Previous studies have suggested that the corticoreticular tract (CRT) has an important role in motor function almost next to the corticospinal tract (CST) in the human brain. Herein, the CRT is reviewed with regard to its anatomy, function, and recovery mechanisms after injury, with particular focus on previous diffusion tensor tractography-based studies. The CRT originates from several cortical areas but mainly from the premotor cortex. It descends through the subcortical white matter anteromedially to the CST with a 6- to 12-mm separation in the anteroposterior direction, then passing through the mesencephalic tegmentum and the pontine and pontomedullary reticular formations. Regarding its motor functions, the CRT appears to be mainly involved in the motor function of proximal joint muscles accounting for ~30–40% of the motor function of these joint muscles. In addition, the CRT is involved in gait function and postural stability. However, further studies that clearly rule out the effects of other motor function-related neural tracts are necessary to clarify the precise portion of the total motor function for which the CRT is responsible. With regard to recovery mechanisms for an injured CRT, three recovery mechanisms were suggested in five previous studies: recovery through the original pathway, recovery through perilesional reorganization, and recovery through the transcallosal pathway. However, each of those studies was single-case reports; therefore, further original studies including a larger number of patients are warranted.

Background: We report on a patient with a mild traumatic brain injury (TBI) who developed abdominal pain due to spinothalamic tract (STT) injuries revealed by diffusion tensor tractography (DTT). Case presentation: A 53-year-old female patient suffered head trauma resulting from a backward fall. While bathing at a public bathhouse, she fell backward and struck the occipital area of her head against the floor. After the head trauma, she experienced pain in the abdomen and in both hands and feet. She underwent evaluations including conventional brain MRI, abdominal and pelvic ultrasonography, and stomach and intestine endoscopy. No abnormality was observed in her brain or abdomen. In addition, her abdominal pain had not been relieved by medical management. When she came to our hospital 4 years after the head trauma, her pain characteristics and severity were as follows: intermittent pain without allodynia or hyperalgesia; squeezing and warm creeping-like pain in the abdomen (visual analog scale score: 7); tingling pain in both hands and feet (visual analog scale score: 7). She was prescribed pregabalin and gabapentin, and her abdominal and limb pain was well-controlled at a tolerable level. On DTT 4 years after head trauma, the upper portion of the spinothalamic tracts (STTs) in both hemispheres showed partial tearing. Discussion and conclusions: Injury of the STT was demonstrated by using DTT in a patient who showed abdominal pain that was refractory to medical management following mild TBI. Our results suggest that central pain due to STT injury might be suspected in patients with abdominal pain that is refractory to medical management following TBI.

We report on a patient with tinnitus who showed injury of auditory radiation following whiplash injury, demonstrated by diffusion tensor tractography (DTT). A 48-year-old male patient suffered from a car crash resulting in flexion-hyperextension injury of his head after being hit from behind by a moving car while waiting at a signal while driving a car. Three days after the car crash, he began to feel tinnitus in both ears and his tinnitus became aggravated with the passage of time. No specific lesion was observed on a conventional brain MRI performed two weeks after the car crash. Although he visited several hospitals, the precise cause of his tinnitus was not detected. Two years after the car crash, he underwent evaluation for his tinnitus at the ear, nose and throat department of a university hospital. The pure tone audiometry was evaluated in a sound-proof room to screen his hearing status for the frequencies of 250–8000 Hz and no specific abnormality was detected. Although he was also tested for speech audiometry, there was also no specific abnormality. In order to assess his tinnitus, a tinnitogram was conducted to evaluate the frequency content and the loudness. His tinnitus was characterized at an intensity of 40 dB and a frequency of 4000 Hz. However, no abnormality was observed in either ear on physical examination. On DTT, the auditory radiation showed severe narrowing and tearing in both hemispheres. To summarize, neural injury of the auditory radiation was demonstrated in a patient with tinnitus following whiplash injury, using DTT.

Background and Purpose: We investigated white matter abnormalities in patients with spontaneous subarachnoid hemorrhage following aneurysmal rupture, by using tract-based spatial statistics. Methods: Sixteen patients with spontaneous subarachnoid hemorrhage due to aneurysmal rupture and 18 age- and sex-matched healthy control subjects were recruited. Voxel-wise statistical analysis of fractional anisotropy data was performed by using tract-based spatial statistics as implemented in the Functional Magnetic Resonance Imaging of the Brain Software Library. We calculated mean fractional anisotropy values across the tract skeleton and within 48 regions of interest based on the intersections between the fractional anisotropy skeleton and the probabilistic Johns Hopkins University white matter atlases. Results: Comparing the patient and control groups, the fractional anisotropy values of 44 regions of interest among the 48 regions of interest showed significant differences ( P <0.05). However, significant differences were not observed in the remaining 4 regions of interest (both retrolenticular parts of the internal capsule, the right superior longitudinal fasciculus, and the right superior corona radiata; P >0.05). Conclusions: By undertaking tract-based spatial statistics analysis, we detected wide-ranging white matter abnormalities in patients with spontaneous subarachnoid hemorrhage. REGISTRATION: URL: http://www.e-irb.com/index.jsp . Unique identifier: 2019-06-032.

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