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
Frequency

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. 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.

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). Classical thalamic (ventral posterior nucleus) lesions produce contralateral hemianesthesia and can evolve into central post-stroke pain (Dejerine–Roussy syndrome).

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.

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.

Functional neurological presentations

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

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). Parietal lobe lesions can impair higher-order tactile processing and contribute to hemibody sensory loss.

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. Differentials include hemispatial neglect (an attentional disorder rather than sensory loss), peripheral neuropathies, and spinal cord syndromes such as Brown–Séquard.

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.

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.

See also

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