Alternating leg muscle activation (ALMA), first described by Chervin and colleagues in 2003, is characterized by brief activation of the anterior tibialis muscle in one leg alternating with similar activation in the other leg, usually lasting up to 20 s and occurring in all sleep stages, but particularly during arousals [43]. In 2006, Consentino and colleagues [44] described a patient with ALMA whose condition responded to pramipexole. Our group [45] documented ALMA in wakefulness, all stages of NREM, and also though less in REM sleep, in patients with a variety of sleep disorders. We observed ALMA also in gastrocnemius and sometimes in quadriceps muscles alternating between two sides. The significance of ALMA remains undetermined but may be a variant of PLMS.

PLMS is a well-known polysomnographic finding, characterized by repetitive, often stereotyped, and sometimes complex involuntary movements of the limbs, trunk, and occasionally cranially innervated muscles . The first description of this condition was in 1953 by Symonds [46], who used the term “nocturnal myoclonus” to distinguish the phenomenon from hypnic jerking, which he described as “nocturnal jerking.” It had been his opinion that both these conditions were associated with an increased risk of epilepsy . A review of his clinical description suggests that Symonds included cases of familial RLS, sleep starts, and myoclonic epilepsy. It was not until 1980 that the term “nocturnal myoclonus” was replaced by “periodic limb movements in sleep” after Coleman et al. [47] clarified that the movements were too prolonged to be classified as myoclonic, and that there was no epileptiform potential associated with them. The association between impaired renal function and PLMS was established in 1985 [48]. The first polygraphic study of PLMS was published by Lugaresi and Coccagna and their collaborators [9, 49, 50] and they demonstrated the common association with RLS as well as the presence of PLMS in normal subjects. An electrophysiological study of PLMS was published later by Wechsler et al. in 1986 [51]. Studying lower limb H-waves, blink responses, and median nerve somatosensory-evoked responses, they postulated that PLMS was likely secondary to a disorder of the central nervous system producing increased excitability of segmental reflexes at the pontine level or rostral to it. In 2001, Provini et al. [52] studied the motor pattern of PLMS neurophysiologically with EMG/nerve conduction studies, somatosensory-evoked potentials, and transcranial magnetic stimulation, all of which were normal . They found that in PLMS, leg muscles were most frequently involved, often with alternation of sides. Axial muscles were rarely involved and upper limb muscles were involved only sometimes. The tibialis anterior muscle was the most frequent to show the onset of PLMS. There was no constant recruitment pattern from one PLMS episode to another, even in the same patient. There was no orderly caudal or rostral spread of the EMG activity. They speculated about the presence of several generators at various levels of the spinal cord, released by a supraspinal generator . In 2004, de Weerd and colleagues [53] studied activity patterns in patients with PLMS and found that the classic pattern of movement (extensor digitorum brevis, EDB–tibialis anterior, TA–biceps femoris, BF–tensor fascia lata, TFL) or its direct variants was found in only 12 % of the total 469 movements analyzed. The most frequent sequences were characterized by contraction of only the TA, TA–EDB only, or TA–EDB followed by all other combinations (32 %). In 1991, Ali et al. [54] reported the first observation of sympathetic hyperactivity caused by PLMS, noting a mean increase in systolic blood pressure following leg movements of 23 %, comparable to that noted in obstructive sleep apnea . In 1993, Pollmächer and Schulz [55] reviewed PSG characteristics of PLMS and found them most frequent at sleep–wake transition, attenuated during deep NREM sleep and even more during REM sleep. The first description of periodic arm movements in association with periodic leg movements in sleep was made by Chabli et al. in 2000, [56] when they studied 15 cases of patients with RLS who exhibited this phenomenon. That same year, Nofzinger and colleagues [57] described the distinctive characteristic of bupropion of improving rather than worsening PLMS unlike other antidepressants. It is notable that bupropion has some dopaminergic function which may be responsible for this effect. There is currently no scientific evidence that PLMS per se are responsible for insomnia or hypersomnia but they are noted in at least 80 % of cases of RLS. The scoring criteria for PLMS have been updated recently [31] .

REM sleep is associated with a variety of phasic phenomena, such as phasic eye movements, body and limb movements, transient muscle bursts (fragmentary myoclonus), and irregular heart rate and respiration. Less-well-defined and less commonly recognized phasic events in REM sleep include spontaneous middle ear muscle activity (MEMA) in human described by Pessah and Roffwarg in 1972 [58], and phasic movements of the tongue. In 1980, Megirian et al. [59] described rhythmic activity of the tongue in rats during REM sleep. Similar complex tongue movements during REM sleep in human occurring irregularly and lasting for 2–10 s were reported by Chokroverty in 1980 [60]. These complex movements may counteract posterior displacement of the tongue, which may otherwise occur in supine REM sleep because of genioglossal hypotonia, thus functioning as nature’s defense against upper airway obstructive sleep apnea during REM sleep.

Catathrenia , or nocturnal groaning, is a relatively new isolated symptom characterized by loud expiratory vocalization, whose exact pitch and timber may vary from individual to individual but is fairly stereotyped in a given patient. While far more frequent in REM sleep, it may also occur in NREM sleep and alternate with normal breathing. It was actually first described by Pevernagie et al. [61], but was first named by Vetrugno et al. [62] in 2001. The same group subsequently reported in 2007 [63] that the groaning was accompanied by disproportionately prolonged expiration causing reduced tidal volume and bradypnea without oxygen desaturation, and that patients experienced no additional symptoms after a mean follow-up of 4.9 years. They speculated that catathrenia was due to persistence of a vestigial type of breathing pattern. In 2011, Ott and colleagues [64] performed laryngoscopy under deep sedation in a patient with catathrenia and found that while the glottis was open at inspiration, there was subtotal closure of the glottis at expiration, resulting in the characteristic groaning. The following year, Koo et al. [65] performed acoustic analysis of catathrenia and found that it had morphologic regularity, with two types of sound pitches (either a monotonous sinusoidal pattern or a sawtooth-shaped signal with higher fundamental frequency), as opposed to snoring which was distinct from catathrenia and had an irregular signal. Several authors have reported the efficacy of continuous positive airway pressure (CPAP) in treating this benign but socially awkward condition [66, 67] .

Excessive fragmentary myoclonus (EFM) is a predominantly PSG finding, currently described as being present if EMG bursts of at least 150 ms occur at a rate of at least 5/min sustained over 20 min of NREM sleep [31]. The first description of EFM was published by Broughton and colleagues in 1985, based on the PSG findings in NREM sleep in 38 consecutive patients [68]. They reported an association with sleep-related respiratory problems, PLMS, narcolepsy, insomnia, and excessive daytime sleepiness. Prior to this, Broughton and Tolentino [69] described what they called fragmentary pathologic myoclonus in a 42-year-old man presenting with excessive daytime sleepiness. In 1993, Lins et al. [70] reported that EFM occurred at high rates in all stages of sleep (including REM) but at a somewhat lower frequency in slow-wave sleep (SWS) explaining, as well, a significantly lower rate in the first hour after onset compared to later hours. More recently, Hoque et al. [71] reported that EFM rates increase with SWS and total REM with the highest EFM rates occurring during phasic REM. The clinical significance and pathophysiology of EFM remain undetermined. A neurophysiologic analysis by Vetrugno et al. failed to disclose any cortical prepotential on EEG–EMG backaveraging suggesting a subcortical origin [72].

While nocturnal bruxism may occur in patients with daytime tooth grinding, it is clearly a distinct entity in its own right, and can lead to excessive dental wear, autonomic arousals, and sleep fragmentation. One of the earliest works regarding the phenomenon was in 1964 by Reding [73], who predicted a relationship between sleep bruxism and dreaming based on its occurrence in REM sleep. The close association between bruxism and REM sleep was further commented upon by Clarke and Townsend in 1984 [74]. Shortly thereafter, Wieselmann and colleagues [75] analyzed the duration and amount of pressing and grinding jaw movements in ten patients with bruxism, and found that the highest level of activity was during stage N3 and wakefulness, with no difference seen with regard to percentages of the sleep stages. In 2001, Lavigne and colleagues [76] coined the term “rhythmic masticatory muscle activity” (RMMA) in sleep, and found that while the number of episodes of RMMA was comparable between bruxers and controls, the number of EMG bursts per episode was more frequent in the former group. In 2008, Manconi et al. [77] published an interesting case report of a patient with sleep bruxism and catathrenia occurring in a synchronized fashion. They hypothesized about the presence of a common trigger mechanism for both phenomena.