A triad of hypokalemic periodic paralysis, potentially fatal cardiac ventricular ectopy and characteristic physical features is known as Anderson-Tawil Syndrome. It affects the heart, symptoms are a disruption in the rhythm of the heart's lower chambers (ventricular arrhythmia) in addition to the symptoms of long QT syndrome. There are also physical abnormalities associated with Andersen–Tawil syndrome, these typically affect the head, face, and limbs. These features often include an unusually small lower jaw (micrognathia), low-set ears, and an abnormal curvature of the fingers called clinodactyly. Furthermore it causes symptoms which are similar to Long QT syndrome, which Andersen's is also known as. Long QT syndrome, a hereditary disorder that usually affects children or young adults, slows the signal that causes the ventricles to contract. Another electrical signal problem, atrial flutter, happens when a single electrical wave circulates rapidly in the atrium, causing a very fast but steady heartbeat. Heart block involves weak or improperly conducted electrical signals from the upper chambers that can't make it to the lower chambers, causing the heart to beat too slowly. These conditions can put you at risk for cardiac arrest. Treatment might involve medication, ablation, or an implanted device to correct the misfiring, such as a pacemaker or defibrillator. Here are some common physical abnormalities, but keep in mind these do vary (in severity) between each patient:

Some more severe issues can be caused via the potassium channelopathy. These include paralysis (mostly temporary and can last from several seconds to several minutes), inability to perform long distance/interval exercises and sudden exhaustion- although this can be a sign of cardiac arrhythmia- which should be immeditaley checked out by a GP, whether you have been diagnosed with ATS or not.

Andersen–Tawil syndrome, also called Andersen syndrome and Long QT syndrome 7, is a form of long QT syndrome. It is a rare genetic disorder, and is inherited in an autosomal dominant pattern and predisposes patients to cardiac arrhythmias. Jervell and Lange-Nielsen Syndrome is a similar disorder which is also associated with sensorineural hearing loss. It was first described by Ellen Damgaard Andersen.

Many people with long QT syndrome have no signs or symptoms.

Some people may experience the following symptoms:

- Fainting (or syncope). This may occur when the patient is emotionally or physically stressed. It is unusual in QT syndrome to have any signs before the person actually faints.

- Seizures

- Sudden death. If there is sudden death, and doctors suspect long QT syndrome as the cause, they may recommend that the family members of the deceased get tested for the disease.

Long QT syndrome (LQTS) is a condition which affects repolarization of the heart after a heartbeat. This results in an increased risk of an irregular heartbeat which can result in fainting, drowning, or sudden death. These episodes can be triggered by exercise or stress. Other associated symptoms may include hearing loss.

Long QT syndrome may be present at birth or develop later in life. The inherited form may occur by itself or as part of larger genetic disorder. Onset later in life may result from certain medications, low blood potassium, low blood calcium, or heart failure. Medications that are implicated include certain antiarrhythmic, antibiotics, and antipsychotics. Diagnosis is based on an electrocardiogram (EKG) finding a corrected QT interval of greater than 440 to 500 milliseconds together with clinical findings.

Management may include avoiding strenuous exercise, getting sufficient potassium in the diet, the use of beta blockers, or a implantable cardiac defibrillator. Without treatment there is a 50%, 10 year risk of death, for the inherited versions. With treatment this decreases to less than 1% over 20 years.

Long QT syndrome is estimated to affect 1 in 7,000 people. Females are affected more often than males. Most people with the condition develop symptoms before they are 40 years old. It is a relatively common cause of sudden death along with Brugada syndrome and arrhythmogenic right ventricular dysplasia. In the United States it results in about 3,500 deaths a year. The condition was first clearly described in 1957.

Although much less publicized, hyperkalemic periodic paralysis has been observed in humans. In humans the disorder causes episodes of extreme muscle weakness, with attacks often beginning in infancy. Depending on the type and severity of the HyperKPP, it can increase or stabilize until the fourth or fifth decade where attacks may cease, decline, or, depending on the type, continue on into old age. Factors that can trigger attacks include rest after exercise, potassium-rich foods, stress, fatigue, weather changes, certain pollutants (e.g., cigarette smoke) and fasting. Muscle strength often improves between attacks, although many affected people may have increasing bouts of muscle weakness as the disorder progresses (abortive attacks). Sometimes with HyperKPP those affected may experience degrees of muscle stiffness and spasms (myotonia) in the affected muscles. This can be caused by the same things that trigger the paralysis, dependent on the type of myotonia.

Some people with hyperkalemic periodic paralysis have increased levels of potassium in their blood (hyperkalemia) during attacks. In other cases, attacks are associated with normal blood potassium levels (normokalemia). Ingesting potassium can trigger attacks in affected individuals, even if blood potassium levels do not rise in response.

In contrast to HyperKPP, hypokalemic periodic paralysis (noted in humans) refers to loss-of-function mutations in channels that prevent muscle depolarisation and therefore are aggravated by low potassium ion concentrations.

This inherited disease is characterized by violent muscle twitching and substantial muscle weakness or paralysis among affected horses. HYPP is a dominant genetic disorder; therefore, heterozygotes bred to genotypically normal horses have a statistic probability of producing clinically affected offspring 50% of the time.

Horses with HYPP can be treated with some possibility of reducing clinical signs, but the degree that medical treatment helps varies from horse to horse. There is no cure. Horses with HYPP often lose muscle control during an attack.

Some horses are more affected by the disease than others and some attacks will be more severe than others, even in the same horse. Symptoms of an HYPP attack may include:

- Muscle trembling

- Prolapse of the third eyelid — this means that the third eyelid flickers across the eye or covers more of the eye than normal

- Generalized weakness

- Weakness in the hind end — the horse may look as though it is 'dog-sitting'

- Complete collapse

- Abnormal whinny — because the muscles of the voicebox are affected as well as other muscles

- Death — in a severe attack the diaphragm is paralyzed and the horse can suffocate

HYPP attacks occur randomly and can strike a horse standing calmly in a stable just as easily as during exercise. Following an HYPP attack, the horse appears normal and is not in any pain which helps to distinguish it from Equine Exertional Rhabdomyolysis (ER), commonly known as "Azoturia," "Monday Morning Sickness" or "tying up." Horses that are tying up usually suffer attacks in connection with exercise and may take anywhere from 12 hours to several days to recover. Muscle tissue is damaged in an attack of ER, and the horse will be in pain during and following an attack. A blood test will reveal elevations in certain muscle enzymes after an episode of ER and so the two diseases, while superficially similar, are easily distinguished from one another in the laboratory.

Unlike with seizures, horses with HYPP are fully conscious and lucid during an attack. Horses may suffocate during an HYPP attack due to paralysis of the respiratory system. Horses that collapse during an episode are clearly distressed as they repeatedly struggle to get to their feet. If this occurs while the horse is being ridden or otherwise handled, the human handler or rider may be at risk of being injured by the movement of the horse.

Congenital myotonia, also called myotonia congenita, is a congenital neuromuscular channelopathy that affects skeletal muscles (muscles used for movement). It is a genetic disorder. The hallmark of the disease is the failure of initiated contraction to terminate, often referred to as delayed relaxation of the muscles (myotonia) and rigidity. Symptoms include delayed relaxation of the muscles after voluntary contraction (myotonia), and may also include stiffness, hypertrophy (enlargement), transient weakness in some forms of the disorder (from certain genetic mutations), and cramping. The condition is sometimes referred to as fainting goat syndrome, as it is responsible for the eponymous 'fainting' seen in fainting goats when presented with a sudden stimulus.

The prolonged muscle contractions, which occur most commonly in the leg muscles in recessive mutations, and more commonly in the hands, face, and eyelids in dominant mutations, are often enhanced by inactivity, and in some forms are relieved by repetitive movement known as "the warm-up effect". This effect often diminishes quickly with rest. Some individuals with myotonia congenita are prone to falling as a result of hasty movements or an inability to stabilize themselves after a loss of balance. During a fall, a person with myotonia congenita may experience partial or complete rigid paralysis that will quickly resolve once the event is over. However, a fall into cold water may render the person unable to move for the duration of submergence. As with myotonic goats, children are more prone to falling than adults, due to their impulsivity.

The two major types of myotonia congenita are distinguished by the severity of their symptoms and their patterns of inheritance. Becker disease usually appears later in childhood than Thomsen disease, and causes more severe myotonia, muscle stiffness and transient weakness. Although myotonia in itself is not normally associated with pain, cramps or myalgia may develop. People with Becker disease often experience temporary attacks of muscle weakness, particularly in the arms and hands, brought on by movement after periods of rest. They may also develop mild, permanent muscle weakness over time. This muscle weakness is not observed in people with Thomsen disease. However, in recent times, as more of the individual mutations that cause myotonia congenita are identified, these limited disease classifications are becoming less widely used.

Early symptoms in a child may include:

- Difficulty swallowing

- Gagging

- Stiff movements that improve when they are repeated

- Frequent falling

- Difficulties opening eyelids after strenuous contraction or crying (von Graefe's sign)

Possible complications may include:

- Aspiration pneumonia (caused by swallowing difficulties)

- Frequent choking or gagging in infants (also caused by swallowing difficulties)

- Abdominal muscle weakness

- Chronic joint problems

- Injury due to falls

Paramyotonia congenita (PC), also known as paramyotonia congenita of von Eulenburg or Eulenburg disease, is a rare congenital autosomal dominant neuromuscular disorder characterized by “paradoxical” myotonia. This type of myotonia has been termed paradoxical because it becomes worse with exercise whereas classical myotonia, as seen in myotonia congenita, is alleviated by exercise. PC is also distinguished as it can be induced by cold temperatures. Although more typical of the periodic paralytic disorders, patients with PC may also have potassium-provoked paralysis. PC typically presents within the first decade of life and has 100% penetrance. Patients with this disorder commonly present with myotonia in the face or upper extremities. The lower extremities are generally less affected. While some other related disorders result in muscle atrophy, this is not normally the case with PC. This disease can also present as hyperkalemic periodic paralysis and there is debate as to whether the two disorders are actually distinct.

A syndrome is a set of medical signs and symptoms occurring together, constitutes a particular disease or disorder. The word derives from the Greek σύνδρομον, meaning "concurrence". In some instances, a syndrome is so closely linked with a pathogenesis or cause that the words "syndrome", "disease", and "disorder" end up being used interchangeably for them. This is especially true of inherited syndromes. For example, Down syndrome, Wolf–Hirschhorn syndrome, and Andersen syndrome are disorders with known pathogeneses, so each is more than just a set of signs and symptoms, despite the "syndrome" nomenclature. In other instances, a syndrome is not specific to only one disease. For example, toxic shock syndrome can be caused by various toxins; premotor syndrome can be caused by various brain lesions; and premenstrual syndrome is not a disease but simply a set of symptoms.

If an underlying genetic cause is suspected but not known, a condition may be referred to as a genetic association (often just "association" in context). By definition, an association indicates that the collection of signs and symptoms occurs in combination more frequently than would be likely by chance alone.

Syndromes are often named after the physician or group of physicians that discovered them or initially described the full clinical picture. Such eponymous syndrome names are examples of medical eponyms. Recently, there has been a shift towards naming conditions descriptively (by symptoms or underlying cause) rather than eponymously, but the eponymous syndrome names often persist in common usage.

Channelopathies are diseases caused by disturbed function of ion channel subunits or the proteins that regulate them. These diseases may be either congenital (often resulting from a mutation or mutations in the encoding genes) or acquired (often resulting from autoimmune attack on an ion channel).

There are a large number of distinct dysfunctions known to be caused by ion channel mutations. The genes for the construction of ion channels are highly conserved amongst mammals and one condition, hyperkalemic periodic paralysis, was first identified in the descendants of Impressive, a registered Quarter Horse (see AQHA website).

The channelopathies of human skeletal muscle include hyper- and hypokalemic (high and low potassium blood concentrations) periodic paralysis, myotonia congenita and paramyotonia congenita.

Channelopathies affecting synaptic function are a type of synaptopathy.

Patients typically complain of muscle stiffness that can continue to focal weakness. This muscle stiffness cannot be walked off, in contrast to myotonia congenita. These symptoms are increased (and sometimes induced) in cold environments. For example, some patients have reported that eating ice cream leads to a stiffening of the throat. For other patients, exercise consistently induces symptoms of myotonia or weakness. Typical presentations of this are during squatting or repetitive fist clenching. Some patients also indicate that specific foods are able to induce symptoms of paramyotonia congenita. Isolated cases have reported that carrots and watermelon are able to induce these symptoms. The canonical definition of this disorder precludes permanent weakness in the definition of this disorder. In practice, however, this has not been strictly adhered to in the literature.

Psychiatric syndromes often called "psychopathological syndromes" (psychopathology is a psychic dysfunction occurring in mental disorder, also it's the study of the origin, diagnosis, development, and treatment of mental disorders).

In Russia those psychopathological syndromes are used in modern clinical practice and described in psychiatric literature in the details: asthenic syndrome, obsessive syndrome, emotional syndromes (for example, manic syndrome, depressive syndrome), Cotard's syndrome, catatonic syndrome, hebephrenic syndrome, delusional and hallucinatory syndromes (for example, paranoid syndrome, paranoid-hallucinatory syndrome, Kandinsky-Clérambault's syndrome also known as syndrome of psychic automatism, hallucinosis), paraphrenic syndrome, psychopathic syndromes (includes all personality disorders), clouding of consciousness syndromes (for example, twilight clouding of consciousness, amential syndrome also known as amentia, delirious syndrome, stunned consciousness syndrome, oneiroid syndrome), hysteric syndrome, neurotic syndrome, Korsakoff's syndrome, hypochondriacal syndrome, paranoiac syndrome, senestopathic syndrome, encephalopathic syndrome.

There are some examples of the psychopathological syndromes used in modern Germany: psychoorganic syndrome, depressive syndrome, paranoid-hallucinatory syndrome, obsessive-compulsive syndrome, autonomic syndrome, hostility syndrome, manic syndrome, apathy syndrome.

Also well known Münchausen syndrom, Ganser syndrome, neuroleptic-induced deficit syndrome, olfactory reference syndrome.

The types in the following table are commonly accepted. Channelopathies currently under research, like Kir4.1 potassium channel in multiple sclerosis, are not included.

Avellis syndrome is a neurological disorder characterized by a peculiar form of alternating paralysis. There is paralysis of the soft palate and vocal cords on one side and loss of pain sensation and temperature sense on the other side, including the extremities, trunk, and neck. It usually results from occlusion of the vertebral artery in lesions of the nucleus ambiguous and pyramidal tract. Horner's syndrome may be associated. In the original description, the vagus and glossopharyngeal nerves were involved; concomitant involvement of the neighbouring cranial nerves was observed later.

Typically an attack occurs without warning leading to sudden loss of consciousness. Prior to an attack, a patient may be pale with hypoperfusion. Normal periods of unconsciousness last approximately thirty seconds; if abnormal movements are present, they will consist of twitching after 15–20 seconds (The movements, which are not seizures occur because of brainstem hypoxia and not due to cortical discharge as evident by EEG findings which show no epileptiform activities). Breathing continues normally throughout the attack, and upon recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation, which has become dilated due to hypoxia.

As with any syncopal episode that results from a cardiac dysrhythmia, the faints do not depend on the patient's position. If they occur during sleep, the presenting symptom may simply be feeling hot and flushed on waking.

Stokes-Adams attacks may be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic. The ECG will show asystole, an AV block, or ventricular fibrillation during the attacks.

Periodic paralysis (also known as myoplegia paroxysmalis familiaris) is a group of rare genetic diseases that lead to weakness or paralysis from common triggers such as cold, heat, high carbohydrate meals, not eating, stress or excitement and physical activity of any kind. The underlying mechanism of these diseases are malfunctions in the ion channels in skeletal muscle cell membranes that allow electrically charged ions to leak in or out of the muscle cell, causing the cell to depolarize and become unable to move.

The symptoms of periodic paralysis can also be caused by hyperthyroidism, and are then labeled thyrotoxic periodic paralysis; however, if this is the underlying condition there are likely to be other characteristic manifestations, enabling a correct diagnosis.

Periodic paralysis is an autosomal dominant myopathy with considerable variation in penetrance, leading to a spectrum of familial phenotypes (only one parent needs to carry the gene mutation to affect the children, but not all family members who share the gene are affected to the same degree). Specific diseases include:

- Hypokalemic periodic paralysis (), where potassium leaks into the muscle cells from the bloodstream.

- Hyperkalemic periodic paralysis (), where potassium leaks out of the cells into the bloodstream.

- Paramyotonia congenita (), a form which often accompanies hyperkalemic periodic paralysis, but may present alone. The primary symptom of paramyotonia congenita is muscle contracture which develops during exercise or activity. Paramyotonia congenita attacks may also be triggered by a low level of potassium in the bloodstream. This means people with both hyperkalemic periodic paralysis and paramyotonia congenita can have attacks with fluctuations of potassium up or down.

- Andersen-Tawil syndrome (), a form of periodic paralysis that includes significant heart rhythm problems, fainting and risk of sudden death. Potassium levels may be low, high, or normal during attacks of ATS. Patients with ATS may also have skeletal abnormalities like scoliosis (curvature of the spine), webbing between the second and third toes or fingers (syndactyly), crooked fingers (clinodactyly), a small jaw (micrognathia) and low-set ears. Patients need to have another form of periodic paralysis to have the Andersen-Tawil. If a patient has hypo or hyper periodic paralysis they have a 50% chance of getting Andersen-Tawil. They just have to have the gene that causes it. This is a rare occurrence of having this. Only around 100 people in the world are recorded to have it.

Signs and symptoms of CBPS typically appear in infancy or at birth, but can appear later in childhood. These include facial diplegia (paralysis on both sides), facial muscle spasms, pseudobulbar palsy, dysarthria (difficulty speaking), difficulty chewing, dysphagia (difficulty swallowing), epilepsy, and intellectual disability. Epileptic seizures in individuals with CBPS are different between individuals and can vary between episodes.

Several disorders may appear similar to CBPS and need to be distinguished in the process of diagnosing CBPS. These include pachygyria, double cortex syndrome, and lissencephaly, all of which are classified along with CBPS as neuronal migration disorders. Diagnostic tests for CBPS include electroencephalograms, CT scanning, and magnetic resonance imaging.

An attack often begins with muscle pain, cramping, and stiffness. This is followed by weakness or paralysis that tends to develop rapidly, usually in late evening or the early hours of the morning. The weakness is usually symmetrical; the limb muscles closer to the trunk (proximal) are predominantly affected, and weakness tends to start in the legs and spread to the arms. Muscles of the mouth and throat, eyes, and breathing are usually not affected, but occasionally weakness of the respiratory muscles can cause life-threatening respiratory failure. Attacks typically resolve within several hours to several days, even in the absence of treatment. On neurological examination during an attack, flaccid weakness of the limbs is noted; reflexes are usually diminished, but the sensory system is unaffected. Mental status is not affected.

Attacks may be brought on by physical exertion, drinking alcohol, or eating food high in carbohydrates or salt. This may explain why attacks are more common in summer, when more people drink sugary drinks and engage in exercise. Exercise-related attacks tend to occur during a period of rest immediately after exercise; exercise may therefore be recommended to abort an attack.

There may be symptoms of thyroid overactivity, such as weight loss, a fast heart rate, tremor, and perspiration; but such symptoms occur in only half of all cases. The most common type of hyperthyroidism, Graves' disease, may additionally cause eye problems (Graves' ophthalmopathy) and skin changes of the legs (pretibial myxedema). Thyroid disease may also cause muscle weakness in the form of thyrotoxic myopathy, but this is constant rather than episodic.

Hypokalemic periodic paralysis (hypoKPP) is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood. In individuals with this mutation, attacks often begin in adolescence and most commonly occur on awakening or after sleep or rest following strenuous exercise (attacks during exercise are rare), high carbohydrate meals, meals with high sodium content, sudden changes in temperature, and even excitement, noise, flashing lights and cold temperatures. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. During an attack reflexes may be decreased or absent. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.

Some people only develop symptoms of periodic paralysis due to hyperthyroidism (overactive thyroid). This entity is distinguished with thyroid function tests, and the diagnosis is instead called thyrotoxic periodic paralysis.

TNF receptor associated periodic syndrome presents with the following signs and symptoms:

- Episodic fever

- Erythrocyte sedimentation rate(increased)

- Pericarditis

- Splenomegaly

- Uveitis

- Vertigo

Hypokalemia (low blood potassium levels) commonly occurs during attacks; levels below 3.0 mmol/l are typically encountered. Magnesium and phosphate levels are often found to be decreased. Creatine kinase levels are elevated in two thirds of cases, usually due to a degree of muscle injury; severe elevations suggestive of rhabdomyolysis (muscle tissue destruction) are rare. Electrocardiography (ECG/EKG) may show tachycardia (a fast heart rate) due to the thyroid disease, abnormalities due to cardiac arrhythmia (atrial fibrillation, ventricular tachycardia), and conduction changes associated with hypokalemia (U waves, QRS widening, QT prolongation, and T wave flattening). Electromyography shows changes similar to those encountered in myopathies (muscle diseases), with a reduced amplitude of the compound muscle action potentials (CMAPs); they resolve when treatment has commenced.

TPP is distinguished from other forms of periodic paralysis (especially hypokalemic periodic paralysis) with thyroid function tests on the blood. These are normal in the other forms, and in thyrotoxicosis the levels of thyroxine and triiodothyronine are elevated, with resultant suppression of TSH production by the pituitary gland. Various other investigations are usually performed to separate the different causes of hyperthyroidism.