New-Onset PTSD After Thalamic Infarct
To the Editor: The onset of symptoms of posttraumatic stress disorder (PTSD) and the reawakening of old traumatic memories after brain injury have been cited (1); there are anecdotal reports relating thalamic dysfunction to PTSD on neuroimaging (1–3). However, as there are no reports, to our knowledge, of PTSD as a sequel of a thalamic lesion, a similar case is described.
Mr. A, a 70-year-old Korean War veteran with a history of hypertension, was treated for a pure sensory stroke after a lacunar infarct in the left posterior thalamus. Although his sensory symptoms gradually improved, a year after the stroke he started losing interest in his hobbies and became aloof. However, he reported no other depressive symptoms. Four months later, Mr. A suddenly started experiencing repetitive thoughts about a colleague’s suicide, which he had witnessed in 1953. This colleague, although not Mr. A’s buddy or close friend, had the same rank as Mr. A and shared the same dormitory.
Mr. A began feeling anxious and jittery and had difficulty falling asleep. He was startled by the ring of the telephone and began avoiding television programs displaying war scenes. No depressive cognitions, obsessions, flashbacks, delusions, or hallucinations were elicited. His family history was unremarkable, and so was his past psychiatric history, including that for PTSD symptoms, such as reexperiencing, avoidance, or hyperarousal. There was no history of recent trauma or stressors, and he had never thought about this incident before. A repeat cranial computerized tomography scan showed no new findings. Mr. A was diagnosed with PTSD with delayed onset.
This case provides an opportunity to study the role of thalamic amygdalar and thalamic cortical pathways in PTSD. After a brain infarct, there is a surge in glutamate (4), which in turn increases glutamatergic transmission in the thalamic amygdalar pathway (5). Of interest, this pathway is involved in long-term potentiation, which induces plastic changes in the amygdala; the amygdala is involved in fear conditioning and in the processing of traumatic memories (5). Moreover, with the infarction of the left thalamus, there could be a partial disconnection in the thalamic cortical connection, which would parallel the functional dissociation between the thalamus and cortex during sleep. Hippocampal cells have been shown to have a higher rate of synchronous discharge during this phase, which contributes to memory consolidation (6). Thus, integrating these observations, one can hypothesize that the possible thalamic cortical disconnection, with its resultant greater availability of hippocampal information, compounded by an enhanced thalamic amygdalar transmission, may contribute to a greater conscious awareness of old, unwanted traumatic memories.
This notion is supported by the role of thalamic-cortical connections in modulating the content of consciousness (7). Moreover, thalamic hypofunction in PTSD has been shown in a recent functional neuroimaging study (3), while two individual case reports have indicated greater thalamic activity in PTSD (1, 2). Thus, future studies are needed to clarify the role of the thalamus in PTSD. Finally, the role of glutamate in PTSD, as highlighted previously (4), deserves further exploration.
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