Sleep attacks

Side effects include dyskinesias, orthostatic hypotension, dizziness, nausea, insomnia, sleep attacks, pathologic gambling, discoloration of urine/sweat, and psychiatric effects (confusion, hallucinations, nightmares, and altered behavior). Dyskinesias caused by adding other PD drugs to levodopa may be improved by decreasing the levodopa dose. Motor complications occur in about 40% of patients within 4 to 6 years of starting levodopa.1,8,24,25,37... 

Evaluate potential side effects of therapy, including nausea, drowsiness, sleep attacks, and headaches for the DA agents. 

Pacchetti C., Martignoni E., Terzaghi M. et al. (2003). Sleep attacks in Parkinson s disease a clinical and polysomnographic study. Neurol Sci. 24, 195-6. 

Rye D., Daley J., Freeman A., Bliwise D. (2003). Daytime sleepiness and sleep attacks in idiopathic parkinson s disease. In Bedard M-A., Agid Y., Chouinard S. et al. editors. Mental and Behavioral Dysfunction in Movement Disorders. Totawa, NJ Humana Press pp. 527-38. 

Ulivelli M., Rossi S Lombard C. et at (2002). Polysomnographic characterization of pergolide-induced sleep attacks in an idiopathic PD patient. Neurology 58(3), 462-5. 

Excessive daytime sleepiness, the irresistible need for sleep during the day, is associated with a chronically low level of alertness. The term sleep attack describes these unavoidable brief naps. Cataplexy, an abrupt decrease or loss in... 

Excessive daytime sleepiness and sleep attacks Very high (95) Very low (5) Wide differential diagnosis for this complaint Diagnosed clinically very disabling symptom... 

Figure 15.3 EEG/EMG recordings showing the differences between cataplexy (A) in an orexin l mouse, and a sleep attack (B) in an OX-jR mouse. Note how cataplexy (i.e. an abrupt arrest) is associated with a transition to REM sleep, but the sleep attack (i.e. a gradual arrest) shows the characteristics of non-REM sleep after the transition. In fact, based only on these EEG/EMG records, the sleep attack would not appear unusual, and it is the associated behavior, as revealed on the concurrent video recordings (i.e. the collapse into sleep without the typical preparatory behaviors), that reveals how this type of attack is similar to the overwhelming sleepiness experienced by the narcoleptic patient. Vertical arrows denote the times at which an arrest is behaviorally evident. Scale bar is 10 sec. Adapted from Willie et al. (2003).

Common side effects of dopamine agonists are nausea, confusion, hallucinations, lightheadedness, lower-extremity edema, postural hypotension, sedation, and vivid dreams. Less common are compulsive behaviors, psychosis, and sleep attacks. Hallucinations and delusions can be managed using a stepwise approach (Table 55-4). When added to L-dopa, dopamine agonists may worsen dyskinesias. 

The essential features are sleep attacks, cataplexy, hypnagogic hallucinations, and sleep paralysis. Individuals with narcolepsy complain of excessive daytime sleepiness, sleep attacks that last up to 30 minutes, fatigue, impaired performance, and disturbed nighttime sleep. They have multiple arousals during the night. 

Narcolepsy is sometimes termed a dyssomnia, but whatever classification is used, it essentially represents an intrusion of REM sleep into wakefulness. Narcolepsy is comprised of a quartet of potential symptoms, but only a few individuals exhibit all four narcolepsy symptoms. The most common symptom of narcolepsy is the sleep attack. Sleep attacks consist of an irresistible urge to fall asleep and can occur several times each day. Patients with narcolepsy usually feel refreshed and energized after a 10-20 minute nap however, their sleepiness returns after just a few hours. 

To fulfill the diagnostic criteria for narcolepsy, a person must have sleep attacks occurring at least daily for 3 months. In addition, at least one of the so-called... 

The first symptoms of narcolepsy usually begin during childhood or in the early teen years and commonly involve excessive drowsiness and sleep attacks. Several years later, one or more of the auxiliary symptoms arise. 

Other Hypersomnias. Narcolepsy is not the only hypersomnia, but it is by far the most common. Primary hypersomnia shares sleep attacks and excessive daytime sleepiness with narcolepsy but does not feature cataplexy or REM-associated abnormalities. Another rare hypersomnia is Kleine-Levin syndrome (KLS), which most often occurs in teenage boys. KLS consists of intermittent bouts of hypersomnia and bizarre behaviors including compulsive eating and sexual inappropriateness. Distinguishing these hypersomnias from narcolepsy may help clarify the patient s prognosis, but the treatment alternatives are very similar. 

Seizure Disorders. Narcolepsy is not a form of epilepsy. Although the sleep attacks and cataplexy resemble certain forms of seizures, narcolepsy can easily be distinguished from epilepsy. In particular, those with narcolepsy remain aware of their surroundings during an attack of cataplexy, whereas the epilepsy patient has no recall of events associated with a seizure. Furthermore, the EEC recording during a sleep study typically distinguishes narcolepsy from seizures. 

Stimulants. Treatment for narcolepsy has focused on its most disabling symptoms namely, sleep attacks and daytime drowsiness. The mainstay of treatment has... 

Pemoline is a less potent stimulant than methylphenidate or dextroamphetamine. It should be initiated at 18.75 mg taken each morning with breakfast and can be increased in increments of 18.75mg every week or so. Typical dosing for pemoline ranges from 60 to 200mg/day in treating narcolepsy. Because pemoline is less potent than other stimulants, it is more likely to be ineffective, even at its higher doses. When pemoline does not relieve daytime sleepiness or sleep attacks, then the patient should be switched to a different stimulant. 

Short-Term Treatment. In the acute phase of treatment, a stepwise approach is often warranted. The medication should be targeted at the most distressing symptom of narcolepsy first. This is almost invariably the sleep attacks and daytime drowsiness. 

Should the first medication fail to provide satisfactory relief from the drowsiness and sleep attacks of narcolepsy, the patient should be switched to an alternative... 

One change that is sometimes made during long-term treatment is the addition of a second medication to treat the auxiliary symptoms of narcolepsy. For many patients, these other symptoms do not occur often enough or are not severe enough to require treatment. However, the auxiliary symptoms (especially cataplexy) can be a big problem for some narcolepsy patients. The stimulants used to treat the sleep attacks can also provide some mild relief of cataplexy, but the benefit is often not sufficient. 

Narcolepsy is another medically recognized indication for the use of the psychomotor stimulants. This disorder is characterized by sleep attacks, particularly during the day, sudden loss of muscle tone cataplexy), sleep paralysis, and vivid visual and auditory nightmares that may persist into the waking state. Drugs that influence the central action of adrenomimetic amines re-... 

Narcolepsy (ICD G47.4) and other types of hypersomnia are severe disturbances of vigilance expressed as a sudden and irresistible requirement for sleep during the day, so-called sleep attacks (Aldrich. 1990). Apart from sleep attacks, the classical tetrad of narcolepsy includes cataplexy (sudden loss of muscular tone), sleep paralysis (waking from sleep with the feeling of not being able to move) and hypnagogic hallucinations (linages or sequences of... 

In narcolepsy, subjects may reverse the normal trajectory as shown in figure 2.8 and enter REM directly from waking at both nocturnal sleep onset and during daytime sleep attacks. This propensity is caused by a combination of relatively weak aminergic drive and reciprocally intensified cholinergic drive, which result in a marked lowering of the wake-REM threshold. 

Figure 7 PVT reaction times prior to the first uncontrolled sleep attack during total sleep deprivation. Fourteen subjects completed 42 hr of total sleep deprivation and completed a 20-min PVT every 2 hr (represented by the closed circles) 19 subjects completed 88 hr of total sleep deprivation and completed a 10-min PVT every 2 hr (represented by the open circles). The number of test bouts (up to 30) prior to an uncontrolled sleep attack (failure to respond for 30 sec on the PVT) is represented on the bottom abscissa, with time prior to the sleep attack (up to 6 min) represented on the top abscissa. In both subject groups a progressive decline in performance on the visual PVT was evident within minutes of an uncontrolled sleep attack on console. This study also demonstrated an increase in subjective sleepiness (measured using the Stanford Sleepiness Scale) in the test bouts prior to the one in which the first sleep attack occurred. Taken together, these findings suggest that even a very sleepy subject cannot fall asleep while performing computerized tasks without some levels of awareness. (From Ref. 95.)...

Excessive daytime sleepiness is found in approximately 15% of Parkinson s patients (104). This is compared with an incidence of approximately 1% in the general population. Excessive daytime sleepiness is typically associated with the anti-Parkinson s medication being taken, such as L-dopa (113). The occurrence of daytime sleep attacks is not commonly associated with Parkinson s disease, but their incidence increases in association with administration of dopaminergic medications (104,113). 

Studies (42 14) showed that patients treated with antiparkinsonian drugs suffer from sleep attacks. These attacks were responsible for traffic accidents (45) modafinil can efficiently counterbalance this symptom in patients suffering from Parkinson s disease (46). 

Ferreira JJ, Galitzky M, Montastruc JL, Rascol O. Sleep attacks and Parkinson s disease treatment. Lancet 2000 355 1333-1334. 

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