It is really interesting, newer neurology textbooks all have large areas discussing benign fasciculation syndrome, where older textbooks bearly mention anything. Here is a section from a neurology textbook we use in medical school. Let me know what you guys thinkPersistent Benign FasciculationsA few random fasciculations in the muscles of the calf, small muscles of the hand or of the face, or elsewhere are seen in most normal individuals. They are of no significance but can be a source of worry to physicians and nurses who have heard or read that fasciculations are an early sign of amyotrophic lateral sclerosis. A simple clinical rule is that fasciculations in relaxed muscle are not indicative of motor system disease unless there is associated weakness, atrophy, or reflex change.Frequently a healthy individual experiences intermittent twitching of a muscle (or even part of a muscle), such as one of the muscles of the thenar eminence, eyelids, calves, or orbicularis oculi. It may continue for days. Lay persons refer to it as "live flesh." Also, penicillin may destabilize the polarization of distal motor endings and cause twitching. Electromyographically, these benign fasciculations tend to be more constant in location and more frequent and rhythmic than the ominous fasciculations of amyotrophic lateral sclerosis, but such distinctions are not entirely reliable. Quantitative study of the motor unit size may be helpful in these circumstances by demonstrating normally modeled units in the benign form and abnormally large units due to reinnervation in the case of motor neuron disease (see Motor Unit Potentials in Denervation).Occasionally, benign fasciculations are widespread and may last for months or even years. In several of our patients they have recurred in bouts separated by months and lasting several weeks. No reflex changes, sensory loss, nerve conduction, EMG abnormality (other than fasciculations), or increase in serum muscle enzymes are found. Low energy and fatigability in some of these patients may suggest an endogenous depressive illness, yet the fasciculations are not explained by this mechanism. Commonly, patients report a sense that the muscles affected by the twitching are weak but this cannot be confirmed by testing, and several of our patients, curiously the majority of whom were physicians, have complained of equally troubling migratory zones of paresthesias (Romero et al). Pain, of aching or burning type, may increase after activity and cease during rest. Fatigue and a sense of weakness are frequent complaints. We suspect that this fasciculatory state reflects a disease of the terminal motor nerves, for a few of our patients have shown slowing of distal latencies, and Cöers and associates have found degeneration and regeneration of motor nerve terminals. However, the majority of these cases are of a benign nature and settle down in a matter of weeks or months. In the cases reported by Hudson and colleagues, the condition, even after years, did not progress to spinal muscular atrophy, a polyneuropathy, or amyotrophic lateral sclerosis. Eventual recovery can be expected. This conforms to our experience and to that reported from the Mayo Clinic where 121 patients with benign fasciculations, followed in some cases for more than 30 years, showed no progression of symptoms and did not acquire motor neuron disease or neuropathy (Blexrud et al). It should be acknowledged, however, that there are infrequent patients with seemingly benign fasciculations in whom the EMG shows some abnormal features (e.g., rare fibrillations) in numerous muscles and who later develop the other features of motor neuron disease. Carbamazepine, and to a lesser extent phenytoin, has been helpful in reducing the fasciculations and sensations of weakness.Cramp-Fasciculation SyndromeThis is a variant of the aforementioned entity in which fasciculations are conjoined with cramps, stiffness, and systemic features such as exercise intolerance, fatigability, and muscle aches. Although affected individuals may be to some degree disabled by these symptoms, the prognosis is good. The salient finding on physiologic studies is that stimulation of peripheral nerves results in sustained muscle firing due to prolonged trains of action potentials in the distal motor nerve. This may be brought out in special electrophysiologic testing as described by Tahmoush and colleagues. In effect, this is a mild form of neuromyotonia (see later). In a small number of patients with cramp-fasciculation syndrome it is possible to demonstrate the presence of autoantibodies directed against voltage-gated axonal potassium channels. Carbamazepine or gabapentin may be beneficial.