Abstracts

Rationale: Delayed recovery of consciousness after hypoxic/anoxic brain injury from cardiac arrest is not well characterized. Some patients in the minimally conscious state (MCS) or vegetative state (VS) may harbor high-level covert cognitive abilities which are not evident at the bedside. Cardiac arrest followed by therapeutic hypothermia may lead to graded rescue of neuronal populations vulnerable to hypoxia, such as the posterior occipital cortex, hippocampus, primary motor cortex and striatum with relative preservation of other brain areas. Our previous work suggests that functional integrity of thalamic and fronto-parietal cortical connections is necessary and sufficient for the possibility of covert command-following in patients with disorders of consciousness. Methods: Report of an index case of a young patient with cardiac arrest followed by therapeutic hypothermia. 2.7 years after the cardiac arrest patient was evaluated by standardized behavioral exam, long-term wake-sleep EEG and FDG-PET. Spectral analysis of wakeful EEG and different sleep stages were performed. Quantitative EEG-based methods were used to detect motor imagery to a verbal command as a proxy for conscious awareness. MRI was contraindicated because of the presence of a pacemaker. Results: On clinical exam, patient did not respond to visual stimuli, did not exhibit goal-directed movements or evidence of a communication channel. Resting wakeful EEG showed normal frontal beta activity and absent posterior alpha rhythm. Sleep EEG showed normal vertex waves, K-complexes, sleep spindles and slow wave sleep. FDG-PET showed intact brain metabolism throughout most of the fronto-temporo-parietal cortex and the bilateral thalami. Bilateral motor cortex, occipital cortex and mesial temporal cortex show marked reduction of metabolic signal. In sharp contrast to the bedside behavioral exam, spectral analysis of the EEG demonstrated evidence of willful modulation of brain activity during command-following paradigms. Conclusions: Neuronal recovery in the setting of therapeutic hypothermia after cardiac arrest may lead to a clinical syndrome of isolation: combining blindness, impaired memory and loss of motor functions with preserved consciousness in the chronic stage of hypoxic/anoxic brain injury. Qualitative and quantitative EEG analysis is the potential mainstay of evaluation of these patients who will often have cardiac pacemakers precluding MRI studies. Our results call for a systematic assessment of cardiac arrest patients treated with therapeutic hypothermia in both the acute and chronic stages. Such studies should aim to assess the risk of such dissociation of covert cognition and observable behavior and may provide further insight into the mechanisms of neuronal recovery.