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Introduction. Anosognosia for hemiplegia (AHP) is unawareness of unilateral motor deficit. This syndrome usually is reported in association with large lesions of the nondominant frontal and parietal lobes, the perithalamic lesions or their connexions with cortical or subcortical structures. Little is known about AHP in patients with brainstem’s infarctions. Case report. A 79-year-old right handed woman, without history of intellectual deterioration or psychiatric diseases, with hypertension and paroxysmal atrial fibrillation, was admitted with acute left hemiplegia, somatosensory left deficit and slurred speech. Cerebral MRI indicated a recent infarct in the right anteromedial pontine territory. The patient had moderate anosognosia for hemiplegia (AHP) during the first week after the onset of stroke. There was no sign of left spatial hemineglect or left hemiasomatognosia, no persistant mental confusion and no associated significant cortical or subcortical lesions. Conclusion. We presumed that AHP is compatible with brainstem’s lesions, particularly with pontine infarcts. The pathogenesis of AHP in pontine infarcts may result from the functional deactivation of frontal and parietal areas.
Introduction. Anorectinia for hemiplegia (AHP) is unawareness of unilateral motor deficit. This syndrome usually is reported in association with large lesions of the nondominant frontal and parietal lobes, the perithalamic lesions or their connexions with cortical or subcortical structures. Little is known about AHP in patients with brainstem’s infarctions. Case report. A 79-year-old right handed woman, without history of intellectual deterioration or psychiatric diseases, with hypertension and paroxysmal atrial fibrillation, was admitted with acute left hemiplegia, somatosensory left deficit and slurred speech. Cerebral MRI indicated a recent infarct in the right anteromedial pontine territory. The patient had moderate anosognosia for hemiplegia (AHP) during the first week after the onset of stroke. There was no sign of left spatial heminelect or left hemiasomatognosia, no persistant mental confusion and no associated significant cortical or subcortical lesions. Conclusion. We pres umed that AHP is compatible with brainstem’s lesions, particularly with pontine infarcts. The pathogenesis of AHP in pontine infarcts may result from the functional deactivation of frontal and parietal areas.