Reduced evoked motor and sensory potential amplitudes in obstructive sleep apnea patients

Mihalj, Mario; Lušić, Linda; Đogaš, Zoran

doi:10.1111/jsr.12368

Cited by 10 publications

(9 citation statements)

References 35 publications

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“…Our study shows a relationship among axonal neuropathy, hypoxia parameters and nerve conduction in OSA patients, which is consistent with previous reports (9,10,13). These studies also reported that subjects with severe OSA, min SaO 2 ≤80%, and ST 90 have lower amplitude for sensory and mixed nerve action potentials, and that sural nerve velocity is slower in OSA patients (8,9).…”

Section: Discussionsupporting

confidence: 93%

“…Prevalence of polyneuropathy due to chronic hypoxia have been reported in a similar range of 28% to 70% in patients with OSA and COPD (5,(9)(10)(11). Previous studies have reported that peripheral nerve sensory amplitudes are impaired in OSA patients, but the relationship with hypoxemia has not been fully elucidated (9,12,13). We hypothesized that patients with severe OSA and hypoxia show significantly impaired peripheral nerve conduction compared to controls.…”

Section: Introductionmentioning

confidence: 91%

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Peripheral Nerve Function Changes Due to Hypoxia in Obstructive Sleep Apnea

Avci¹,

Avci²

2019

jtsm

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Periferik nöropati için risk faktörlerinden birinin kronik hipoksi olduğu bilinmektedir. Bununla birlikte, aralıklı hipoksinin periferal sinirler üzerindeki etkisi tam olarak anlaşılamamıştır. Bu çalışmada Obstrüktif Uyku Apnesi (OSA) hastalarında aralıklı hipoksi ve periferik sinir fonksiyonu arasındaki ilişki değerlendirildi. Gereç ve Yöntem: Bu retrospektif çalışmaya polisomnografi (PSG) ve elektronöromiyografi uygulanmış 86 hasta alındı. Periferik sinirleri ve akciğer fonksiyonlarını etkileyen hastalıkları olan katılımcılar çalışma dışı bırakıldı. Hipoksi parametreleri PSG çalışmasından elde edildi. Tüm hastaların alt ekstremite motor ve duyu siniri iletim çalışmaları değerlendirildi. Bulgular: OSA'lı hastalarda kontrollere göre peroneal sinir distal motor latansı ve sural duyusal sinir aksiyon potansiyeli amplitüdü düşük ve hızı anlamlı olarak yavaştı (p<0,001, p<0,04, p<0,001, sırasıyla). Yaş ve vücut kitle indeksi için ayarlama yapıldıktan sonra, sonuçlar anlamlı kaldı (p<0,001, p<0,01, p<0,001, sırasıyla). Sinir iletim sonuçları hipoksi parametreleri ile anlamlı olarak korele idi. Karıştırıcı faktörler ayarlandıktan sonra, lojistik regresyon analizleri, hipoksi parametrelerinin sinir iletimi sonuçlarıyla bağımsız olarak ilişkili olduğunu gösterdi. Sonuç: OSA ve aralıklı hipoksi, hem motor hem de duyusal sinir iletimini etkileyebilmekte, bu da subklinik sensorimotor periferik nöropatinin OSA ile ilişkili olduğunu düşündürmektedir. OSA ve ilgili aralıklı hipoksi, aksonal ve demiyelinizan nöropatinin bir nedeni olabilir.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 91%

Peripheral Nerve Function Changes Due to Hypoxia in Obstructive Sleep Apnea

Avci¹,

Avci²

2019

jtsm

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“…[3][4][5] OSAS is associated with a range of medical conditions such as hypertension, obesity, type 2 diabetes, depression, peripheral neuropathy, as well as with psychological and cognitive deficits. [4][5][6][7][8][9][10] However, the pathophysiologic mechanisms of OSAS are still challenging to disentangle. Transcranial magnetic stimulation (TMS) studies proposed an altered motor cortical excitability as part of the mechanisms underlying OSAS in terms of a dysfunctional cortico-motoneuronal system.…”

Section: Introductionmentioning

confidence: 99%

<p>Obstructive Sleep Apnea Syndrome: A Preliminary Navigated Transcranial Magnetic Stimulation Study</p>

Vidaković

Šoda

Jerković

et al. 2020

NSS

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Purpose: An increase in resting motor threshold (RMT), prolonged cortical silent period duration (CSP), and reduced short-latency afferent inhibition (SAI), confirmed with previous transcranial magnetic stimulation (TMS), suggest decreased cortical excitability in obstructive sleep apnea syndrome (OSAS). The present study included MRI of OSAS patients for navigated TMS assessment of the RMT, as an index of the threshold for corticospinal activation at rest, and SAI as an index of cholinergic neurotransmission. We hypothesize to confirm findings on SAI and RMT with adding precision in the targeting of motor cortex in OSAS. Subjects and Methods: After acquiring head MRIs for 17 severe right-handed OSAS and 12 healthy subjects, the motor cortex was mapped with nTMS to assess the RMT and SAI, with motor evoked potentials (MEPs) recorded from the abductor-pollicis brevis (APB) muscle. The 120%RMT intensity was used for the SAI by a paired-pulse paradigm in which the electrical stimulation to the median nerve is followed by magnetic stimulation of the motor cortex at inter-stimulus intervals (ISIs) of 18-28 ms (ISIs 18-28). The SAI control condition included a recording of MEPs without peripheral stimulation. Latency and amplitude of MEP at RMT at 120%RMT for eleven different at ISIs 18-28 were analyzed. Results: The study showed a significantly lower percentage deviation of MEP amplitude at ISIs (18-28ms) from the control condition between OSAS and healthy subjects (U=44.0, p=0.01). The intensity of stimulation at RMT was significantly higher in OSAS subjects (U=55.0, p=0.04*). Correlation analysis showed that BMI significantly negatively correlated (ρ=−0.47) with MEP amplitude percentage deviation in OSAS patients. Conclusion: The nTMS study results in increased RMT, and reduced cortical afferent inhibition in OSAS patients for SAI at ISIs 18-28 , confirming previous findings of impaired cortical afferent inhibition in OSAS. Future nTMS studies are desirable to elucidate the role of RMT and SAI in diagnostics and treatment of OSAS, and to elucidate the usefulness of nTMS in OSAS research.

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“…But is the neuropathy of OSAS, the cause or a consequence of the disease? It is unknown to what extent chronic intermittent hypoxemia in OSAS causes damage to the motor and sensory peripheral nerve, but muscle action potential and sensory nerve action potential amplitudes are significantly reduced in the nerves outside UA in patients with OSAS suggesting that axonal damage exists in patients with OSAS to a greater extent than previously thought [24]. On the other hand, association between OSAS and sensory neuropathy, and nerve damage outside the UA [18,[25][26][27], type 2 or type 1A diabetic neuropathy, and axonal subtypes of Charcot-Marie-Tooth disease [28][29][30][31] has been also demonstrated.…”

Section: The Neurological Theory Of Osas and The Upper Airways Remodementioning

confidence: 58%

Nerve and Muscle Changes in the Upper Airways of Subjects with Obstructive Sleep Apnea: Structural Basis for the Neurogenic Theory

Cobo¹,

Macías²,

Alvarez³

et al. 2017

Sleep Apnea - Recent Updates

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Obstructive sleep apnea syndrome (OSAS) is a widely diffused disease associated with specific genetics, age, gender, craniofacial and upper airways anatomy, obesity, and endocrine conditions, but not with ethnicity profiles. The so-called neurogenic neurogenic theory of OSAS postulates that the collapse of the upper airways that characterize this disease is due to peripheral nerve degeneration that leads to muscle atrophy and collapse. This review attempts to summarize the structural and functional changes in both the sensory and motor innervation of the walls of the upper air ways in patients suffering from OSAS.

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Reduced evoked motor and sensory potential amplitudes in obstructive sleep apnea patients

Cited by 10 publications

References 35 publications

Peripheral Nerve Function Changes Due to Hypoxia in Obstructive Sleep Apnea

Peripheral Nerve Function Changes Due to Hypoxia in Obstructive Sleep Apnea

<p>Obstructive Sleep Apnea Syndrome: A Preliminary Navigated Transcranial Magnetic Stimulation Study</p>

Nerve and Muscle Changes in the Upper Airways of Subjects with Obstructive Sleep Apnea: Structural Basis for the Neurogenic Theory

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