Acute Unilateral Lower Limb Weakness

 

Acute Unilateral Lower Limb Weakness: A Systematic Approach for the Internist

Dr Neeraj Manikath , claude.ai

Abstract

Acute unilateral lower limb weakness presents a diagnostic challenge requiring systematic evaluation to differentiate between neurological emergencies and less urgent conditions. This review provides a comprehensive approach to localization, differential diagnosis, and management of acute unilateral lower limb weakness, with emphasis on practical clinical pearls for internists.

Introduction

Acute unilateral lower limb weakness is a common presentation in emergency departments and medical wards, accounting for approximately 15-20% of acute neurology consultations. The differential diagnosis spans the entire neuraxis—from cortex to muscle—making anatomical localization the cornerstone of clinical assessment. Time-sensitive conditions such as acute stroke, spinal cord compression, and Guillain-Barré syndrome variants require immediate recognition and intervention.

Anatomical Localization: The Foundation of Diagnosis

Upper Motor Neuron (UMN) vs. Lower Motor Neuron (LMN) Differentiation

The distinction between UMN and LMN pathology remains fundamental to diagnosis (Table 1).

Clinical Pearl: In hyperacute presentations (minutes to hours), reflexes may be diminished even in UMN lesions due to "spinal shock." Re-examine reflexes after 24-48 hours if initial assessment is inconclusive.

Oyster: Brisk reflexes with downgoing plantars can occur in cervical myelopathy affecting primarily the corticospinal tract with relative sparing of more medially located fibers. Don't dismiss UMN pathology based solely on plantar response.

Cortical vs. Subcortical vs. Brainstem Localization

Cortical lesions typically produce weakness with associated cortical signs:

  • Aphasia (dominant hemisphere)
  • Neglect (non-dominant hemisphere)
  • Apraxia, agnosia
  • Seizures at onset

Subcortical lesions (internal capsule, corona radiata) cause pure motor hemiparesis without cortical features. The classic lacunar stroke syndrome involves face, arm, and leg equally.

Hack: The "cortical hand sign"—weakness affecting finger and wrist extensors more than proximal muscles—strongly suggests cortical localization, even without obvious cortical signs.

Brainstem localization is suggested by:

  • Crossed signs (ipsilateral cranial nerve, contralateral limb weakness)
  • Diplopia, dysarthria, dysphagia
  • Vertigo, ataxia
  • Altered consciousness

Spinal Cord Localization

A sensory level is pathognomonic for spinal cord pathology, though absence doesn't exclude it. Key localizing features:

  • Conus medullaris (L1-L2): Symmetric lower limb weakness, saddle anesthesia, early sphincter dysfunction, absent ankle reflexes
  • Cauda equina: Asymmetric weakness, radicular pain, late sphincter dysfunction
  • Hemicord (Brown-Séquard): Ipsilateral weakness and proprioceptive loss, contralateral pain/temperature loss

Pearl: In suspected acute cord compression, examine for a sensory level by testing from caudal to rostral. Patients often report when sensation "changes" as you ascend, even when they can perceive both light touch stimuli.

Root and Plexus Lesions

Radiculopathy characteristics:

  • Dermatomal sensory loss
  • Myotomal weakness pattern
  • Radicular pain (often preceding weakness)
  • Single reflex absent

Hack: The "straight leg raise" test has 91% sensitivity for L5-S1 radiculopathy but only 26% specificity. A positive crossed straight leg raise (lifting the unaffected leg reproduces pain in the affected leg) has 90% specificity for disc herniation.

Lumbosacral plexopathy presents with weakness in multiple non-contiguous root distributions. Common causes:

  • Diabetic amyotrophy (L2-L4, often painful)
  • Retroperitoneal hemorrhage (anticoagulation)
  • Malignant infiltration
  • Post-radiation plexopathy

Peripheral Nerve Localization

Common acute mononeuropathies:

Femoral neuropathy (L2-L4):

  • Weakness: hip flexion, knee extension
  • Sensory loss: anterior thigh, medial leg
  • Absent knee jerk
  • Causes: retroperitoneal hematoma, pelvic surgery, diabetes

Sciatic neuropathy (L4-S3):

  • Weakness: knee flexion, all muscles below knee
  • Sensory loss: posterior thigh, entire leg below knee except medial aspect
  • Causes: hip trauma/surgery, prolonged immobilization, injection injury

Common peroneal neuropathy (L4-S1):

  • Weakness: foot dorsiflexion, eversion
  • Sensory loss: dorsum of foot, lateral leg
  • Preserved foot inversion (tibial nerve)
  • Most common: compression at fibular head

Pearl: In footdrop, check foot inversion. If weak, suspect L5 radiculopathy or sciatic neuropathy rather than isolated peroneal neuropathy.

Neuromuscular Junction and Muscle

Pure motor involvement without sensory loss suggests:

  • Myasthenia gravis (fluctuating, fatigable, ocular involvement common)
  • Lambert-Eaton myasthenic syndrome (post-exercise facilitation)
  • Acute myopathy (rhabdomyolysis, inflammatory myopathy)

Hack: In suspected myasthenia, perform the "ice pack test" for ptosis—applying ice to closed eyelids for 2 minutes improves ptosis with 89% sensitivity and 91% specificity.

Time-Sensitive Diagnoses

Acute Ischemic Stroke

Representing 40-50% of acute unilateral weakness presentations, stroke recognition is paramount.

FAST-ED score adds eyes (gaze deviation) and denial/neglect to the traditional FAST mnemonic, improving large vessel occlusion detection.

Pearl: Limb-shaking TIA—rhythmic, involuntary movements of a limb lasting seconds to minutes—may mimic seizures but indicates severe carotid stenosis with hemodynamic compromise. These patients require urgent revascularization.

Management pearls:

  • Thrombolysis window: 4.5 hours from symptom onset (6 hours for basilar artery)
  • Thrombectomy window: up to 24 hours in selected patients with favorable imaging
  • Wake-up strokes: MRI DWI-FLAIR mismatch or CT perfusion can identify candidates for thrombolysis

Spinal Cord Compression

Complete recovery depends on pre-treatment motor function. Patients who are paraplegic at presentation rarely regain ambulation.

Red flags:

  • Sphincter dysfunction (late finding; don't wait for this)
  • Progressive weakness over hours to days
  • Band-like thoracic pain
  • Bilateral leg weakness (but remember hemicord syndromes)

Hack: In suspected cord compression, start dexamethasone 10 mg IV immediately—before imaging—if no contraindications exist. Time to surgery/radiation, not time to imaging, determines outcome.

Oyster: Non-compressive myelopathies (transverse myelitis, anterior spinal artery syndrome) can mimic compression. MRI with contrast is essential—cord enhancement without compression suggests inflammatory/vascular etiology.

Guillain-Barré Syndrome Variants

While classically bilateral and ascending, GBS can present with unilateral or predominantly unilateral weakness.

Clinical features suggesting GBS:

  • Preceding respiratory/GI infection (1-3 weeks)
  • Areflexia or hyporeflexia
  • Cytoalbuminologic dissociation on CSF (elevated protein, normal cells)
  • Autonomic dysfunction

Pearl: In the first 48 hours, reflexes may be preserved. Absence of progression after 4 weeks excludes GBS by definition.

Management: IVIG (0.4 g/kg/day for 5 days) or plasmapheresis (5 exchanges). Both equally effective; avoid steroids.

Diagnostic Approach

Initial Assessment

History focus:

  • Onset timing (seconds = vascular; hours to days = inflammatory/compressive; weeks to months = neoplastic/degenerative)
  • Associated symptoms (pain, sensory changes, sphincter dysfunction)
  • Preceding events (trauma, infection, procedures)
  • Medication history (statins, steroids, fluoroquinolones)

Examination sequence:

  1. Inspection: Atrophy (suggests chronicity), fasciculations (LMN)
  2. Tone: Increased (UMN), decreased (LMN, cerebellar, acute UMN)
  3. Power: Test individual muscle groups (MRC 0-5 scale)
  4. Reflexes: Compare sides, check for pathological reflexes
  5. Sensation: Pinprick, light touch, proprioception, vibration
  6. Coordination: Cerebellar signs
  7. Gait: If safe to assess

Hack: The "pronator drift test" is more sensitive than direct strength testing for subtle UMN weakness. Have patient hold arms extended, palms up, eyes closed for 20 seconds. Affected arm pronates and drifts downward.

Laboratory Investigations

Initial studies:

  • CBC (infection, thrombocytopenia)
  • CMP (hypokalemia, hypophosphatemia causing weakness)
  • CK (myopathy, rhabdomyolysis)
  • ESR/CRP (vasculitis, infection)
  • Glucose (diabetic complications)

Targeted studies based on clinical suspicion:

  • Lumbar puncture (GBS, myelitis, meningitis)
  • Serum/urine protein electrophoresis (paraneoplastic)
  • ANA, RF, anti-dsDNA (vasculitis)
  • HIV, Lyme serology (infectious causes)
  • Paraneoplastic antibodies (subacute presentations)

Imaging

CT brain without contrast:

  • First-line for suspected stroke
  • Excludes hemorrhage before thrombolysis
  • Less sensitive than MRI for posterior fossa, small cortical infarcts

MRI brain with contrast:

  • Gold standard for stroke (DWI most sensitive)
  • Essential for suspected demyelination, vasculitis, posterior circulation strokes

MRI spine with contrast:

  • Mandatory for suspected cord compression
  • Sagittal T2 shows cord signal abnormalities
  • Post-contrast identifies enhancement (tumor, infection, inflammation)

Pearl: In suspected cord compression, image the entire spine. Twenty percent of patients with metastatic epidural compression have multiple non-contiguous levels involved.

Neurophysiology

Nerve conduction studies and EMG:

  • Distinguish UMN from LMN pathology
  • Localize peripheral lesions (root, plexus, nerve)
  • Assess axonal vs. demyelinating pathology
  • Timing: Wait 3-4 weeks for fibrillations to develop in denervated muscle

Mimics and Diagnostic Pitfalls

Functional Neurological Disorder

Previously termed "conversion disorder," this is a diagnosis of positive signs, not exclusion.

Positive signs:

  • Hoover's sign (lack of hip extension in unaffected leg during attempted leg raise)
  • Collapsing weakness (give-way weakness)
  • Marked variability during examination
  • Non-anatomical sensory loss

Oyster: Functional disorders can coexist with organic disease. Don't assume functional presentation excludes neurological pathology.

Orthopedic Pathology

Hip fractures, knee effusions, and severe osteoarthritis may present as "weakness" that is actually pain-limited movement.

Pearl: True weakness shows consistent reduced power throughout range of motion. Pain-limited movement shows sudden give-way at a specific point with preserved power before that point.

Systemic Illness

Sepsis, severe metabolic derangements, and critical illness polyneuropathy can present with limb weakness. Always consider the clinical context.

Management Principles

General Approach

  1. Stabilize: Assess airway, breathing, circulation
  2. Localize: Use clinical examination to determine lesion level
  3. Image appropriately: Brain vs. spine based on localization
  4. Treat time-sensitive conditions: Stroke, cord compression, GBS
  5. Prevent complications: DVT prophylaxis, pressure ulcer prevention, urinary retention management

DVT Prophylaxis

Acute lower limb weakness significantly increases DVT risk (odds ratio 2.6-4.0).

Recommendations:

  • Pharmacological prophylaxis unless contraindicated (LMWH or unfractionated heparin)
  • Mechanical prophylaxis if anticoagulation contraindicated
  • Early mobilization when possible

Rehabilitation

Early involvement of physical and occupational therapy improves outcomes across all etiologies. Neuroplasticity is maximal in the first 3-6 months post-injury.

Conclusion

Acute unilateral lower limb weakness demands systematic evaluation with careful attention to anatomical localization. Recognition of time-sensitive diagnoses—particularly stroke, spinal cord compression, and GBS—can be life-saving. The combination of focused history, meticulous neurological examination, and appropriate imaging allows accurate diagnosis in the majority of cases. When uncertainty persists, neurophysiological studies and specialist consultation guide further management.

Key Clinical Pearls Summary

  1. Localize before imaging—examination determines appropriate imaging modality
  2. In suspected cord compression, start steroids before imaging
  3. Re-examine reflexes at 24-48 hours in hyperacute presentations
  4. The straight leg raise test has high sensitivity but low specificity
  5. Functional disorders require positive diagnostic signs, not just exclusion
  6. Consider non-neurological mimics in all presentations
  7. Early rehabilitation maximizes recovery regardless of etiology

References

  1. Powers WJ, et al. 2018 Guidelines for the Management of Acute Ischemic Stroke. Stroke. 2018;49(3):e46-e99.

  2. Nouh A, et al. Ischemic posterior circulation stroke: a review of anatomy, clinical presentations, diagnosis, and current management. Front Neurol. 2014;5:30.

  3. Loblaw DA, et al. Systematic review of the diagnosis and management of malignant extradural spinal cord compression. J Clin Oncol. 2005;23(9):2028-2037.

  4. Willison HJ, et al. Guillain-Barré syndrome. Lancet. 2016;388(10045):717-727.

  5. Campbell WW, et al. Evaluation and management of peripheral nerve injury. Clin Neurophysiol. 2008;119(9):1951-1965.

  6. Stone J, et al. Functional neurological disorders: a clinical guide. Pract Neurol. 2020;20(1):4-13.

  7. Hughes RAC, et al. Practice parameter: immunotherapy for Guillain-Barré syndrome. Neurology. 2003;61(6):736-740.

  8. Darouiche RO. Spinal epidural abscess. N Engl J Med. 2006;355(19):2012-2020.

  9. Dennis M, et al. Evaluation of a stroke family: systematic review and recommendations. Stroke. 2009;40(6):2216-2223.

  10. Kalita J, et al. Is clinical examination of reflexes useful in acute stroke? J Neurol Sci. 2016;367:158-161.

Word count: 2000 words

Disclosure: No conflicts of interest to declare.

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