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.

PLMD is estimated to occur in approximately 4% of adults (aged 15–100), but is more common in the elderly, especially females, with up to 11% experiencing symptoms. PLMD appears to be related to restless legs syndrome (RLS) - a study of 133 people found that 80% of those with RLS also had PLMD. However the opposite is not true: many people who have PLMD do "not" also have restless legs syndrome.

Polysomnography is also used to aid in the diagnosis of other sleep disorders such as obstructive sleep apnea (OSA), narcolepsy, and restless leg syndrome (RLS). Normal test results show little to no episodes of sleep apnea and normal electrical activity in the individual's brain and muscles during sleep.

Polysomnography is a study conducted while the individual being observed is asleep. A polysomnograph (PSG) is a recording of an individual's body functions as they sleep. Complete sleep studies are most commonly facilitated at a designated sleep center. Specialized electrodes and monitors are connected to the individual and remain in place throughout study. Video cameras can be used in certain cases to record physical behaviors occurring while the individual is asleep. Typically the unwanted sexual behaviors do not present on film, therefore the majority of information is taken from a sleep study.

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.

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:

Treatments for sleep disorders generally can be grouped into four categories:

- Behavioral and psychotherapeutic treatment

- Rehabilitation and management

- Medication

- Other somatic treatment

None of these general approaches is sufficient for all patients with sleep disorders. Rather, the choice of a specific treatment depends on the patient's diagnosis, medical and psychiatric history, and preferences, as well as the expertise of the treating clinician. Often, behavioral/psychotherapeutic and pharmacological approaches are not incompatible and can effectively be combined to maximize therapeutic benefits. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.

Medications and somatic treatments may provide the most rapid symptomatic relief from some sleep disturbances. Certain disorders like narcolepsy, are best treated with prescription drugs such as Modafinil. Others, such as chronic and primary insomnia, may be more amenable to behavioral interventions, with more durable results.

Chronic sleep disorders in childhood, which affect some 70% of children with developmental or psychological disorders, are under-reported and under-treated. Sleep-phase disruption is also common among adolescents, whose school schedules are often incompatible with their natural circadian rhythm. Effective treatment begins with careful diagnosis using sleep diaries and perhaps sleep studies. Modifications in sleep hygiene may resolve the problem, but medical treatment is often warranted.

Special equipment may be required for treatment of several disorders such as obstructive apnea, the circadian rhythm disorders and bruxism. In these cases, when severe, an acceptance of living with the disorder, however well managed, is often necessary.

Some sleep disorders have been found to compromise glucose metabolism.

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.

Nocturnal awakenings are more common in older patients and have been associated with depressive disorders, chronic pain, obstructive sleep apnea, obesity, alcohol consumption, hypertension, gastroesophageal reflux disease, heart disease, menopause, prostate problems, and bipolar disorders.

Nocturnal awakenings can be mistaken as shift work disorder.

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.

The effects of myoclonus in an individual can vary depending on the form and the overall health of the individual. In severe cases, particularly those indicating an underlying disorder in the brain or nerves, movement can be extremely distorted and limit ability to normally function, such as in eating, talking, and walking. In these cases, treatment that is usually effective, such as clonazepam and sodium valproate, may instead cause adverse reaction to the drug, including increased tolerance and a greater need for increase in dosage. However, the prognosis for more simple forms of myoclonus in otherwise healthy individuals may be neutral, as the disease may cause few to no difficulties. Other times the disease starts simply, in one region of the body, and then spreads.

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.

Benign neonatal sleep myoclonus (BNSM) is the occurrence of myoclonus (jerky movements) during sleep. It is not associated with seizures.

Occurs in the first few weeks of life, usually resolves in first 2–3 months of life. Often worries parents because they appear like seizures, but they are not. Features that can help distinguish this condition from seizures include: The myoclonic movements only occur during sleep, when baby is woken up the myoclonic movements stop, normal EEG, normal neurological examination, normal developmental examination. The myoclonic jerks occur during non-REM sleep

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.

There is no laboratory test for serotonin syndrome. Therefore, diagnosis is by symptom observation and investigation of the patient's history. Several diagnostic criteria have been proposed. The first rigorously evaluated criteria were introduced in 1991 by Harvey Sternbach, a professor of psychiatry at UCLA. Researchers in Australia later developed the Hunter Toxicity Criteria Decision Rules, which have better sensitivity and specificity, 84% and 97%, respectively, when compared with the gold standard of diagnosis by a medical toxicologist. As of 2007, Sternbach's criteria were still the most commonly used.

The most important symptoms for diagnosing serotonin syndrome are tremor, extreme aggressiveness, akathisia, or clonus (spontaneous, inducible and ocular). Physical examination of the patient should include assessment of deep-tendon reflexes and muscle rigidity, the dryness of the mucosa of the mouth, the size and reactivity of the pupils, the intensity of bowel sounds, skin color, and the presence or absence of sweating. The patient's history also plays an important role in diagnosis, investigations should include inquiries about the use of prescription and over-the-counter drugs, illicit substances, and dietary supplements, as all these agents have been implicated in the development of serotonin syndrome. To fulfill the Hunter Criteria, a patient must have taken a serotonergic agent and meet one of the following conditions:

- Spontaneous clonus, or

- Inducible clonus plus agitation or diaphoresis, or

- Ocular clonus plus agitation or diaphoresis, or

- Tremor plus hyperreflexia, or

- Hypertonism plus temperature > plus ocular clonus or inducible clonus

Deep brain stimulation (DBS) has been found to be an effective and safe treatment for myoclonus dystonia patients, whose severe and debilitating symptoms are resistant to drug treatments. Electrical stimulation within the brain is a common treatment for many movement disorders because of the ability to excite or inhibit neurons within the brain. Deep brain stimulation patients have electrodes inserted into the brain and then an electrical signal is sent from an external source to elicit a response. The frequency and intensity of this signal can be changed to monitor the effects on neuronal activity using voltage recordings or neuroimaging, like functional MRIs. By re-positioning the electrodes in different areas or changing the size or timing of the stimulus, varying effects can be seen on the patient depending on the origin of the disorder.

In one study, five patients with genetically determined epsilon sarcoglycan protein deficiency underwent deep brain stimulation of the internal pallidum. Each patient’s movement and disability symptoms were assessed before and after treatment using the Burke-Fahn-Marsden Dystonia Rating Scale and the Unified Myoclonus Rating Scale. Upon completion of the surgery, both the myoclonus and dystonia symptoms of the disorder had decreased by 70%, with no report of unfavorable side effects. Therefore, deep brain stimulation has been shown to effectively improve both myoclonus and dystonia, unlike many drug treatments which may improve one or the other.

Other studies examined the effects of DBS to both the ventrointermediate nucleus of the thalamus, Vim, and the globus pallidus interna, GPi. Following deep brain stimulation of GPi and Vim, the Unified Myoclonus Rating Scale disability score improved 61-66%. In addition, the Dystomia Rating Scale score improved by 45-48%. While there was no significant difference in improvement between GPi-Vim stimulation and GPi stimulation, GPi-Vim stimulation was significantly more effective than Vim deep brain stimulation alone. Overall, Deep brain stimulation shows promise as a viable treatment for myoclonus dystonia.

Although myoclonus and dystonia are present in myoclonus dystonia patients, optimum treatment for myoclonus dystonia differs from the treatment for myoclonus or dystonia alone. Myoclonus improved significantly more than dystonia when Deep brain stimulation was applied. In addition, myoclonus improved regardless of whether Deep brain stimulation was applied to GPi or Vim. However, GPi stimulation was more effective at reducing the symptoms of dystonia than Vim stimulation.

Many drugs used to treat myoclonus dystonia do not have a significant impact individually, but when combined, can work on different brain mechanisms to best alleviate symptoms. The method of treatment used depends on the severity of the symptoms presented in the individual, and whether the underlying cause of the syndrome is known.

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.

Daytime wetting is more common in girls than in boys, but bedwetting is three times as prevalent in boys (i.e., around 75% of sufferers are male). At the age of 7 approximately 3% of girls and 2% of boys experience functional daytime wetting at least once a week.

There are a number of management options for bedwetting. The following options apply when the bedwetting is not caused by a specifically identifiable medical condition such as a bladder abnormality or diabetes. Treatment is recommended when there is a specific medical condition such as bladder abnormalities, infection, or diabetes. It is also considered when bedwetting may harm the child's self-esteem or relationships with family/friends. Only a small percentage of bedwetting is caused by a specific medical condition, so most treatment is prompted by concern for the child's "emotional" welfare. Behavioral treatment of bedwetting overall tends to show increased self-esteem for children.

Parents become concerned much earlier than doctors. A study in 1980 asked parents and physicians the age that children should stay dry at night. The average parent response was 2.75 years old, while the average physician response was 5.13 years old.

Punishment is not effective and can interfere with treatment.

Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.

Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes. and or basal ganglia hypermetabolism. Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.

Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition. Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis. There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.

The diagnosis can be confirmed when the characteristic centrotemporal spikes are seen on electroencephalography (EEG). Typically, high-voltage spikes followed by slow waves are seen. Given the nocturnal activity, a sleep EEG can often be helpful. Technically, the label "benign" can only be confirmed if the child's development continues to be normal during follow-up. Neuroimaging, usually with an MRI scan, is only advised for cases with atypical presentation or atypical findings on clinical examination or EEG.

The disorder should be differentiated from several other conditions, especially centrotemporal spikes without seizures, centrotemporal spikes with local brain pathology, central spikes in Rett syndrome and fragile X syndrome, malignant Rolandic epilepsy, temporal lobe epilepsy and Landau-Kleffner syndrome.

Thorough history regarding frequency of bedwetting, any period of dryness in between, associated daytime symptoms, constipation, and encopresis should be sought.

Upon the discontinuation of serotonergic drugs, most cases of serotonin syndrome resolve within 24 hours, although in some cases delirium may persist for a number of days. Symptoms typically persist for a longer time frame in patients taking drugs which have a long elimination half-life, active metabolites, or a protracted duration of action.

Cases have reported muscle pain and weakness persisting for months, and antidepressant discontinuation may contribute to ongoing features. Following appropriate medical management, serotonin syndrome is generally associated with a favorable prognosis.

Treatment of primary dystonia is aimed at reducing symptoms such as involuntary movements, pain, contracture, embarrassment, and to restore normal posture and improve the patient’s function. This treatment is therefore not neuroprotective. According to the European Federation of Neurological Sciences and Movement Disorder Society, there is no evidence-based recommendation for treating primary dystonia with antidopaminergic or anticholinergic drugs although recommendations have been based on empirical evidence. Anticholinergic drugs prove to be most effective in treating generalized and segmental dystonia, especially if dose starts out low and increases gradually. Generalized dystonia has also been treated with such muscle relaxants as the benzodiazepines. Another muscle relaxant, baclofen, can help reduce spasticity seen in cerebral palsy such as dystonia in the leg and trunk. Treatment of secondary dystonia by administering levodopa in dopamine-responsive dystonia, copper chelation in Wilson’s disease, or stopping the administration of drugs that may induce dystonia have been proven effective in a small number of cases. Physical therapy has been used to improve posture and prevent contractures via braces and casting, although in some cases, immobilization of limbs can induce dystonia, which is by definition known as peripherally induced dystonia. There are not many clinical trials that show significant efficacy for particular drugs, so medical of dystonia must be planned on a case-by-case basis. Botulinum toxin B, or Myobloc, has been approved by the US Food and Drug Administration to treat cervical dystonia due to level A evidential support by the scientific community. Surgery known as GPi DBS (Globus Pallidus Pars Interna Deep Brain Stimulation) has come to be popular in treating phasic forms of dystonia, although cases involving posturing and tonic contractions have improved to a lesser extent with this surgery. A follow-up study has found that movement score improvements observed one year after the surgery was maintained after three years in 58% of the cases. It has also been proven effective in treating cervical and cranial-cervical dystonia.