Anatomy and Physiology of Normal Sleep

Schneider, Logan

doi:10.1016/b978-0-12-804074-4.00001-7

Cited by 7 publications

(5 citation statements)

References 194 publications

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“…This potentially suggests that strong emotions very selectively activate the sublaterodorsal nucleus-ventral medullary atonia circuitry, rather than other parts of the REM sleep flip-flop switch. 12 As such, despite generalized and severe weakness during this patient's cataplectic events, she was able to volitionally move her eyes, which has not been previously demonstrated during a cataplectic attack, even though it is apparent that this should be the case. Still images from the video of facial cataplexy demonstration volitional leftward (A) and rightward (B) gaze despite facial muscle paralysis.…”

Section: Report Of Casementioning

confidence: 52%

“…10,11 It may be that the main generators of REM sleep atonia-the pontine sublaterodorsal nucleus and the more caudal ventral medulla-reside below the main eye-movement brainstem nuclei in the midbrain and upper pons. 12 Nonetheless, cataplexy, serves as a marker of the sleepwake state instability that results from hypocretin deficiency, as the spells clearly recapitulate the atonia of REM sleep without necessarily inducing sleep or dream-like mentation. This potentially suggests that strong emotions very selectively activate the sublaterodorsal nucleus-ventral medullary atonia circuitry, rather than other parts of the REM sleep flip-flop switch.…”

Section: Report Of Casementioning

confidence: 99%

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Images: Facial cataplexy with demonstration of persistent eye movements

Schneider

Ellenbogen

2020

Journal of Clinical Sleep Medicine

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A patient was transferred for management of "medication-refractory seizures" after failure of levetiracetam and valproate dual therapy. She had a life-long history of two types of events: periods in which she would rapidly and uncontrollably lapse into unconsciousness, and spells in which she would "pass out" but maintain consciousness, the latter happening with increasing frequency in association with laughing, as of late. She also reported hypnogogic/hypnopompic hallucinations, sleep paralysis, and disrupted nocturnal sleep. A clinical diagnosis of narcolepsy was made. The prevailing pathophysiological concept of narcolepsy details "partial intrusions of REM" sleep into wakefulness. Healthy REM sleep includes generalized atonia, but with preservation of eye movements, respiratory function, and sphincter tone. Cataplexy recapitulates this pattern, and is often induced by extreme emotions, laughter in this case. Despite generalized and severe weakness and areflexia during this patient's cataplectic events, she was able to volitionally move her eyes, which is consistent with the physiology of REM sleep. The diagnosis of cataplexy is often missed, due to clinicians being unfamiliar with the findings and the lack of ability to induce sufficient emotional responses to trigger an episode. This example of cataplexy is also quite characteristic of the "cataplectic facies." The ability to observe the infrequently observed phenomenon of cataplexy serves as a reminder that consciousness is preserved, as are extra-ocular muscle movements.

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Section: Report Of Casementioning

confidence: 52%

Section: Report Of Casementioning

confidence: 99%

Images: Facial cataplexy with demonstration of persistent eye movements

Schneider

Ellenbogen

2020

Journal of Clinical Sleep Medicine

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“…The metabolic defect in SSADHD, an inability to catabolise γ‐aminobutyrate (GABA), results in a pathological elevation of GABA and related metabolites (Maitre et al, 2016; Snead III & Gibson, 2005). There is well‐established evidence that GABAergic neurotransmission facilitates the initiation and maintenance of physiological and pharmacological sleep (Harrison, 2007; Schneider, 2017). It is, therefore, reasonable that sleep disturbances constitute a core clinical manifestation of SSADHD, in addition to cognitive deficits, behavioural disturbances, movement disorders, and epilepsy (Pearl, Gibson, et al, 2003; Pearl, Novotny, et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…neurotransmission facilitates the initiation and maintenance of physiological and pharmacological sleep (Harrison, 2007;Schneider, 2017). It is, therefore, reasonable that sleep disturbances constitute a core clinical manifestation of SSADHD, in addition to cognitive deficits, behavioural disturbances, movement disorders, and epilepsy .…”

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confidence: 99%

Glymphatic dysfunction coincides with lower GABA levels and sleep disturbances in succinic semialdehyde dehydrogenase deficiency

Tokatly Latzer,

Yang,

Afacan

et al. 2023

Journal of Sleep Research

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SummarySuccinic semialdehyde dehydrogenase deficiency (SSADHD) is an inherited metabolic disorder of γ‐aminobutyrate (GABA) catabolism. Cerebral waste clearance along glymphatic perivascular spaces depends on aquaporin 4 (AQP4) water channels, the function of which was shown to be influenced by GABA. Sleep disturbances are associated independently with SSADHD and glymphatic dysfunction. This study aimed to determine whether indices of the hyperGABAergic state characteristic of SSADHD coincide with glymphatic dysfunction and sleep disturbances and to explicate the modulatory effect that GABA may have on the glymphatic system. The study included 42 individuals (21 with SSADHD; 21 healthy controls) who underwent brain MRIs and magnetic resonance spectroscopy (MRS) for assessment of glymphatic dysfunction and cortical GABA, plasma GABA measurements, and circadian clock gene expression. The SSADHD subjects responded to an additional Children's Sleep Habits Questionnaire (CSHQ). Compared with the control group, SSADHD subjects did not differ in sex and age but had a higher severity of enlarged perivascular spaces in the centrum semiovale (p < 0.001), basal ganglia (p = 0.01), and midbrain (p = 0.001), as well as a higher MRS‐derived GABA/NAA peak (p < 0.001). Within the SSADHD group, the severity of glymphatic dysfunction was specific for a lower MRS‐derived GABA/NAA (p = 0.04) and lower plasma GABA (p = 0.004). Additionally, the degree of their glymphatic dysfunction correlated with the CSHQ‐estimated sleep disturbances scores (R = 5.18, p = 0.03). In the control group, EPVS burden did not correlate with age or cerebral and plasma GABA values. The modulatory effect that GABA may exert on the glymphatic system has therapeutic implications for sleep‐related disorders and neurodegenerative conditions associated with glymphatic dysfunction.

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“…2 in the sleepwake neurocircuitry. 10 Three characteristic features define bladder abnormalities in MSA. These include large postvoid residual urine volumes of > 100 mL, an open bladder neck during fillingphase video urodynamics, and sphincter denervation attributed to neuronal cell loss in Onuf's nucleus in the sacral spinal segment.…”

Section: Introductionmentioning

confidence: 99%

The Non-motor Symptoms, Disability Progression, and Survival Analysis of Atypical Parkinsonism: Case Series from Eastern India and Brief Review of Literature

Pani

Nayak

2022

JNRP

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Objective The objectives of this study are (1) to describe the non-motor profile, the motor disability progression, and survival analysis of atypical parkinsonism in a tertiary care hospital of eastern India and (2) to elucidate the neurocircuitry and the putative substrates responsible for non-motor manifestations. Methods In this prospective observational study, patients were diagnosed based on Consensus Criteria for Progressive Supranuclear Palsy (PSP), The Fourth Consensus Report of the Dementia with Lewy Body (DLBD) Consortium 2017, The Autonomic Neuroscience 2018 Criteria for Multiple System Atrophy (MSA), and Armstrong 2013 Criteria for Corticobasal Degeneration (CBD). Disease severity was assessed at baseline and 6 months of follow-up using the Unified Parkinson's Disease Rating Scales (UPDRS). For PSP and MSA, the PSP-Clinical Deficits Scale (PSP-CDS) and the Unified MSA Rating Scale (UMSARS), respectively, were used. Cox regression analysis and the hazard ratio were calculated. Results Out of 27 patients, the diagnosis was probable PSP in 12, probable MSA in 7, probable CBD in 5, and probable DLBD in 3. Non-motor symptoms were highly prevalent across all subtypes. Motor disability progression as assessed by UPDRS parts 2 and 3 showed significant deterioration over 6-month follow-up across all groups (p < 0.05). Disease progression assessed by PSP-CDS and UMSARS over 6 months was significant (p < 0.05). One PSP and two MSA patients died during a 6-month follow-up period. The hazard ratio in MSA was 3.5 (95% confidence interval: 0.31–0.38) with p = 0.306. Conclusion Atypical parkinsonian disorders are rare, and usually more severe than idiopathic parkinsonism. As no definitive treatment is available, symptomatic management involving a multidisciplinary team approach must be prioritized.

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Anatomy and Physiology of Normal Sleep

Cited by 7 publications

References 194 publications

Images: Facial cataplexy with demonstration of persistent eye movements

Images: Facial cataplexy with demonstration of persistent eye movements

Glymphatic dysfunction coincides with lower GABA levels and sleep disturbances in succinic semialdehyde dehydrogenase deficiency

The Non-motor Symptoms, Disability Progression, and Survival Analysis of Atypical Parkinsonism: Case Series from Eastern India and Brief Review of Literature

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