This condition is characterized by a short-term loss of voluntary muscle control during arousal or sleep onset. 

Sleep paralysis is associated with a sleeper's inability to move or speak despite complete consciousness. Durations of sleep paralysis span for several minutes and after arousal, the ability to move or speak is restored. 

An estimate of 25% persons with narcolepsy encounter the condition of sleep paralysis [8]. Incidence of REM sleep typically occurs 60 to 90 minutes after sleep onset. REM phase involves elevated brain activity, lucid dreaming and atonia-a short-term muscle paralysis. Acting out the dreams is prevented by atonia and it usually ends after waking up from the sleep. 

In the case of persons with narcolepsy, entry to the REM phase is quite quicker (15 minutes after sleep onset). Consequently, the experiences usually developed in the REM phase may turn into wakefulness. Sleep paralysis occurs due to the persistent prevalence of atonia during the awakening. 

Hallucinations affect one-third of narcolepsy patients and it frequently develops during the periods of sleep onset or arousals. Hallucinations are visually perceptive in general, but in some instances multiple senses may also be involved. 

Cataplexy can be defined as the rapid loss of muscle tone during awakenings. Individuals encountering cataplexy continue to stay fully alert unlike the conditions like fainting and seizure disorders. 

Cataplexy is precipitated by intense emotions [9] such as annoyance, laughter, surprise and exhilaration. Cataplexy is associated with Narcolepsy Type 1 only. Mild cataplexy episodes span for a few seconds and consist of a lesser count of muscle groups like eyelids. 

Severe cataplexy episodes may persist for several minutes and encompass a complete loss of voluntary control of muscles, leading to a short-term, total paralysis.

This can be considered as a common symptom of narcolepsy although it does not include in standard tetrad of narcolepsy symptoms. About 30-95% of patients [10] are affected with disrupted nighttime sleep. 

This symptom might be a stand-alone one or could be developed due to an underlying sleep dysfunction. Narcolepsy patients generally sleep for the same duration as individuals without this disorder but the former category lacks the consolidation of sleep.

The fundamental aspect of NT1 is the loss of hypocretin-generating hormones, known as orexins. A significant loss of about 90% of hypocretin-producing hormones characterizes NT1 condition leading to the poor regulation of sleep and wakefulness [2]. 

A genetically vulnerable person may encounter loss of these neurons in an autoimmune manner following an environmental activator. Some research studies explore the correlation of NT1 with influenza virus. Though exceptionally rare, possibilities of NT1 onset could be noticeable after the H1N1 epidemic and with a specific vaccine brand administered for H1N1. 

Probabilistic links with other infection categories have been observed as well. On the grounds of these analytical data, it can be perceived that an external triggering factor stimulates the immune system and makes it to damage hypocretin-making neurons. This sort of autoimmune response is not the sole cause as its nature is quite inconsistent. 

A genetic mutation, known as DQB1*0602 which plays a prominent role in immune function is linked with the genetic vulnerability in 98% of the NT1 cases [11]. 

This justification is not conclusively validated yet broadly recognized. Individuals with family history of NT1 have a 1-2% probability of experiencing this neurological sleep disorder. In rare cases, underlying medical conditions that damage the brain parts that constitute orexins. This can happen from brain trauma or infection in Central Nervous System.

The biology of NT2 and its risk factors are poorly understood. According to some experts, NT2 is a less evident loss of hypocretin-making hormones even though the persons with NT2 are typically not deficient in hypocretin [2]. 

Others believe that NT2 is an antecedent to NT1 but Cataplexy condition tends to develop in 10% of instances with initial prognosis of NT2. NT2 can even develop due to some medical issues affecting the brain including head trauma and multiple sclerosis.

In PSG, the breathing pattern, eye movements, muscle action and brain function are taken into account through an overnight sleep analysis. PSG tracks the sleep phases and arousals and it can unveil the presence of other sleep dysfunctions.

MSLT is conducted in the daytime soon after doing PSG. MSLT involves measuring the sleep onset time and time required to enter REM sleep at five distinct intervals by making use of the same sensors employed in PSG.

The outcomes of these sleep studies are significant in narcolepsy diagnosis. The test results become valid only if preparations such as stabilization of sleep cycle for a week, cessation of sleep-interfering drugs or substances and usage of sleep log for documenting sleep are done properly.

In addition to these sleep studies, testing the level of hypocretin-producing hormones by the lumbar puncture procedure. In this, a small quantity of Cerebrospinal Fluid is removed from the lower spinal area. Low levels of hypocretin indicate the presence of NT1. Human Leukocyte Antigen (HLA) is another test to find out whether the mutation is noticeable in a gene DQB1*06:02. 

This variation in gene cannot provide a prognostic result for narcolepsy because the mutation can occur in people without narcolepsy.

The patients must satisfy both of these criteria

All these 5 criteria must be met

There is a possibility of changing the diagnosis over time. Reclassification of narcolepsy occurs in approximately 10% of individuals. At the outset, they may be diagnosed with NT2, but with the incidence of cataplexy, the diagnostic decision can be changed to NT1.