“We” is used here to include application at the PNI “we” is also used generically, for example, in broader recognitions of symptoms by researchers. Keywords: Age Armodafinil Auto-Immune Bilateral Bipolarity Cataplexy Cerebrospinal Fluid Children CSF Crying Day-Time Sleepiness Diplopia DSM-V DTS Dyssomnia EEG Ego-Boundary Emotion Episodes Epworth Sleepiness Scale ESS False Negative False Positive FISS FISS-1 FISS-2 Gold Standard HLA HLA DR DQB2 06:02 HLA-DQ6 DQA1*01:02 DQB1*06:02 Hallucination HCRT H1N1 Hypersomnia Hypothalamus Hypnagogic Hallucinations Hypnopompic Hallucinations Hypocretin Hypocretin (Orexin) Neuropeptide Precursor ICSD Illusion International Classification of Sleep Disorders Laughing Loci Modafinil Modified Epworth Sleepiness Scale MESS “Multiple Sleep-Latency Test” Muscle Tone Mythology Narcolepsy Narcolepsy Type 1 Narcolepsy Type 2 Neppe Neppe Narcolepsy Questionnaire NNQ NNQ-4R Neuro-Excitatory Neurological Neuropsychiatry Nocturnal Polysomnography Nortriptyline NPSG Nuvigil Oxybate OSA Orexin Periodic Leg Movements PLM Pharmacological Responsiveness PNI Modified Fatigue Severity Scale Primary Narcolepsy Provigil Rapid Eye Movement RAS Reticular Activating System, REM Schizophrenia Sleep Sleep Apnea Sleep-Onset Sleep-Onset REM Period Seizure SOREMP Sleep Paralysis Sleep-Wake Cycle Symptomatic Narcolepsy Tetrad Transition Tricyclic Uncontrollable Sleepiness Venlafaxine Wakefulness Weakness Xyremī“PNI” refers to the Pacific Neuropsychiatric Institute in Seattle, WA. The various ICSD and DSM criteria are re-examined.
some require proof by MSTL or Orexin levels and some do not). On the others hand, some old classifications have used the previous terms “Type 1 Narcolepsy” for narcolepsy with cataplexy, and “Type 2 Narcolepsy” for narcolepsy without demonstrated cataplexy: this classification appears redundant and has ambiguities (e.g. This accentuates the need for proposing two new terms, namely “primary narcolepsy” for the most common narcolepsy condition that appears to be hypothalamically linked to an auto-immune process involving hypocretin, and “symptomatic narcolepsy” due to infectious or tumor or trauma events involving the hypocretin / reticular activating system/ hypothalamus. I suggest a new model of hypocretin deficiency being slightly down-stream from the actual cause of narcolepsy-cataplexy. These may reflect multifactorial etiologies: some of these may be linked with narcolepsy, and others unassociated.
#TRAINING FOR NARCOLEPSY CATAPLEXY ANXIETY SERVICE DOGS PLUS#
This is pertinent because, in the USA, insurance approval of costly medications such as modafinil, armodafinil and sodium oxybate are often dependent on the insurances applying a positive MSLT as a requirement when it is negative, the insurances might tragically deny coverage of these medications: This might deprive many in the narcolepsy population of their essential life-sustaining treatment, even though they might have definite clinical features plus the gene expression, and often, already, response to wakefulness drugs.
Secondly, the multiple sleep-latency test (MSLT) may be overemphasized for definitive diagnosis, because the genetic test is as important or even more relevant.
However, the DQA1*01:02 gene should also be measured 1:02. These genes include particularly DQB1*06:02. First, the genes for narcolepsy have been largely ignored when applying the recognized criteria for diagnosing narcolepsy.The classical standard narcolepsy research criteria confirming a narcolepsy diagnosis consist of either a positive multiple sleep-latency tests (MSLT), or an abnormally low cerebrospinal fluid (CSF) Orexin (hypocretin) level. Diplopia and nocturnal insomnia are two other often ignored common symptoms.
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