Post-traumatic narcolepsy and injury of the ascending reticular activating system

A review of sleep disturbances following traumatic brain injury

“…Subsequently, the development of hypocretin deficient narcolepsy is questionable given the lack of specificity in damage to hypocretin neurons, as well as inconsistent presentation with regards to CSF hypocretin levels in hypersomnolence post TBI patients (Baumann et al 2005). This is further reinforced by the demonstration of one such patient with narcolepsy following TBI in whom diffuse tensor imaging demonstrated injury to the ascending reticular activating system between the pons and hypothalamus, rather than the hypothalamus itself (Jang et al 2016). The pathophysiology behind development of narcolepsy in post-TBI patients is likely of heterogeneous etiologies, and appears to differ from narcolepsy type I.…”

“…The authors suggested that these patients were genetically predisposed to the development of narcolepsy with cataplexy prior to TBI rather than cataplexy developing from TBI itself. Diagnostic testing with PSG and MSLT is often positive in patients with narcolepsy following TBI, with most studies using criteria of mean sleep latency < 5 min and ≥ 2 sleep onset rapid eye movement periods (Baumann et al 2007;Castriotta et al 2007;Poryazova et al 2011;Jang et al 2016). In light of these contrasting findings, it would seem that the use of PSG and MSLT for diagnosis for narcolepsy would be a more consistent diagnostic tool than use of CSF hypocretin levels.…”

Relation between injury of the hypothalamus and subjective excessive daytime sleepiness in patients with mild traumatic brain injury: Table 1

“…A recent diffusion tensor tractography study reported on two patients with post-traumatic fatigue and SEDS due to injury of the two lower portions of the ascending reticular activating system which is responsible for regulation of consciousness between the pontine reticular formation and the thalamus, and between the pontine reticular formation and the hypothalamus following mild TBI. 5 Thus, to the best of our knowledge, this is the first study to demonstrate the association between SEDS and injury of the hypothalamus in patients with mild TBI. However, the limitations of this study should be considered.…”

“…However, only a few DTI studies on the hypothalamus and sleep disorders have been reported. [3][4][5] In 2012, Menzler et al 3 demonstrated microstructural white matter abnormalities in the right hypothalamus as well as in the left mesencephalon, pons and medulla oblongata in eight patients with idiopathic narcolepsy with cataplexy using Tract-Based Spatial Statistics. A recent diffusion tensor tractography study reported on two patients with post-traumatic fatigue and SEDS due to injury of the two lower portions of the ascending reticular activating system which is responsible for regulation of consciousness between the pontine reticular formation and the thalamus, and between the pontine reticular formation and the hypothalamus following mild TBI.…”

Hypersomnia due to injury of the ventral ascending reticular activating system following cerebellar herniation

“…Although this patient showed injury of both the lower dorsal and ventral ARAS, the injury of the lower ventral ARAS was more severe. Subsequently, Jang et al [11] demonstrated injury of the lower ventral ARAS in a patient who showed hypersomnia and narcolepsy following mild traumatic brain injury. During the same year, Jang et al [12] reported on a patient who showed recovery of hypersomnia concurrent with the recovery of an injured lower dorsal and ventral ARAS following spontaneous subarachnoid hemorrhage.…”