Those who suffer from idiopathic hypersomnia have recurring episodes of excessive daytime sleepiness (EDS). These occur in spite of "adequate, or more typically, extraordinary sleep amounts (e.g., greater than 10 hours per night)." Sleep is usually deep, with significant difficulty arousing from sleep, even with use of several alarm clocks. In fact, patients with IH often must develop elaborate rituals to wake, as alarm clocks and even physical attempts by friends/family to wake them may fail. Despite getting more hours of sleep than typically required by the human body, patients awake unrefreshed and may also suffer sleep inertia, known more descriptively in its severe form as sleep drunkenness (significant disorientation upon awakening). Daytime naps are generally very long (up to several hours) and are also unrefreshing, as opposed to the short refreshing naps associated with narcolepsy. Sleep paralysis and hypnagogic hallucinations may also occur, as well as motor hyper-reactivity.

Several studies have shown increased frequencies of other symptoms in patients with idiopathic hypersomnia, although it is not clear whether these symptoms are caused by the idiopathic hypersomnia. These symptoms include palpitations, digestive problems, difficulty with body temperature regulation, and cognitive problems, especially deficits in memory, attention, and concentration. Anxiety and depression are often increased in idiopathic hypersomnia, most likely as a response to chronic illness. A large case series in 2010 found that peripheral vascular symptoms, such as cold hands and feet (Raynaud’s-type phenomena) were significantly more common in people with idiopathic hypersomnia than in controls. In addition to difficulty with temperature regulation and Raynaud’s type symptoms, other symptoms associated with autonomic dysfunction were noted to occur in idiopathic hypersomnia. These included: fainting episodes (syncope); dizziness upon arising (orthostatic hypotension); and headaches (possibly migrainous in quality). Food cravings and impotence have also been reported.

Symptom intensity often varies between weeks, months, or years, and symptoms can worsen just prior to menses in women. Many patients are chronically tardy to work, school or social engagements and, over time, may lose the ability to function in family, social, occupational or other settings altogether. (See Prognosis section below).

In addition to differentiating between the primary and secondary hypersomnias, the 2001 International Classification of Sleep Disorders (ICSD) further classified the primary hypersomnia syndromes. These included idiopathic hypersomnia, narcolepsy, and the recurrent hypersomnias (like Klein-Levin syndrome).

The 2001 ICSD defines idiopathic hypersomnia as "a disorder of presumed central nervous system cause that is associated with a normal or prolonged major sleep episode and excessive sleepiness consisting of prolonged (1- to 2-hour) sleep episodes of N-REM"(non-rapid eye movement sleep). The ICSD initially described two clinical forms of idiopathic hypersomnia: "1) a polysymptomatic form with nocturnal sleep and naps of abnormally long duration with ‘sleep drunkenness’ on awakening, and 2) a monosymptomatic form manifested by isolated EDS." These forms were later described as idiopathic hypersomnia with long sleep time and idiopathic hypersomnia without long sleep time, respectively.

This classification has steadily evolved, as further research has shown overlap between narcolepsy and idiopathic hypersomnia. The 3rd edition of the ICSD labels narcolepsy caused by hypocretin deficiency as "type 1 narcolepsy," which is almost always associated with cataplexy. The other hypersomnias remain subdivided based on the presence of sleep-onset rapid eye movement periods (SOREMPs). They are labeled: "type 2 narcolepsy," with 2 or more SOREMPs on mean sleep latency testing (MSLT); and "idiopathic hypersomnia," with less than 2 SOREMPS.

However, "there is no evidence that the pathophysiology or therapeutic response is substantially different for hypersomnia with or without SOREMPs on the MSLT." Given the newly understood overlap of idiopathic hypersomnia and narcolepsy, the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders also updated its classification of the primary hypersomnias. It reclassified both idiopathic hypersomnia with and without long sleep time as major somnolence disorder (MSD). Additionally, MSD encompasses all syndromes of hypersomnolence not explained by low hypocretin, including not only idiopathic hypersomnia, but also narcolepsy without cataplexy, and long sleepers (patients requiring >10 hours sleep/day).

Further complicating these updated classification schemes, overlap between narcolepsy with cataplexy and idiopathic hypersomnia has also been reported. A subgroup of narcoleptics with long sleep time, comprising 18% of narcoleptics in one study, had symptoms of both narcolepsy with cataplexy and idiopathic hypersomnia (long sleep time and unrefreshing naps). It is felt that this subgroup might have dysfunction in multiple arousal systems. (See Causes section below).

The true primary hypersomnias include these: narcolepsy (with and without cataplexy); idiopathic hypersomnia; and recurrent hypersomnias (like Klein-Levin syndrome).

Hypersomnia can be primary (of central/brain origin), or it can be secondary to any of numerous medical conditions. More than one type of hypersomnia can coexist in a single patient. Even in the presence of a known cause of hypersomnia, the contribution of this cause to the complaint of EDS needs to be assessed. When specific treatments of the known condition do not fully suppress EDS, additional causes of hypersomnia should be sought. For example, if a patient with sleep apnea is treated with CPAP (continuous positive airway pressure) which resolves their apneas but not their EDS, it is necessary to seek other causes for the EDS. Obstructive sleep apnea “occurs frequently in narcolepsy and may delay the diagnosis of narcolepsy by several years and interfere with its proper management.”

There are two main characteristics of narcolepsy: excessive daytime sleepiness and abnormal REM sleep. The first, excessive daytime sleepiness (EDS), occurs even after adequate night time sleep. A person with narcolepsy is likely to become drowsy or fall asleep, often at inappropriate times and places, or just be very tired throughout the day. Narcoleptics are not able to experience the amount of restorative deep sleep that healthy people experience – they are not "over-sleeping". In fact, narcoleptics live their entire lives in a constant state of extreme sleep deprivation.

Daytime naps may occur with little warning and may be physically irresistible. These naps can occur several times a day. They are typically refreshing, but only for a few hours or less. Vivid dreams may be experienced on a regular basis, even during very brief naps. Drowsiness may persist for prolonged periods or remain constant. In addition, night-time sleep may be fragmented, with frequent awakenings. A second prominent symptom of narcolepsy is abnormal REM sleep. Narcoleptics are unique in that they enter into the REM phase of sleep in the beginnings of sleep, even when sleeping during the day.

The classic symptoms of the disorder, often referred to as the "tetrad of narcolepsy," are cataplexy, sleep paralysis, hypnagogic hallucinations, and excessive daytime sleepiness. Other symptoms may include automatic behaviors and night-time wakefulness. These symptoms may not occur in all patients.

- Cataplexy is an episodic loss of muscle function, ranging from slight weakness such as limpness at the neck or knees, sagging facial muscles, weakness at the knees often referred to as "knee buckling", or inability to speak clearly, to a complete body collapse. Episodes may be triggered by sudden emotional reactions such as laughter, anger, surprise, or fear, and may last from a few seconds to several minutes. The person remains conscious throughout the episode. In some cases, cataplexy may resemble epileptic seizures. Usually speech is slurred and vision is impaired (double vision, inability to focus), but hearing and awareness remain normal. Cataplexy also has a severe emotional impact on narcoleptics, as it can cause extreme anxiety, fear, and avoidance of people or situations that might elicit an attack. Cataplexy is generally considered to be unique to narcolepsy and is analogous to sleep paralysis in that the usually protective paralysis mechanism occurring during sleep is inappropriately activated. The opposite of this situation (failure to activate this protective paralysis) occurs in rapid eye movement behavior disorder.

- Periods of wakefulness at night

- Sleep paralysis is the temporary inability to talk or move when waking (or less often, when falling asleep). It may last a few seconds to minutes. This is often frightening but is not dangerous.

- Hypnagogic hallucinations are vivid, often frightening, dreamlike experiences that occur while dozing or falling asleep. Hypnopompic hallucinations refer to the same sensations while awakening from sleep. These hallucinations may manifest in the form of visual or auditory sensations.

- Automatic behaviors occur when a person continues to function (talking, putting things away, etc.) during sleep episodes but awakens with no memory of performing such activities. It is estimated that up to 40 percent of people with narcolepsy experience automatic behavior during sleep episodes.

In most cases, the first symptom of narcolepsy to appear is excessive and overwhelming daytime sleepiness. The other symptoms may begin alone or in combination months or years after the onset of the daytime naps. There are wide variations in the development, severity, and order of appearance of cataplexy, sleep paralysis, and hypnagogic hallucinations in individuals. Only about 20 to 25 percent of people with narcolepsy experience all four symptoms. The excessive daytime sleepiness generally persists throughout life, but sleep paralysis and hypnagogic hallucinations may not. A rare subset of narcoleptics also experience a heightened sense of taste and smell known as the supertaster phenomenon.

Many people with narcolepsy also suffer from insomnia for extended periods of time. The excessive daytime sleepiness and cataplexy often become severe enough to cause serious problems in a person's social, personal, and professional life. Normally, when an individual is awake, brain waves show a regular rhythm. When a person first falls asleep, the brain waves become slower and less regular, which is called non-rapid eye movement (NREM) sleep. After about an hour and a half of NREM sleep, the brain waves begin to show a more active pattern again, called REM sleep (rapid eye movement sleep), when most remembered dreaming occurs. Associated with the EEG-observed waves during REM sleep, muscle atonia is present called REM atonia.

In narcolepsy, the order and length of NREM and REM sleep periods are disturbed, with REM sleep occurring at sleep onset instead of after a period of NREM sleep. Also, some aspects of REM sleep that normally occur only during sleep, like lack of muscular control, sleep paralysis, and vivid dreams, occur at other times in people with narcolepsy. For example, the lack of muscular control can occur during wakefulness in a cataplexy episode; it is said that there is intrusion of REM atonia during wakefulness. Sleep paralysis and vivid dreams can occur while falling asleep or waking up. Simply put, the brain does not pass through the normal stages of dozing and deep sleep but goes directly into (and out of) rapid eye movement (REM) sleep.

As a consequence night time sleep does not include as much deep sleep, so the brain tries to "catch up" during the day, hence EDS. People with narcolepsy may visibly fall asleep at unpredicted moments (such motions as head bobbing are common). People with narcolepsy fall quickly into what appears to be very deep sleep, and they wake up suddenly and can be disoriented when they do (dizziness is a common occurrence). They have very vivid dreams, which they often remember in great detail. People with narcolepsy may dream even when they only fall asleep for a few seconds. Along with vivid dreaming, people with narcolepsy are known to have audio or visual hallucinations prior to falling asleep.

Narcoleptics can gain excess weight; children can gain 20 to 40 lb (9 to 18 kg) when they first develop narcolepsy; in adults the body-mass index is about 15% above average.

The most common sleep disorders include:

- Bruxism, involuntarily grinding or clenching of the teeth while sleeping.

- Catathrenia, nocturnal groaning during prolonged exhalation.

- Delayed sleep phase disorder (DSPD), inability to awaken and fall asleep at socially acceptable times but no problem with sleep maintenance, a disorder of circadian rhythms. Other such disorders are advanced sleep phase disorder (ASPD), non-24-hour sleep–wake disorder (non-24) in the sighted or in the blind, and irregular sleep wake rhythm, all much less common than DSPD, as well as the situational shift work sleep disorder.

- Hypopnea syndrome, abnormally shallow breathing or slow respiratory rate while sleeping.

- Idiopathic hypersomnia, a primary, neurologic cause of long-sleeping, sharing many similarities with narcolepsy.

- Insomnia disorder (primary insomnia), chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for these symptoms. Insomnia can also be comorbid with or secondary to other disorders.

- Kleine–Levin syndrome, a rare disorder characterized by persistent episodic hypersomnia and cognitive or mood changes.

- Narcolepsy, including excessive daytime sleepiness (EDS), often culminating in falling asleep spontaneously but unwillingly at inappropriate times. About 70% of those who have narcolepsy also have cataplexy, a sudden weakness in the motor muscles that can result in collapse to the floor while retaining full conscious awareness.

- Night terror, "Pavor nocturnus", sleep terror disorder, an abrupt awakening from sleep with behavior consistent with terror.

- Nocturia, a frequent need to get up and urinate at night. It differs from enuresis, or bed-wetting, in which the person does not arouse from sleep, but the bladder nevertheless empties.

- Parasomnias, disruptive sleep-related events involving inappropriate actions during sleep, for example sleep walking, night-terrors and catathrenia.

- Periodic limb movement disorder (PLMD), sudden involuntary movement of arms and/or legs during sleep, for example kicking the legs. Also known as nocturnal myoclonus. See also Hypnic jerk, which is not a disorder.

- Rapid eye movement sleep behavior disorder (RBD), acting out violent or dramatic dreams while in REM sleep, sometimes injuring bed partner or self (REM sleep disorder or RSD).

- Restless legs syndrome (RLS), an irresistible urge to move legs. RLS sufferers often also have PLMD.

- Shift work sleep disorder (SWSD), a situational circadian rhythm sleep disorder. (Jet lag was previously included as a situational circadian rhythm sleep disorder, but it doesn't appear in DSM-5 (see Diagnostic and Statistical Manual of Mental Disorders)).

- Sleep apnea, obstructive sleep apnea, obstruction of the airway during sleep, causing lack of sufficient deep sleep, often accompanied by snoring. Other forms of sleep apnea are less common. When air is blocked from entering into the lungs, the individual unconsciously gasps for air and sleep is disturbed. Stops of breathing of at least ten seconds, 30 times within seven hours of sleep, classifies as apnea. Other forms of sleep apnea include central sleep apnea and sleep-related hypoventilation.

- Sleep paralysis, characterized by temporary paralysis of the body shortly before or after sleep. Sleep paralysis may be accompanied by visual, auditory or tactile hallucinations. Not a disorder unless severe. Often seen as part of narcolepsy.

- Sleepwalking or "somnambulism", engaging in activities normally associated with wakefulness (such as eating or dressing), which may include walking, without the conscious knowledge of the subject.

- Somniphobia, one cause of sleep deprivation, a dread/ fear of falling asleep or going to bed. Signs of the illness include anxiety and panic attacks before and during attempts to sleep.

There are over 30 recognized kinds of dyssomnias. Major groups of dyssomnias include:

- Intrinsic sleep disorders – 12 disorders recognized, including

- idiopathic hypersomnia,

- narcolepsy,

- periodic limb movement disorder,

- restless legs syndrome,

- sleep apnea,

- sleep state misperception.

- Extrinsic sleep disorders – 13 disorders recognized, including

- alcohol-dependent sleep disorder,

- food allergy insomnia,

- inadequate sleep routine.

- Circadian rhythm sleep disorders, both intrinsic and extrinsic – 6 disorders recognized, including

- advanced sleep phase syndrome,

- delayed sleep phase syndrome,

- jetlag,

- shift work sleep disorder.

Narcolepsy is a long-term neurological disorder that involves a decreased ability to regulate sleep-wake cycles. Symptoms include periods of excessive daytime sleepiness that usually last from seconds to minutes and may occur at any time. About 70% of those affected also experience episodes of sudden loss of muscle strength, known as cataplexy. These spells can be brought on by strong emotions. Less commonly there may be inability to move or vivid hallucinations while falling asleep or waking up. People with narcolepsy tend to sleep about the same number of hours per day as people without, but the quality of sleep tends to be worse.

The exact cause of narcolepsy is unknown with potentially several causes. In up to 10% of cases there is a family history of the disorder. Often those affected have low levels of the neuropeptide "orexin" which may be due to an autoimmune disorder. Trauma, infections, toxins, or psychological stress may also play a role. Diagnosis is typically based on the symptoms and sleep studies, after ruling out other potential causes. Excessive daytime sleepiness can also be caused by other sleep disorders such as sleep apnea, major depressive disorder, anemia, heart failure, drinking alcohol, and not getting enough sleep. Cataplexy may be mistaken for seizures.

While there is no cure, a number of lifestyle changes and medications may help. Lifestyle changes include taking regular short naps and sleep hygiene. Medications used include modafinil, sodium oxybate, and methylphenidate. While initially effective, tolerance to the benefits may develop over time. Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) may improve cataplexy.

About 0.2 to 600 per 100,000 people are affected. The condition often begins in childhood. Men and women are affected equally. Untreated narcolepsy increases the risk of motor vehicle collisions and falls. The term "narcolepsy" is from the French "narcolepsie". The French term was first used in 1880 by Jean-Baptiste-Édouard Gélineau who used the Greek νάρκη ("narkē") meaning "numbness" and λῆψις ("lepsis") meaning "attack".

Dyssomnias are a broad classification of sleeping disorders involving difficulty getting to sleep, remaining asleep, or of excessive sleepiness.

Dyssomnias are primary disorders of initiating or maintaining sleep or of excessive sleepiness and are characterized by a disturbance in the amount, quality, or timing of sleep.

Patients may complain of difficulty getting to sleep or staying asleep, intermittent wakefulness during the night, early morning awakening, or combinations of any of these. Transient episodes are usually of little significance. Stress, caffeine, physical discomfort, daytime napping, and early bedtimes are common factors.

Excessive daytime sleepiness (EDS) is characterized by persistent sleepiness and often a general lack of energy, even during the day after apparently adequate or even prolonged nighttime sleep. EDS can be considered as a broad condition encompassing several sleep disorders where increased sleep is a symptom, or as a symptom of another underlying disorder like narcolepsy, sleep apnea or a circadian rhythm sleep disorder.

Some persons with EDS, including those with hypersomnias like narcolepsy and idiopathic hypersomnia, are compelled to nap repeatedly during the day; fighting off increasingly strong urges to sleep during inappropriate times such as while driving, while at work, during a meal, or in conversations. As the compulsion to sleep intensifies, the ability to complete tasks sharply diminishes, often mimicking the appearance of intoxication. During occasional unique and/or stimulating circumstances, a person with EDS can sometimes remain animated, awake and alert, for brief or extended periods of time. EDS can affect the ability to function in family, social, occupational, or other settings. A proper diagnosis of the underlying cause and ultimately treatment of symptoms and/or the underlying cause can help mitigate such complications.

This sleep disorder frequently applies when patients report not feeling tired despite their subjective perception of not having slept. Generally, they may describe experiencing several years of no sleep, short sleep, or non-restorative sleep. Otherwise, patients appear healthy, both psychiatrically and medically. (That this condition is often asymptomatic could explain why it is relatively unreported.)

However, upon clinical observation, it is found that patients may severely overestimate the time they took to fall asleep—often reporting having slept half the amount of time indicated by polysomnogram or electroencephalography (EEG), which may record normal sleep. Observing such discrepancy between subjective and objective reports, clinicians may conclude that the perception of poor sleep is primarily illusionary.

Alternatively, some people may report excessive daytime sleepiness or chronic disabling sleepiness, while no sleep disorder has been found to exist. Methods of diagnosing sleepiness objectively, such as the Multiple Sleep Latency Test do not confirm the symptom"true" sleepiness is not observed despite the complaint. (It may be speculated that such reports of daytime sleepiness may be a result of the nocebo response —the reverse of the placebo effect—due to patient expectations of adverse effects from their subjective perception of poor sleep.)

Finally, on the opposite end of the spectrum, other patients may report feeling that they have slept much longer than is observed. It has been proposed that this experience be subclassified under sleep state misperception as "positive sleep state misperception", "reverse sleep state misperception", and "negative sleep state misperception".

Sleep state misperception is classified as an intrinsic dyssomnia. While SSM is regarded a sub-type of insomnia, it is also established as a separate sleep-condition, with distinct pathophysiology. Nonetheless, the value of distinguishing this type of insomnia from other types is debatable due to the relatively low frequency of SSM being reported.

Sleep state misperception can also be further broken down into several types, by patients who—

- report short sleep (subjective insomnia complaint without objective findings)

- or no sleep at all (subjective "total" insomnia)

- report excessive daytime sleepiness (subjective sleepiness complaint without objective findings)

- report sleeping too much (subjective hypersomnia without objective findings)

A systematic review found that traumatic childhood experiences (such as family conflict or sexual trauma) significantly increases the risk for a number of sleep disorders in adulthood, including sleep apnea, narcolepsy, and insomnia. It is currently unclear whether or not moderate alcohol consumption increases the risk of obstructive sleep apnea.

In addition, an evidence-based synopses suggests that the sleep disorder, idiopathic REM sleep behavior disorder (iRBD), may have a hereditary component to it. A total of 632 participants, half with iRBD and half without, completed self-report questionnaires. The results of the study suggest that people with iRBD are more likely to report having a first-degree relative with the same sleep disorder than people of the same age and sex that do not have the disorder. More research needs to be conducted to gain further information about the hereditary nature of sleep disorders.

A population susceptible to the development of sleep disorders is people who have experienced a traumatic brain injury (TBI). Because many researchers have focused on this issue, a systematic review was conducted to synthesize their findings. According to their results, TBI individuals are most disproportionately at risk for developing narcolepsy, obstructive sleep apnea, excessive daytime sleepiness, and insomnia. The study's complete findings can be found in the table below:

An adult who is compelled to nap repeatedly during the day may have excessive daytime sleepiness; however, it is important to distinguish between occasional daytime sleepiness and excessive daytime sleepiness, which is chronic.

A number of tools for screening for EDS have been developed. One is the Epworth Sleepiness Scale which grades the results of a questionnaire. The ESS generates a numerical score from zero (0) to 24 where a score of ten [10] or higher may indicate that the person should consult a specialist in sleep medicine for further evaluation.

Another tool is the Multiple Sleep Latency Test (MSLT), which has been used since the 1970s. It is used to measure the time it takes from the start of a daytime nap period to the first signs of sleep, called sleep latency. The test is based on the idea that the sleepier people are, the faster they will fall asleep.

The Maintenance of Wakefulness Test (MWT) is also used to quantitatively assess daytime sleepiness. This test is performed in a sleep diagnostic center. The test is similar to the MSLT. However, during this test the patient is instructed to try to stay awake.

Patients with Kleine–Levin syndrome (KLS) experience reoccurring episodes of prolonged sleep (hypersomnia). In most cases, patients sleep 15 to 21 hours a day during episodes.

Excessive appetite (hyperphagia) and unusual cravings are present in half to two thirds of cases. About half of patients, mainly male patients, experience dramatically increased sexual urges (hypersexuality). Several other symptoms usually accompany the syndrome, including marked changes in mood and cognitive ability. Derealization and severe apathy are present in at least 80 percent of cases. About one third of patients experience hallucinations or delusions. Depression and anxiety occur less commonly; one study found them in about 25 percent of patients. Individuals usually cannot remember what happened during episodes. Repetitive behaviors and headaches are commonly reported. Some patients act very childlike during episodes, and communication skills and coordination sometimes suffer.

Sleep studies of KLS show varying results based on the amount of time the patient is observed. Slow wave sleep is often reduced at the beginning of episodes, and REM sleep is reduced near the end. Conversely, REM sleep is often normal at the beginning, and slow wave sleep is often normal by the conclusion. Stage two non-rapid eye movement sleep is often interrupted during KLS. Studies also show that stage one and three non-rapid eye movement sleep become more efficient when the episodes end. The Multiple Sleep Latency Test has yielded inconsistent results when given to KLS patients. In many cases, hours are spent in a withdrawn sleep-like state while awake during episodes. Most sleep studies have been performed while subject are near the end of their episodes. Some patients experience brief insomnia and become very happy and talkative after the episode ends.

The first time a patient experiences KLS, it usually occurs along with symptoms that are similar to those of the flu or encephalitis. In at least 75 percent of cases, symptoms occur after an airway infection or a fever. Viruses observed before the development of the condition include Epstein-Barr virus, varicella zoster virus, herpes zoster virus, Influenza A virus subtypes, and adenovirus. Several days after symptoms first occur, patients become very tired. In cases that occur after an infection, KLS usually starts within three to five days for teenagers and fewer for children. In other cases, alcohol consumption, head injury, or international travel precede symptoms. Lifestyle habits, such as stress, alcohol abuse and lack of sleep and stress, have also been proposed as possible triggers. First episodes of KLS are preceded by a clear event in about 90 percent of cases. Recurrences generally do not have clear triggers; only about 15 percent have a precipitating event.

The condition generally disrupts the social lives and academic or profession obligations of sufferers. Some patients also gain weight during episodes. The most severe cases cause a long-term impact on mood and cognitive attention. In rare cases, patients experience long-term memory problems.

In patients with KLS, MRI and CT scans show normal brain morphology. When SPECT is performed, hypoperfusion can often be observed in the brain, particularly in the thalamic and frontotemporal areas. The hypoperfusion is significantly diminished between episodes. Serum biology, c-reactive proteins and leptins, the hormonal pituitary axis, and protein in the cerebral spinal fluid (CSF) are normal in KLS patients.

The frequency of KLS episodes can vary from attacks one week in length occurring twice a year to dozens of episodes that follow each other in close succession. The median duration of KLS episodes is about ten days, but some last several weeks or months. A study of 108 patients found an average of 19 episodes over the duration of the disease. Another study found a median of 3.5 months between episodes. Outside of episodes, there is no disturbance in patients' sleep patterns and they are generally asymptomatic. Patients do not experience the same symptoms in each episode.

About 80 percent of patients are adolescents when they first experience KLS. On some occasions though, its first occurrence comes in childhood or adulthood. In most adolescent-onset patients, symptoms cease by the time they are 30 years old. A French study of 108 patients found a median duration of 13 years, but a review of 186 cases found a median duration of 8 years. Unusually young or old patients and those who experience hypersexuality tend to have a more severe course. Patients who initially have frequent attacks generally see the disease cease earlier than others. The condition spontaneously resolves, and the patient is considered to be cured if there have been no symptoms for six years.

The symptoms include many of the symptoms associated with milder degrees of hypoglycemia, especially the adrenergic symptoms, but do not progress to objective impairment of brain function, seizures, coma, or brain damage.

- Shakiness

- Sense of weakness

- Altered or depressed mood

- Confusion

- Fatigue

- Anxiety

- Paleness

- Perspiration

- Increased pulse or respiratory rate

- Hunger

Epilepsy is most commonly recognised by involuntary movements of the head and limbs, however other characteristics include salivation, lack of and anxiety. Animals often lose consciousness and are not aware of their surroundings.

There is some evidence of the existence of a so-called "adrenergic postprandial syndrome": the glycemia is normal, and the symptoms are caused through autonomic adrenergic counterregulation. Often, this syndrome is associated with emotional distress and anxious behaviour of the patient.

Watching an animal have a seizure can be quite frightening. There is not much that can be done during a seizure except to remain calm and not leave the animal alone. If your pet is having a seizure it is important to make sure they are laying down on the floor away from any water, stairs or other animals. When an animal has a seizure, do not try to grab their tongue or clear their mouth as there is a high chance you will be bitten; contrary to popular myth, neither humans nor animals can "swallow their tongue" during a seizure so it is safest to stay well away from their mouth during one. Timing seizures is also crucial. Take notes of seizures - what time they occur, how often and any other specific information which can be passed onto the vet or emergency animal clinic.

Juvenile myoclonic epilepsy (JME) is an idiopathic generalized epilepsy that occurs in patients aged 8 to 20 years. Patients have normal cognition and are otherwise neurologically intact. The most common seizure is myoclonic jerks, although generalized tonic-clonic seizures and absence seizures may occur as well. Myoclonic jerks usually cluster in the early morning after awakening. The EEG reveals generalized 4–6 Hz spike wave discharges or multiple spike discharges. These patients are often first diagnosed when they have their first generalized tonic-clonic seizure later in life, when they experience sleep deprivation (e.g., freshman year in college after staying up late to study for exams). Alcohol withdrawal can also be a major contributing factor in breakthrough seizures, as well. The risk of the tendency to have seizures is lifelong; however, the majority have well-controlled seizures with anticonvulsant medication and avoidance of seizure precipitants.

Childhood absence epilepsy (CAE) is an idiopathic generalized epilepsy that affects children between the ages of 4 and 12 years of age, although peak onset is around five to six years old. These patients have recurrent absence seizures, brief episodes of unresponsive staring, sometimes with minor motor features such as eye blinking or subtle chewing. The EEG finding in CAE is generalized 3 Hz spike and wave discharges. Some go on to develop generalized tonic-clonic seizures. This condition carries a good prognosis because children do not usually show cognitive decline or neurological deficits, and the seizures in the majority cease spontaneously with ongoing maturation.

Seizures are purely occipital and primarily manifest with elementary visual hallucinations, blindness or both.

They are usually frequent and diurnal, develop rapidly within seconds and are brief, lasting from a few seconds to 1–3 min, and, rarely, longer.

Elementary visual hallucinations are the most common and characteristic ictal symptoms, and are most likely to be the first and often the only clinical manifestation. They consist mainly of small multicoloured circular patterns that often appear in the periphery of a visual field, becoming larger and multiplying during the course of the seizure, frequently moving horizontally towards the other side.

Other occipital symptoms, such as sensory illusions of ocular movements and ocular pain, tonic deviation of the eyes, eyelid fluttering or repetitive eye closures, may occur at the onset of the seizures or appear after the elementary visual hallucinations. "Deviation of the eyes", often associated with ipsilateral turning of the head, is the most common (in about 70% of cases) nonvisual ictal symptom. It is often associated with ipsilateral turning of the head and usually starts after visual hallucinations, although it may also occur while the hallucinations still persist. It may be mild, but more often it is severe and progresses to hemiconvulsions and secondarily generalised tonic clonic seizures (GTCS). Some children may have seizures of eye deviation from the start without visual hallucinations.

"Forced eyelid closure and eyelid blinking" occur in about 10% of patients, usually at a stage at which consciousness is impaired. They signal an impending secondarily GTCS.

"Ictal blindness", appearing from the start or, less commonly, after other manifestations of occipital seizures, usually lasts for 3–5 min. It can occur alone and be the only ictal event in patients who could, at other times, have visual hallucinations without blindness.

Complex visual hallucinations, visual illusions and other symptoms resulting from more anterior ictal spreading rarely occur from the start. They may terminate in hemiconvulsions or generalised convulsions.

Ictal headache, or mainly orbital pain, may occur and often precedes visual or other ictal occipital symptoms in a small number of patients.

Consciousness is not impaired during the visual symptoms (simple focal seizures), but may be disturbed or lost in the course of the seizure, usually before eye deviation or convulsions.

Occipital seizures of ICOE-G may rarely progress to extra-occipital manifestations, such as hemiparaesthesia. Spread to produce symptoms of temporal lobe involvement is exceptional and may indicate a symptomatic cause.

Post-ictal headache, mainly diffuse, but also severe, unilateral and pulsating, or indistinguishable from migraine headache, occurs in half the patients, in 10% of whom it may be associated with nausea and vomiting.

Circadian distribution: Visual seizures are predominantly diurnal and can occur at any time of the day. Longer seizures, with or without hemi or generalised convulsions, tend to occur either during sleep, causing the patient to wake up, or after awakening. Thus, some children may have numerous diurnal visual seizures and only a few seizures that are exclusively nocturnal or occur on awakening.

Frequency of seizures: If untreated, patients experience frequent and brief visual seizures (often several every day or weekly). However, propagation to other seizure manifestations, such as focal or generalised convulsions, is much less frequent.

Recurrent brief depression (RBD) defines a mental disorder characterized by intermittent depressive episodes, not related to menstrual cycles in women, occurring between approximately 6-12 times per year, over at least one year or more fulfilling the diagnostic criteria for major depressive episodes (DSM-IV and ICD-10) except for duration which in RBD is less than 14 days, typically 2–4 days. Despite the short duration of the depressive episodes, such episodes are severe and suicidal ideation and impaired function is rather common. The majority of patients with RBD also report symptoms of anxiety and increased irritability. Hypersomnia is also rather frequent. About 1/2 of patients fulfilling diagnostic criteria for RBD may have additional short episodes of brief hypomania which is a severity marker of RBD. RBD may be the only mental disorder present, but RBD may also occur as part of a history of recurrent major depressive episodes or bipolar disorders. RBD is also seen among some patients with personality disorders.

One major symptom of a mental breakdown is depression. When someone is depressed they may experience weight loss or gain (often due to changes in appetite), suicidal thoughts, loss of interest in social, family or work life, insomnia or hypersomnia, exhaustion or fatigue and feelings of hopelessness or worthlessness. Another symptom of a breakdown is anxiety, which can produce an increase in blood pressure, dizziness, trembling, or feeling sick to the stomach. Panic attacks are very similar to mental breakdowns, but can also be a symptom in some cases. Difficulty with breathing and extreme fear, alongside rapid heartbeat may occur in those who are experiencing a panic attack. In more severe cases of mental breakdown, a person may experience mood swings, hallucinations, paranoia, and flashbacks. In each of these more severe cases there can be a more serious underlying problem that caused the mental breakdown. Hallucinations may suggest schizophrenia or other disorders involving psychosis, mood swings may suggest bipolar disorder or other mood disorders (or personality disorders such as BPD), and flashbacks may suggest posttraumatic stress disorder. The severity of each of these disorders and symptoms may vary based upon the person and their background.