**9.1 Excessive daytime sleepiness in PD**

Excessive daytime sleepiness (EDS) involves symptoms of frequent napping, feeling abnormally sleepy and sleep attacks. It is seen in 33–76% of patients with PD [100, 107] and is likely a result of damaged to the orexin-producing neurons from the posterior lateral hypothalamus involved in the wakefulness [108]. Other brainstem stimulating monoaminergic neurons are also implicated in promoting wakefulness in damaged in PD [109]. EDS is common in advanced PD and is a marker of dopamine loss [110, 111]. **Table 6** display the condition more commonly associated with EDS in PD.

**65**

**Table 7.**

*The Relationship between Amyotrophic Lateral Sclerosis and Parkinson's Disease and Sleep…*

Sleep attacks, which are defined as sudden irresistible drowsiness without awareness of falling sleep, are seen in 21% of PD patients. These are particularly concerning as they can cause serious injuries or even death, for example, as a result of a car accident when the patient falls asleep while driving [45, 55]. The Inappropriate Sleep Composite Score (ISCS) have a high specificity to detect the risk of car accidents related to EDS while driving [112]. A study with drug-naïve patients with early PD showed that patient who developed EDS after 5 years of

Management of EDS includes improving sleep hygiene, daytime regular exercises, avoid strenuous exercises a few hours before bedtime, reducing sedating medications both psychiatric (i.e. antidepressants, benzodiazepines, antipsychotics, etc.) as well as anti-Parkinson medications (particularly dopaminergic medications and levodopa), especially when used in combination [45, 114]. Stimulating anti-Parkinson medication earlier into the day such as amantadine and selegeline may help with EDS and if appropriate may be used instead of DAs [115]. If above plan

• Sodium oxybate at a dose of 3–9 grams per night at bedtime and 4 hours

treatment had higher baseline levels of drowsiness [113].

fails, consider starting stimulants such as:

later [120].

Increase total sleep time Increase sleep efficiency Reduce sleep fragmentation

Improve restless leg syndrome Improve daytime sleepiness

*Deep brain stimulation, sleep architecture and sleep disorders.*

Decrease WASO Increased slow wave sleep Increase REM sleep Improve insomnia

• Caffeine at a dose of 200 mg twice a day [116]

• Modafanil at a dose of 100–400 mg/day [117, 118].

Treatment of co-existent sleep disorders is essential.

• Methylphenidate at a dose of 1 mg/kg TID [119]

*DOI: http://dx.doi.org/10.5772/intechopen.98934*

Severe PD PD-related disability Cognitive decline Frequent hallucinations

Dementia Depression Polypharmacy

**Table 6.**

Co-existence sleep disorders High comorbid disease burden High doses of antiparkinsonian Drugs

*Cause of excessive daytime sleepiness in PD.*

*The Relationship between Amyotrophic Lateral Sclerosis and Parkinson's Disease and Sleep… DOI: http://dx.doi.org/10.5772/intechopen.98934*


#### **Table 6.**

*Updates in Sleep Neurology and Obstructive Sleep Apnea*

mic expression of melanopsin in retina ganglion cells [88].

melatonin production and sleep-awake disruption.

patients [100].

below list:

dian rhythm.

expression]

[104–106].

**9. Diurnal sleep disorders**

associated with EDS in PD.

**9.1 Excessive daytime sleepiness in PD**

blunted in PD patients [98] which correlates with the self-reported symptoms of EDS [97]. The amplitude in melatonin decreases and melatonin phase advanced in PD treated patients compared with non-treated patients indicating that as PD progresses melatonin decreases with a phase advancement [99]. Dopamine drugs affect the regulation of melatonin circadian pattern and sleep onset patients in PD

Circadian rhythm changes affect also visual performance in PD [101] most likely caused by impairment in retinal dopamine content that follows a circadian rhythm independent of light/dark cycles [102] Dopamine agonists may regulate the rhyth-

In summery the causes of CRD in PD are multifactorial and some are included

• Hypothalamic dysregulation with a decline of the SCN that lead to reduction in

• Dysregulation of the genes that control the awake-sleep cycles such as Bmal1 gene and clock genes expression [dopamine regulates the Bmal1/clock activity]

• Striatum dysregulation [dopamine controlled clock proteins Per1/Per2 gene

• Decrease rhythmic expression of retinal melanopsin [regulated by dopamine]

• Animal models of PD revealed changes in the neurons firing pattern of the SCN associated with changes in the circadian rhythm amplitude [86, 87, 103]

Light therapy is a non-invasive technique proven to be safe, well tolerated, and effective on the treatment of daily drowsiness and impair alertness in PD

Excessive daytime sleepiness (EDS) involves symptoms of frequent napping, feeling abnormally sleepy and sleep attacks. It is seen in 33–76% of patients with PD [100, 107] and is likely a result of damaged to the orexin-producing neurons from the posterior lateral hypothalamus involved in the wakefulness [108]. Other brainstem stimulating monoaminergic neurons are also implicated in promoting wakefulness in damaged in PD [109]. EDS is common in advanced PD and is a marker of dopamine loss [110, 111]. **Table 6** display the condition more commonly

• Disconnection of SCN with neuronal circuitries and hormonal signals

• SCN degeneration associated with clock gene dysregulation

that affect the entrainment of diurnal circadian rhythm

• Disorders of the sleep-awake neuronal circuity controlling the circa-

**64**

*Cause of excessive daytime sleepiness in PD.*

Sleep attacks, which are defined as sudden irresistible drowsiness without awareness of falling sleep, are seen in 21% of PD patients. These are particularly concerning as they can cause serious injuries or even death, for example, as a result of a car accident when the patient falls asleep while driving [45, 55]. The Inappropriate Sleep Composite Score (ISCS) have a high specificity to detect the risk of car accidents related to EDS while driving [112]. A study with drug-naïve patients with early PD showed that patient who developed EDS after 5 years of treatment had higher baseline levels of drowsiness [113].

Management of EDS includes improving sleep hygiene, daytime regular exercises, avoid strenuous exercises a few hours before bedtime, reducing sedating medications both psychiatric (i.e. antidepressants, benzodiazepines, antipsychotics, etc.) as well as anti-Parkinson medications (particularly dopaminergic medications and levodopa), especially when used in combination [45, 114]. Stimulating anti-Parkinson medication earlier into the day such as amantadine and selegeline may help with EDS and if appropriate may be used instead of DAs [115]. If above plan fails, consider starting stimulants such as:


Treatment of co-existent sleep disorders is essential.

Increase total sleep time Increase sleep efficiency Reduce sleep fragmentation Decrease WASO Increased slow wave sleep Increase REM sleep Improve insomnia Improve restless leg syndrome Improve daytime sleepiness

#### **Table 7.**

*Deep brain stimulation, sleep architecture and sleep disorders.*
