2. Ekbom syndrome aka Anxietas tibiarum
Leg jitters- colloquial term
Periodic limb movements in sleep (PLMS)
Motor counterpart of RLS
Formerly nocturnal myoclonus and periodic
leg movements in sleep.
3. Affects about 10% of adults
Approximately one third-symptoms prior to
age of 18
Prevalence-increases with age
More common in females
Family history-frequently in those who
experience early symptoms.
4. Early-onset RLS-starts before age of 45
years, progress gradually.
Late-onset RLS-advances more quickly and
occurs more often.
Primary RLS- occurs independently of other
disorders.
Secondary RLS- precipitated by other
disorders and resolves when other disorders
treated.
7. Characterised-irresistible urge to move legs
especially at rest.
Symptoms worsen in evening and night and
improve with activity such as walking.
Sensations described as crawling, pins and
needles, tingling, prickly, painful, or worming
or other indescribable feelings in their legs.
May simply have a need to move.
Sensation decreased by movement,
massaging.
8. Rarely occur on arms
Can cause sleep disturbances
Most have mild or intermittent symptoms
30 percent-moderate to severe symptoms.
Severe-15 days or more per month.
Often associated with depression and anxiety
Can have negative effect on quality of life.
9. Periodic limb movements of sleep (PLM or
PLMS)
Brief repetitive movements
Mostly of legs
Occur every 20-40 seconds.
Often present in RLS patients
Initial jerk followed by tonic spasm.
Dorsiflexion of big toe, foot and even leg
Occurs during stage I and II of sleep
10. Underlying causes of RLS or PLMS remain unclear
Central dopaminergic system, particularly
striatonigral system, implicated
Hypothesis supported by beneficial effects of
dopaminergic agents
SPECT and PET-reduced striatal D2 receptor
binding using123I-IBZM and 11C-raclopride.
18F-DOPA PET-decrease in striatal18F-DOPA
uptake
Decrease in cerebral blood flow in caudate nuclei
and increase in anterior cingulate gyrus-familial
RLS.
11. Reduced CSF ferritin and increased transferrin
concentrations in idiopathic RLS
Serum iron concentrations exhibit circadian
variation with up to 50% drop in iron
concentration at night
Iron-cofactor for hydroxylation of tyrosine
hydroxylase-rate limiting enzyme for
dopamine production.
12. PLMS and spinal flexor reflexes share
common spinal origin
Disinhibition of reticulospinal excitatory
responses may lead to pathological
recruitment of spinal motor neurons.
Spinal flexor reflexes seem to be under
partial dopaminergic control and levodopa
depresses both facilitatory and inhibitory
flexor reflex afferents.
13. Coexistence of RLS and Parkinson's disease is
controversial
Increased PLM index-reported in untreated
patients with Parkinson's disease.
Misdiagnosis of RLS-nocturnal dyskinesias
and akathisia in PD
Genetic basis for RLS-positive family history
in 63%-92% & autosomal dominant pattern
of inheritance
Associated with spinocerebellar ataxia (type
3).
14. Panic attacks
Akathisia
Painful legs and moving toes syndrome-similar
distribution but not relieved by movement.
“Vesper’s curse”-associated with congestive heart
failure, in which engorgement of lumbar veins at
night brings transient stenosis of lumbar cord
causing nocturnal pain in lower limbs extending
to lumbosacral region.
Polyneuropathies
Meralgia paraesthetica
Sleep onset myoclonus and nocturnal myoclonus
15. Essential criteria
Urge to move or Urge to move legs, usually
accompanied/caused by uncomfortable/
unpleasant sensations in legs.
Unpleasant sensations begin or worsen during
periods of rest or inactivity.
Urge to move or unpleasant sensations are
partially/totally relieved by movement, at least as
long as activity continues.
Urge to move or unpleasant sensations worse in
evening/night than during day, or only occur in
evening/night.
16. Positive family history of RLS.
Positive response to dopaminergic Drugs.
PLMS as assessed with polysomnography or
leg activity devices.
17. Natural clinical course of disorder.
Sleep disorders-frequent but unspecific
symptom of the RLS.
Medical evaluation/physical examination:
neurological examination usually normal.
Probable causes for secondary RLS should be
excluded.
18. POLYSOMNOGRAPHY
Records PLMS
Correlates strongly but indirectly with RLS
Useful measure for diagnosing RLS and
monitoring of treatment.
Tibialis anterior muscle-recorded
PLM scoring-pathological value >five
PLM/hour of sleep.
Evidence of arousal.
19. ACTIGRAPHY
Muscle activity monitored by small portable
meter
Usually worn at ankle.
Allows monitoring in patient’s own home
Actigraphical devices do not differentiate
between PLM and other involuntary
movements associated with apnoea.
20. IMMOBILISATION TESTS
Suggested immobilisation test (SIT)-Patients
attempt to maintain seated posture without
moving their legs
Forced immobilisation test (FIT)-legs are
physically restrained while anterior tibial
EMGs record PLM
Discomfort of patients.
21. Primary RLS-require treatment throughout
their lives
Secondary RLS -remit underlying condition
resolved
RLS treatment symptomatic, not preventive.
Non-pharmacological measures-advice on
improvement of sleep hygiene and avoidance
of stimulants or aggravating drugs (caffeine,
alcohol, hot baths).
22. Levodopa
In primary RLS and at short-term follow-up-
effective in reducing symptoms of RLS and
improving sleep quality and quality of life and
reducing PLMS (level A rating).
Adverse events minor (level A).
In long-term follow-up its still effective
30–70% dropped out due to adverse events or
lack of efficacy (level C).
23. Augmentation-20-82%
In RLS secondary to uraemia, at short-term
follow-up, levodopa probably effective in
reducing symptoms, improving quality of life
and reducing PLMS (level B).
24. Ergot derivatives
In primary RLS pergolide effective at mean
dosages of 0.4–0.55 mg/day (level A)
Possibly effective in long term (level C).
Cabergoline effective at 0.5–2 mg/day (level
A) and possibly effective in long term (level
C).
Bromocriptine 7.5 mg probably effective
(level B).
25. In secondary RLS associated with chronic
haemodialysis, pergolide probably ineffective
at 0.25 mg/day (level B).
Adverse events- nausea, headache, nasal
congestion, dizziness and orthostatic
hypotension
Augmentation not assessed with pergolide in
class I studies
26. Non ergot derivatives
Primary RLS ropinirole effective 1.5–4.6 mg/day
(level A)
Rotigotine transdermal patch delivery effective
in short term (level A)
Pramipexole probably effective (level B).
In RLS secondary to uraemia ropinirole probable
effective (level B).
Augmentation-7% with ropinirole (class I
evidence).
Insufficient evidence about use of non-ergot in
PLMD.
27. Gabapentin 800–1800 mg/day effective in
primary RLS (level A) and probably effective in
secondary RLS after haemodialysis (level B).
Carbamazepine 100–300 mg and valproate
slow release 600 mg/day-probably effective
in primary RLS (level B).
Pregabalin also effective.
28. Clonidine-probably effective in reducing
symptoms and sleep latency in primary RLS at
short term (level B).
Mean dosage 0.5 mg 2 h before onset of
symptoms) for 2–3 weeks
Adverse events (dry mouth, decreased
cognition and libido, lightheadedness,
sleepiness, headache
Other drugs-talipexole, propranolol and
phenoxybenzamine
29. Clonazepam -probably effective for
improving symptoms in primary RLS when
given at 1 mg before bedtime
Probably ineffective when given at four doses
(level B).
For PLMD, clonazepam at 0.5–2 mg/daily
probably effective (level B)
Triazolam (0.125–0.50 mg/day)-probably
effective in ameliorating sleep efficiency and
probably ineffective in reducing PLMS (level
B).
30. Adverse events-morning sedation, memory
dysfunction, daytime somnolence and
muscle weakness
No recommendation for other
benzodiazepines/hypnotics and in secondary
RLS.
31. Primary RLS oxycodone at 11.4 mg probably
effective in improving RLS symptoms, PLMS and
sleep efficiency on short-term basis (level B).
Adverse events-mild sedation and rare nocturnal
respiratory disturbances on long-term use
Insufficient evidence about morphine, tramadol,
codeine and dihydrocodeine, tilidine, and
methadone and intrathecal route
Insufficient evidence in secondary RLS.
32. Primary RLS iron sulphate at daily dose
325mg probably ineffective (level B).
Insufficient evidence to about use of
intravenous iron dextran, magnesium oxide
and amantadine.
In RLS secondary to uraemia, iron dextran
1000 mg in single intravenous dose is
probably effective in short term (<1 month)
(level B).
Iron sucrose ineffective.
33. PLMS- transdermal oestradiol ineffective
(level A)
Modafinil and 1-day nocturnal haemodialysis
probably ineffective(level B)
Cognitive-behavioural therapy as effective as
clonazepam (level B).
5-OH-tryptophan, trazodone possibly
ineffective
Apomorphine and physical exercise (in
myelopathy) possibly effective (level C).
36. Algorithms for the diagnosis and treatment of restless legs
syndrome in primary care; Garcia-Borreguero et al. BMC
Neurology 2015, 11:28
Hornyak M et al; What treatment works best for restless
legs syndrome? Meta-analyses of dopaminergic and non-
dopaminergic medications. Sleep Med Rev. 2014
Apr;18(2):153-64.
Rios R. Et al; Treatment of restless legs syndrome. Curr
Treat Options Neurol. 2013 Aug;15(4):396-409.
The Treatment of Restless Legs Syndrome and Periodic
Limb Movement Disorder in Adults—An Update for 2012:
Practice Parameters with an Evidence-Based Systematic
Review and Meta-Analyses; SLEEP, Vol. 35, No. 8, 2012
EFNS guidelines on management of restless legs syndrome
and periodic limb movement disorder in sleep; European
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