The Parkinson's-Reversing Breakthrough

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This is due to degeneration and loss of dopamine in the basal ganglia and causes bradykinesia, tremor and rigidity. There are two main forms which are discussed below.

Idiopathic Parkinsonism (Parkinson's disease) This is due to degeneration in the basal ganglia and related structures. The substantia nigra in the mid-brain has close relationships with the LDT/PPT in the pons which controls REM sleep, and with the raphe nuclei and locus coeruleus which are involved with NREM sleep. The initial degeneration probably occurs in the pons, which may explain the frequency of postural hypotension and the appearance of the REM sleep behaviour disorder often several years before other features of Parkinsonism appear. As the disease advances it may extend into the dorsolateral prefrontal cerebral cortex.

Several sleep abnormalities are associated with idiopathic Parkinsonism.

1 Excessive daytime sleepiness (page 158).

2 Insomnia (page 182).

3 Hallucinations and vivid dreams (page 191).

4 Motor abnormalities.

The Parkinsonian tremor is most prominent at the moment of arousal from sleep, or at transitions from a deeper to a lighter stage of sleep, and in stages 1 and 2 NREM sleep. In 10-25% of subjects the dyskinesias improve initially after sleep for between 30 min and 3 h ('sleep benefit') and then deteriorate during the day [21]. The mechanism whereby sleep may be beneficial is uncertain.

Periodic limb movements are rarely seen once treatment with dopaminergic agents has been initiated, but in untreated subjects they are frequent and often associated with the symptoms of the restless legs syndrome. Iron deficiency is often present and iron supplementation, as well as dopaminergic agents, may be of help.

Obstructive sleep apnoeas are said to be more frequent in Parkinsonism than in normal subjects, but there is no evidence to support this. The REM sleep behaviour disorder is, however, a frequent association. It occurs in around one-third of those with idiopathic Parkinsonism and often appears many years before other features of Parkinsonism. This is probably due to degeneration of the LDT/PPT and the locus subcoeruleus, leading to failure of normal motor inhibition during REM sleep. Dopaminergic treatment is ineffective, suggesting that there may be degeneration in noradrenergic or cholinergic mechanisms. Interestingly the vigorous physical enactment of dreams during REM sleep behaviour disorder is not impaired by any bradykinesia, tremor or other motor abnormality present in wakefulness.

Polysomnography characteristically shows a reduction in total sleep time and in sleep efficiency, an increase in wakefulness after sleep onset and sleep fragmentation. There is often a reduction in amplitude and frequency of sleep spindles, which can be reversed by L-dopa therapy. Sleep-onset REM sleep is common both during overnight polysomnography and during naps in the day. Muscle tone is increased in REM sleep in those with the REM sleep behaviour disorder, and REM sleep-onset blepharospasm is recognized. Periodic limb movements and sleep apnoeas may be seen.

Secondary Parkinsonism

Patients with these disorders, such as multiple system atrophy and Lewy body disease, have the same difficulties with sleep as those with idiopathic Parkinsonism, but with additional problems specific to their condition. The effects of post-encephalitic Parkinsonism are described in Chapter 6.

Multiple system atrophy. In this condition there is widespread CNS degeneration with loss of control of the autonomic nervous system. Insomnia occurs with frequent awakenings, reduction in stages 3 and 4 NREM sleep and, especially in the olivopontocere-bellar atrophy variant, loss of REM sleep duration and density, and prolonged episodes which are difficult to classify either as NREM or as REM sleep.

REM sleep behaviour disorder may appear early in its natural history and precede other features by as long as 2-3 years, and eventually appears in around 90% of subjects.

Involvement of the nucleus ambiguus impairs control of the vocal cords and leads to episodes of adduction associated with stridor and choking, often at night, but also occasionally during the day. These respond to a proton pump inhibitor since they are triggered by occult gastro-oesophageal reflux. They cause obstructive sleep apnoeas and occasionally a tracheostomy may be required. An irregular respiratory pattern with prolonged central apnoeas also develops.

Lewy body disease. This degenerative disorder is associated with Parkinsonism, progressive cognitive defects and visual hallucinations. The REM sleep behaviour disorder is present in around 25% of subjects.

Progressive supranuclear palsy (PSP). In this condition Parkinsonism is combined with dementia, dystonic gait, a disturbance of axial rigidity and a vertical voluntary gaze palsy. Degeneration develops in the core (tegmentum) of the pons and midbrain, particularly in the region of the locus coeruleus.

The sleep disturbance is proportional to the degree of motor abnormalities and can be severe. Depression, nocturia and discomfort due to immobility may all contribute to the sleep disruption. There is difficulty in maintaining sleep and early morning awakening. The REM sleep behaviour disorder occurs in 10% of subjects. Dream recall is reduced or absent due to damage to the REM sleep generating mechanisms, and there is little response of the sleep disturbances to L-dopa or dopamine receptor agonists. The main symptoms are difficulty maintaining wakefulness and early morning waking.

Polysomnography shows a reduction in total sleep time, increased sleep latency, frequent awakenings, reduction of sleep spindles, fewer REM sleep episodes and a shortened total duration of REM sleep, and there may be loss of muscle atonia during REM sleep [22].

Insomnia is more marked than in other dementias, such as Alzheimer's disease or idiopathic Parkinson-ism, and is related to the severity of the disorder.

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