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.