PATTERNS OF NEUROPHYSIOLOGICAL ABNORMALITY IN PROLONGED CRITICAL ILLNESS

Objective: To describe the various patterns of neurophysiological abno rmalities which may complicate prolonged critical illness and identify possible aetiological factors, Design: Prospective case series of neu rophysiological studies, severity of illness scores, organ failures, d rug therapy and hospital outcome. Some patients also had muscle biopsi es, Setting: General intensive care unit (ICU) in a University Hospita l. Patients: Forty-four patients requiring intensive care unit stay of more than 7 days. The median age was 60 (range 27-84 years), APACHE I I score 19 (range 8-33), organ failures 3 (range 1-6), and mortality w as 23 %, Results: Seven patients had normal neurophysiology (group I), 4 had a predominantly sensory axonal neuropathy (group II), 11 had mo tor syndromes characterised by markedly reduced compound muscle action potentials and sensory action potentials in the normal range (group I II) and 19 had combinations of motor and sensory abnormalities (group IV). Three patients had abnormal studies but could not be classified i nto the above groups (group V). All patients had normal nerve conducti on velocities. Electromyography revealed evidence of denervation in fi ve patients in group III and five in group IV. There was no obvious re lationship between the pattern of neurophysiological abnormality and t he APACHE II score, organ failure score, the presence of sepsis or the administration of muscle relaxants and steroids, A wide range of hist ological abnormalities was seen in the 24 patients who had a muscle bi opsy; there was no clear relationship between these changes and the ne urophysiological abnormalities, although histologically normal muscle was only found in patients with normal neurophysiology. Only three of the eight patients from group III in whom muscle biopsy was performed had histological changes compatible with myopathy, Conclusions: Neurop hysiological abnormalities complicating critical illness can be broadl y divided into three types - sensory abnormalities alone, a pure motor syndrome and a mixed motor and sensory disturbance. The motor syndrom e could be explained by an abnormality in the most distal portion of t he motor axon, at the neuromuscular junction or the motor end plate an d, in some cases, by inexcitable muscle membranes or extreme loss of m uscle bulk. The mixed motor and sensory disturbance which is character istic of 'critical illness polyneuropathy' could be explained by a com bination of the pure motor syndrome and the mild sensory neuropathy. M ore precise identification of the various neurophysiological abnormali ties and aetiological factors may lead to further insights into the ca uses of neuromuscular weakness in the critically ill and ultimately to measures for their prevention and treatment.