The reporting of this study confirms to the CARE guidelines. The need for patient consent was waived by the Jeonbuk National University institutional review board because no information was collected that could identify the patient, and because the report was based on existing data and documentation (IRB number CUH 2023-04-002)
This case study patient was a 51-year-old man with mild TBI who had no known chronic disease without any medication history before the accident. His head was injured by shaking effect of the car when crushing into guardrails. Right after the car accident, he had a loss of consciousness for < 10 minutes, but had no neurologic sequelae such as motor deficits. After the car accident, headache and depression had started and been treated at hospital despite of no specific findings on twice conventional brain magnetic resonance images (MRI). He complained headache focused on vertex area, depressive mood, cognitive impairment including concentration, working memory deficit, posterior neck and right-side pain, and sleep disturbance. These symptoms persisted despite of medication and injection therapy in other hospitals for 13 months.
He visited our hospital for further evaluation and treatment. His main complaints were headache and posterior neck pain commonly more on vertex area with a burning sensation and also accompanied central pain and right-side pain. Also, after the trauma he was easily irritated and depressed. We conducted physical sensory examination. When pain, temperature, crude touch, and pressure tests were performed, he showed decreased sensation on right side. There were no other abnormal findings on physical examination (Fig. 1).
We checked the headache and right central pain through a NRS, which is expressed as a score from 0 to 10, 0 means no pain, and 10 means maximum imaginable pain [19]. Also, we checked depression intensity through a BDI score, which is evaluated from 0 to 63, 0 means no depressive mood, and 63 means maximum depressive mood [20]. We performed the motor and sensory-evoked potential studies (MEP, SEP), nerve conduction study (NCS), and electromyography (EMG) to confirm the neural compromise. We conducted brain diffusion tensor imaging (DTI) three times to investigate the cause of pain; before, during and after rTMS treatment. We acquired 49 contiguous slices parallel to the anterior commissure-posterior commissure line. Imaging parameters were as follows: acquisition time = approximately 3 min; acquisition matrix = 128 x 128; field of view = 220mm x 220mm; TR = 6600ms; TE 95ms; parallel acquisition factor GRAPPA = 2 bandwidth = 1562 Hz/Px; EPI factor = 128; b = 1000 s/mm2; slice gap = 0 mm; and a slice thickness = 3mm (acquired isotropic voxel size = 0.9mm x 0.9mm x 3.0mm) [21]. After DTI, fiber tracking was performed with fractional anisotropy (FA) threshold of 0.20 and a tract turning angle of 60◦ using the DTI studio software v.1.02 (CMRM, John Hopkins Medical Institute, Baltimore, MD, USA). We performed several DTI reconstructions by selecting three regions of interest (ROIs) from the brain MRI axial slice; (1) STT (the first target ROI was set the ventro-postero-lateral nucleus of the thalamus, the second ROI was both posterolateral to the inferior olivary nucleus and anterior to the inferior cerebellar peduncle in the medulla), (2) SLF (the seed ROI was set the superior parietal lobule, the target ROI was the supplementary motor area along with the dorsal part of premotor area), (3) ILF (the first target ROI was set the posterior border of anterior temporal lobe, the second target was around the occipital lobe), (4) IFOF (the first target ROI was set the inferior frontal region, the second target was in the occipital region), (5) uncinate from coronal slice (the first ROI was set the entire temporal lobe, the second target was the entire fiber projections in the frontal lobe on the posterior-most coronal slice) [13, 22–25]. Subsequently, we selected fiber bundles that passed through the ROI. Then, the FA and tract volume (TV) of the reconstructed tracts were obtained, and the values of the left and right side were compared [14, 26, 27]. The FA values represented the directionality of water diffusion and was quantified from 0 (completely isotropic diffusion) to 1 (completely anisotropic diffusion) [26, 28]. The TV represents the number of voxels included in the neural tract [29, 30].
We applied rTMS as a treatment for central pain and depression. The following rTMS protocol was employed based on a previous study: high-frequency rTMS (10 Hz rTMS, 1500 pulses, 30 seconds cycles, 4 seconds on, 26 seconds off) applied to the left dorsolateral prefrontal cortex daily for 15 days, and intensity was 120% of motor threshold [31, 32]. rTMS was applied total 15 times; once a day and five times a week for three weeks.
We checked headache, central pain NRS and BDI at three time points: admission, discharge and 1 month after discharge. NRS scores showed decrease from 6 to 3 and then to 3 (headache) and from 4 to 2 and then to 2 (right central pain). Also, BDI score showed improvement from 34 to 23 and then to 23 (Table 1). These scores were maintained after a year after discharge. Before rTMS, the FA and TV values of the contralateral STT, ILF, SLF and IFOF on the more painful side were lower than on the other side. The FA and TV values during and after rTMS treatment were increased compared to the results before rTMS treatment (Fig. 2). During the rTMS treatment, there was no change in medications, other interventions and there was no adverse effect such as headache or dizziness.
Table 1
The NRS and BDI of patient before and after rTMS
| Admission | Discharge | 1 month after discharge |
NRS for headache | 6 | 3 | 3 |
NRS for right central pain | 4 | 2 | 2 |
BDI | 34 | 23 | 23 |
NRS: numeric rating scale, BDI: beck depression inventory, rTMS: repetitive transcranial magnetic stimulation.