The amplitude of the cortically generated somatosensory evoked potential (SSEP) is used to predict outcome in comatose patients. The relationship between epileptiform discharges and SSEP amplitude has not been elucidated in those patients.

Bilateral median nerve SSEP and electroencephalograph (EEG) studies were performed in a comatose patient (patient 1) 1 day after cardiac surgery and repeated 4 days later. He had tranexamic acid administered before and during surgery. Another comatose patient (patient 2) had the same studies performed 1 day after sustaining 10 minutes of pulseless electrical cardiac activity.

Both comatose patients had epileptiform discharges (on EEG) that were coincident with giant cortically generated SSEPs. In patient 1, the EEG and SSEP studies repeated 5 days postoperatively showed no epileptiform discharges, and the cortically generated SSEP amplitude was decreased (normalized) compared with that obtained one day postoperatively. He emerged from coma and had a good recovery. Patient 2 died shortly after EEG and SSEP testing.

Epileptiform discharges were associated with giant cortically generated median nerve SSEP amplitude (tranexamic acid was implicated in patient 1 and anoxic brain injury in patient 2). Accordingly, those who use the amplitude of cortically generated SSEPs for predicting outcome in comatose patients should consider the presence of epileptiform discharges (detected by EEG) as a potential confounding factor.

Depression frequently co-occurs with somatization, and somatic complaints have been reported as a vulnerability marker for affective disorders observable before disease onset. Somatization is thought to result from an increased attention to somatic sensations, which should be reflected in long-latency somatosensory evoked electroencephalogram (EEG) potentials (SSEPs) at the physiological level. Previous studies revealed that SSEPs are altered in depressed patients and suggested late SSEP components as vulnerability markers for affective disorders. Neurotransmitters such as serotonin, γ-aminobutyric acid (GABA) and the neuropeptide substance P may play an important role for both affective disorders and somatosensory processing.

We investigated the associations between SSEPs and polymorphisms within candidate genes of the serotonergic, GABAergic as well as the substance P system in subjects at high risk for affective disorders. The sample was composed of high-risk families participating in the Munich Vulnerability Study and genetic association analyses were calculated using qfam (family-based association tests for quantitative traits) implemented in PLINK 1.05.

We observed significant associations (false discovery rate <0.05) withstanding correction for multiple testing between late SSEP components (response strength 170–370 ms after stimulation) and four single nucleotide polymorphisms within the GABA transaminase (ABAT) gene region coding for a protein responsible for GABA degradation. No effects were found with the classical disease trait approach, suggesting SSEP marker specificity of the observed associations.

Our findings point to a possible role of ABAT gene-regulated GABA catabolism for an altered processing of somatosensory stimuli as a potential vulnerability marker for affective disorders.

The generation of shunt criteria by somatosensory evoked potentials is controversial. This study was designed to validate somatosensory evoked potentials’ tracings and their derived shunt criteria compared with clinical-neurological examination.

We prospectively studied the somatosensory evoked potentials’ tracing in 102 patients who underwent carotid endarterectomy under cervical plexus blockade, comparing different somatosensory evoked potentials’ derived thresholds of impaired cerebral blood flow with the neurological examination.

The 50% reduction of the primary cortical response to median nerve stimulation as threshold of critical cerebral blood flow showed a sensitivity of 87% and a specificity of 66%. In case of total collapse of primary cortical response, we observed a sensitivity of 85% and a specificity of 89%. Concerning the prolongation of central conduction time between the spinal response at N13 and the cortical response at N20/P25 as critical threshold of impaired cerebral blood flow, the sensitivity was 87% and specificity 40%. The need-to-shunt index with its threshold at >0.5 showed a sensitivity of 85% and a specificity of 88%.

Compared to other studies, we have shown a much lower sensitivity and specificity of somatosensory evoked potentials in detecting critical cerebral perfusion; thus its use remains controversial and has to be assessed in further investigations.