Experienced and physiological fatigue in neuromuscular disorders

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Clin Neurophysiol. 2007 Feb;118(2):292-300.

Experienced and physiological fatigue in neuromuscular disorders.

Schillings ML, Kalkman JS, Janssen HM, van Engelen BG, Bleijenberg

G, Zwarts MJ.

Department of Clinical Neurophysiology, Radboud University Nijmegen

Medical Centre, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands;

Institute for Fundamental and Clinical Human Movement Sciences

(IFKB), The Netherlands.

OBJECTIVE: Fatigue has been described as a typical symptom of

neurological diseases. It might be caused both by changes at the

peripheral and at the central level. This study measured the level

of experienced fatigue and physiological correlates of fatigue in

three genetically defined neuromuscular disorders.

METHODS: Sixty-five facioscapulohumeral dystrophy (FSHD), 79

classical myotonic dystrophy (DM), 73 hereditary motor and sensory

neuropathy type I (HMSN) patients and 24 age-matched healthy

controls made a 2-min sustained maximal voluntary contraction of the

biceps brachii muscle. Experienced fatigue at the current moment was

assessed with the abbreviated fatigue questionnaire just before the

physiological measurement. Peripheral fatigue was quantified by

comparing the amplitudes of an initial and a final stimulated force

response during rest. Muscle fibre conduction velocity was

determined from a 5-channel surface EMG recording in order to show

peripheral changes during the contraction. Central aspects of

fatigue were measured using superimposed electrical endplate

stimulation.

RESULTS: Patients showed an increased level of experienced fatigue.

Total physiological and peripheral fatigue were smaller in patients

compared to controls, and central fatigue was normal. The most

interesting result of this study was the presence of a large central

activation failure (CAF) in all groups of neuromuscular patients;

they showed CAF values of 36-41% already directly at the start of

sustained contraction, whereas the control group showed only 12%.

CAF slightly correlated with the level of experienced fatigue just

before the test.

CONCLUSIONS: The cause of the large CAF in patients is unclear.

Reduced concentration, motivation or effort can lead to lower

central activation. In neuromuscular patients especially fear of

physical activity or fear to damage the muscle or nerve tissue may

contribute. Besides, also physiological feedback mechanisms or

changes at the motocortical level may be a cause of reduced central

activation.

SIGNIFICANCE: For the clinician it is important to know that

experienced fatigue is part of the clinical spectrum of

neuromuscular patients. Besides, the weakness in these patients is

aggravated by reduced central activation. Potentially, both problems

could be subject of an intervention.