Hemianesthesia

Hemianesthesia
Other names	Hemianaesthesia; hemisensory loss
Specialty	Neurology
Symptoms	Loss or marked reduction of somatic sensation on one side of the body
Complications	Central post-stroke pain
Causes	Stroke (especially thalamic), lesions of the parietal cortex or internal capsule, Brainstem or spinal cord disorders (e.g., Brown–Séquard syndrome), Functional neurological disorder
Differential diagnosis	Hemispatial neglect, Hemiplegia, Peripheral neuropathy, Brown–Séquard syndrome

Hemianesthesia (also spelled hemianaesthesia) is a neurological sign consisting of loss or marked impairment of somatic sensation (e.g., touch, pain, temperature, vibration, proprioception) on one side of the body.^[1] It most commonly follows lesions that interrupt thalamocortical sensory pathways, particularly the ventral posterior thalamic nuclei, but may also arise from cortical, subcortical, brainstem, or hemicord pathology, or occur as part of a functional neurological presentation.^[2][3][4]

Presentation

Patients typically report unilateral numbness, tingling, or loss of all sensory modalities affecting the face, arm, and leg on the same side (a "complete" hemisensory pattern), or a partial distribution (e.g., Cheiro-oral syndrome).^[4] Classical thalamic (ventral posterior nucleus) lesions produce contralateral hemianesthesia and can evolve into central post-stroke pain (Dejerine–Roussy syndrome).^[2]

Causes

Cerebral lesions

Pure sensory strokes most often involve the thalamus, but similar hemisensory patterns may arise from small infarcts in the posterior limb of the internal capsule, parietal cortex, corona radiata, or pons.^[4][3]

Brainstem and spinal cord

Hemisection or partial lesions of the spinal cord produce dissociated sensory loss patterns; classically, Brown–Séquard syndrome causes ipsilateral loss of vibration/proprioception and contralateral loss of pain/temperature below the lesion, which may be misinterpreted as “hemibody” sensory loss.^[5][6]

Functional neurological presentations

A proportion of “hemisensory syndromes” represent functional (conversion) symptoms, often with non-dermatomal distribution and normal neuroimaging.^[7][8]

Pathophysiology

Contralateral hemianesthesia from thalamic stroke reflects interruption of the ventral posterolateral and ventral posteromedial relay nuclei and their projections to primary somatosensory cortex; precise somatotopy explains incomplete variants (e.g., face–hand patterns).^[2] Parietal lobe lesions can impair higher-order tactile processing and contribute to hemibody sensory loss.^[3]

Diagnosis

Bedside examination assesses modality-specific loss (light touch, pinprick, temperature, vibration, joint position) and distribution (face, arm, leg). Neuroimaging is often performed to exclude ischemia; studies of isolated hemisensory syndrome show a relatively low yield of acute ischemic lesions overall, with higher likelihood when symptom onset is hyperacute (≤24 h), in older patients, and in smokers.^[7][4] Differentials include hemispatial neglect (an attentional disorder rather than sensory loss), peripheral neuropathies, and spinal cord syndromes such as Brown–Séquard.^[5]

Management

Treatment targets the underlying cause (e.g., secondary prevention after stroke, management of demyelinating or compressive lesions). When hemianesthesia evolves into central post-stroke pain, pharmacologic options supported by reviews include tricyclic antidepressants (e.g., amitriptyline) and anticonvulsants (e.g., lamotrigine), alongside non-pharmacologic approaches; high-quality evidence remains limited and individualized management is recommended.^[9][10][11]

History

Nineteenth-century neurologists described “hysterical hemianesthesia” in lectures on hysteria; Jean-Martin Charcot’s Lecture X, “Hysterical Hemianaesthesia,” is an early example linking hemibody sensory loss to functional presentations.^[12]

See also

• Thalamus
• Somatosensory system
• Dejerine–Roussy syndrome
• Functional neurological disorder
• Brown–Séquard syndrome

References

1. Venes D, ed. (2025). "hemianesthesia". Taber's Cyclopedic Medical Dictionary (25th ed.). F.A. Davis. Retrieved October 13, 2025.
2. Schmahmann JD (August 21, 2003). "Vascular Syndromes of the Thalamus". Stroke. 34 (9). American Heart Association: 2264–2278. doi:10.1161/01.STR.0000087786.38997.9E. PMID 12933968. Retrieved October 13, 2025.
3. Bassetti C, Bogousslavsky J, Regli F (October 1993). "Sensory syndromes in parietal stroke". Neurology. 43 (10). American Academy of Neurology: 1942–1949. doi:10.1212/WNL.43.10.1942. PMID 8413950. Retrieved October 13, 2025.
4. Koh PX, Ti J, Saffari SE, Lim ZY, Tu T (2021). "Hemisensory syndrome: Hyperacute symptom onset and age differentiates ischemic stroke from other aetiologies". BMC Neurology. 21 (1) 179. Springer Nature: Article 179. doi:10.1186/s12883-021-02206-8. PMC 8077773. PMID 33906637.
5. Roth EJ, Park T, Oken J, Burton A, Mirocha J (1991). "Traumatic cervical Brown-Sequard and Brown-Sequard-plus syndromes: the spectrum of presentations and outcomes". Spinal Cord. 29 (9). Nature Publishing Group: 582–589. doi:10.1038/sc.1991.86. PMID 1787982. Retrieved October 13, 2025.
6. Shams S (2024). "Brown-Séquard Syndrome". StatPearls. StatPearls Publishing. PMID 30844162. Retrieved October 13, 2025.
7. Toth C (August 2003). "Hemisensory syndrome is associated with a low diagnostic yield and a nearly uniform benign prognosis". Journal of Neurology, Neurosurgery & Psychiatry. 74 (8). BMJ Publishing Group: 1113–1116. doi:10.1136/jnnp.74.8.1113. PMC 1738619. PMID 12876246. Retrieved October 13, 2025.
8. Milano BA, Moutoussis M, Convertino L (March 16, 2023). "The neurobiology of functional neurological disorders characterised by impaired awareness". Frontiers in Psychiatry. 14 1122865. Frontiers Media. doi:10.3389/fpsyt.2023.1122865. PMC 10060839. PMID 37009094.
9. Klit H, Finnerup NB, Jensen TS (2009). "Central post-stroke pain: clinical characteristics, pathophysiology, and management". Lancet Neurology. 8 (9). Elsevier: 857–868. doi:10.1016/S1474-4422(09)70176-0. PMID 19679277.
10. Kumar B, Kalita J, Misra UK (2009). "Central poststroke pain: a review of pathophysiology and treatment". Neurology India. 57 (2). Medknow: 149–154. doi:10.4103/0028-3886.51281. PMID 19372350.
11. Betancur DF, Henao AE, Puentes AV (2021). "Central Post-Stroke Pain: An Integrative Review of Somatotopic Damage, Clinical Symptoms, and Neurophysiological Measures". Frontiers in Neurology. 12 678198. Frontiers Media. doi:10.3389/fneur.2021.678198. PMC 8416310. PMID 34484097.
12. Goetz CG (April 21, 2025). "Charcot, Impressionism, and Functional Dyschromatopsia". World Neurology (World Federation of Neurology). World Federation of Neurology. Retrieved October 13, 2025.