Cortical Excitability Changes in Patients with Sleep-Wake Disturbances after Traumatic Brain Injury

Department of Neurology, Christian Doppler Clinic, Paracelsus Medical University, Salzburg, Austria.
Journal of neurotrauma (Impact Factor: 3.71). 03/2011; 28(7):1165-71. DOI: 10.1089/neu.2010.1748
Source: PubMed


Although chronic sleepiness is common after head trauma, the cause remains unclear. Transcranial magnetic stimulation (TMS) represents a useful complementary approach in the study of sleep pathophysiology. We aimed to determine in this study whether post-traumatic sleep-wake disturbances (SWD) are associated with changes in excitability of the cerebral cortex. TMS was performed 3 months after mild to moderate traumatic brain injury (TBI) in 11 patients with subjective excessive daytime sleepiness (EDS; defined by the Epworth Sleepiness Scale ≥10), 12 patients with objective EDS (as defined by mean sleep latency <5 on multiple sleep latency tests), 11 patients with fatigue (defined by daytime tiredness without signs of subjective or objective EDS), 10 patients with post-traumatic hypersomnia "sensu strictu," and 14 control subjects. Measures of cortical excitability included central motor conduction time, resting motor threshold (RMT), short-latency intracortical inhibition (SICI), and intracortical facilitation to paired-TMS. RMT was higher and SICI was more pronounced in the patients with objective EDS than in the control subjects. In the other patients all TMS parameters did not differ significantly from the controls. Similarly to that reported in patients with narcolepsy, the cortical hypoexcitability may reflect the deficiency of the excitatory hypocretin/orexin-neurotransmitter system. These observations may provide new insights into the causes of chronic sleepiness in patients with TBI. A better understanding of the pathophysiology of post-traumatic SWD may also lead to better therapeutic strategies in these patients.

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    • "ICI is markedly reduced [49,52e55,59,60] whereas facilitation is normal or increased in RLS [49] [52] [55] [60]. Conversely, paired-pulse curves of patients with OSAS and chronic insomnia are reported to be basically similar to controls [44] [45] [63] [88]. "
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    ABSTRACT: Altered responses to transcranial magnetic stimulation (TMS) in obstructive sleep apnea syndrome (OSAS), restless legs syndrome (RLS), insomnia, and sleep-deprived healthy subjects have been reported. We have reviewed the relevant literature in order to identify eventual distinctive electrocortical profiles based on single and paired-pulse TMS, sensory-motor modulation, plasticity-related and repetitive TMS measures. Although obtained from heterogeneous studies, the detected changes might be the result of the different pathophysiological substrates underlying OSAS, RLS, insomnia and sleep deprivation rather than reflect the general effect of non-specific sleep loss and instability. OSAS tends to exhibit an increased motor cortex inhibition, which is reduced in RLS; intracortical excitability seems to be in favor of an “activating” profile in chronic insomnia and in sleep-deprived healthy individuals. Abnormal plasticity-related TMS phenomena have been demonstrated in OSAS and RLS. This review provides a perspective of TMS techniques by further understanding the role of neurotransmission pathways and plastic remodeling of neuronal networks involved in common sleep disorders. TMS might be considered a valuable tool in the assessment of sleep disorders, the evaluation of the effect of therapy and the design of non-pharmacological approaches.
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    ABSTRACT: Traumatic brain injury is a frequent condition worldwide, and sleep-wake disturbances often complicate the course after the injuring event. Current evidence suggests that the most common sleep-wake disturbances following traumatic brain injury include excessive daytime sleepiness and posttraumatic hypersomnia, that is, increased sleep need per 24 h. The neuromolecular basis of posttraumatic sleep pressure enhancement is not entirely clear. First neuropathological and clinical studies suggest that impaired hypocretin (orexin) signalling might contribute to sleepiness, but direct or indirect traumatic injury also to other sleep-wake modulating systems in the brainstem and the mesencephalon is likely. Posttraumatic insomnia may be less common than posttraumatic sleepiness, but studies on its frequency revealed conflicting results. Furthermore, insomnia is often associated with psychiatric comorbidities, and some patients with posttraumatic disruption of their circadian rhythm may be misdiagnosed as insomnia patients. The pathophysiology of posttraumatic circadian sleep disorders remains elusive; however, there is some evidence that reduced evening melatonin production due to traumatic brain damage may cause disruption of circadian regulation of sleep and wakefulness.
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