Multi-modal intervention for neuropsychological symptoms following traumatic brain injury: A case report

To the Editor, Neuropsychological symptoms are common presentations in patients with traumatic brain injury (TBI) in the long run. The manifestations range from cognitive deficits to anxiety, depression, personality changes (impulsivity, irritability, apathy, lability of affect), suicidality, and several other behavioral changes that interfere with their socio-occupational functioning.[1,2] Treatment of the neuropsychological sequel of TBI is heterogeneous as concluded from the analysis of several randomized controlled trials.[3] In this case study, we highlight the role of multi-modal intervention (pharmacotherapy, transcranial random noise stimulation, and cognitive remediation) in the management of the cognitive and behavioral symptoms following TBI. A 28-year-old man visited the neuro-psychiatric clinic due to persistent forgetfulness and increased irritability over the past 4 years. Initially, he suffered a head injury in December 2019 from a road traffic accident, resulting in hemorrhages on bilateral frontal lobes. After a right frontal craniotomy, he spent 38 days in a coma and showed disorientation upon regaining consciousness. Despite consultations with neurologists and neurosurgeons, along with treatments like multi-vitamins, piracetam, and citicoline, his forgetfulness and behavioral issues persisted. At the time of consultation, he was on citicoline 1000 mg/day, piracetam 800 mg/day, and multi-vitamins. Cognitive assessments using Hindi mini-mental status examination (HMSE) and Addenbrooke's cognitive examination III (ACE-III) revealed scores of 19/30 and 61/100, respectively. He was diagnosed with "Mild neurocognitive disorder due to known physiological condition" and prescribed memantine (10 mg/day), donepezil (10 mg/day), escitalopram (5 mg/day), and quetiapine (25 mg/day). The placement of the anode was done over the left dorsolateral prefrontal cortex (DLPFC) and the cathode over the cerebellar vermis using 2.0 milliampere current with an offset of 0.1 milliamperes (mA) for 20 min. The patient received two sessions of tRNS in a day and 5 to 6 days in a week. At the end of ten sessions, his ACE-III score improved to 82/100, and the HMSE score reached 24/30. At the end of 20 sessions of tRNS over 10 days, it resulted in an ACE-III score of 84/100 and an HMSE score of 28/30. After 30 tRNS sessions, the ACE-III score increased to 86/100, while the HMSE score remained at 28/30. He was taking a longer time in completing the tasks during the initial assessment, which improved substantially later during the course of treatment. Cognitive enhancement strategies, such as trail-making tests and puzzle solving, were incorporated during tRNS and drug therapy. Follow-up after 2 weeks showed improved scores of HMSE (29/30) and ACE-III (90/100). Maintenance tRNS sessions were recommended for periodic cognitive evaluations. The cognitive domains affected more profoundly (as reflected in HMSE score) were time orientation, concentration, and recent memory (registration and recall), following sequence of commands. The improvement in total HMSE score following intervention occurred due to improvement in those domains. Our patient had prominent cognitive symptoms that were interfering with day-to-day functioning. The impairments mostly affected the memory, attention, and concentration domain. He was also slow in performing the tasks, which was indicative of a slow processing speed. In many clinical set-ups, pharmacotherapy is the mainstay of treatment due to unavailability of facilities of neuromodulation and cognitive remediation. We used multi-modal intervention involving pharmacotherapy, accelerated transcranial random noise stimulation, and cognitive remediation strategies, which improved the cognitive as well as behavioral symptoms significantly. Repeat assessment using a particular tool may have a practice effect. This can be minimized by using multiple exhaustive baseline evaluation and increasing the time interval between the re-tests. In our case, we did HMSE and ACE-III at the baseline and repeat assessments were spaced adequately to control the practice effect. A Cochrane database systematic review reports that there is insufficient evidence in favor of pharmacotherapy for the cognitive symptoms following TBI.[4] Hence, adding alternative strategies like neuromodulation and cognitive remediation may be beneficial. Evidence supports that transcranial direct current stimulation may be useful in the management of the cognitive impairments following mild TBI; but, the pieces of evidence are mixed.[5] Various combinations of treatment modalities have been tried in the management of cognitive symptoms following mild TBI; however, the results are not encouraging.[6] Add on tRNS has been used in patients with prominent cognitive impairments associated with TBI and encephalitis, with improvement of cognitive functions.[7] Murphy et al.[8] reported superiority of tRNS over tDCS in improving cognitive function, particularly working memory performance. In our case study, we found significant improvement in cognitive performance as reflected in the scores of cognitive function assessment tools. The combination adopted in our case study is a reasonably feasible option that can be tried in future research on TBI patients. Choosing an appropriate protocol for tRNS may be another deciding factor for therapeutic efficacy, what the future research should explore about. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and that due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.