Hemianesthesia
Hemianesthesia is a neurological sign consisting of loss or marked impairment of somatic sensation 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, or a partial distribution. Classical thalamic lesions produce contralateral hemianesthesia and can evolve into central post-stroke pain.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.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 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. Parietal lobe lesions can impair higher-order tactile processing and contribute to hemibody sensory loss.Diagnosis
Bedside examination assesses modality-specific loss and distribution. 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, in older patients, and in smokers. Differentials include hemispatial neglect, peripheral neuropathies, and spinal cord syndromes such as Brown–Séquard.Management
Treatment targets the underlying cause. When hemianesthesia evolves into central post-stroke pain, pharmacologic options supported by reviews include tricyclic antidepressants and anticonvulsants, 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.