperacute phase
  2. Functional doesn't mean feigned: Avoid dismissive attitudes toward FND
  3. Coexisting pathology: Functional symptoms can overlay organic disease
  4. Time sensitivity: Delayed spinal decompression can result in permanent disability

Diagnostic Hacks:

  1. Pronator drift test: Perform with eyes closed; functional weakness often improves
  2. Heel-to-shin test: Difficult to fake; preserved in functional hemiparesis
  3. Tandem gait: Often preserved in functional disorders
  4. Distraction techniques: Improvement during distraction suggests functional etiology

Prognosis and Outcomes

Spinal Pathology:

  • Cervical myelopathy: Surgery within 6 months optimizes outcomes
  • Cord infarction: Variable recovery; complete lesions have poor prognosis
  • Traumatic cord injury: ASIA scale predicts functional recovery

Functional Disorders:

  • Early diagnosis: Improves outcomes and prevents chronicity
  • Multidisciplinary care: Neurology, psychiatry, and rehabilitation
  • Patient education: Understanding diagnosis reduces healthcare utilization

Future Directions

Advances in neuroimaging, including high-resolution spinal MRI and functional connectivity studies, may improve diagnostic accuracy. The development of biomarkers for functional neurological disorders remains an active area of research. Artificial intelligence applications in pattern recognition may assist in differentiating functional from organic presentations.

Conclusion

Hemiparesis with normal brain imaging requires a systematic approach that extends beyond traditional cerebrovascular evaluation. Spinal cord pathology, particularly cervical myelopathy and cord infarction, represents treatable causes that demand urgent recognition. Functional neurological disorders, while lacking structural correlates, require careful diagnosis and appropriate management to prevent chronicity and disability.

The critical care physician must maintain clinical vigilance for time-sensitive spinal pathology while developing competency in recognizing functional presentations. A collaborative approach involving neurology, neurosurgery, and psychiatry services optimizes patient outcomes in this challenging clinical scenario.

The key to successful management lies in systematic evaluation, appropriate imaging utilization, and avoiding both overinvestigation and premature diagnostic closure. As our understanding of functional neurological disorders evolves, the integration of positive diagnostic criteria with traditional exclusionary approaches will continue to improve patient care and outcomes.


References

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  2. Kalsi-Ryan S, Karadimas SK, Fehlings MG. Cervical spondylotic myelopathy: the clinical phenomenon and the current pathobiology of an increasingly prevalent and devastating disorder. Neuroscientist. 2013;19(4):409-421.

  3. Ono K, Ebara S, Fuji T, et al. Myelopathy hand. New clinical signs of cervical spinal cord damage. J Bone Joint Surg Br. 1987;69(2):215-219.

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  6. Stone J, Carson A, Duncan R, et al. Symptoms 'unexplained by organic disease' in 1144 new neurology out-patients: how often does the diagnosis change at follow-up? Brain. 2009;132(10):2878-2888.

  7. Johnston SC, Rothwell PM, Nguyen-Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007;369(9558):283-292.

  8. Headache Classification Committee of the International Headache Society. The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018;38(1):1-211.

  9. Espay AJ, Aybek S, Carson A, et al. Current concepts in diagnosis and treatment of functional neurological disorders. JAMA Neurol. 2018;75(9):1132-1141.

  10. Fehlings MG, Wilson JR, Kopjar B, et al. Efficacy and safety of surgical decompression in patients with cervical spondylotic myelopathy: results of the AOSpine North America prospective multi-center study. J Bone Joint Surg Am. 2013;95(18):1651-1658.

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