|
Parasomnias are a group of disorders which take place around sleep. They
may occur with arousal, partial arousal, or sleep transition. Most
parasomnias are a manifestation of central nervous system activations, and
as a result they are expressed primarily through motor behaviors or
autonomic arousal.
Introduction. Parasomnias are a group of disorders which take
place around sleep. They may occur with arousal, partial arousal, or sleep
transition. Most parasomnias are a manifestation of central nervous system
activations, and as a result they are expressed primarily through motor
behaviors or autonomic arousal.
Sleep Terrors and Nightmares. Sleep terrors consist of sudden arousals from
Stage 3/4 sleep, usually the first third of the night. A patient will
suddenly scream or cry out and then display an intense autonomic response to
perceived panic and fear. There is marked tachycardia, tachypnea,
diaphoresis, and mydriasis sometimes accompanied by incomprehensible
vocalizations. Episodes last up to 15 minutes after which a patient will
promptly fall back to sleep. The patient is amnestic for the event the
following day.
Sleep terrors typically occur in children, but may rarely persist or present
in adults in the third decade. A male predominance has been noted.1
Nightmares are distinguished from sleep terrors by time of onset and
clinical behavior.
Nightmares occur in REM (not Stage 3/4) sleep and usually in the last (not
first) third of sleep. Screaming is infrequent and autonomic activity is
minimal. Patients are frightened, awake, coherent, and describe
detailed imagery when recalling their nightmare. The following day, rather
than being amnestic for the event, the patient has vivid recall of the
nightmare. In some cases, when nightmares recur frequently, a patient may
even come to fear sleep.
The differential diagnosis for sleep terrors and nightmares includes
nocturnal sleep related seizures. A polysomnogram (PSG) will show episodes
occurring in the appropriate stage of sleep. An electroencephalogram (EEG)
should show epileptiform activity only in patients with epilepsy. Sleep
terrors occur in slow wave sleep (first third), night terrors in REM (last
third), and complex partial seizures in any stage. Autonomic symptoms are
seen primarily in sleep terrors, sleep phobia, and nightmares. Postictal
confusion with amnesia for the event can be either a sleep terror or a
complex partial seizure.
The treatment of sleep terrors includes patient and family education, sleep
hygiene, and possibly family counseling, psychotherapy, or relaxation
techniques. Diazepam (Valium)
2 mg to 10 mg at bedtime can be a temporary treatment. Imipramine may also
suppress episodes.1
REM Behavioral Disorder. Rapid eye movement sleep behavioral disorder (RBD)
is characterized by intermittent loss of REM sleep muscle inhibition.2
Normally during REM sleep, there is muscle atonia and the patient lies
still. In RBD, REM sleep is associated with elaborate motor activity. While
a patient is dreaming, there may be punching, kicking, leaping, or running
as a patient acts out his or her dreams.
RBD primarily occurs in the sixth and seventh decade with a large male
prominence. Etiology in half of cases is idiopathic, whereas half are due to
neurological causes.3 These illnesses include olivopontocerebellar atrophy (OPCA),
subarachnoid hemorrhage, dementia, Parkinson’s disease, cerebrovascular
disease, multiple sclerosis, brain stem lesions, or neoplasms. Hence, a
brain MRI may be indicated in a patient diagnosed with RBD to rule out an
underlying structural lesion.
The diagnosis of RBD is made using polysomnogram and clinical data.
Polysomnogram criteria include augmentation of chin muscle tone, excessive
chin or limb phasic muscle twitching, limb or body jerking, complex violent
behaviors, and absence of any electroencephalogram seizure pattern, or any
epileptic activity during REM sleep. The PSG is otherwise completely normal.
Clinically, a patient displays violent behaviors in sleep which may lead to
injuries such as bruises, fractures, or lacerations. Body movement
associated with dreaming and behavior disrupting sleep continuity are also
noted. There is lack of association with any psychiatric disorder. Other
sleep disorders, such as sleep walking, can be present, but are not the
cause of the nocturnal behaviors.
Benzodiazepines are the treatment of choice for RBD. Clonazepam (Klonopin)
doses of 0.5 mg to 1.5 mg at bedtime are effective in controlling the
inappropriate motor behaviors. The risk of dosage tolerance, adverse
affects, or abuse, has been shown to be low in patients treated long term.4
A safe bedroom environment should also be maintained.
Nocturnal Paroxysmal Dystonia and Epilepsy. Nocturnal paroxysmal dystonia (NPD)
consists of recurrent stereotype dystonic episodes occurring during non-REM
sleep. NPD is also known as extrapyramidal seizures, Choreoathetosis
seizures, paroxysmal kinesogenic dystonia, or hypnogenic paroxysmal dystonia.
Clinically a patient displays dystonia or dyskinetic movements in sleep
which may be brief and last from 15 to 60 seconds in non-REM sleep, but is
otherwise normal. The movements in NPD do not meet criteria for other sleep
disorders, such as sleep terrors or RBD.
The differential diagnosis of NPD includes sleep related frontal lobe
epilepsy and there are arguments that they represent the same entity. In one
study of patients with nocturnal paroxysmal arousals with motor behaviors,
80% demonstrated epileptiform abnormalities on EEG.5 While the presence of
epileptiform activity can confirm the diagnosis of epilepsy, its absence
does not exclude frontal lobe epilepsy (FLE). Abnormalities in FLE may
originate in orbital frontal or medial frontal regions which are difficult
to record with surface EEG.6
Clinically FLE and NPD are similar with dystonia often seen in three or four
limbs. Confirmed cases of nocturnal FLE demonstrate seizures with abrupt
onset, rapid, often dystonic, movements, and nocturnal clustering. There is
a spectrum of behaviors ranging from brief arousal to nocturnal wandering.
An autosomal dominant FLE has recently been described.7, 8 Attacks occur in
non-REM sleep (especially Stage II), as is seen in NPD.
Sleep Apnea Syndrome and Epilepsy. There exists a complex relationship
between sleep and epilepsy. Patients with epilepsy are more prone to sleep
disorders. Sleep disruption may in turn aggravate a person seizures. Many
patients with epilepsy complain of daytime somnolence. Although sleepiness
is often blamed upon antiepileptic medications, poor seizure control, or
sleep related seizures, it appears these factors may be totally uninvolved.
Instead the presence of concurrent sleep disorders, such as sleep apnea
syndrome or restless legs syndrome was the main predictor or daytime
sleepiness in one study of persons with epilepsy.9 High risk patients are
obese and have a history of snoring, apnea, and daytime somnolence.
Sleep apnea syndrome is characterized by numerous apneic episodes resulting
in oxygen desaturation, hypoxemia, and arousal. Chronic sleep deprivation
develops and daytime sleepiness ensues. Diagnosis is by polysomnogram, which
usually shows an elevated respiratory disturbance index (number of apneas
and hypopneas per hour), usually with significant oxygen desaturation. The
resulting sleep deprivation, hypoxemia, impaired cardiac output and
decreased cerebral blood flow may all exacerbate a patient’s seizures.
Treating the sleep apnea may improve seizure control.10,11
Mild to moderate sleep apnea may be treated with protriptyline (Vivactil) or
acetazolamide (Diamox). Moderate to severe cases, however, require more
definitive treatment such as nasal continuous positive airway pressure (CPAP).
In patients unable to tolerate or comply with CPAP, one may try dental
prosthesis, bilevel positive airway pressure, or uvulopalatopharyngoplasty.
|
References
1. Thorpy MJ, Clovinsky PB. Parasomnias. In: The psychiatric clinics of
North America. WB Sauders Company. December 1987. Vol4:623-639.
2. Schenck CH, Bundlie SR, Ettinger MG, Mahowald MW. Chronic behavior
disorders of human REM sleep: A new category of parasomnia. Sleep
1986;9(2):293 308.
3. Tan A, Salgado M, Fahn S. Rapid eye movement sleep behavior disorder
preceding parkinson disease with therapeutic response to levodopa. Movement
Disorders. 1996;11(2):214-216.
4. Schenck CH, Mahowald MW. Long term nightly benzodiazepine treatment of
injury as parasominas and other disorders of disruptive nocturnal sleep in
170 adults. Am J Med. 1996;100(3):333-337.
5. Zucconi M, Oldania, Ferini-Strambi L, Bizzoero D, Ferini S. Nocturnal
paroxysmal arousal with motor behaviors during sleep; frontal lobe epilepsy,
or parasomnia? J Cln Neurophysiology. 1997;14(6):513-522.
6. Tinuper P, Cerullo A, Cirignotta F, Corelli P, Lugaresi E, Montagenia P.
Nocturnal paroxysmal dystonia with short lasting attacks, three cases with
evidence for an epileptic frontal lobe origin of the seizures. Epilepsia.
1990;31:548-556.
7. Scheffer IE, Bhatia KP, Lopescends I, et al. Autosomal dominant, frontal
epilepsy misdiagnosed as sleep disorder. Lancet. 1994;343:151-157.
8. Oldani A, Zucconi M, Ferini-Stamabi L, Bizzorzero D, Smirene S.
Autosominal dominant, nocturnal frontal lobe epilepsy: Electroclinical
picture. Epilepsia. 1996;37(10):964-976.
9. Malow BA, Bowes RJ, Lin X. Predictors of sleepiness in an epilepsy
patient. Sleep. 1997;20(12):1105-1110.
10. Devinsky O, Eherienberg B, Barthlen GM, Abrahamson HS, Luciano D.
Epilepsy and sleep apnea syndrome. Neurology. 1994;44:2060-2064.
|
|
