OBJECTIVES: Bilateral loss of the cortical somatosensory evoked potentials (SEP) is usually regarded as a strong predictor for a very poor clinical outcome. We present four patients with a favorable recovery from bilaterally absent cortical SEP. DESIGN: Case series. SETTING: Neurocritical care unit at the University of Heidelberg. PATIENTS: Four patients with viral encephalitis, carbamazepine intoxication, head trauma, and left-side, space-occupying hemispheric infarction, respectively. INTERVENTIONS: Serial recording of somatosensory and auditory evoked potentials, therapy of increased intracranial pressure, including decompressive surgery, hypothermia, and barbiturate coma. MEASUREMENTS AND MAIN RESULTS: Three patients had an excellent outcome (Glasgow Outcome Scale 4 and 5). In those three patients, the SEP became completely normal during the clinical course. In one patient who remained severely disabled, the SEP became detectable again over the contralateral hemisphere, but remained abnormal. Possible influencing factors were sedative and analgetic drugs in all patients, and hypothermia and barbiturate coma in one of the patients. CONCLUSIONS: The absence of cortical SEP does not invariably imply an unfavorable prognosis. Absent cortical SEP indicates a severe neuronal dysfunction, which may be completely reversible if the underlying disease does not lead to permanent structural damage.
OBJECTIVES: Bilateral loss of the cortical somatosensory evoked potentials (SEP) is usually regarded as a strong predictor for a very poor clinical outcome. We present four patients with a favorable recovery from bilaterally absent cortical SEP. DESIGN: Case series. SETTING: Neurocritical care unit at the University of Heidelberg. PATIENTS: Four patients with viral encephalitis, carbamazepine intoxication, head trauma, and left-side, space-occupying hemispheric infarction, respectively. INTERVENTIONS: Serial recording of somatosensory and auditory evoked potentials, therapy of increased intracranial pressure, including decompressive surgery, hypothermia, and barbituratecoma. MEASUREMENTS AND MAIN RESULTS: Three patients had an excellent outcome (Glasgow Outcome Scale 4 and 5). In those three patients, the SEP became completely normal during the clinical course. In one patient who remained severely disabled, the SEP became detectable again over the contralateral hemisphere, but remained abnormal. Possible influencing factors were sedative and analgetic drugs in all patients, and hypothermia and barbituratecoma in one of the patients. CONCLUSIONS: The absence of cortical SEP does not invariably imply an unfavorable prognosis. Absent cortical SEP indicates a severe neuronal dysfunction, which may be completely reversible if the underlying disease does not lead to permanent structural damage.