A hypnic jerk, hypnagogic jerk, sleep start, sleep twitch or night start is an involuntary twitch which occurs when a person is beginning to fall asleep, often causing them to awaken suddenly for a moment. Physically, hypnic jerks resemble the "jump" experienced by a person when startled, sometimes accompanied by a falling sensation. Hypnic jerks are associated with a rapid heartbeat, quickened breathing, sweat, and sometimes "a peculiar sensory feeling of 'shock' or 'falling into the void. A higher occurrence is reported in people with irregular sleep schedules.

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.

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. While cataplexy worsens with fatigue, it is different from narcoleptic sleep attacks and is usually, but not always, triggered by strong emotional reactions such as laughter, anger, surprise, awe, and embarrassment, or by sudden physical effort, especially if the person is caught off guard. One well known example of this was the reaction of 1968 Olympic long jump medalist Bob Beamon on understanding that he had broken the previous world record by over 0.5 meters (2 feet). Cataplectic attacks may occasionally occur spontaneously, with no identifiable emotional trigger.

According to the American Academy of Sleep Medicine there is a wide range of potential causes, including anxiety, caffeine, stress and strenuous activities in the evening. However, most hypnic jerks occur essentially at random in healthy people.

Another hypothesis is evolutionary, stretching back to our primate ancestors. A study at the University of Colorado has suggested that a hypnic jerk could be "an archaic reflex to the brain's misinterpretation of muscle relaxation with the onset of sleep as a signal that a sleeping primate is falling out of a tree. The reflex may also have had selective value by having the sleeper readjust or review his or her sleeping position in a nest or on a branch in order to assure that a fall did not occur."

During an epilepsy and intensive care study, the lack of a preceding spike discharge measured on an epilepsy monitoring unit, along with the presence only at sleep onset, helped differentiate hypnic jerks from epileptic myoclonus.

According to a study on sleep disturbances in the "Journal of Neural Transmission", a hypnic jerk occurs during the non-rapid eye movement sleep cycle and is an "abrupt muscle action flexing movement, generalized or partial and asymmetric, which may cause arousal, with an illusion of falling". Hypnic jerks are more frequent in childhood with 4 to 7 per hour in the age range from 8 to 12 years old, and they decrease toward 1 or 2 per hour by 65 to 80 years old.

The central symptom of sleep paralysis is being aware but being unable to move during awakening.

Imagined sounds such as humming, hissing, static, zapping and buzzing noises are reported during sleep paralysis. Other sounds such as voices, whispers and roars are also experienced. These symptoms are usually accompanied by intense emotions: such as fear, and panic. People also have sensations of being dragged out of bed or of flying, numbness, and feelings of electric tingles or vibrations running through their body.

Sleep paralysis may include hallucinations, such as a supernatural creature suffocating or terrifying the individual, accompanied by a feeling of pressure on one's chest and difficulty breathing. Another example of a hallucination involves a menacing shadowy figure entering one's room or lurking outside one's window, while the subject is paralyzed.

The body image distortion (affecting parietal regions and the temporoparietal junction) may result in the sleeper having bodily hallucinations, such as illusory limbs and out-of-body experiences. The content and interpretation of these hallucinations are driven by fear, somatic sensations, REM-induced sexual arousal, and REM mentation which are embedded in the sleeper's cultural narrative.

REM sleep physiology and somatic symptoms coupled with the awareness that one is paralyzed, can generate a variety of psychological symptoms during sleep paralysis, including fear and worry that are aggravated by catastrophic cognitions about the attack. This can activate a fight-flight reaction and panic-like arousal. Consequently, when the person attempts to escape the paralysis, somatic symptoms and arousal are exacerbated, as execution of motor programs in the absence of dampening proprioceptive feedback can lead to heightened sensations of bodily tightness and pressure, and even pain and spasms in limbs.

The diagnosis of narcolepsy and cataplexy is usually made by symptom presentation. Presenting with the tetrad of symptoms (Excessive daytime sleepiness, sleep onset paralysis, hypnogogic hallucinations, cataplexy symptoms) is strong evidence of the diagnosis of narcolepsy. A Multiple Sleep Latency Test (MSLT) is often conducted in order to quantify daytime sleepiness.

Sleep paralysis is when, during awakening or falling asleep, one is aware but unable to move. During an episode, one may hear, feel, or see things that are not there. It often results in fear. Episodes generally last less than a couple of minutes. It may occur as a single episode or be recurrent.

The condition may occur in those who are otherwise healthy, those with narcolepsy, or may run in families as a result of specific genetic changes. The condition can be triggered by sleep deprivation, psychological stress, or abnormal sleep cycles. The underlying mechanism is believed to involve a dysfunction in REM sleep. Diagnosis is based on a person's description. Other conditions that can present similarly include narcolepsy, atonic seizure, and hypokalemic periodic paralysis.

Treatment options for sleep paralysis have been poorly studied. People should generally be reassured that the condition is common and not serious. Other efforts that may be tried include sleep hygiene, cognitive behavioral therapy, and antidepressants.

Between 8% and 50% of people experience sleep paralysis at some time. About 5% of people have regular episodes. Males and females are affected equally. Sleep paralysis has been described throughout history. It is believed to have played a role in the creation of stories about alien abduction and other paranormal events.

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.

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).

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.

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).

Myoclonic seizure can be described as "jumps" or "jolts" experienced in a single or even the entire body. The feeling experienced by the individual is described as uncontrollable jolts common to receiving a mild electric shock. The sudden jerks and twitching of the body can often be so severe that it can cause a small child to fall.

A myoclonic seizure ("myo" "muscle", "clonic" "jerk") is a sudden involuntary contraction of muscle groups. The muscle jerks consist of symmetric, mostly generalized jerks, localized in the arms and in the shoulders and also simultaneously with a head nod; both the arms may fling out together and simultaneously a head nod may occur. Symptoms have some variability amongst subjects. Sometimes the entire body may jerk, just like a startle response. As is the case with all generalised seizures, the patient is not conscious during the event but the seizure is so brief that the person appears to remain fully conscious.

In reflex epilepsies, myoclonic seizures can be brought on by flashing lights or other environmental triggers (see photosensitive epilepsy).

Familiar examples of normal myoclonus include hiccups and hypnic jerks that some people experience while drifting off to sleep. Severe cases of pathologic myoclonus can distort movement and severely limit a person's ability to sleep, eat, talk, and walk. Myoclonic jerks commonly occur in individuals with epilepsy.

The most common types of myoclonus include action, cortical reflex, essential, palatal, those seen in the progressive myoclonus epilepsies, reticular reflex, sleep and stimulus-sensitive.

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".

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:

Myoclonus dystonia includes the rapid contractions of myoclonus alongside the abnormal postures classified under dystonia, as well as neurological and psychiatric issues. This disease typically begins during childhood with symptoms of myoclonus and slight dystonia, most commonly cervical dystonia or writer’s cramp. Dystonia symptoms tend to not get exaggerated over the course of the disease and is rarely the only associated symptom, while the myoclonus symptoms can become more severe. Psychiatric issues are clinically diagnosed with the aforementioned symptoms and include depression, anxiety, personality disorders and addiction. Obsessive-compulsive disorder is associated with myoclonus dystonia as both have been found to have a commonality on chromosome 7 in various studies.

Neurological symptoms are relatively common in those with myoclonus dystonia. Any neurological abnormalities won’t normally be present in those affected at a young age. Neurological testing has been performed to determine the origins of these symptoms and multiple parts of the brain have been pinpointed including the brainstem, neocortex, pallidum, and thalamus. These cause various effects in those diagnosed with myoclonus dystonia including changes in posture and tremors, and very rarely dementia and ataxia.

Dystonia is a response to simultaneous contraction of agonist and antagonist muscles seen as twisting and contorting that affect posture and stance. Other symptoms can include tremors and muscle spasms due to various interactions of muscle, contractions and movement. Dystonia can be either primary or secondary with the latter being more common. Primary dystonia or “pure” dystonia is only physiological in origin. Secondary dystonia has multiple origins that are physiological, pathological or neurological.

A hiccup is an involuntary contraction (myoclonic jerk) of the diaphragm that may repeat several times per minute. In Latin it is called singultus for the act of catching one's breath while sobbing. The hiccup is an involuntary action involving a reflex arc. Once triggered, the reflex causes a strong contraction of the diaphragm followed about 0.25 second later by closure of the vocal cords, which results in the classic "hic" sound.

Hiccups may occur individually, or they may occur in bouts. The rhythm of the hiccup, or the time between hiccups, tends to be relatively constant.

A bout of hiccups, in general, resolves itself without intervention, although many home remedies are often used to attempt to shorten the duration. Medical treatment is occasionally necessary in cases of chronic hiccups.

The clinical manifestations of absence seizures vary significantly among patients. Impairment of consciousness is the essential symptom, and may be the only clinical symptom, but this can be combined with other manifestations. The hallmark of the absence seizures is abrupt and sudden-onset impairment of consciousness, interruption of ongoing activities, a blank stare, possibly a brief upward rotation of the eyes. If the patient is speaking, speech is slowed or interrupted; if walking, they stand transfixed; if eating, the food will stop on its way to the mouth. Usually, the patient will be unresponsive when addressed. In some cases, attacks are aborted when the patient is called. The attack lasts from a few seconds to half a minute, and evaporates as rapidly as it commenced. Absence seizures generally are not followed by a period of disorientation or lethargy (post-ictal state), in contrast to the majority of seizure disorders.

1. Absence with impairment of consciousness only as per the above description.

2. Absence with mild clonic components. Here the onset of the attack is indistinguishable from the above, but clonic components may occur in the eyelids, at the corner of the mouth, or in other muscle groups which may vary in severity from almost imperceptible movements to generalised myoclonic jerks. Objects held in the hand may be dropped.

3. Absence with atonic components. Here there may be a diminution in tone of muscles subserving posture as well as in the limbs leading to dropping of the head, occasionally slumping of the trunk, dropping of the arms, and relaxation of the grip. Rarely tone is sufficiently diminished to cause this person to fall.

4. Absence with tonic components. Here during the attack tonic muscular contraction may occur, leading to increase in muscle tone which may affect the extensor muscles or the flexor muscles symmetrically or asymmetrically. If the patient is standing, the head may be drawn backward and the trunk may arch. This may lead to retropulsion, which may cause eyelids to twitch rapidly, eyes may jerk upwards or the patients head may rock back and forth slowly, as if nodding. The head may tonically draw to one or another side.

5. Absence with automatisms. Purposeful or quasipurposeful movements occurring in the absence of awareness during an absence attack are frequent and may range from lip licking and swallowing to clothes fumbling or aimless walking. If spoken to, the patient may grunt, and when touched or tickled may rub the site. Automatisms are quite elaborate and may consist of combinations of the above described movements or may be so simple as to be missed by casual observation.

6. Absence with autonomic components. These may be pallor, and less frequently flushing, sweating, dilatation of pupils and incontinence of urine.

Mixed forms of absence frequently occur.

These seizures can happen a few times a day or in some cases hundreds of times a day, to the point that the person cannot concentrate in school or in other situations requiring sustained, concentrated attention.

Hiccups may be triggered by a number of common human conditions. In rare cases, they can be a sign of serious medical problems.

Absence seizures are one of several kinds of seizures. These seizures are sometimes referred to as petit mal seizures (from the French for "little illness", a term dating from the late 18th century). Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy (i.e. without a notable postictal state).

Patients with stiff person syndrome (SPS) suffer progressive stiffness in their truncal muscles, which become rigid and stiff because the lumbar and abdominal muscles engage in constant contractions. Initially, stiffness occurs in the thoracolumbar paraspinal and

abdominal muscles. It later affects the proximal leg and abdominal wall muscles. The stiffness leads to a change in posture, and patients develop a rigid gait. Persistent lumbar hyperlordosis often occurs as it progresses. The muscle stiffness initially fluctuates, sometimes for days or weeks, but eventually begins to consistently impair mobility. As the disease progresses, patients sometimes become unable to walk or bend. Chronic pain is common and worsens over time but sometimes acute pain occurs as well. Stress, cold weather, and infections lead to an increase in symptoms, and sleep decreases them.

SPS patients suffer superimposed spasms and extreme sensitivity to touch and sound. These spasms primarily occur in the proximal limb and axial muscles. There are co-contractions of agonist and antagonist muscles. Spasms usually last for minutes and can recur over hours. Attacks of spasms are unpredictable and are often caused by fast movements, emotional distress, or sudden sounds or touches. In rare cases, facial muscles, hands, feet, and the chest can be affected and unusual eye movements and vertigo occur. There are brisk stretch reflexes and clonus occurs in patients. Late in the disease's progression, hypnagogic myoclonus can occur. Tachycardia and hypertension are sometimes also present.

Because of the spasms, patients may become increasingly fearful, require assistance, and lose the ability to work, leading to depression, anxiety, and phobias, including agoraphobia and dromophobia. Most patients are psychologically normal and respond reasonably to their situations.

Paraneoplastic SPS tends to affect the neck and arms more than other variations. It progresses very quickly, is more painful, and is more likely to include distal pain than classic SPS. Patients with paraneoplastic SPS generally lack other autoimmune issues but may have other paraneoplastic conditions.

Stiff-limb syndrome is a variant of SPS. This syndrome develops into full SPS about 25 percent of the time. Stiffness and spasms are usually limited to the legs and hyperlordoisis generally does not occur. The stiffness begins in one limb and remains most prominent there. Sphincter and brainstem issues often occur with stiff-limb syndrome. Progressive encephalomyelitis with rigidity, another variant of the condition, includes symptoms of SPS with brainstem issues and autonomic disturbances. It involves polio-encephalomyelitis in the spine and brainstem. There is cerebellar and brainstem involvement. In some cases, the limbic system is affected, as well. Most patients have upper motoneuron issues and autonomic disturbances. Jerking man syndrome or jerking SPS is another subtype of the condition. It begins like classical SPS and progresses for several years, up to 14 in some cases. It is then distinguished by the development of myoclonus as well as seizures and ataxia in some cases.

Signs and symptoms of pseudobulbar palsy include:

- Slow and indistinct speech

- Dysphagia (difficulty in swallowing)

- Small, stiff and spastic tongue

- Brisk jaw jerk

- Dysarthria

- Labile affect

- Gag reflex may be normal, exaggerated or absent

- Examination may reveal upper motor neuron lesion of the limbs

Jactitation is an archaic medical term (derived, perhaps as a corruption, from "jactation", meaning a restless tossing and turning of the body, and derived itself from Latin "jactare" or "jacere", both meaning "to throw or hurl") referring to the involuntary spasm of a limb, muscle, or muscle group. This is sometimes seen in fever patients or other situations of physical distress, but may occur in healthy individuals in a hypnogogic state. This hypnagogic jactitation often occurs in the legs, and may occasion a short explanatory dream about stumbling or missing the bottom stair.

Focal impaired awareness seizures are seizures which impair consciousness to some extent: they alter the person's ability to interact normally with their environment. They usually begin with a focal aware seizure, then spread to a larger portion of the temporal lobe, resulting in impaired consciousness. They may include autonomic and psychic features present in focal aware seizures.

Signs may include:

- Motionless staring

- Automatic movements of the hands or mouth

- Confusion and disorientation

- Altered ability to respond to others, unusual speech

- Transient aphasia (losing ability to speak, read, or comprehend spoken word)

These seizures tend to have a warning or aura before they occur, and when they occur they generally tend to last only 1–2 minutes. It is not uncommon for an individual to be tired or confused for up to 15 minutes after a seizure has occurred, although postictal confusion can last for hours or even days. Though they may not seem harmful, due to the fact that the individual does not normally seize, they can be extremely harmful if the individual is left alone around dangerous objects. For example, if a person with complex partial seizures is driving alone, this can cause them to run into the ditch, or worse, cause an accident involving multiple people. With this type, some people do not even realize they are having a seizure and most of the time their memory from right before or after the seizure is wiped. First-aid is only required if there has been an injury or if this is the first time a person has had a seizure.

"Focal aware" means that the level of consciousness is not altered during the seizure. In temporal lobe epilepsy, a focal seizure usually causes abnormal sensations only.

These may be:

- Sensations such as déjà vu (a feeling of familiarity), jamais vu (a feeling of unfamiliarity)

- Amnesia; or a single memory or set of memories

- A sudden sense of unprovoked fear and anxiety

- Nausea

- Auditory, visual, olfactory, gustatory, or tactile hallucinations.

- Visual distortions such as macropsia and micropsia

- Dissociation or derealisation

- Synesthesia (stimulation of one sense experienced in a second sense) may transpire.

- Dysphoric or euphoric feelings, fear, anger, and other emotions may also occur. Often, the patient cannot describe the sensations.

Olfactory hallucinations often seem indescribable to patients beyond "pleasant" or "unpleasant".

Focal aware seizures are often called "auras" when they serve as a warning sign of a subsequent seizure. Regardless an "aura" is actually a seizure itself, and such a focal seizure may or may not progress to a focal impaired awareness seizure. People who only experience focal aware seizures may not recognize what they are, nor seek medical care.