Guillain-Barré Syndrome Guillain-Barré syndrome

)ften difficult. Often, clinical tésting of the sensory :uflctions is neither reliable nor helpful in the determination. Theoretically, predominant proximal . veakness, neck flexor weakness, and facial weakness occur more often in patients with myopathy. Dn needle electromyography, low amplitudes and short duration of the motor unit potentials suggest myopathy. Normal sensory nerve action potential amplitudes and decreased compound motor action potential (CMAP) amplitudes are usually present in the conduction study. However, absent or decreased ensory nerve action potential amplitudes do not exclude a myopathy. Because of tissue edema, sensory nerve action potential amplitudes may be spuriously low. If serious edema is absent, serial examinations may reveal a significant fall in sensory nerve action potential amplitudes in CIP. Reliable examination of the motor unit potentials on voluntary activation is also difficult in patients with severe muscle weakness. Rich and associates (1997) described in neuropathy or endplate dysfunction that the excitability of the muscle remains normal, which appeared not to be the case in acute quadriplegic myopathy. We postulate that direct muscle stimulation can be helpful in the distinction of polyneuropathy and myopathy in the spectrum of CIP. Determination of the creatinine phosphokinase serum concentration is also helpful in revealing myopathic changes. Elevated levels of creatine pllosphokinase sggest a necrotizing myopathy; furthermore, severe uyopathy is associated with myoglobinurea. The best method to differentiate between underlying polyneuropathy or myopathy is a muscle biopsy using standard light microscopic examination of the muscle tissue. As mentioned in the introductory paragraphs, we prefer to consider critical illness myopathy as part of CIPNM.