Fasciculation potentials (FPs) are a spontaneous discharge of a motor units, frequently, but not invariably, visible as a muscle contraction.1 There are probably different neural generators involved, from the motor cortex to the distal nerve terminal, which differs depending on the associated neuromuscular disease.2 FPs bear special relevance to amyotrophic lateral sclerosis (ALS), a disease in which FPs are frequently generalised and profuse, associated with muscle cramping, and may even precede the development of lower motor neuron dysfunction. Indeed, absence of clinical and electrophysiologically recorded FPs raises concern about the diagnosis of ALS. Importantly, FPs evident in ALS appear to exhibit a unique morphology, being described as complex, of longer duration, and possessing a slower firing frequency.3 In addition, the FP waveform evident in ALS is unstable exhibiting increased jitter. Taken together, such morphological characteristics of ALS-related FPs, may serve as a diagnostic biomarker for ALS, and are an integral part of the sensitive Awaji diagnostic criteria.4 ,5 Patience, however, may be required to detect FPs, since the discharge rate may be slow at any given site, perhaps as slow as once every 2 min. Surface recording with the active electrode over the end plate region of the muscle is a useful trick to record FPs if they are sparse, although such a technique provides no information regarding FP morphology.

Recently, it was reported that FP morphology was an unreliable biomarker in distinguishing ALS-related FPs from benign fasciculations that may be evident in mimic disorders, such as cramp fasciculation syndrome, or even in healthy controls.6 Given that benign fasciculations may be diffuse, even affecting facial musculature, this could result in overwhelming anxiety as to the possibility of ALS on the part of the patient.

de Carvalho and Swash, describe that FPs may be a very early feature of motor unit dysfunction in ALS, preceding other electromyographic abnormalities. Of importance, these early FPs were clearly distinguishable from benign FPs based on their relative complexity and increased waveform instability. The complexity of ALS-related FPs appeared to increase with disease progression, perhaps reflecting compensatory reinnervation. These findings would seem to corroborate clinical observations that complex-looking FPs may be evident in ALS patients even when the morphology of recruited motor units at the same needle site appears normal. In addition, ALS physicians are aware that occasionally FPs may be the presenting features of ALS. While this is seldom by more than a few months, it does highlight the fact that patients presenting with generalised FPs, even without neurological deficit, should be followed-up prior to excluding the diagnosis of ALS. Taken together, complex FPs appear to be an early feature of ALS, clearly distinguishing ALS from mimic disorders, and thereby implying that FPs may be of diagnostic utility in early ALS.