Hemiparesis is a weakness affecting one side of the body, less severe than a hemiplegia. Characteristically this affects the extensor muscles of the upper limb more than flexors, and the flexors of the leg more than extensors ("pyramidal" distribution of weakness), producing the classic hemiparetic/hemiplegic posture with flexed arm and extended leg, the latter permitting standing and a circumducting gait.
Hemiparesis results from damage (most usually vascular) to the corticospinal pathways anywhere from motor cortex to the cervical spine. Accompanying signs may give clues as to localization, the main possibilities being hemisphere, brainstem, or cervical cord. Hemisphere lesions may also cause hemisensory impairment, hemianopia, aphasia, agnosia or apraxia; headache, and incomplete unilateral ptosis, may sometimes feature. Spatial neglect, with or without anosognosia, may also occur, particularly with right-sided lesions producing a left hemiparesis. Pure motor hemiparesis may be seen with lesions of the internal capsule, corona radiata, and basal pons (lacunar/small deep infarct), in which case the face and arm are affected more than the leg; such facio-brachial predominance may also be seen with cortico-subcortical lesions laterally placed on the contralateral hemisphere. Crural predominance suggests a contralateral paracentral cortical lesion or one of the lacunar syndromes.
Brainstem lesions may produce diplopia, ophthalmoplegia, nystagmus, ataxia, and crossed facial sensory loss or weakness in addition to hemiparesis ("alternating hemiplegia").
Spinal lesions are more likely to show bilateral long tract signs (e.g., bilateral Babinksi’s sign) and may have accompanying spinal or root pain, sphincter disturbance, and a sensory or motor level.
Hemiparesis is most usually a consequence of a vascular event (cerebral infarction). Tumor may cause a progressive hemiparesis (although meningiomas may produce transient "stroke-like" events). Hemiparetic multiple sclerosis is rare but well described. Transient hemiparesis may be observed as an ictal phenomenon (Todd’s paresis), or in familial hemiplegic migraine which is associated with mutations in a voltage-gated Ca2+ ion channel gene.