Narcolepsy with cataplexy 1 G47.411 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes. 2 The 2020 edition of ICD-10-CM G47.411 became effective on October 1, 2019. 3 This is the American ICD-10-CM version of G47.411 - other international versions of ICD-10 G47.411 may differ.
Cataplexy without narcolepsy is rare and the cause is unknown. The term cataplexy originates from the Greek κατά (kata, meaning "down"), and πλῆξις (plak, meaning "strike") and it was first used around 1880 in German physiology literature to describe the phenomenon of tonic immobility also known as «playing possum».
Signs and symptoms. Cataplexy manifests itself as muscular weakness which may range from a barely perceptible slackening of the facial muscles to complete muscle paralysis with postural collapse.
Previous treatments include tricyclic antidepressants such as imipramine, clomipramine or protriptyline. Monoamine oxidase inhibitors may be used to manage both cataplexy and the REM sleep-onset symptoms of sleep paralysis and hypnagogic hallucinations.
G47. 4 - Narcolepsy and cataplexy | ICD-10-CM.
G47. 411 is a billable/specific ICD-10-CM code that can be used to indicate a diagnosis for reimbursement purposes.
ICD-10 code G47. 419 for Narcolepsy without cataplexy is a medical classification as listed by WHO under the range - Diseases of the nervous system .
The 2022 edition of ICD-10-CM G47. 41 became effective on October 1, 2021. This is the American ICD-10-CM version of G47.
Cataplexy. This sudden loss of muscle tone while a person is awake leads to weakness and a loss of voluntary muscle control. It is often triggered by sudden, strong emotions such as laughter, fear, anger, stress, or excitement. The symptoms of cataplexy may appear weeks or even years after the onset of EDS.
The sleepiness combined with muscle weakness is called narcolepsy with cataplexy. It's not dangerous, but the sudden attacks of sleepiness and weakness can have a big impact on your quality of life.
Cataplexy is associated with narcolepsy. Narcolepsy is a neurological condition that causes extreme sleepiness during the day. You can also have unexpected episodes of falling asleep, even in the middle of a conversation or in the middle of an activity.
Narcolepsy without cataplexy is a subtype, also known as narcolepsy type 2. It means someone experiences sleepiness and other symptoms of narcolepsy, but not cataplexy, which is a sudden loss of muscle tone. Only a healthcare professional can diagnose and treat narcolepsy.
ICD-10 code G47. 10 for Hypersomnia, unspecified is a medical classification as listed by WHO under the range - Diseases of the nervous system .
ICD-10 code F51. 01 for Primary insomnia is a medical classification as listed by WHO under the range - Mental, Behavioral and Neurodevelopmental disorders .
ICD-9 Code Transition: 327.23 Code G47. 33 is the diagnosis code used for Obstructive Sleep Apnea. It is a sleep disorder characterized by pauses in breathing or instances of shallow breathing during sleep.
Narcolepsy is excessive daytime sleepiness combined with sudden muscle weakness. The ICD-10-CM code is G47.
Cataplexy is associated with narcolepsy. Narcolepsy is a neurological condition that causes extreme sleepiness during the day. You can also have unexpected episodes of falling asleep, even in the middle of a conversation or in the middle of an activity.
Narcolepsy type 2 (narcolepsy without cataplexy) is characterized by excessive daytime sleepiness and abnormal manifestations of REM sleep on polysomnography and multiple sleep latency testing. Cataplexy is absent.
People with narcolepsy often experience a temporary inability to move or speak while falling asleep or upon waking. These episodes are usually brief — lasting a few seconds or minutes — but can be frightening.
33 – Obstructive Sleep Apnea (Adult) (Pediatric) ICD-Code G47. 33 is a billable ICD-10 code used for healthcare diagnosis reimbursement of Obstructive Sleep Apnea (Adult) (pediatric).
Cataplexy attacks are self-limiting and resolve without the need for medical intervention. If the person is reclining comfortably, he or she may transition into sleepiness, hypnagogic hallucinations, or a sleep-onset REM period.
The treatments for narcolepsy and cataplexy can be divided in treatments that act on the excessive daytime sleepiness (ESD) and those which improve the cataplexy. For most of the patients, this will represent a lifelong medication. Nevertheless, most of the treatments in humans will act only symptomatically and do not target the loss of the orexin producing neurons.
Cataplexy manifests itself as muscular weakness which may range from a barely perceptible slackening of the facial muscles to complete muscle paralysis with postural collapse. Attacks are brief, most lasting from a few seconds to a couple of minutes, and typically involve dropping of the jaw, neck weakness, and/or buckling of the knees. Even in a full-blown collapse, people are usually able to avoid injury because they learn to notice the feeling of the cataplectic attack approaching and the fall is usually slow and progressive. Speech may be slurred and vision may be impaired (double vision, inability to focus), but hearing and awareness remain normal.
Not to be confused with Catalepsy. Cataplexy is a sudden and transient episode of muscle weakness accompanied by full conscious awareness, typically triggered by emotions such as laughing, crying, or terror. Cataplexy affects approximately 70% of people who have narcolepsy, and is caused by an autoimmune destruction of hypothalamic neurons ...
When treating cataplexy, all three systems: adrenergic, cholinergic and dopaminergic must be considered.
Secondary cataplexy is associated with specific lesions located primarily in the lateral and posterior hypothalamus. Cataplexy due to brainstem lesions is uncommon particularly when seen in isolation. The lesions include tumors of the brain or brainstem and arterio-venous malformations.
In mouse models, cataplexy is regulated by the dopaminergic system via the D2-like receptor, which when blocked decreases cataplectic attacks. The role of the cholinergic system was also observed in canine models, where it was suggested that stimulation of this system led to severe cataplexy episodes.