During my clinical rotation in the Emergency Department, I encountered a patient whose case has continued to fascinate me months later. He was a pleasant young man in his mid-20s, cooperative despite his frustration and confusion about being in the ED. I noticed nothing strange about him during the interview, and also struggled to figure out why he had been brought to us. Police notes simply stated that he’d had a fight with his father and needed to be evaluated. I figured we would let him cool off for a bit and send him on his way. A bit later, I returned to his room to let him know two visitors had arrived.
“T. and S. are here to see you,” I told him. “Are they your parents?”
Suddenly, he became confused and furrowed his brow. He crossed his arms across his chest, frowning.
“Yeah I guess so,” he said. He was guarded when pressed, but finally burst out: “I just have so many of them! They’re always changing. Wearing wigs, trying to confuse me. There are at least four S’s, and those are just the ones I know of!”
I got a far more detailed picture when I met with his parents. Three years ago, he had been in a severe motor vehicle accident during which he sustained head trauma, among other injuries. Prior to the accident, he had been living on his own for some time, had recently been promoted at work, and had a steady girlfriend. Gradually though, his parents started noting changes in his behavior. He complained about people spying on him: co-workers, neighbors, even his girlfriend. He eventually lost his job after getting into a fight with his boss, the girlfriend left him, and he moved back home with his parents.
Always friendly and caring, he became volatile. He had angry outbursts, and began threatening his parents with violence. He spent most of the day sitting in the dark in his room. When his Mother entered his room to do laundry, she found spoiled food hidden in his closet: he was afraid the imposters who had taken the place of his parents were poisoning him. He often stayed up all night, and woke up his parents screaming at them to quiet down and stop laughing so loudly. He had been brought to the ED after holding a knife to his father’s throat, demanding to know where his real father was.
This case has stayed with me not because it is particularly unique in terms of a psychotic presentation, but because the timing of his symptoms so closely aligned with his head injury. I wondered whether a traumatic brain injury (TBI) could cause this type of frank psychosis. As I dug into the literature, I found that TBI is indeed closely correlated with a range of neuropsychiatric issues, psychosis among them. In fact, about 40% of TBI victims experience at least two psychiatric disorders and a literature review by Vashnavi, et. al., shows that between 3% and 8% of those with TBI develop psychotic symptoms (2009).
So what is it that underlies these troubling symptoms? Like most other psychiatric disorders, the exact cause is unknown, and in the case of the psychiatric consequences of TBI, sufficient research is still scarce. However, there are some neuroanatomical correlates that have been found. Multiple studies have concluded that while the severity of the TBI does not directly correlate with the likelihood of developing psychosis, the location of the injury may be directly related (Vashnavi 2009).
Fujii and Fujii offer the most comprehensive review of studies of psychotic disorders due to TBI (PD-TBI) reported in psychiatry and neurology journals (2012). What I found most interesting in their review was some of the ways PD-TBI can be differentiated from schizophrenia in terms of brain dysfunction:
PD-TBI is more likely to show positive findings on MRI/CT than schizophrenia (70% vs. 12%-35%). For PD-TBI, findings are more focal in nature, with frontal (74%) and temporal (47%) lesions the most prevalent. By contrast, schizophrenia is most commonly associated with whole-brain and hippocampal atrophy and enlarged ventricles. On PET/SPECT scans, PD-TBI demonstrates abnormalities in both temporal (46%) and frontal areas (38%), whereas, in schizophrenia, hypo- frontality is the most common finding, and temporal areas are generally normal. EEG abnormalities are more prevalent in PD-TBI (77%) versus schizophrenia (20%–60%). The most common EEG finding in PD-TBI is temporal spiking or slowing, whereas schizophrenia is associated with general slowing (Fujii and Fujii 2012: 283).
The frontal lobe is a major center of brain activity, involved in motor function, judgment, executive processing, emotional regulation, language, memory, among many other things. Damage to this area can cause a wide range of issues, and unfortunately, the frontal lobe is particularly vulnerable to injury given its location at the very front of our heads. The temporal lobe has more distinct functions; it is associated with processing auditory input, interpreting visual stimuli, and memory, as well as comprehension and naming. It would make sense that lesions in each of these areas could indeed cause many of the auditory and perceptual disturbances associated with PD-TBI, as well as much of the cognitive dysfunction and behavioral dysregulation.
While all these differences are fascinating from a neuroscientific standpoint, they are unlikely to be useful in clinical practice. What is more interesting from a clinical standpoint is the difference in presentation between PD-TBI and schizophrenia. Compared to those with schizophrenia, people with PD-TBI are much less likely to show negative symptoms (14% versus 25-84%). Of the positive symptoms typically associated with schizophrenia, PD-TBI patients most commonly present with persecutory delusions (22%-80%) and auditory hallucinations (47%-84%) (Fujii and Fujii 2012).
My experience with my patient seems to mirror these findings. While his affect might have been described as somewhat blunted, for the most part negative symptoms were not the major issue. Rather, his delusions of persecution and auditory hallucinations were at the root of his distress. Though it would be a stretch to rule out a first psychotic break associated with schizophrenia, it is clinically interesting to consider these differences when approaching his treatment. Witnessing how devastating this situation was for his family, I can only hope that future research will provide more guidance about early interventions for victims of head injury that may prevent TBI from progressing to serious psychiatric disorders.
Fujii, D., Ahmed, I, & Hishinuma, E. (2004). A Neuropsychological Comparison of Psychotic Disorder Following Traumatic Brain Injury, Traumatic Brain Injury Without Psychotic Disorder, and Schizophrenia. The Journal of Neuropsychiatry and Clinical Neurosciences, 16, 306–314.
Fujii, D. & Fujii, D. (2012). Psychotic Disorder Due To Traumatic Brain Injury: Analysis of Case Studies in the Literature. The Journal of Neuropsychiatry and Clinical Neurosciences, 24, 278–289.
Vaishnavi, S., Rao, V., & Fann, R. (2009). Neuropsychiatric Problems after Traumatic Brain Injury: Unraveling the Silent Epidemic. Psychosomatics, 50, 198-205.