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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_41_библиотеки_им_акад_М_И_Перельмана
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Demographics
Sleep-related leg cramps appear to occur at any age but are more common and frequent in the elderly. In an epidemiologic study in children, an overall incidence of
7.3% was reported [58]. In a general practice-based study of 233 people older than
age 60, almost one-third had cramps during the previous 2months, and this increased
to one-half in those older than 80. In addition, 40% had cramps more than 3 times a
week and 6% reported daily cramps [59]. A study of outpatient veterans found that
56% reported leg cramps [60]. Sleep-related leg cramps may appear or worsen during pregnancy and were reported in 75% of women in their third trimester in a study
of 12 women [61].
Differential Diagnosis
The differential diagnosis of sleep-related leg cramps includes muscle strain, dystonia, claudication, RLS, PLMS, and nocturnal myoclonus. The pain associated with
muscle strain is often associated with overuse or injury and does not usually occur
only at night. The pain associated with claudication is usually relieved by rest. RLS
involves an urge to move the legs with temporary relief with movement and does not
require stretching of the muscle. PLMS occur during sleep and are not associated
with pain or muscle hardening. Muscle cramps may also be a feature of a number of
other neurologic conditions; however these cramps are not usually restricted to
nighttime or the legs alone.
Associated Features
During the cramp the muscles are rm and tender. Tenderness and discomfort in the
muscle may persist for several hours after the cramping. Delayed sleep onset and
awakenings from sleep are often present with persistent discomfort delaying return
to sleep. Patients may need to get out of bed to stand and stretch to alleviate symptoms. Sleep-related leg cramps are not sleep-stage specic as they may occur in any
sleep stage. Although sleep-related leg cramps are idiopathic in most individuals, a
large number of potential contributing factors have been reported. Medications that
have been reported to cause leg cramps include diuretics, nifedipine, statins,
β-agonists, steroids, morphine, cimetidine, penicillamine, and lithium. Medical
conditions associated with sleep-related leg cramps include uremia, diabetes, thyroid disease, hypoparathyroidism, hypomagnesemia, hypocalcemia, hyponatremia,
and hypokalemia. Additional predisposing factors include vigorous exercise during
the day, oral contraceptive use, peripheral vascular disease, and dehydration. PSG is
not routinely recommended for the evaluation of sleep-related leg cramps, but may
show bursts of increased electromyographic activity over the affected area.
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Treatment
A careful history to identify and treat any precipitating factors is important in
patients with sleep-related leg cramps. Patients should be reassured regarding the
benign nature of the disease. Adjustment of possible contributing medications
should be considered. Cramps, once present, can be aborted by forcible dorsiexion
of the foot with the knee extended. This is often discovered by patients while dealing with cramps acutely at night and may be all that is required when sleep-related
leg cramps are infrequent. Passive massage or stretching may also help. However,
research data on the efcacy of stretching exercises are contradictory. A randomized
controlled trial of 80 adults above 55years found that stretching of the calves and
hamstrings before sleep effectively reduced the frequency and severity of leg
cramps, while a previous trial found this treatment to be ineffective [62].
Pharmacological treatment of leg cramps may be necessary when symptoms are
severe and frequent. A number of treatments have been investigated. Quinine, an
alkaloid agent, reduces the excitability of the motor end plate to nerve stimulation
and increases the refractory period of skeletal muscle contraction. It has been used
with great efcacy to treat leg cramps since 1940 though there were signicant
concerns regarding the risk/benet ratio with this drug [63, 64]. In 1995, the FDA
concluded that the risks of quinine outweighed any possible benet and ordered a
stop to the marketing of quinine for off-label use for prevention or treatment of
sleep-related leg cramps. Quinine-induced thrombocytopenia and hypersensitivity
reactions are among the most serious complications of quinine. Naftidrofuryl oxalate, a vasodilator, signicantly reduced the frequency of cramps and increased the
number of cram-free days by a third in a double-blind, placebo-controlled trial in 14
patients [65]. Orphenadrine citrate, an anticholinergic, reduced the frequency of leg
cramps by a third in the majority of patients in a double-blind crossover trial [66].
Verapamil at 120mg given at bedtime for 8weeks resulted in an improvement in
cramp symptoms in seven out of eight patients during an uncontrolled study [67].
Magnesium was effective in treating sleep-related leg cramps in pregnant women in
several double-blind, randomized, placebo-controlled studies [68–70]; however, no
signicant effect was seen in the study of nonpregnant adults [71–73]. It was suggested that possible underlying pregnancy-induced magnesium deciency may
have led to positive results in pregnant patients and measurements of baseline and
posttreatment serum magnesium in all patients should be conducted to highlight
that nding. Vitamin E use yielded conicting results among two randomized
blinded studies [74, 75]. In the only randomized, double-blind, placebo-controlled
study evaluating the efcacy of vitamin B complex capsules, 86% of the patients
had prominent remission of leg cramps at 3 months compared to placebo [76].
Several studies have demonstrated the effectiveness of gabapentin in the treatment
of leg cramps in those with neurologic conditions though its usefulness in idiopathic
leg cramps remains unclear [77, 78]. The effectiveness of lidocaine injection at the
gastrocnemius trigger point and botulinum injection into calf muscles for treatment
of sleep-related leg cramps has also been reported [79, 80]. Finally, continuous
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positive airway pressure (CPAP) cured leg cramps in patients in a report of four
patients with comorbid obstructive sleep apnea (OSA) [81]. More research in this
area is needed.
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Sleep-Related Bruxism
One of the rst reports of bruxism was from Black in 1886; however, the term bruxism was introduced by Miller in 1938 [82, 83]. Sleep-related bruxism is an oral
activity characterized by grinding or clenching of the teeth during sleep usually
associated with sleep arousals. Jaw activity during sleep includes tonic contractions
and rhythmic masticatory muscle activity (RMMA) that occurs at about 1 Hz.
Teeth-grinding sounds occur when these contractions are strong during sleep and
are present in about 20% of episodes [84].
Demographics
Bruxism has the highest prevalence in childhood which decreases with increasing
age. One study reported an overall prevalence of 8% with a frequency of 13% in
those 18–29years of age and only 3% in older individuals [85]. No gender differences have been found [86]. A familial pattern is seen in approximately 20–35% of
patients [87]. Moderate to severe tooth wear and jaw discomfort is seen in about
5–10% of the population [84].
Diagnosis
The diagnosis of sleep-related bruxism according to the ICSD-3 requires the following: (a) The patient reports or is aware of tooth-grinding sounds or tooth clenching during sleep. (b) One or more of the following are present: abnormal wear of the
teeth, transient morning jaw muscle discomfort, fatigue or pain, and/or jaw locking
[1] (Table18.6). Although PSG is not required for diagnosis, bruxism is ideally
recorded via the masseter EMG showing characteristic RMMA either a phasic pattern of activity at 1Hz frequency lasting 0.25–2s, sustained tonic activity lasting
longer than 2s, or a mixed pattern. Simultaneous audiovisual recording increases
diagnostic reliability distinguishing between RMMA episodes and orofacial and
other muscular activities that occur during sleep (swallowing, sleep talking, etc.).
The RMMA episodes are associated with sleep arousal and are preceded by signs of
increased autonomic activity (such as increased heart rate). PSG will also assess
comorbid sleep disorders that may worsen bruxism such as OSA or RBD [88].
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Differential Diagnosis
Sleep-related bruxism must be distinguished from other nocturnal faciomandibular
activities including idiopathic myoclonus, RBD, parasomnias such as night terrors
and confusional arousals, and dyskinetic jaw movements persisting in sleep. Very
rarely, nocturnal partial or complex seizures may present as isolated bruxism.
Associated Features
Sleep-related bruxism can lead to abnormal wear of the teeth, tooth pain, jaw muscle pain, or temporal headache. Fractured teeth and buccal lacerations and temporomandibular joint pain can also occur as a consequence. Sleep disruption is also
prevalent. Over time, hypertrophy of the masseter and other facial muscles can
develop. Sleep bruxism has been attributed to several etiologies though the theory
that malocclusion was the cause has fallen out of favor. Presumed mechanisms
include sleep arousal, autonomic sympathetic cardiac activation, genetic predisposition, psychological components, and comorbidities such as sleep-disordered breathing and acid reux. Medications such as selective serotonin reuptake inhibitors
(SSRI) and amphetamines have been associated with bruxism. Bruxism is frequently associated with Down’s syndrome, autism, and ADHD [89, 90]. Although
bruxism can occur during any sleep stage, including REM sleep, it is most often
seen during arousals from stage N1 and N2 sleep.
Management
Therapies for sleep-related bruxism can be divided into orthodontic, behavioral, and
pharmacologic. Non-pharmacological treatments include occlusal bite splints that
are extensively used in clinical practice to provide protection against tooth damage,
although there is a lack of evidence to support their role in halting bruxism [88].
Furthermore, side effects of such treatment include changes in dental occlusion,
dental hypersensitiveness, and worsening of orofacial pain and SDB by reducing the
intraoral cavity space [91]. Patients should be followed by a dentist who can
Table 18.6 Diagnostic criteria for sleep-related bruxism
Tooth-grinding sounds or tooth clenching during sleep
One or more of the following are present: abnormal wear of the teeth, jaw muscle discomfort,
fatigue or pain, and jaw lock upon awakening
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monitor dental wear. Excessively worn teeth may need to be crowned. OSA is a risk
factor for sleep-related bruxism, and successful treatment of sleep-disordered
breathing may eliminate bruxism during sleep [92]. Psychological counseling may
be helpful in stress-related cases of bruxism. Albeit, there is little evidence to support the use of antidepressants to treat bruxism. Amitriptyline (a tricyclic antidepressant) was found to be ineffective, and SSRI worsened bruxism in some reports
[93, 94]. Benzodiazepines and muscle relaxants may be necessary in more severe
cases though they may contribute to daytime sleepiness. Randomized, controlled,
and double-blinded studies investigating the pharmacologic therapies for sleeprelated bruxism are lacking. Other medications that have been reported to be used
for bruxism include propranolol, -dopa, pergolide, bromocriptine, clonidine, and
gabapentin [95–99]. A recent systematic review of four randomized controlled trials
assessing the effect of botulinum toxin in the treatment of bruxism concluded that
botulinum toxin injection in the masseter muscles resulted in a signicant reduction
of the frequency and severity of bruxism episodes, as well as pain intensity and
improved patients’ quality of life. In addition, doses <100IU are safe and effective
treatment with a low risk of adverse side effects. Therefore the authors recommended botulinum toxin in patients with severe bruxism who did not respond to
conventional therapy [100].
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Sleep-Related Rhythmic Movement Disorder
Described in 1905 by Zappert as “jactatio capitis nocturna” and independently by
Cruchet as “rhythmie du sommeil,” the term “rhythmic movement disorder” was
adopted by the ICSD in 1990. RMD is characterized by repetitive, stereotyped, and
rhythmic motor behaviors that occur predominantly during drowsiness or sleep and
involve large muscle groups. Initially classied as a sleep-wake transition disorder,
the revised ICSD reclassied RMD under the heading of sleep-related movement
disorders. Sleep-related rhythmic movements are normal in children, and a disorder
should be diagnosed when signicant consequences are present. RMD is typically
seen in infants and children. Body rocking, head banging, and head rolling are subtypes of RMD.Combined types may also be observed.
Demographics
RMD is most commonly observed in children. The incidence of RMD is 66% in
9-month-old infants and decreases to 8% in 4-year-olds [101]. In one study, head
banging persisted beyond the age of 4in 30% of patients but usually ended by age 10
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Table 18.7 Diagnostic criteria for sleep-related rhythmic movement disorder (RMD)
Repetitive, stereotyped, and rhythmic motor behaviors
Involving large muscle groups
Movements are predominantly sleep related or occur near nap or bedtime
A signicant complaint such as interference with sleep, signicant impairment in daytime
function, or self-inicted bodily injury is present
Rhythmic movements are not better explained by another disorder
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[102]. Though most common in children, RMD has also been reported in adolescents
and adults. When observed in older children and adults, there have been conicting
reports regarding persistent RMD and its association with neurodevelopmental and
psychiatric disorders as cases in adults of normal intelligence have been reported
[103–105]. Therefore, there is insufcient evidence to fully understand the true natural history of the condition. No sex differences have been found in patients with RMD.
Diagnosis
RMD can be recognized by its characteristic clinical features. However, in some
instances PSG may be useful. The diagnosis of RMD according to the ICSD-3
requires the following: (a) The patient exhibits repetitive, stereotyped, and rhythmic
motor behaviors involving large muscle groups. (b) The movements are predominantly sleep related, occurring near nap or bedtime or when the individual appears
drowsy or asleep. (c) The behaviors result in a signicant complaint as manifest by
at least one of the following: interference with normal sleep, signicant impairment
in daytime function, or self-inicted bodily injury or likelihood of injury if preventive measures are not used. (d) The rhythmic movements are not better explained by
another movement disorder or epilepsy [1] (Table18.7).
Associated Features
While PSG have shown rhythmic movements to occur most often in stage N1 and
N2 sleep, there have been reports of RMD in REM (24%) [104, 106, 107]. In the
case of RMD occurring in REM sleep, concurrent RBD has not been reported
[104, 107, 108]. Exclusively REM-RMD occurs more frequently in adults. The
most common subtypes of RMD are body rocking (19.1%), head banging (5.1%),
and head rolling (6.3%). Body rolling, head rolling, and leg banging subtypes have
also been described. As noted previously patients may also have combinations of
the noted subtypes. Sleep is not fragmented by RMD and sleep stages do not
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usually change as a result of movement. RMD does not usually interrupt sleep and
patients have minimal recall. A review of ten subjects with RMD persisting beyond
5years of age found a strong association with ADHD [104]. Several studies have
reported RMD in adults with OSA with RMD initiated by arousals at the termination of the apneas. Improvement in RMD was noted with treatment of OSA with
CPAP [109–111]. PSG is useful to uncover RMD aggravated by another sleep
disorder, such as OSA, RBD, and RLS.On PSG the frequency of movements
ranges from 0.5 to 2Hz.
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Differential Diagnosis
The clinical history of RMD is usually clear though the differential diagnosis of
RMD includes RLS and sleep-related epilepsy. In contrast to RLS, the movements
of RMD are continuous for short periods of time rather than periodic jerking.
Electroencephalographic studies are normal between RMD episodes in most individuals. Polysomnographic ndings of RMD may be confused with bruxism, thumb
sucking, and rhythmic sucking of the lips or a pacier. RMD should also be distinguished from akathisia which is not sleep related and involves a feeling of generalized restlessness.
Treatment
For the majority of RMD patients, no treatment other than reassurance is required.
Parents should be advised that neurologic damage is unlikely and that the child will
outgrow the problem. RMD has rarely been associated with head injury, carotid
artery dissection, and ocular injury [112–114]. In cases where there is concern
regarding serious injury, treatment is warranted. There is a lack of systematic studies assessing the risk of injury or daytime consequences of RMD and clinical trials
evaluating its treatment. Contemporary management of RMD is guided by clinical
experience and reports of case studies. Hypnosis was reported as an effective treatment in a 26-year-old woman with body rocking since infancy [115]. Other treatments that have been used include behavioral interventions [116]. Almost complete
resolution of rhythmic movements was noted in six children with 3weeks of controlled sleep restriction with hypnotic administration in the rst week [117].
Tricyclic antidepressants have also been used to treat RMD.One study documented
failure of doxepin, amitriptyline, and imipramine, while another reported success
with imipramine [118, 119] . In one report citalopram at a dose of 20 mg was
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effective in eliminating head banging in a 5-year-old with ADHD [120]. Several
studies have demonstrated the utility of low-dose clonazepam. Clonazepam at a
starting dose of 0.5mg was not sufcient to decrease the intensity or frequency of
events, but 1mg was found to be effective [121, 122]. The use of the dopamine
antagonists haloperidol and pimozide decreased the intensity and duration of head
punching in a 17-year-old boy [123].
S. Zeineddine and N. S. Undevia
Propriospinal Myoclonus at Sleep Onset
Propriospinal myoclonus at sleep onset (PSM) was rst described in 1997in
three patients with jerks occurring only during relaxed wakefulness preceding
sleep and at the sleep-wake transition (N1 sleep) and quickly disappears when
N2 sets in [124–126]. Few reports showed persistence of jerks during sleep
[127, 128]. Myoclonus is termed “propriospinal” when it doesn’t remain
restricted to its segmental origin and it propagates along the spinal cord with a
slow conduction velocity. PSM usually originates from the thoracoabdominal
myelomere and less often from cervical ones. It provokes spontaneous and
repetitive exion of the trunk and neck. Less frequently an extension pattern has
been reported.
Finally, a striking shift came with the rst description of a case of functional
(psychogenic) PSM and with the paper by Kang and Shon reporting that the typical
pattern of PSM may be mimicked voluntary by healthy volunteers [129, 130].
Afterward, a number of cohorts with functional PSM have been described and so
far, and more than 50% of all the reported cases of PSM appear to be functional
[131]. Hence, our current knowledge of PSM presents heterogeneous features that
are difcult to disentangle.
Diagnosis
PSM was previously classied among the “isolated symptoms, apparently normal
variants and unresolved issues.” ICSD-3 reclassied PSM at sleep onset among the
“sleep-related movement disorders” since it is very rarely associated with spinal
injury or disease and most patients with this disorder have a normal spinal MRI.Its
diagnosis compromises a combination of all the following criteria: (a) A complaint
of sudden jerks, mainly of the abdomen, trunk, and neck. (b) The jerks appear during relaxed wakefulness and during sleep-wake transition. (c) The jerks disappear
upon mental activation and with onset of stable sleep. (d) The jerks are so bothersome, and they preclude sleep onset. (e) The disorder is not better explained by
another sleep, mental, medical, or neurological disorder, as well as by a medication
or substance use disorder [1] (Table18.8).
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Table 18.8 Diagnostic criteria for propriospinal myoclonus at sleep onset
Sudden jerks, mainly of the abdomen, trunk, and neck
The jerks appear during relaxed wakefulness and during sleep-wake transition
The jerks disappear upon mental activation and with onset of stable sleep
The jerks are so bothersome, and they preclude sleep onset
The disorder is not better explained by another sleep, mental, medical, or neurological disorder,
as well as by a medication or substance use disorder
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Demographics
Epidemiologic data are lacking. PSM appears to be typical of middle-aged subjects
and extremely rare in children [131]. PSM is considered position dependent, with
worsening in the supine position in >50% of the cases. In at least one-third of the
cases, the movements are stimulus-sensitive.
Associated Features
PSM appears to be idiopathic in around 80% of cases. Etiology is postulated to
involve a functional abnormality of the spinal generator with afferent stimuli from
the distal part of the spinal cord triggering hyperexcitability of the myoclonic volleys [131]. The remainder consists of “symptomatic forms” that include a wide
range of organic lesions of the spine or other central nervous system levels and
medical conditions such as herpes zoster, Lyme disease, hepatitis C, myasthenia
gravis, breast cancer, and Escherichia coli infection. Isolated reports associated the
development of PSM with use of certain drugs such as interferon-alpha, intrathecal
bupivacaine, ciprooxacin, and cannabis; however, causality remains to be proven
[132–136]. Sleep-onset insomnia is a common and peculiar feature of PSM.The
movements disappear once stable sleep is reached but may reappear during arousals or awakenings with similar features. Patients may develop a fear of falling
asleep, anxiety, and depression. PSM has also been described in association with
RLS [137]. Remarkably, in those patients PSM coexisted with prominent PLM
during relaxed wakefulness and signicant restlessness and leg discomfort, typical of RLS.
Differential Diagnosis
The sleep-wake transition stage appears to act as a pacemaker for many sleep- related
movement disorders besides PSM, such as hypnic jerks and restless legs syndrome
(RLS). Hypnic jerks similarity to PSM might be the caudal propagation from facial
and cervical muscles but is easily differentiated given the absence of periodicity and
slow propagation velocity. Hypnic jerks do not typically cause sleep-onset insomnia, a
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hallmark feature of PSM.PLMS generally spare the trunk and abdomen and are longer
in duration. RLS is differentiated from PSM given associated prominent leg discomfort. Functional (psychogenic) PSM mimics a typical PSM presentation in healthy
adults; however the muscle recruitment pattern and the spread velocity differ [130].
Associated psychological disturbances as well as intraindividual variability over time
are also common features on functional PSM.Differentiating PSM and tic disorders
should also be taken into account. The “tic-like” myoclonus with jerks, involving the
trunk and arms, if present, lacks the positional triggering (supine position) and is not
usually limited to the trunk. Finally, epileptic myoclonus is not conned to relaxed
wakefulness, and electroencephalography may show epileptic discharges.
S. Zeineddine and N. S. Undevia
Treatment
There are no current guidelines for idiopathic PSM treatment. Treatment of underlying condition is mainstay of symptomatic PSM management, even if this doesn’t
lead to a complete PSM resolution in most cases [131]. For example, almost complete resolution of PSM anterior cervical discectomy with fusion signicantly
improved PSM in a patient with cord compression in the absence of myelopathy
[138]. Clonazepam at doses 0.5–2mg given at bedtime to 65 patients was an effective treatment in 52% of patients [139]. Anecdotal use of other medical treatments
that were sporadically effective in some cases include valproate, SSRI, zonisamide,
and intrathecal infusion of baclofen [131, 140–142]. A case study of a 62-year-old
male patient with comorbid PSM at sleep onset and OSA reported that CPAP
decreased the frequency of the events [143].
Sleep-Related Movement Disorder DuetoaMedical Disorder
The ICSD-3 intends this diagnosis for sleep-related movement disorders due to an
underlying medical or neurological condition that does not meet criteria for another
specic movement disorder. Often, this is a transient diagnosis until the underlying
medical or neurological condition is fully diagnosed, and therefore the latter will
take precedence in terms of the nal diagnosis.
Diagnosis
According to ICSD-3, all the three following criteria must be met for diagnosis: (a)
The patient manifests sleep-related movements that disturb sleep or its onset. (b)
The movement disorder occurs as a consequence of a signicant underlying medical
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