We identified the DRTT in the human brain using probabilistic tractography. Our results could be useful in research on movement control.

It appears that the proximal weakness of this patient was attributed to injury of both CRPs following head trauma. It is assumed that the mild weakness at the onset of head trauma was caused by the primary traumatic axonal injury and the aggravated weakness that started from 29 days might be ascribed to the secondary traumatic axonal injury.

We report on patients with post-traumatic fatigue and hypersomnia who showed injury of the lower portion of the ascending reticular activating system (ARAS) between the pontine reticular formation (RF) and the intralaminar thalamic nucleus (ILN) following mild traumatic brain injury (TBI), using diffusion tensor tractography (DTT).Two patients with mild TBI resulting from a car accident were enrolled in this study. Patient 1 was a 51-year-old woman showed abnormalities as 6.9 (cut off: 3.7 points) and 18 (cut off: 10) on the Fatigue Severity Scale and the Epworth Sleepiness Scale at 11 months after onset. Patient 2 was a 64-year-old woman who revealed abnormalities on the Fatigue Severity Scale and the Epworth Sleepiness Scale with 6.8 and 19 at 3 months after onset.In both patients, the upper ARAS in which the neural connectivity of the ILN to the cerebral cortex did not show significant abnormalities. However, we observed the narrowing of the left dorsal lower ARAS between the pontine RF and the ILN in both patients and the tearing (patient 1) and narrowing (patient 2) of the left ventral lower ARAS between the pontine RF and the hypothalamus.Injuries of the dorsal and ventral lower ARAS were demonstrated in patients with fatigue and hypersomnia following mild TBI. We believe that these injuries of the ARAS might be a pathogenetic mechanism of fatigue and hypersomnia in patients with TBI.

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Objectives: Many animal and a few human studies have reported on the neural connectivity of the substantia nigra (SN) and the ventral tegmental area (VTA). However, it has not been clearly elucidated so far. We attempted to investigate any differences in neural connectivity of the SN/VTA in the human brain, using diffusion tensor imaging (DTI).Methods: Sixty-three healthy subjects were recruited for this study. DTIs were acquired using a sensitivity-encoding head coil at 1. 5T. Connectivity was defined as the incidence of connection between the SN/VTA and each brain regions in the brain.Results: The connectivity of SN was higher than that of the VTA. This included in the primary motor cortex, primary somatosensory cortex, premotor cortex, prefrontal cortex, caudate nucleus, globus pallidus, putamen, nucleus accumbens, temporal lobe, amygdala, pontine basis, occipital lobe, anterior and posterior lobe of cerebellum, corpus callosum, and external capsule (p < 0.05). However, no significant differences were observed in the red nucleus, thalamus, pontine tegmentum, and medial temporal lobe between the SN and VTA (p > 0.05).Conclusions: We found the differences in neural connectivity of the SN/VTA in the human brain. The method and results of this study can provide useful information for clinicians and researchers in neuroscience, especially who work for Parkinson’s disease and patients with brain injury.

Background:We report on a patient who developed aggravation of excessive daytime sleepiness (EDS) concurrent with aggravation of an injured ascending reticular activating system (ARAS) following mild traumatic brain injury (TBI), demonstrated by follow-up diffusion tensor tractographies (DTTs).Methods:A 42-year-old male patient experienced head trauma resulting from flexion-hyperextension injury after collision with another vehicle from behind while stopped at an intersection. The patient lost consciousness for approximately 10 seconds and experienced no post-traumatic amnesia following the accident. The patient's Glasgow Coma Scale score was 15. No specific lesion was observed on the conventional brain MRI performed at 10 weeks after onset. The patient complained of EDS after the head trauma and aggravation of EDS with passage of time. The Epworth Sleepiness Scale indicated abnormality with a score of 12 at 10 weeks after onset (cut-off: 10 points full mark: 24 score) and it was aggravated with a score of 18 at 16 months.Results:On 10-week DTT, decreased neural connectivity of the intralaminar thalamic nucleus to the prefrontal cortex and basal forebrain was observed in both hemispheres. However, no significant abnormality was observed in the dorsal and ventral lower ARAS. On 16-month DTT, the upper portion of the left dorsal lower ARAS showed partial tearing and the ventral lower ARAS showed thinning (both sides) and partial tearing (right side).Conclusions:Aggravation of EDS concurrent with aggravation of an injured ARAS was demonstrated in a patient with mild TBI using DTT.

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