PLMD is often treated with anti-Parkinson medication; it may also respond to anticonvulsants, benzodiazepines, and narcotics. Patients must stay on these medications in order to experience relief, because there is no known cure for this disorder.

PLMs tend to be exacerbated by tricyclic antidepressants, SSRIs, stress, and sleep deprivation. It is also advised not to consume caffeine, alcohol, or antidepressants as these substances could worsen the PLMD symptoms.

Other medications aimed at reducing or eliminating the leg jerks or the arousals can be prescribed. Non-ergot derived dopaminergic drugs (pramipexole and ropinirole) are preferred. Other dopaminergic agents such as co-careldopa, co-beneldopa, pergolide, or lisuride may also be used. These drugs decrease or eliminate both the leg jerks and the arousals. These medications are also successful for the treatment of restless legs syndrome.

In one study, co-careldopa was superior to dextropropoxyphene in decreasing the number of leg kicks and the number of arousals per hour of sleep. However, co-careldopa and, to a lesser extent, pergolide may shift the leg movements from the nighttime to the daytime.

Clonazepam (Klonopin), in doses of 1 mg has been shown to improve objective and subjective measures of sleep.

Research suggests that hypnosis may be helpful in alleviating some types and manifestations of sleep disorders in some patients. "Acute and chronic insomnia often respond to relaxation and hypnotherapy approaches, along with sleep hygiene instructions." Hypnotherapy has also helped with nightmares and sleep terrors. There are several reports of successful use of hypnotherapy for parasomnias specifically for head and body rocking, bedwetting and sleepwalking.

Hypnotherapy has been studied in the treatment of sleep disorders in both adults and children.

A review of the evidence in 2012 concluded that current research is not rigorous enough to make recommendations around the use of acupuncture for insomnia. The pooled results of two trials on acupuncture showed a moderate likelihood that there may be some improvement to sleep quality for individuals with a diagnosis insomnia. This form of treatment for sleep disorders is generally studied in adults, rather than children. Further research would be needed to study the effects of acupuncture on sleep disorders in children.

Middle-of-the-night insomnia is often treated with medication, although currently Intermezzo (zolpidem tartrate sublingual tablets) is the only Food and Drug Administration-approved medication specifically for treating MOTN awakening. Because most medications usually require 6–8 hours of sleep to avoid lingering effects the next day, these are often used every night at bedtime to prevent awakenings. Medication may not be prescribed in some cases, especially if the cause turns out to be the patient ingesting too much fluid during the day or just before they go to sleep.

Sleep restriction therapy and stimulus control therapy as described in insomnia have shown significance in treating middle of night insomnia.

Some studies have shown that zaleplon, which has a short elimination half-life, may be suitable for middle-of-the-night administration because it does not impair next day performance.

Treatment for sexsomnia involves one or more of the following:

- prescription medications

- CPAP

- lifestyle changes

Since there is not an FDA-approved medication on the market specifically designed for the treatment of sexsomnia, health professionals attempt to treat the disorder through a variety of approaches. Among the first line of prevention for sexsomnia involves creating and maintaining a safe environment for all who are affected as a result of the disorder. Precautionary measures include, but are not limited to, the individual in question sleeping in a separate bedroom and the installation of locks and alarms on doors.

Concerning more serious afflictions, the complex origins of myoclonus may be treated with multiple drugs, which have a limited effect individually, but greater when combined with others that act on different brain pathways or mechanisms. Treatment is most effective when the underlying cause is known, and can be treated as such. Some drugs being studied in different combinations include clonazepam, sodium valproate, piracetam, and primidone. Hormonal therapy may improve responses to antimyoclonic drugs in some people.

Some studies have shown that doses of 5-hydroxytryptophan (5-HTP) leads to improvement in patients with some types of action myoclonus and PME. These differences in the effect of 5-HTP on patients with myoclonus have not yet been explained.

Many of the drugs used for myoclonus, such as barbiturates, phenytoin and primidone, are also used to treat epilepsy. Barbiturates slow down the central nervous system and cause tranquilizing or antiseizure effects. Phenytoin and primidone are effective antiepileptics drugs, although phenytoin can cause liver failure or have other harmful long-term effects in patients with PME. Sodium valproate is an alternative therapy for myoclonus and can be used either alone or in combination with clonazepam. Some people have adverse reactions to clonazepam and/or sodium valproate.

When patients are taking multiple medications, the discontinuation of drugs suspected of causing myoclonus and treatment of metabolic derangements may resolve some cases of myoclonus. When pharmacological treatment is indicated anticonvulsants are the main line of treatment. Paradoxical reactions to treatment are notable. Drugs which most people respond to may in other individuals worsen their symptoms. Sometimes this leads to the mistake of increasing the dose, rather than decreasing or stopping the drug. Treatment of myoclonus focuses on medications that may help reduce symptoms. Drugs used include sodium valproate, clonazepam, the anticonvulsant levetiracetam, and piracetam. Dosages of clonazepam usually are increased gradually until the patient improves or side effects become harmful. Drowsiness and loss of coordination are common side effects. The beneficial effects of clonazepam may diminish over time if the patient develops a tolerance to the drug.

In forms of myoclonus where only a single area is affected, and even in a few other various forms, Botox injections (OnabotulinumtoxinA) may be helpful. The chemical messenger responsible for triggering the involuntary muscle contractions is blocked by the Botulinum toxins of the Botox.

Surgery is also a viable option for treatment if the symptoms are caused by a tumor or lesion in the brain or spinal cord. Surgery may also correct symptoms in those where myoclonus affects parts of the face or ear. While DBS is still being studied for use with myoclonus, Deep Brain Stimulation has also been tried in those with this and other movement disorders.

Botulinum toxin injections also act upon acetylcholine to reduce dystonia symptoms. The neurotoxin is active in presynaptic terminals and blocks exocytosis of acetylcholine into the synaptic cleft which reduces muscle activity. Botulinum may also have a role in inhibiting glutamate and changing muscle movement. Studies have also shown possible axon transport of this neurotoxin as well as its function as a pain reliever without affect on overactive muscle movement in myoclonus dystonia patients.

Before prescribing medication for these conditions which often resolve spontaneously, recommendations have pointed to improved skin hygiene, good hydration via fluids, good nutrition, and installation of padded bed rails with use of proper mattresses. Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine which block dopamine receptors; these are the first line of treatment for hemiballismus. Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and tardive dyskinesia. Tetrabenazine works by depleting presynaptic dopamine and blocking postsynaptic dopamine receptors, while reserpine depletes the presynaptic catecholamine and serotonin stores; both of these drugs treat hemiballismus successfully but may cause depression, hypotension and parkinsonism. Sodium valproate and clonazepam have been successful in a limited number of cases. Stereotactic ventral intermediate thalamotomy and use of a thalamic stimulator have been shown to be effective in treating these conditions.

Antiepileptics like valproate must act upon GABA receptors and manipulate ionic conductance to reduce tremors and spasms in myoclonus dystonia. GABA neurons that fire rapidly and affect the motor cortex are blocked by antiepileptics in addition to changes in sodium and calcium concentrations that can excite the neuron. Different antiepileptics vary in sufficiency to control ionic conductance and can also produce seizures or myoclonus symptoms in some patients.

The medical treatment of essential tremor at the Movement Disorders Clinic at Baylor College of Medicine begins with minimizing stress and tremorgenic drugs along with recommending a restricted intake of beverages containing caffeine as a precaution, although caffeine has not been shown to significantly intensify the presentation of essential tremor. Alcohol amounting to a blood concentration of only 0.3% has been shown to reduce the amplitude of essential tremor in two-thirds of patients; for this reason it may be used as a prophylactic treatment before events during which one would be embarrassed by the tremor presenting itself. Using alcohol regularly and/or in excess to treat tremors is highly unadvisable, as there is a purported correlation between tremor and alcoholism. Alcohol is thought to stabilize neuronal membranes via potentiation of GABA receptor-mediated chloride influx. It has been demonstrated in essential tremor animal models that the food additive 1-octanol suppresses tremors induced by harmaline, and decreases the amplitude of essential tremor for about 90 minutes.

Two of the most valuable drug treatments for essential tremor are propranolol, a beta blocker, and primidone, an anticonvulsant. Propranolol is much more effective for hand tremor than head and voice tremor. Some beta-adrenergic blockers (beta blockers) are not lipid-soluble and therefore cannot cross the blood–brain barrier (propranolol being an exception), but can still act against tremors; this indicates that this drug’s mechanism of therapy may be influenced by peripheral beta-adrenergic receptors. Primidone’s mechanism of tremor prevention has been shown significantly in controlled clinical studies. The benzodiazepine drugs such as diazepam and barbiturates have been shown to reduce presentation of several types of tremor, including the essential variety. Controlled clinical trials of gabapentin yielded mixed results in efficacy against essential tremor while topiramate was shown to be effective in a larger double-blind controlled study, resulting in both lower Fahn-Tolosa-Marin tremor scale ratings and better function and disability as compared to placebo.

It has been shown in two double-blind controlled studies that injection of botulinum toxin into muscles used to produce oscillatory movements of essential tremors, such as forearm, wrist and finger flexors, may decrease the amplitude of hand tremor for approximately three months and that injections of the toxin may reduce essential tremor presenting in the head and voice. The toxin also may help tremor causing difficulty in writing, although properly adapted writing devices may be more efficient. Due to high incidence of side effects, use of botulinum toxin has only received a C level of support from the scientific community.

Deep brain stimulation toward the ventral intermediate nucleus of the thalamus and potentially the subthalamic nucleus and caudal zona incerta nucleus have been shown to reduce tremor in numerous studies. That toward the ventral intermediate nucleus of the thalamus has been shown to reduce contralateral and some ipsilateral tremor along with tremors of the cerebellar outflow, head, resting state and those related to hand tasks; however, the treatment has been shown to induce difficulty articulating thoughts (dysarthria), and loss of coordination and balance in long-term studies. Motor cortex stimulation is another option shown to be viable in numerous clinical trials.

For those patients who have not been able to stop this disorder on their own, doctors have been working to discover a treatment that will work for everyone. One treatment that Schenck and Mahowald studied consisted of psychotherapy combined with "environmental manipulation". This was usually done separately from the weight-reducing diets. However, during this study only 10 percent of the patients were able to lose more than one third of their initial excess weight, which was not a viable percentage. In addition, they reported that many of the patients experienced "major depression" and "severe anxiety" during the attempted treatments. This was not one of the most successful attempts to help those with NSRED.

However, Dr. R. Auger reported on another trial treatment where patients were treated utilizing pramipexole. Those conducting the treatment noticed how the nocturnal median motor activity was decreased, as was assessed by actigraphy, and individual progress of sleep quality was reported. Nevertheless, Augur also said, "27 percent of subjects had RLS (restless legs syndrome, a condition known to respond to this medication), and number and duration of waking episodes related to eating behaviors were unchanged." Encouraged by the positive response verified in the above-mentioned trial treatment, doctors and psychiatrists conducted a more recent study described by Auger as "efficacy of topiramate [an antiepileptic drug associated with weight loss] in 17 consecutive patients with NSRED." Out of the 65 percent of patients who continued to take the medication on a regular basis, all confirmed either considerable development or absolute remission of "night-eating" in addition to "significant weight loss" being achieved. This has been one of the most effective treatments discovered so far, but many patients still suffered from NSRED. Therefore, other treatments were sought after.

Such treatments include those targeted to associated sleep disorders with the hope that it would play an essential part of the treatment process of NSRED. In Schenck and Mahowald's series, combinations of cardibopa/L-dopa, codeine, and clonazepam were used to treat five patients with RLS and one patient with somnambulism and PLMS (periodic limb movements in sleep). These patients all were suffering from NSRED as well as these other disorders, and they all experienced a remission of their NSRED as a result of taking these drugs. Two patients with OSA (obstructive sleep apnea) and NSRED also reported as having a "resolution of their symptoms with nasal continuous positive airway pressure (nCPAP) therapy." Clonazepam monotherapy was also found to be successful in 50 percent of patients with simultaneous somnambulism. Interestingly, dopaminergic agents such as monotherapy were effective in 25 percent of the NSRED subgroup. Success with combinations of dopaminergic and opioid drugs, with the occasional addition of sedatives, also was found in seven patients without associated sleep disorders. In those for whom opioids and sedatives are relatively contraindicated (e.g., in those with histories of substance abuse), two case reports were described as meeting with success with a combination of bupropion, levodopa, and trazodone. Notably, hypnotherapy, psychotherapy, and various behavioral techniques, including environmental manipulation, were not effective on the majority of the patients studied. Nevertheless, Auger argue that behavioral strategies should complement the overall treatment plan and should include deliberate placement of food to avoid indiscriminate wandering, maintenance of a safe sleep environment, and education regarding proper sleep hygiene and stress management. Even with their extensive studies, Schenck and Mahowald did not find the success as Auger found by treating his patients with topiramate.

Treatment for hyperthermia includes reducing muscle overactivity via sedation with a benzodiazepine. More severe cases may require muscular paralysis with vecuronium, intubation, and artificial ventilation. Suxamethonium is not recommended for muscular paralysis as it may increase the risk of cardiac dysrhythmia from hyperkalemia associated with rhabdomyolysis. Antipyretic agents are not recommended as the increase in body temperature is due to muscular activity, not a hypothalamic temperature set point abnormality.

Like other forms of epilepsy, nocturnal epilepsy can be treated with anti-convulsants.

Despite the effectiveness of anti-convulsants in people who suffer from nocturnal epilepsy, the drugs are shown to disrupt a person's sleeping structure. This may cause concern in people who suffer specifically from nocturnal epilepsy because undisrupted sleep is important for these people, as it lowers the likeliness of epileptic symptoms to arise.

One particular study by V. Bradley and D. O'Neill analysed the different forms of epilepsy, including nocturnal epilepsy and its relationship with sleep. They found that some patients only experienced epileptic symptoms while they are asleep (nocturnal epilepsy), and that maintaining good sleep helped in reducing epileptic symptoms. Another study determined that anti-convulsant medications can minimize epilepsy not just in people who are awake, but also in people who are asleep. However, some of these anti-convulsant medications did also have adverse effects on subjects' sleeping structures, which can exacerbate epileptic symptoms in people who suffer from nocturnal epilepsy.

To minimize epileptic seizures in these people, it is important to find an anti-convulsant medication that does not disrupt a person's sleeping structure. The anti-convulsant medications that were tested to meet this criteria are: phenobarbital, phenytoin, carbamazepine, valproate, ethosuximide, felbamate, gabapentin, lamotrigine, topiramate, vigabatrin, tiagabine, levetiracetam, zonisamide, and oxcarbazepine. Oxcarbazepine is shown to have the least amount of adverse effects on sleep. Another study shows that it enhances slow wave-sleep and sleep continuity in patients with epilepsy.

Periodic limb movement disorder (PLMD), previously known as nocturnal myoclonus, is a sleep disorder where the patient moves limbs involuntarily during sleep, and has symptoms or problems related to the movement.

PLMD should not be confused with restless legs syndrome (RLS). RLS occurs while awake as well as when asleep, and when awake, there is a voluntary response to an uncomfortable feeling in the legs. PLMD on the other hand is involuntary, and the patient is often unaware of these movements altogether.

Research on myoclonus is supported through the National Institute of Neurological Disorders and Stroke (NINDS). The primary focus of research is on the role of neurotransmitters and receptors involved in the disease. Identifying whether or not abnormalities in these pathways cause myoclonus may help in efforts to develop drug treatments and diagnostic tests. Determining the extent that genetics play in these abnormalities may lead to potential treatments for their reversal, potentially correcting the loss of inhibition while enhancing mechanisms in the body that would compensate for their effects.

Simple behavioral methods are recommended as initial treatment. Enuresis alarm therapy and medications may be more effective but have potential side effects.

- Motivational therapy in nocturnal enuresis mainly involves parent and child education. Guilt should be allayed by providing facts. Fluids should be restricted 2 hours prior to bed. The child should be encouraged to empty the bladder completely prior to going to bed. Positive reinforcement can be initiated by setting up a diary or chart to monitor progress and establishing a system to reward the child for each night that he or she is dry. The child should participate in morning cleanup as a natural, nonpunitive consequence of wetting. This method is particularly helpful in younger children (<8 years) and will achieve dryness in 15-20% of the patients.

- Waiting: Almost all children will outgrow bedwetting. For this reason, urologists and pediatricians frequently recommend delaying treatment until the child is at least six or seven years old. Physicians may begin treatment earlier if they perceive the condition is damaging the child's self-esteem and/or relationships with family/friends.

- Bedwetting alarms: Physicians also frequently suggest bedwetting alarms which sound a loud tone when they sense moisture. This can help condition the child to wake at the sensation of a full bladder. These alarms are considered effective, with study participants being 13 times more likely to become dry at night. There is a 29% to 69% relapse rate, however, so the treatment may need to be repeated.

- DDAVP (desmopressin) tablets are a synthetic replacement for antidiuretic hormone, the hormone that reduces urine production during sleep. Desmopressin is usually used in the form of desmopressin acetate, DDAVP. Patients taking DDAVP are 4.5 times more likely to stay dry than those taking a placebo. The drug replaces the hormone for that night with no cumulative effect. US drug regulators have banned using desmopressin nasal sprays for treating bedwetting since the oral form is considered safer.

- DDAVP is most efficient in children with nocturnal polyuria (nocturnal urine production greater than 130% of expected bladder capacity for age) and normal bladder reservoir function (maximum voided volume greater than 70% of expected bladder capacity for age). Other children who are likely candidates for desmopressin treatment are those in whom alarm therapy has failed or those considered unlikely to comply with alarm therapy. It can be very useful for summer camp and sleepovers to prevent enuresis.

- Tricyclic antidepressants: Tricyclic antidepressant prescription drugs with anti-muscarinic properties have been proven successful in treating bedwetting, but also have an increased risk of side effects, including death from overdose. These drugs include amitriptyline, imipramine and nortriptyline. Studies find that patients using these drugs are 4.2 times as likely to stay dry as those taking a placebo. The relapse rates after stopping the medicines are close to 50%.

In most of the reported cases, the treatment options were very similar. Plasmapheresis alone or in combination with steroids, sometimes also with thymectomy and azathioprine, have been the most frequently used therapeutic approach in treating Morvan’s Syndrome. However, this does not always work, as failed response to steroids and to subsequently added plasmapheresis have been reported. Intravenous immunoglobulin was effective in one case.

In one case, the dramatic response to high-dose oral prednisolone together with pulse methylprednisolone with almost complete disappearance of the symptoms within a short period should induce consideration of corticosteroids.

In another case, the subject was treated with haloperidol (6 mg/day) with some improvement in the psychomotor agitation and hallucinations, but even high doses of carbamazepine given to the subject failed to improve the spontaneous muscle activity. Plasma Exchange (PE) was initiated, and after the third such session, the itching, sweating, mental disturbances, and complex nocturnal behavior improved and these symptoms completely disappeared after the sixth session, with improvement in insomnia and reduced muscle twitching. However, one month after the sixth PE session, there was a progressive worsening of insomnia and diurnal drowsiness, which promptly disappeared after another two PE sessions.

In one case there high dose steroid treatment resulted in a transient improvement, but aggressive immuno-suppressive therapy with cyclophosphamide was necessary to control the disease and result in a dramatic clinical improvement.

In another case, the subject was treated with prednisolone (1 mg/kg body weight) with carbamazepine, propanolol, and amitriptyline. After two weeks, improvement with decreased stiffness and spontaneous muscle activity and improved sleep was observed. After another 7–10 days, the abnormal sleep behavior disappeared completely.

In another case, symptomatic improvement with plasmapheresis, thymectomy, and chronic immunosuppression provide further support for an autoimmune or paraneoplastic basis.

Although thymectomy is believed to be a key element in the proposed treatment, there is a reported case of Morvan’s Syndrome presenting itself post-thymectomy.

Major changes in the management of daytime wetting came about in the 1990s. In most current programs, non-invasive treatments incorporate hydration, timed voiding, correction of constipation and in some cases, computer assisted pelvic floor retraining. These methods have been extremely successful in correcting daytime wetting. Bladder stretching exercises (where the person tries to hold their urine as long as possible) are no longer recommended. In fact, some urologists actually believe that this can be dangerous because the person could develop the long-term habit of tightening the urethral sphincter muscle, which can cause bladder or kidney problems. Urinating on a regular basis is much preferred.

Ruling out infections can also be a part of the differential.

Specific treatment for some symptoms may be required. One of the most important treatments is the control of agitation due to the extreme possibility of injury to the person themselves or caregivers, benzodiazepines should be administered at first sign of this. Physical restraints are not recommended for agitation or delirium as they may contribute to mortality by enforcing isometric muscle contractions that are associated with severe lactic acidosis and hyperthermia. If physical restraints are necessary for severe agitation they must be rapidly replaced with pharmacological sedation. The agitation can cause a large amount of muscle breakdown. This breakdown can cause severe damage to the kidneys through a condition called rhabdomyolysis.

The most commonly effective treatment is clonazepam, which leads to the increased efficacy of another inhibitory neurotransmitter, GABA. There are anecdotal reports of the use of Levetiracetam in genetic and acquired hyperekplexia. During attacks of hypertonia and apnea, the limbs and head may be flexed towards the trunk in order to dissipate the symptoms. This is named the Vigevano maneuver after the doctor who invented it.

There is no known definitive cure for OMS. However, several drugs have proven to be effective in its treatment.

Some of medication used to treat the symptoms are:

- ACTH has shown improvements in symptoms but can result in an incomplete recovery with residual deficits.

- Corticosteroids (such as "prednisone" or "methylprednisolone") used at high dosages (500 mg - 2 g per day intravenously for a course of 3 to 5 days) can accelerate regression of symptoms. Subsequent very gradual tapering with pills generally follows. Most patients require high doses for months to years before tapering.

- Intravenous Immunoglobulins (IVIg) are often used with varying results.

- Several other immunosuppressive drugs, such as cyclophosphamide and azathioprine, may be helpful in some cases.

- Chemotherapy for neuroblastoma may be effective, although data is contradictory and unconvincing at this point in time.

- Rituximab has been used with encouraging results.

- Other medications are used to treat symptoms without influencing the nature of the disease (symptomatic treatment):

- Trazodone can be useful against irritability and sleep problems

- Additional treatment options include plasmapheresis for severe, steroid-unresponsive relapses.

The National Organization for Rare Disorders (NORD) recommends FLAIR therapy consisting of a three-agent protocol involving front-loaded high-dose ACTH, IVIg, and rituximab that was developed by the National Pediatric Myoclonus Center, and has the best-documented outcomes. Almost all patients (80-90%) show improvement with this treatment and the relapse rate appears to be about 20%.

A more detailed summary of current treatment options can be found at Treatment Options

The following medications should probably be avoided:

- Midazolam - Can cause irritability.

- Melatonin - Is known to stimulate the immune system.

- Also, see for more details

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.

Given the benign nature of the condition and the low seizure frequency, treatment is often unnecessary. If treatment is warranted or preferred by the child and his or her family, antiepileptic drugs can usually control the seizures easily. Carbamazepine is the most frequently used first-line drug, but many other antiepileptic drugs, including valproate, phenytoin, gabapentin, levetiracetam and sultiame have been found effective as well. Bedtime dosing is advised by some. Treatment can be short and drugs can almost certainly be discontinued after two years without seizures and with normal EEG findings, perhaps even earlier.

Parental education about Rolandic epilepsy is the cornerstone of correct management. The traumatizing, sometimes long-lasting effect on parents is significant.

It is unclear if there are any benefits to clobazam over other seizure medications.

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.