SYNOPSIS:

INTRODUCTION:
Cataplexy is a brain disorder that causes a sudden and temporary loss of
muscle tone and control. The episodes (or “cataplectic attacks”) are, in most
cases, triggered by strong or extreme emotions, including anger, stress, anxiety,
fear, a depressed mood, joy, and laughter.
The vast majority of people who experience cataplexy do so as a result of
having type 1 narcolepsy, a chronic sleep and neurological disorder in which
the brain has trouble properly controlling wake and sleep cycles. In very rare
cases, cataplexy has been reported in individuals without narcolepsy.
Living with cataplexy is challenging. You cannot always control your emotions
or emotional response, so cataplectic attacks can occur randomly. For some, it
means being constantly vigilant about how to avoid losing control of their
bodies.
Here are some important things to know about why cataplexy happens, its
connection to narcolepsy, and how to manage the potentially debilitating
symptoms.

DEFINITION:
Cataplexy, from the Greek ‘kata’ and ‘plexis’, meaning ‘down’ and ‘strike’
respectively, is a sudden episode of weakness combined with full awareness
and consciousness. It is triggered by a strong emotion like surprise, anger,
laughter, crying, or fear. More often, an episode of cataplexy will be triggered
by positive emotions, but negative emotions can occasionally be a trigger too.
In simple words, it is defined as sudden loss of muscle power following a strong
emotional stimulus

PREVALENCE:
Only one in every 2,000 people have narcolepsy and only 75% of these have
cataplexy, it’s not at all common. As many as 30,000 people in the UK have
narcolepsy, which means that approximately 22,500 suffer from associated
cataplexy.

TYPES:

CAUSES:
Autoimmune conditions.
Brain tumours growing near the areas of the brain that control sleep patterns.
Brain injuries or head injuries.
Infections like swine flu.
Medications used for insomnia

SYMPTOMS:
What are the symptoms?
Symptoms of cataplexy can be different for each person. Most people start to
notice their symptoms as teenagers or as young adults. This is usually when
you enter college, the workforce, or other new, potentially stressful
environments.

Some possible symptoms of cataplexy episodes include:

Drooping eyelids
Jaw dropping
Head falling to the side due to neck muscle weakness
Whole body falling to the ground
Various muscles around your body twitching without an obvious cause
Cataplexy is often mistaken for a seizure when it’s more severe. But unlike a
seizure, you will likely remain conscious and remember everything that
happens during an episode. Cataplectic episodes also vary in length. They may
last only a few seconds or go on for up to a few minutes.

Cataplexy usually happens after you feel a strong emotion. Emotional triggers
can include:

Excitement
Happiness
Stress
Fear
Anger
Laughter
Not everyone with cataplexy has the same triggers. They may also not be
consistent. Laughing may cause cataplexy in certain situations, but not others.
Anger may trigger an episode in one case, but not another.

Cataplexy can be one of the first noticeable symptomsTrusted Source in people

who have narcolepsy. It often shows up as a minor muscle abnormality, such as
your eyelid drooping or your head falling over briefly because your neck
muscles weaken. As a result, you may not even realize you have cataplexy or
narcolepsy.

ETIOLOGY:
While the cause of cataplexy is still being investigated, most people with
cataplexy show a loss of certain brain cells that produce the hormone orexin
(also called hypocretin). Orexin plays an important role in the sleep-wake cycle.

Much of what we know about the relationship between orexin (hypocretin)

and cataplexy comes from type 1 narcolepsy research. This research suggests
that several factors may contribute to a loss of orexin in people with type 1
narcolepsy.

Autoimmune disorders: A loss of cells that produce orexin may be related to

dysfunction in the immune system. In autoimmune disorders, the body attacks
its own healthy tissue by mistake. There is increasing evidence that type 1
narcolepsy may be caused by the immune system attacking cells that produce
orexin.

Family history: While potential genetic links aren’t fully understood, around
10% of people with type 1 narcolepsy have a close relative with similar
symptoms.

Brain injury: Some people with type 1 narcolepsy lose orexin-containing brain
cells due to brain injuries, tumors, and other acquired diseases.

Cataplexy isn’t always linked to narcolepsy. Around 30% of cataplexy episodes

are related to other disorders
, including:

Niemann-Pick type C Disease (NPC): NPC is a rare genetic disorder

characterized by the body’s inability to transport lipids such as cholesterol
within cells, leading to accumulations of fatty substances in body tissues.
People diagnosed with NPC may experience a variety of neurologic symptoms
, including cognitive impairment, dementia, and cataplexy.
Prader-Willi Syndrome: Prader-Willi syndrome is a genetic condition that begins
in childhood, leading to early feeding challenges, delayed growth and
development, and an insatiable appetite. In this condition, both excitement
and food may cause cataplexy.

Angelman Syndrome: This genetic disorder affects the nervous system , leading
to intellectual disability, speech impairment, and problems with movement and
balance. Cataplexy has been reported in many children with this disorder.

In rare cases, cataplexy can also be a side effect of medications. Suvorexant, a

medication for insomnia that blocks orexin, can cause cataplexy in rare cases.
Fortunately, cataplexy typically disappears after patients stop taking these
medications.

Psychopathogenesis:

Differential Diagnosis:

Cataplexy is all but unique to type 1 narcolepsy; therefore, the differential

diagnosis of this feature is sparse. Pseudocataplexy, a feature of conversion
disorder, is characterized by cataplexy-like attacks; however, the other defining
characteristics of narcolepsy are often absent.

Although rare, cataplexy can occur in the presence of lateral hypothalamic

lesions implicated in the development of secondary narcolepsy. Such lesions
may arise in the setting of arteriovenous malformations, cerebrovascular
accidents, inflammatory processes, and neoplasms.[8][9] Again, if cataplexy
were to occur in such situations, other neurological deficits will likely be
evident, as neuronal destruction does not typically remain confined to the
hypothalamus

Psychiatric intervention:
While behavior modifications (i.e., planned naps, a sufficient night’s sleep) play
a role in the management of the excessive daytime sleepiness associated with
type 1 narcolepsy, treatment of cataplexy is purely pharmacological. The
duration of therapy is indefinite, as type 1 narcolepsy is incurable. It bears
mentioning that treatment options include various combinations of
medications, often creating an individualized treatment. Clinicians can use the
Epworth Sleepiness Scale to follow the response to treatment. For
completeness, the pharmacologic treatment of type 1 narcolepsy, as a whole, is
presented below:

Successful management of excessive daytime sleepiness often requires the use

of wakefulness-promoting agents, as behavioral modifications fail to provide
complete relief.[14] Modafinil (100 to 400 mg by mouth once daily every
morning) and its isolated R-enantiomer, armodafinil (150 to 250 mg by mouth
once daily every morning), are considered first-line pharmacologic agents in
the management of excessive daytimes sleepiness. While the mechanism of
action of these agents is not entirely understood, the thinking is that their
effects are due to an increase in dopaminergic signaling via the inhibition of
dopamine reuptake.[17] Two medications received FDA approval in 2019:
pitolisant and solriamfetol. Pitolisant (8.9 to 35.6 mg by mouth once daily every
morning) is a histamine-3 receptor inverse agonist, while solriamfetol (75 to
300 mg by mouth once daily every morning) is a selective
dopamine/norepinephrine reuptake inhibitor.[18] For breakthrough excessive
daytime sleepiness, the following agents are options on an as-needed basis:
dextroamphetamine-amphetamine (5 to 60 mg by mouth daily in one to three
divided doses) and methylphenidate (5 to 60 mg by mouth daily in two to three
divided doses).[19]

Successful management of cataplexy requires the use of REM sleep-

suppressing drugs. Such agents increase the concentration of norepinephrine
and serotonin. The following pharmacologic agents are considered first-line in
the management of cataplexy: Selective serotonin reuptake inhibitors
(fluoxetine 10 to 80 mg by mouth daily every morning), norepinephrine
reuptake inhibitors (atomoxetine 40 to 80 mg by mouth daily every morning),
serotonin/norepinephrine reuptake inhibitors (venlafaxine extended-release
37.5 to 150 mg by mouth once daily every morning), and tricyclic
antidepressants (clomipramine 10 to 150 mg by mouth daily every morning).
Prescribers of the medications, as mentioned earlier, should keep in mind the
following considerations:

Tricyclic antidepressants (TCAs) have fallen out of favor for the treatment of
cataplexy due to their anticholinergic side effects (i.e., delirium, dry mucous
membranes, hyperthermia, ileus, mydriasis, tachycardia, and urinary
retention). Moreover, TCA overdose can result in a toxidrome: anticholinergic
symptoms, cardiac toxicity, and CNS toxicity. Cardiac toxicity includes
interventricular conduction delay (QRS prolongation), right-axis deviation, and
tachycardia (anticholinergic effect).[20]
Serotonin syndrome is diagnosed clinically using the Hunter criteria:
administration of a serotonergic agent in the setting of inducible clonus with
either agitation or diaphoresis. It can occur with the use of a single
serotonergic agent as prescribed/taken in excess or with the co-ingestion of
multiple serotonergic agents simultaneously. Its manifestations are due to an
increase of serotonin in the central nervous system. Typical presentation
includes altered mental status, increased autonomic activity, and
neuromuscular changes. Great care is necessary to avoid the prescription of
multiple serotonergic agents in a single patient.[21]
Currently, only one medication has FDA approval for the treatment of both
cataplexy and the excessive daytime sleepiness associated with narcolepsy:
Sodium oxybate, the sodium salt of gamma-hydroxybutyrate. The mechanism
of action of this medication is unknown; however, it is a known metabolite of
gamma-aminobutyric acid (GABA). It is therefore thought to work via the
GABA-B receptor. This medication is dosed initially at bedtime with subsequent
dosing 2.5 to 4 hours later and has a significant salt content of 1100 mg to 1640
mg when dosed in the effective range (6 g to 9 g per night in two divided
doses).
The management of type 1 narcolepsy in children differs slightly from
management in adults. In children, the first-line pharmacologic agents for the
treatment of symptoms of excessive daytime sleepiness are stimulants such as
dextroamphetamine-amphetamine (10 to 40 mg by mouth daily in one to two
divided doses) or methylphenidate (10 to 60 mg by mouth daily in two to three
divided doses) rather than wakefulness-promoting agents such as armodafinil
(50 to 250 mg by mouth once daily every morning) and modafinil (50 to 200 mg
by mouth once daily every morning). Moreover, the first-line pharmacologic
agent for the treatment of cataplexy is sodium oxybate (1 to 2 g per night in
two divided doses), rather than REM sleep-suppressing drugs, in children over
the age of seven. In children under seven with cataplexy requiring treatment,
the following REM sleep-suppressing drugs are possible therapies:
clomipramine 25 mg by mouth once daily at bedtime, fluoxetine 5 to 10 mg by
mouth once daily, or venlafaxine extended-release 25 mg by mouth once daily.
Yoga and naturopathy management:
Yoga improves the sleep wake cycle and the hormony of circadian rhythm.
Changing Sleep patterns can disturb your biological clock and thus results in
sleeping disorders like this narcolepsy and cataplexy. Yoga helps to regulate
your circadian rhythm by improving your quality of sleep. Yoga also helps in
strengthening the musculoskeletal system.
There are certain asanas used to treat cataplexy:
1. Shavasana
2. Makrasana
3. Shashankasana
4. Veerasana
5. Matsyakridasana
6. Surya namaskar
7. Pawanmuktasana series-2
8. Veerapadrasana
9. Setubandhasana
10. Bhujangasana

Relaxation techniques:
DRT
MSRT
PET
Yoga nidra
VISAK

Pranayama:
Bhramari
Nadishuddhi
Sandrabedha pranayama

Massage :
Full body massage ( Swedish massage )
Dry head massage

Acupuncture points :
Buddha points – H-7, L-9, P-6, Du -20, TW-17

Hydrotherapy:
Hot foot bath
Full Steam bath
Spinal douch
Neutral hip bath
Chromotherapy
Plantain leaf bath
Blue glass exposure
Green solarised water

Mud therapy:
1. Full mud bath
2. Mud pack to abdomen and eyes

Supplements and Herbs for Narcolepsy

For patients interested in supplements and herbs, there are various evidence-
based solutions that may help reduce symptomatology.

L-Tyrosine for Narcolepsy

L-Tyrosine, a notable amino acid, has been under investigation for its potential
benefits in treating narcolepsy. Preliminary studies suggest it may impart a mild
stimulant effect on the central nervous system, thus potentially reducing
symptoms like excessive daytime sleepiness. However, it is important to note
that these observations were limited due to the study’s small scale.

Dose: 9 g daily

Duration: 4 weeks

Melatonin for Narcolepsy

Melatonin, a hormone that regulates the sleep-wake cycle, could potentially
offer benefits for individuals suffering from narcolepsy. As narcolepsy disrupts
normal sleep patterns, introducing a regulated dose of melatonin might aid in
establishing a healthier, more consistent sleep routine. This, in turn, could
alleviate excessive daytime sleepiness, a hallmark symptom of narcolepsy.

Dose: 2.5-3 mg nightly

Duration: 3-week minimum

Valerian for Narcolepsy

Valerian, a natural herb often used for its sedative properties, may hold
potential benefits for those dealing with narcolepsy. As individuals with
narcolepsy face challenges in achieving consistent and restful sleep,
incorporating valerian could potentially enhance the quality of their sleep. Its
calming effects could also potentially help reduce the instances of cataplexy, a
common symptom of narcolepsy characterized by sudden loss of muscle
control (29,30).

Dose: 1060 mg daily

Duration: 4-week minimum

Conclusion:
Yoga and naturopathy interventions helps to reorder the circadian rhythm by
improving your sleep wake cycle. Cataplexy occurs as a response to an
emotion. Yoga and pranayamam help to overcome your emotional hipe. It
calm down your mind and helps to balance your emotions. And thus, it gives
significant improvements in cataplexy.
Research papers: