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Ann Indian Acad Neurol
Ann Indian Acad Neurol
AIAN
Ann Indian Acad Neurol
Annals of Indian Academy of Neurology
0972-2327
1998-3549
Wolters Kluwer - Medknow India

AIAN-27-450
10.4103/aian.aian_38_24
Letters to the Editor
Sleep Disorders Can Only be a Risk Factor for Breathing Disorders in Amyotrophic Lateral Sclerosis if All Other Risk Factors are Excluded
Finsterer Josef
Neurology Department, Neurology and Neurophysiology Center, Vienna, Austria
Address for correspondence: Dr. Josef Finsterer, Postfach 20, 1180 Vienna, Austria. E-mail: fifigs1@yahoo.de
Jul-Aug 2024
12 4 2024
27 4 450451
15 1 2024
27 2 2024
29 2 2024
Copyright: © 2024 Annals of Indian Academy of Neurology
2024
https://creativecommons.org/licenses/by-nc-sa/4.0/ This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
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pmcDear Editor,

We read with interest Li et al.’s[1] article on a prospective, observational, monocentric study on the influence of sleep quality on respiratory functions in 63 patients with sporadic amyotrophic lateral sclerosis (ALS). Sleep quality was assessed using the Pittsburgh sleep quality index (PSQI), and the respiratory function was assessed using forced vital capacity (FVC).[1] According to PSQI, 38% of patients were poor sleepers and 62% were good sleepers.[1] The proportion of poor sleepers increased to 60% after 6 months and to 75% after 12 months.[1] ΔFVC was higher in poor sleepers than in good sleepers.[1] It has been concluded that poor sleep quality at the time of diagnosis of ALS is associated with rapid deterioration in respiratory function as the disease progresses.[1] The study is impressive, but several points require discussion.

The first point is that poor sleep was thought to cause breathing disorders.[1] We disagree with such a causal relationship. It is more likely the other way round that progressive involvement of the respiratory muscles leads to hypo-oxygenation, and thus sleep disorders. It is also conceivable that pain, a common non-motor symptom in ALS,[2] increases as ALS progresses and subsequently causes sleep disturbances.

The second point is that FCV depends not only on sleep quality, but also on many other factors that were not included in the assessment. These include the degree of bulbar involvement, the degree of respiratory muscle involvement, and comorbidities such as chronic obstructive pulmonary disease (COPD), emphysema, chronic bronchitis, asthma, alveolitis, lung fibrosis, pulmonary hypertension, and heart failure.

The third point is that sleep quality depends not only on respiratory muscle weakness and reduced FVC, but also on several other factors that were not included in the assessment. Poor sleep quality is multi-causal and can result from almost any disorder. Among neurologic diseases, sleep disorders have been reported particularly in epilepsy, ischemic stroke, Parkinson’s disease, pituitary dysfunction, radiculitis, neuropathy, restless leg syndrome, and myasthenia. Among psychiatric diseases, sleep disturbance has been reported in dementia, psychosis, mood and anxiety disorders, obsessive–compulsive disorders, autism spectrum disorders, and eating disorders. Sleep problems can also be due to lung disease (e.g., infection, asthma, COPD, sleep apnea syndrome), cardiac disease (e.g., heart failure, cardiomyopathy, arrhythmias), gastrointestinal disease (e.g., diarrhea, obstipation, reflux), urological disease (e.g., pollakisuria, nocturia), dermatologic disease (e.g., itching), orthopedic disease (e.g., pain), immunological disease (e.g., arthritis, colitis, Crohn’s disease), or peripheral artery disease. In addition, sleep quality also depends heavily on lifestyle and exogenous factors, such as eating habits, timing of water and food intake, taking illegal drugs, and the use of adrenergic stimulants such as nicotine, caffeine, cola, Red Bull, or alcohol abuse.[3] The noisy sleeping place, the personality structure, humidity and temperature at the sleeping place, and the pattern of social interactions were also not taken into account.

The fourth point is that it was not mentioned how many of the 63 ALS patients had bulbar ALS and how many had limb ALS. Respiratory muscle involvement occurs more rapidly in patients with bulbar-onset ALS than in patients with limb-onset ALS.

The fifth point is that oxygen saturation was not measured at night or during the day. It is important to know whether desaturation occurred especially at night, as this may be responsible for poor sleep quality.

The sixth point is that sleep quality was assessed only through subjective assessment and not through systematic sleep studies. To find out the causes of sleep disturbance in ALS patients, it is mandatory to systematically test all the included patients in a sleep laboratory before admission and at follow-up after 6 and 12 months.

The seventh point is that we should know how many of the included patients had sporadic ALS and how many had familial ALS. Some forms of familial ALS are known to be associated with frontotemporal dementia, an increasingly recognized feature and a known risk factor for sleep disturbance.[4]

The eighth point is that current medication was not included in the assessment.[1] Psychotropic drugs (e.g., hypnotics, sedatives, antidepressants, neuroleptics), steroids, adrenergic drugs, antiepileptic drugs, anti-Parkinson’s drugs, beta-blockers, cholinesterase inhibitors (e.g., donepezil, rivastigmine, galantamine), decongestants, and caffeine-containing drugs can heavily influence sleep quality.[5]

To sum up, the excellent study has limitations that should be addressed before final conclusions are drawn. Clarifying the weaknesses would strengthen the conclusions and improve the study. Before respiratory dysfunction in ALS can be attributed to poor sleep quality, all other factors affecting the respiratory function and sleep in ALS must be ruled out as alternative causes.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.
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REFERENCES

1. Li X Liu Q Niu T Jia H Liu T Xin Z Sleep disturbances as a potential risk factor for deterioration of respiratory function in patients with amyotrophic lateral sclerosis Ann Indian Acad Neurol 2023 26 754 60 38022487
2. Shojaie A Al Khleifat A Opie-Martin S Sarraf P Al-Chalabi A Non-motor symptoms in amyotrophic lateral sclerosis Amyotroph Lateral Scler Frontotemporal Degener 2024 25 61 6 37798838
3. Antila H Kwak I Choi A Pisciotti A Covarrubias I Baik J A noradrenergic-hypothalamic neural substrate for stress-induced sleep disturbances Proc Natl Acad Sci USA 2022 119 e2123528119 36331996
4. Dedeene L Van Schoor E Vandenberghe R Van Damme P Poesen K Thal DR Circadian sleep/wake-associated cells show dipeptide repeat protein aggregates in C9orf72-related ALS and FTLD cases Acta Neuropathol Commun 2019 7 189 31791419
5. Jain SV Glauser TA Effects of epilepsy treatments on sleep architecture and daytime sleepiness: An evidence-based review of objective sleep metrics Epilepsia 2014 55 26 37 24299283
