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.

To date, there is no single, universal treatment that has been found to cure myoclonus dystonia. However, there are several treatment methods that have been found to be effective for helping to reduce the symptoms associated with the syndrome.

Consumption of alcohol has also been found to be an effective agent for temporarily easing the severity of the tremors associated with myoclonus dystonia. Alcohol causes an increase in GABA transmission between interneurons and Purkinje cells. This then reduces the transmission of glutamate at granule cell-Purkinje cell synapses, which decreases muscle movements. This treatment only alleviates the strength of the tremors for a short duration and does not change how often tremors will occur. Doctors inform patients of risks associated with the use of alcohol for myoclonus dystonia due to the high susceptibility for alcohol abuse and dependency. Alcoholism itself causes tremors in the hands and degeneration of the Purkinje cells and other parts of the cerebral cortex, counteracting alcohol's original corrective 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

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.

Myoclonic epilepsy refers to a family of epilepsies that present with myoclonus. When myoclonic jerks are occasionally associated with abnormal brain wave activity, it can be categorized as myoclonic seizure. If the abnormal brain wave activity is persistent and results from ongoing seizures, then a diagnosis of myoclonic epilepsy may be considered.

Hyperkinesia, also known as hyperkinesis, refers to an increase in muscular activity that can result in excessive abnormal movements, excessive normal movements, or a combination of both. The word hyperkinesis comes from the Greek "hyper", meaning "increased," and "kinein", meaning "to move." Hyperkinesia is a state of excessive restlessness which is featured in a large variety of disorders that affect the ability to control motor movement, such as Huntington's disease. It is the opposite of hypokinesia, which refers to decreased bodily movement, as commonly manifested in Parkinson's disease. Many hyperkinetic movements are the result of improper regulation of the basal ganglia-thalamocortical circuitry. Overactivity of a direct pathway combined with decreased activity of an indirect pathway results in activation of thalamic neurons and excitation of cortical neurons, resulting in increased motor output. Often, hyperkinesia is paired with hypotonia, a decrease in muscle tone. Many hyperkinetic disorders are psychological in nature and are typically prominent in childhood. Depending on the specific type of hyperkinetic movement, there are different treatment options available to minimize the symptoms, including different medical and surgical therapies.

It is mostly unknown what causes PLMD, but in many cases the patient also suffers from other medical problems such as Parkinson's disease or narcolepsy. Factors that increase the likelihood of PLMD in the absence of restless leg syndrome include being a shift worker, snoring, coffee drinking, stress, and use of hypnotics, particularly in the case of benzodiazepine withdrawal. For women, the presence of musculoskeletal disease, heart disease, obstructive sleep apnea, cataplexy, doing physical activities close to bedtime and the presence of a mental disorder were significantly associated with having a higher risk of both PLMD and restless legs syndrome.

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.

Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

The prognosis for Rolandic seizures is invariably excellent, with probably less than 2% risk of developing absence seizures and less often GTCS in adult life.

Remission usually occurs within 2–4 years from onset and before the age of 16 years. The total number of seizures is low, the majority of patients having fewer than 10 seizures; 10–20% have just a single seizure. About 10–20% may have frequent seizures, but these also remit with age.

Children with Rolandic seizures may develop usually mild and reversible linguistic, cognitive and behavioural abnormalities during the active phase of the disease. These may be worse in children with onset of seizures before 8 years of age, high rate of occurrence and multifocal EEG spikes.

The development, social adaptation and occupations of adults with a previous history of Rolandic seizures were found normal.

PME accounts for less than 1% of epilepsy cases at specialist centres. The incidence and prevalence of PME is unknown, but there are considerable geography and ethnic variations amongst the specific genetic disorders. One cause, Unverricht Lundborg Disease, has an incidence of at least 1:20,000 in Finland.

Currently there are no clinically established laboratory investigations available to predict prognosis or therapeutic response.

Tumors in children who develop OMS tend to be more mature, showing favorable histology and absence of n-myc oncogene amplification than similar tumors in children without symptoms of OMS. Involvement of local lymph nodes is common, but these children rarely have distant metastases and their prognosis, in terms of direct morbidity and mortality effects from the tumor, is excellent. The three-year survival rate for children with non-metastatic neuroblastoma and OMS was 100% according to Children’s Cancer Group data (gathered from 675 patients diagnosed between 1980 and 1994); three-year survival in comparable patients with OMS was 77%. Although the symptoms of OMS are typically steroid-responsive and recovery from acute symptoms of OMS can be quite good, children often suffer lifelong neurologic sequelae that impair motor, cognitive, language, and behavioral development.

Most children will experience a relapsing form of OMS, though a minority will have a monophasic course and may be more likely to recover without residual deficits. Viral infection may play a role in the reactivation of disease in some patients who had previously experienced remission, possibly by expanding the memory B cell population. Studies have generally asserted that 70-80% of children with OMS will have long-term neurologic, cognitive, behavioral, developmental, and academic impairment. Since neurologic and developmental difficulties have not been reported as a consequence of neuroblastoma or its treatment, it is thought that these are exclusively due to the immune mechanism underlying OMS.

One study concludes that: ""Patients with OMA and neuroblastoma have excellent survival but a high risk of neurologic sequelae. Favourable disease stage correlates with a higher risk for development of neurologic sequelae. The role of anti-neuronal antibodies in late sequelae of OMA needs further clarification"."

Another study states that: ""Residual behavioral, language, and cognitive problems occurred in the majority"."

Non-epileptic seizures are paroxysmal events that mimic an epileptic seizure but do not involve abnormal, rhythmic discharges of cortical neurons. They are caused by either physiological or psychological conditions. The latter is discussed more fully in psychogenic non-epileptic seizures.

[Please could somebody add an actual description of what happens when somebody has a seizure or 'paroxysmal event'?!]

The three main signs of hyperekplexia are generalized stiffness, excessive startle beginning at birth and nocturnal myoclonus. Affected individuals are fully conscious during episodes of stiffness, which consist of forced closure of the eyes and an extension of the extremities followed by a period of generalised stiffness and uncontrolled falling at times. Initially, the disease was classified into a "major" and a "minor" form, with the minor form being characterized by an excessive startle reflex, but lacking stiffness. There is only genetic evidence for the existence of the major form.

Other signs and symptoms of hyperekplexia may include episodic neonatal apnea, excessive movement during sleep and the head-retraction reflex. The link to some cases of Sudden Infant Death remains controversial.

Possible causes include:

- Syncope (fainting)

- Reflex anoxic seizures

- Breath-holding spells of childhood

- Hypoglycaemia

- Cataplexy

- Hyperekplexia, also called startle syndrome

- Migraine

- Narcolepsy

- Non-epileptic myoclonus

- Opsoclonus

- Parasomnias, including night terrors

- Paroxysmal kinesigenic dyskinesia

- Repetitive or ritualistic behaviours

- Tics

- AADC Deficiency

Hyperekplexia is known to be caused by a variety of genes, encoding both pre- and postsynaptic proteins. The symptoms displayed, as well as the forms of heritance, vary based on which gene is affected.

The age of onset ranges from 1 to 14 years with 75% starting between 7–10 years. There is a 1.5 male predominance, prevalence is around 15% in children aged 1–15 years with non-febrile seizures and incidence is 10–20/100,000 of children aged 0–15 years

In children, most cases are associated with neuroblastoma and most of the others are suspected to be associated with a low-grade neuroblastoma that spontaneously regressed before detection. In adults, most cases are associated with breast carcinoma or small-cell lung carcinoma. It is one of the few paraneoplastic (meaning 'indirectly caused by cancer') syndromes that occurs in both children and adults, although the mechanism of immune dysfunction underlying the adult syndrome is probably quite different.

It is hypothesized that a viral infection (perhaps St. Louis encephalitis, Epstein-Barr, Coxsackie B, enterovirus, or just a flu) causes the remaining cases, though a direct connection has not been proven, or in some cases Lyme disease.

OMS is not generally considered an infectious disease. OMS is not passed on genetically.

RHS type 1 is caused by the impairment of a regulatory mechanism between cerebellar and brainstem nuclei and has been associated with a wide range of diseases, including Lafora disease, dentatorubropallidoluysian atrophy, and celiac disease.

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.

Juvenile myoclonic epilepsy is responsible for 7% of cases of epilepsy. Seizures usually begin around puberty and usually have a genetic basis. Seizures can be stimulus-selective, with flashing lights being one of the most common triggers.

The progression of SPS depends on whether it is a typical or abnormal form of the condition and the presence of comorbidities. Early recognition and neurological treatment can limit its progression. SPS is generally responsive to treatment, but the condition usually progresses and stabilizes periodically. Even with treatment, quality of life generally declines as stiffness precludes many activities. Some patients require mobility aids due to the risk of falls. About 65 percent of SPS patients are unable to function independently. About ten percent of SPS patients require intensive care at some point; sudden death occurs in about the same number of patients. These deaths are usually caused by metabolic acidosis or an autonomic crisis.

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.