SSD3377 - SECTION 9: INFORMATION THAT INDICATES NARCOLEPSY
Section 9: Information that Indicates Narcolepsy
DSM-5-TR Code: G47.4xx
Prevalence = 0.05%
Can Narcolepsy legitimately be diagnosed by a Master’s level clinician? No. This diagnosis requires referral to a sleep specialist for diagnosis and treatment.
The signs and symptoms of narcolepsy are quite apparent to most people who suffer from this medical condition, and they will most likely already be under the care of a medical specialist in sleep disorders. These signs include an irrepressible need to sleep or a sudden unexpected and unpredictable descent into a sleep state, and may also include either:
1) Episodes of cataplexy, which may be manifested by sudden bilateral loss of muscle tonus (going limp), or spontaneous grimaces or jaw opening episodes with tongue thrusting or a broad reduction in muscle tonus over the whole body; or
2) A clear deficiency of a key sleep related neuropeptide called hypocretin, which is also known as Orexin, usually caused by the destruction of the cells in the brain that secrete this important sleep chemical.
3) Disturbances in REM sleep, including rapid movement to REM sleep upon falling asleep and the presence of REM sleep during daytime naps
The disorder may appear at any time between early childhood and about age 50, according to the National Organization for Rare Disorder (NORD). However, there are two peak periods for the development of Narcolepsy: around age 15 and around age 36, so it is advisable for clinicians to be more aware of the possibility of narcolepsy development with clients at those ages who complain of excessive sleepiness with no other clear causation factors.
In the rare event where a mental health clinician is the initial point of entry to the medical system for a client who presents with signs and symptoms of narcolepsy, it may be helpful to understand the basis of these problems. Hypocretin, or Orexin, is a chemical that helps a person stay awake and avoid falling asleep. It works against (antagonistically) the neurochemicals that push a person into a sleeping state, holding back the descent into a sleeping state and allowing the person to stay awake.
When a person has too much hypocretin in his/her brain, it can work too effectively and cause insomnia. There are a number of factors that can elevate the level of hypocretin and interfere with sleep at a neurochemical level. This will be covered in a later part of this course when challenges to the sleep cycle are examined in more detail.
But this is not the problem in a person who is experiencing narcolepsy. A person with narcolepsy has a shortage of hypocretin, often due to some sort of autoimmune disease, injury, or illness that destroys some or most of their hypocretin secreting cells in their brain.
Without the presence of hypocretin, the other chemicals in a person’s sleep-wake system – the ones that move a person towards sleeping states – are free to operate and push the person into various stages of the sleep cycle. This explains the primary symptom of narcolepsy, which involves the irrepressible urge to sleep.
The other symptoms of narcolepsy are also related to the diminishment in the functioning of hypocretin and the effects of removing this chemical from its role in preventing the sleep related chemicals from taking over. Our bodies have some special chemicals that get released during the part of our sleep cycle where we dream, and for a very good reason.
During REM sleep, when people dream, the body releases chemicals in the brain that prevent a person from moving their muscles, a kind of self-induced paralysis called alpha motor neuron paralysis. This phenomenon has a very important survival purpose: to prevent a person from moving their muscles in dangerous ways in response to the content of their dreams. Without this, people would act out what is happening in their dreams and place themselves in all kinds of danger.
The presence of hypocretin (Orexin) in the brain during times when a person is awake prevents this process from occurring. But when hypocretin is diminished when a person has narcolepsy, the person can be susceptible to alpha motor neuron paralysis during semi-waking states, resulting in cataplexy and loss of muscle tonus (going limp). The person can also move more quickly to REM states when sleep is achieved during daytime naps.
There are also some rare instances in which narcolepsy is present without a measurable hypocretin deficiency based upon tests of the patient’s levels within their cerebrospinal fluid. The DSM-5 notes that this occurs in less than 5% of the cases, and the exact causes of this kind of narcolepsy remain unexplained. (NORD)
When diagnosticians specify which type of narcolepsy is present, they use the diagnosis to describe both symptoms that are present and causative factors. Here are several sub-types of narcolepsy, based upon these factors, shown as follows:
G47.419 Narcolepsy without cataplexy but with hypocretin deficiency
G47.411 Narcolepsy with cataplexy but without hypocretin deficiency
G47.419 Autosomal dominant cerebellar ataxia, deafness and narcolepsy
G47.419 Autosomal dominant narcolepsy, obesity and type 2 diabetes
G47.429 Narcolepsy secondary to another medical condition
As with most sleeping disorders, a diagnosis of narcolepsy should be left to a medical professional with a specialization in sleep disorders. In the record of a mental health clinician, therefore, the diagnosis would be recorded with the specifier, “by history”. The treatment role for the clinician would be to provide support for the emotional repercussions of having this difficult medical condition.