With better survival of critically ill patients, ‘de novo’ arising neuromuscular complications like critical illness myopathy or polyneuropathy have been increasingly observed. Prolonged hospitalization not only imposes risks like pneumonia or thrombosis on patients but also represents a real budget threat to modern intensive-care medicine. Clinical symptoms like muscle weakness and weaning failure are common to critical illness myopathy and critical illness polyneuropathy and do not allow for distinction. Specific therapies are not yet available, and the quest for the pathomechanisms has proved more complicated than anticipated. Especially for critical illness myopathy, multiple sites of disturbances to the excitation–contraction coupling cascade are possible causes of muscle weakness. The present review summarizes the epidemiological, clinical and diagnostic features of critical illness myopathy and then focuses on current concepts of the presumed pathomechanisms of critical illness myopathy. Sepsis was shown to be a major cause of critical illness myopathy and special emphasis will be placed on how sepsis and inflammatory mediators influence (i) the membrane excitability at the level of voltage-gated ion channels and (ii) the intracellular protein signalling that results in selective loss of myosin protein content and muscle wasting. For (i), critical illness myopathy represents a new type of acquired channelopathy affecting the inactivation properties of Na+ channels. For (ii), both protein proteolysis and protein build up at the transcriptional level seem to be involved. Findings from different studies are put into a common context to propose a model for cytokine-mediated failure of muscle in severe sepsis. This can open a series of new possible trials to test specific therapeutic strategies in the future.

In spite of the many tools available for monitoring the central nervous system, there are no clinical trials which prove that continuous monitoring of any single variable in the intensive care unit has had any significant impact on the outcome of patients. Even in the absence of robust evidence proving the efficacy of neuromonitoring tools, we believe it is time to re-examine the basic objectives of neuromonitoring. The main reasons for monitoring neurocritical patients could be summarized as follows: (1) to detect early neurological worsening before irreversible brain damage occurs; (2) to individualize patient care decisions; (3) to guide patient management; (4) to monitor therapeutic response of some interventions and to avoid any consequent adverse effects; (5) to allow clinicians to be able to understand the pathophysiology of complex disorders; (6) to design and implement management protocols; and (7) to improve neurological outcome and quality of life in survivors of severe brain injuries. To reach these goals, there is a need to overcome some obstacles, such as the learning curve needed for any monitor and establishing consensus among experts on how to interpret monitor readings. In this review, the obstacles confronted in running randomized clinical trials in this field are discussed. The lack of equipoise and the ethical concerns in conducting such trials are discussed. In addition, the reasons for failure to improve outcome through the use of some monitoring devices are discussed and potential solutions proposed.