BACKGROUND AND AIM: Thalamic and brainstem strokes are a cause of organic hypersomnia. In thalamic lesions it has been attributed to disruption of ascending activating impulses from the brainstem reticular formation and to insufficient spindling and slow-wave production, which depends upon activities of reticular thalamic nucleus and thalamocortical neurons, respectively. Reported sleep disorders in brainstem lesions have occasionally been contradictory and that is because of the presence of nearby structures in the brainstem with different functions in sleep-waking cycle. The aim of the study is to present the results of polysomnographic records in patients with thalamic and/or brainstem vascular lesions, and to correlate them with the anatomical structures affected. PATIENTS AND METHODS: We have performed a polysomnographic study, (8-channel system), in patients with thalamic and/or brainstem strokes. All of them showed alterations of sleep-wake cycle. Neuroimaging studies were carried out in all patients. RESULTS: We report seven patients, 4 males and 3 females. Two cases presented thalamic strokes, in 3 the lesion was located in the brainstem and 2 patients had thalamo-mesencephalic lesions. All of them developed hypersomnia with an increase of NREM sleep. In patients with bilateral mesencephalic lesions we found that REM sleep was diminished as well. CONCLUSIONS: We have confirmed that lesions affecting thalamus and mesencephalic or pontine tegmental reticular formation are a cause of hypersomnia. The observation that this sleepiness is transient, supports the evidence of an extrathalamic alternative activating route.
BACKGROUND AND AIM: Thalamic and brainstem strokes are a cause of organic hypersomnia. In thalamic lesions it has been attributed to disruption of ascending activating impulses from the brainstem reticular formation and to insufficient spindling and slow-wave production, which depends upon activities of reticular thalamic nucleus and thalamocortical neurons, respectively. Reported sleep disorders in brainstem lesions have occasionally been contradictory and that is because of the presence of nearby structures in the brainstem with different functions in sleep-waking cycle. The aim of the study is to present the results of polysomnographic records in patients with thalamic and/or brainstem vascular lesions, and to correlate them with the anatomical structures affected. PATIENTS AND METHODS: We have performed a polysomnographic study, (8-channel system), in patients with thalamic and/or brainstem strokes. All of them showed alterations of sleep-wake cycle. Neuroimaging studies were carried out in all patients. RESULTS: We report seven patients, 4 males and 3 females. Two cases presented thalamic strokes, in 3 the lesion was located in the brainstem and 2 patients had thalamo-mesencephalic lesions. All of them developed hypersomnia with an increase of NREM sleep. In patients with bilateral mesencephalic lesions we found that REM sleep was diminished as well. CONCLUSIONS: We have confirmed that lesions affecting thalamus and mesencephalic or pontine tegmental reticular formation are a cause of hypersomnia. The observation that this sleepiness is transient, supports the evidence of an extrathalamic alternative activating route.