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.

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.

Myoclonus is characterized by rapid contractions that affect the upper body including the neck, torso and arms, but may also affect the legs. These movements are stimulated by various factors including stress, noise, caffeine, and physical stimuli. Myoclonus can be characterized in multiple ways including neurological basis, muscular activity, and by stimuli. Myoclonus can be positive or negative; positive myoclonus results from brief spurts of muscle activity and negative myoclonus occurs when there is a lack of any muscular activity. Myoclonus is usually classified physiologically to optimize treatment. Myoclonus is a precursor effect to myoclonus dystonia and most commonly begins in childhood or adolescence.

Myoclonus is classified as cortical, subcortical, peripheral or spinal. Cortical myoclonus is the most common of these four and affects the upper limbs and face. Myoclonus dystonia has been characterized under subcortical origin, specifically under nonsegmented myoclonus or brainstem myoclonus. Symptoms within this classification include the startle response and reticular reflex myoclonus. Sudden stimuli like noise or touch to areas around the head or chest cause the startle response which will go up the brain stem and down the spinal cord causing jerk-like movements. Hyperekplexia is a heightened brainstem response where an affected person will continue to elicit the same response to a repeated stimuli. In contrast, reticular reflex myoclonus occurs spontaneously to stimuli applied to distal limbs. Spinal myoclonus is caused by defects in spinal organization or connections, and peripheral myoclonus has symptoms of rhythmic jerks due to a neuron-the most common being the hemifacial spasm.

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

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.

Myoclonic seizures involve brief involuntary muscle twitching, and may become frequent enough to be disabling. Tonic-clonic seizures have two phases: the tonic phase may last a few seconds and involves the muscles tensing, and may lead to the person falling down; the clonic phase involves a convulsion of rapidly alternating muscle tensing and relaxing. Neurological dysfunction includes difficulty coordinating muscle movements (ataxia) and a decline in cognitive ability (dementia).

Myoclonus can be described as brief jerks of the body; it can involve any part of the body, but it is mostly seen in limbs or facial muscles. The jerks are usually involuntary and can lead to falls. EEG is used to read brain wave activity. Spike activity produced from the brain is usually correlated with brief jerks seen on EMG or excessive muscle artifact. They usually occur without detectable loss of consciousness and may be generalized, regional or focal on the EEG tracing. Myclonus jerks can be epileptic or not epileptic. Epileptic myoclonus is an elementary electroclinical manifestation of epilepsy involving descending neurons, whose spatial (spread) or temporal (self-sustained repetition) amplification can trigger overt epileptic activity.

In the early stages, it can be difficult to distinguish progressive myoclonic epilepsy from benign idiopathic generalised epilepsies, such as juvenile myoclonic epilepsy. With PME, the initial effectiveness of anticonvulsant treatment diminishes as seizures become more frequent and neurological decline progresses. However, these can also be signs of anticonvulsant intoxication. The myoclonus in PME is usually severe and is the prominent seizure type.

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

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

The cardinal features of Rolandic epilepsy are infrequent, often single, focal seizures consisting of:

Hemifacial sensorimotor seizures are often entirely localised in the lower lip or spread to the ipsilateral hand. Motor manifestations are sudden, continuous or bursts of clonic contractions, usually lasting from a few seconds to a minute. Ipsilateral tonic deviation of the mouth is also common. Hemifacial sensory symptoms consist of unilateral numbness mainly in the corner of the mouth.

Hemifacial seizures are often associated with an inability to speak and hypersalivation:

"The left side of my mouth felt numb and started jerking and pulling to the left, and I could not speak to say what was happening to me."

Negative myoclonus can be observed in some cases, as an interruption of tonic muscular activity

Oropharyngolaryngeal ictal manifestations are unilateral sensorimotor symptoms inside the mouth. Numbness, and more commonly paraesthesias (tingling, prickling, freezing), are usually diffuse on one side or, exceptionally, may be highly localised even to one tooth. Motor oropharyngolaryngeal symptoms produce strange sounds, such as death rattle, gargling, grunting and guttural sounds, and combinations:

"In his sleep, he was making guttural noises, with his mouth pulled to the right, ‘as if he was chewing his tongue’". "We heard her making strange noises ‘like roaring’ and found her unresponsive, head raised from the pillow, eyes wide open, rivers of saliva coming out of her mouth, rigid."

Arrest of speech is a form of anarthria. The child is unable to utter a single intelligible word and attempts to communicate with gestures.

"My mouth opened and I could not speak. I wanted to say I cannot speak. At the same time, it was as if somebody was strangling me."

Hypersalivation , a prominent autonomic manifestation, is often associated with hemifacial seizures, oro-pharyngo-laryngeal symptoms and speech arrest. Hypersalivation is not just frothing:

"Suddenly my mouth is full of saliva, it runs out like a river and I cannot speak."

Syncope-like epileptic seizures may occur, probably as a concurrent symptom of Panayiotopoulos syndrome:

"She lies there, unconscious with no movements, no convulsions, like a wax work, no life."

Consciousness and recollection are fully retained in more than half (58%) of Rolandic seizures.

"I felt that air was forced into my mouth, I could not speak and I could not close my mouth. I could understand well everything said to me. Other times I feel that there is food in my mouth and there is also a lot of salivation. I cannot speak."

In the remainder (42%), consciousness becomes impaired during the ictal progress and in one third there is no recollection of ictal events.

Progression to hemiconvulsions or generalised tonic–clonic seizures occurs in around half of children and hemiconvulsions may be followed by postictal Todd’s hemiparesis .

Duration and circadian distribution: Rolandic seizures are usually brief, lasting for 1–3 min. Three quarters of seizures occur during nonrapid eye movement sleep, mainly at sleep onset or just before awakening.

Status epilepticus: Although rare, focal motor status or hemiconvulsive status epilepticus is more likely to occur than secondarily generalised convulsive status epilepticus, which is exceptional. Opercular status epilepticus usually occurs in children with atypical evolution or may be induced by carbamazepine or lamotrigine. This state lasts for hours to months and consists of ongoing unilateral or bilateral contractions of the mouth, tongue or eyelids, positive or negative subtle perioral or other myoclonus, dysarthria, speech arrest, difficulties in swallowing, buccofacial apraxia and hypersalivation. These are often associated with continuous spikes and waves on an EEG during NREM sleep.

Other seizure types: Despite prominent hypersalivation, focal seizures with primarily autonomic manifestations (autonomic seizures) are not considered part of the core clinical syndrome of Rolandic epilepsy. However, some children may present with independent autonomic seizures or seizures with mixed Rolandic-autonomic manifestations including emesis as in Panayiotopoulos syndrome.

Atypical forms: Rolandic epilepsy may present with atypical manifestations such early age at onset, developmental delay or learning difficulties at inclusion, other seizure types, atypical EEG abnormalities.

These children usually have normal intelligence and development. Learning can remain unimpaired while a child is afflicted with Rolandic epilepsy.

Patients with Unverricht–Lundborg disease exhibit myoclonic jerks and tonic-clonic seizures at a young age, between ages 6–16. The myoclonic jerks occur in the muscles of the arms and legs closest to the torso, and are triggered due to a variety of common external stimuli. Seizures begin at an average age of 10.8 years, with myoclonus beginning around 12.1 years. It is not currently possible to diagnose without a genetic test, and since early symptoms are general, it is often mistaken for another more common epilepsy, in many cases juvenile myoclonic epilepsy (JME).

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

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'?!]

Restless leg syndrome is a disorder in which patients feel uncomfortable or unpleasant sensations in the legs. These sensations usually occur in the evening, while the patient is sitting or lying down and relaxing. Patients feel like they have to move their legs to relieve the sensations, and walking generally makes the symptoms disappear. In many patients, this can lead to insomnia and excessive daytime sleepiness. This is a very common problem and can occur at any age.

Similarly, the syndrome akathisia ranges from mildly compulsive movement usually in the legs to intense frenzied motion. These movements are partly voluntary, and the individual typically has the ability to suppress them for short amounts of time. Like restless leg syndrome, relief results from movement.

DRPLA is a rare trinucleotide repeat disorder (polyglutamine disease) that can be juvenile-onset ( 40 years). Late adult-onset DRPLA is characterized by ataxia, choreoathetosis and dementia. Early adult-onset DRPLA also includes seizures and myoclonus. Juvenile-onset DRPLA presents with ataxia and symptoms consistent with progressive myoclonus epilepsy

(myoclonus, multiple seizure types and dementia). Other symptoms that have been described include cervical dystonia, corneal endothelial degeneration autism, and surgery-resistant obstructive sleep apnea.

Onset of symptoms usually occur in early adulthood and is characterized by intention tremor, progressive ataxia, convulsions, and myoclonic epileptic jerks.

Tremors usually affect one extremity, primarily the upper limb, and eventually involve the entire voluntary motor system. Overall, the lower extremity is usually disturbed less often than the upper extremity.

Additional features of the syndrome include: an unsteady gait, seizures, muscular hypotonia, reduced muscular coordination, asthenia, adiadochokinesia and errors with estimating range, direction, and force of voluntary movements. Mental deterioration can occur, however it is rare.

An individual displaying MERRFs syndrome will manifest not only a single symptom, but regularly patients display more than one affected body part at a time. It has been observed that patients with MERRF syndrome will primarily display Myoclonus as a first symptom, along with it they can also manifest seizures, cerebellar ataxia and myopathy. Secondary features include dementia, optic atrophy, bilateral deafness, peripheral neuropathy, spasticity or multiple lipomata. Additional symptoms include dementia, optic atrophy, bilateral deafness and peripheral neuropathy, spasticity, lipomatosis, and/or cardiomyopathy with wolff parkinson-white syndrome. Most patients will not exhibit all of these symptoms, however more than one of these symptoms will be present in a patient who has been diagnosed with MERRFS disease. Due to the multi-symptoms presented by the individual, the severity of the syndrome is very difficult to evaluate. Mitochondrial disorders may present at any age, and this holds truth for MERRS, since it forms part of them. Therefore, if a patient is presenting some of these symptoms, the doctor is able to narrow it down to MEERF mitochondrial disorder.

The genetic cause of ULD is known, but research has led to new areas of study that may lead to an increase in knowledge of what causes ULD.

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.

Benign Rolandic epilepsy or benign childhood epilepsy with centrotemporal spikes (BCECTS) is the most common epilepsy syndrome in childhood. Most children will outgrow the syndrome (it starts around the age of 3-13 with a peak around 8–9 years and stops around age 14-18), hence the label benign. The seizures, sometimes referred to as "sylvian seizures", start around the central sulcus of the brain (also called the centrotemporal area, located around the Rolandic fissure, after Luigi Rolando).

Patients with PLMD will complain of excessive daytime sleepiness (EDS), falling asleep during the day, trouble falling asleep at night, and difficulty staying asleep throughout the night. Patients also display involuntary limb movements that occur at periodic intervals anywhere from 20–40 seconds apart. They often only last the first half of the night during non-REM sleep stages. Movements do not occur during REM because of muscle atonia.

Symptoms include:

- opsoclonus (rapid, involuntary, multivectorial (horizontal and vertical), unpredictable, conjugate fast eye movements without intersaccadic [quick rotation of the eyes] intervals)

- myoclonus (brief, involuntary twitching of a muscle or a group of muscles)

- cerebellar ataxia, both truncal and appendicular

- aphasia (a language disorder in which there is an impairment of speech and of comprehension of speech, caused by brain damage)

- mutism (a language disorder in which a person does not speak despite evidence of speech ability in the past, often part of a larger neurological or psychiatric disorder)

- lethargy

- irritability or malaise

- drooling

- strabismus (a condition in which the eyes are not properly aligned with each other)

- vomiting

- sleep disturbances

About half of all OMS cases occur in association with neuroblastoma (a cancer of the sympathetic nervous system usually occurring in infants and children).

In most cases OMS starts with an acute flare-up of physical symptoms within days or weeks, but some less obvious symptoms such as irritability and malaise may begin weeks or months earlier.