Research has shown that a small, yet significant minority of individuals with traumatic brain injuries (TBI) experience psychotic symptoms post-TBI. TBI has also been associated with earlier onset schizophrenia in individuals with a genetic risk for psychosis.

The current case presents a 15-year-old female with pre-existing psychotic symptoms (auditory and visual hallucinations [AVH] and delusions) who stopped experiencing AVH a few weeks post-injury. The, at least temporary, cessation of her hallucinations raises several important questions about the neuroanatomy of pediatric psychosis and the impact of TBI on a potentially divergently developing brain.

Patient is a 15-year-old female who identifies as Hispanic (adopted, of Central American origin). Prior to her injury her developmental history was notable probable neglect prior to adoption, and her psychiatric history was notable for major depressive disorder, anxiety, chronic insomnia, and AVH. AVH were religious in nature and involved command hallucinations. AVH had been attributed to her chronic insomnia, per medical records. Participant was in a motorcycle accident with her caregiver and sustained a severe traumatic brain injury (GCS=3-8). Medical workup, including MRI, indicated a right basal ganglia hemorrhage, right thalamic hemorrhage, as well as injury of the brain stem at the pons, resulting in left-sided hemiparesis. She was ultimately diagnosed with traumatic right-sided intracerebral hemorrhage, traumatic subdural hematoma, traumatic hemorrhage of basal ganglia, traumatic encephalopathy, and a left homonymous hemianopia (left visual field cut) from her right temporal parietal injury. She received a neuropsychological evaluation 10 months post-TBI. Testing included: subtests of the WISC-V, measures of sustained attention and executive functioning, tasks of orientation and memory, and questionnaire measures assessing social-emotional, executive, and adaptive functioning. Parent and adolescent clinical interviews were conducted.

Results indicated appropriate orientation, broadly intact intelligence presumed consistent with premorbid functioning, average sustained attention, and deficits in aspects executive functioning, visual-motor processing speed, and fine motor skills. Although she performed well on objective measures of memory, she reported significant long term social memory loss (e.g., difficulties remembering friends and memories of emotional connectedness) during the clinical interview. Interview and questionnaire measures also indicated continued challenges with depression and anxiety, as well as post-traumatic personality changes, tics, and symptoms of trauma. Patient reported that her hallucinations, both visual and auditory, stopped early in her recovery post-TBI; patient’s premorbid delusions were still present post-TBI.

This case raises questions related to the impact of structural or axonal injury to regions or networks in the brain that may be associated with psychosis. It also adds to a minimal literature examining AVH in pediatric TBI. Using the current literature as a framework we will explore 1) the injury to this patient’s thalamus as it relates to both her emotional memory deficits as well as the interruption of her AVH hallucinations, and 2) the relationship between her visual field cut and the interruption of her visual hallucinations. Overall, this case study highlights the unique nature of the developing brain both in terms of the TBI and psychosis.