What is the most likely cause of new left‑sided sensory changes and how should it be evaluated and managed?

Acute Left-Sided Sensory Changes: Stroke Until Proven Otherwise

New-onset left-sided sensory changes demand immediate evaluation for right hemisphere stroke, particularly involving the right middle cerebral artery (MCA) or thalamic territory, and require urgent neuroimaging within 25 minutes of presentation. 1, 2

Immediate Clinical Assessment

The presentation of left-sided sensory changes most likely represents:

• Right MCA territory infarction causing contralateral hemisensory loss affecting the left face, arm, and potentially leg, with sensory deficits following the same distribution as motor weakness (face and arm > leg) 1
• Right thalamic stroke (posterolateral nucleus ventrocaudalis region) presenting as pure sensory stroke with loss of all sensory modalities in a faciobrachiocrural distribution 3, 4
• Right internal capsule/corona radiata lesion which can produce cortical-type sensory loss despite being subcortical, due to cerebral diaschisis 5

Critical Associated Features to Assess

Look specifically for these accompanying deficits that localize the lesion:

• Left-sided motor weakness (hemiparesis affecting face and arm more than leg suggests right MCA territory) 1
• Left homonymous hemianopia (confirms cortical involvement and right MCA/optic radiation damage) 1
• Left-sided neglect and visuospatial deficits (indicates right hemisphere cortical involvement) 1, 2
• Cortical sensory signs: loss of graphesthesia, stereognosis, two-point discrimination, or position sense (suggests parietal cortex involvement) 6, 4
• Dissociated sensory loss (spinothalamic vs. dorsal column modalities affected differently suggests specific tract involvement) 3, 4

Diagnostic Workup Algorithm

Immediate Imaging (Within 25 Minutes)

1. Non-contrast head CT first to exclude hemorrhage and identify large territory infarction 2

   • Look for hyperdense MCA sign (thrombus in proximal MCA) 1
   • Loss of gray-white differentiation in cortical ribbon (detectable in 82% within 6 hours) 1
   • Early infarct signs involving >1/3 MCA territory predict hemorrhagic transformation risk 1

2. CT angiography from aortic arch to vertex to assess extracranial and intracranial vasculature 2

   • Essential to identify large vessel occlusion amenable to thrombectomy 2

3. CT or MR venography if any suspicion for cerebral venous thrombosis (especially if preceded by weeks of headache) 2

Preferred Advanced Imaging

• Brain MRI with and without contrast provides superior detection of small ischemic lesions, particularly in thalamus, internal capsule, corona radiata, and pons 2, 4
• MRI is critical for identifying very small lacunes (<5mm) that may be missed on CT but cause pure sensory syndromes 3, 4

Anatomical Localization by Sensory Pattern

Pattern 1: All Sensory Modalities Lost (Touch, Pain, Temperature, Vibration, Proprioception)

• Posterolateral thalamus (nucleus ventrocaudalis) with relatively large lacune or hemorrhage 3, 4
• Right parietal operculum and posterior insula with underlying white matter (pseudothalamic sensory syndrome) 6
• Distribution: typically faciobrachiocrural 3

Pattern 2: Isolated Loss of Discriminative Sensation (Stereognosis, Graphesthesia, Position Sense)

• Superior-posterior parietal cortex (cortical sensory syndrome) 6
• Posterolateral nucleus ventrocaudalis when only position sense affected 3
• Distribution: may involve only one or two body parts 6

Pattern 3: Dissociated Sensory Loss (Spinothalamic vs. Dorsal Column)

• Lenticulocapsular region or corona radiata (spinothalamic tract involvement) 4
• Pontine tegmentum (medial lemniscal type deficit) 4
• Inferolateral thalamus (thalamogeniculate arteries) 3

Critical Pitfalls to Avoid

Do Not Assume Benign Etiology

• Never dismiss persistent focal sensory deficits as migraine or peripheral neuropathy without definitive exclusion of stroke 2
• Approximately 19% of cortical strokes lack overt cortical signs initially—sensory changes may be the only manifestation 1

Do Not Delay Imaging

• Any new neurological deficit requires immediate neuroimaging regardless of symptom severity 2
• Time-sensitive interventions (thrombolysis, thrombectomy) depend on rapid diagnosis 1, 2

Recognize Subcortical Lesions Can Mimic Cortical Syndromes

• Internal capsule and corona radiata lesions can produce "cortical" sensory loss (graphanesthesia, impaired two-point discrimination) due to cerebral diaschisis affecting perfusion in distant cortical regions 5
• This resolves as regional cerebral blood flow improves, typically by 4 weeks 5

Pain and Dysesthesia Development

Monitor for delayed central post-stroke pain:

• Develops in patients with nucleus ventrocaudalis involvement (often with nucleus ventro-oralis intermedius damage) 3
• Time lag: 2-15 days post-stroke (mean 10.5 days) 3
• Initial paresthesias present in 72% of thalamic stroke patients with ventrocaudalis involvement 3

Prognosis and Recovery

• Contralateral (left) somatosensory cortex undergoes neuronal circuit remodeling to compensate for right hemisphere damage 7
• Synaptic spine turnover increases at 1 week, with new sensory processing circuits established by 4 weeks 7
• Recovery correlates with improvement in regional cerebral blood flow and normalization of somatosensory evoked potentials 5