Hypokalemic sensory overstimulation is characterized by a subjective experience of sensory overload and a relative resistance to lidocaine local anesthesia. The sensory overload is treatable with oral potassium gluconate. The phenotype overlaps with that of attention deficit disorder, raising the possibility of subtypes of attention deficit disorder that have a peripheral sensory cause and possible new forms of therapy.

Hypokalemic sensory overstimulation is a term coined by MM Segal to describe a syndrome that has been reported in a single case-study by his group. Segal describes the syndrome as a form of neurological disorder that has similarities to attention deficit hyperactivity disorder and has several similarities to disorders of ion channels, in particular to the muscle disorder hypokalemic periodic paralysis.

It is medically related to disorders of ion channels, in particular to the muscle disorder hypokalemic periodic paralysis and is similar in nature to ADHD, as the prominent feature of hypokalemic sensory overstimulation is the feeling of sensory overstimulation that is also characteristic of attention deficit disorder and the over stimulation of the nervous system.. It may also be connected with premenstrual syndrome and the body's natural sodium levels.

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.

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.

Diagnosis can be achieved through a specialized form of electromyographic (EMG) testing called the long exercise test. This test measures the amplitude of a nerve response (called the Compound Muscle Action Potential or CMAP) for 40 to 50 minutes following a few minutes of exercise. In affected patients, there is a progressive fall in the amplitude of the potential. Besides the patient history or a report of serum potassium low normal or low during an attack, the long exercise test is the current standard for medical testing. Genetic diagnosis is often unreliable as only a few of the more common gene locations are tested, but even with more extensive testing 20–37% of people with a clinical diagnosis of hypokalemic periodic paralysis have no known mutation in the two known genes. Standard EMG testing cannot diagnose a patient unless they are in a full blown attack at the time of testing. Provoking an attack with exercise and diet then trying oral potassium can be diagnostic, but also dangerous as this form of PP has an alternate form known as hyperkalemic periodic paralysis. The symptoms are almost the same, but the treatment is different. The old glucose insulin challenge is dangerous and risky to the point of being life-threatening and should never be done when other options are so readily available.

People with hypokalemic periodic paralysis are often misdiagnosed as having a conversion disorder or hysterical paralysis since the weakness is muscle-based and doesn't correspond to nerve or spinal root distributions. The tendency of people with hypokalemic periodic paralysis to get paralyzed when epinephrine is released in "fight or flight" situations further adds to the temptation to misdiagnose the disorder as psychiatric.

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.

The most distinctive clinical feature is the absence of overflow tears with emotional crying after age 7 months. This symptom can manifest less dramatically as persistent bilateral eye irritation. There is also a high prevalence of breech presentation. Other symptoms include weak or absent suck and poor tone, poor suck and misdirected swallowing, and red blotching of skin.

Symptoms in an older child with familial dysautonomia might include:

1. Delayed speech and walking

2. Unsteady gait

3. Spinal curvature

4. Corneal abrasion

5. Less perception in pain or temperature with nervous system.

6. Poor growth

7. Erratic or unstable blood pressure.

8. Red puffy hands

9. Dysautonomia crisis: a constellation of symptoms in response to physical and emotional stress; usually accompanied by vomiting, increased heart rate, increase in blood pressure, sweating, drooling, blotching of the skin and a negative change in personality.

Thyrotoxic periodic paralysis (TPP) is a condition featuring attacks of muscle weakness in the presence of hyperthyroidism (overactivity of the thyroid gland). Hypokalemia (a decreased potassium level in the blood) is usually present during attacks. The condition may be life-threatening if weakness of the breathing muscles leads to respiratory failure, or if the low potassium levels lead to cardiac arrhythmias (irregularities in the heart rate). If untreated, it is typically recurrent in nature.

The condition has been linked with genetic mutations in genes that code for certain ion channels that transport electrolytes (sodium and potassium) across cell membranes. The main ones are the L-type calcium channel α1-subunit and potassium inward rectifier 2.6; it is therefore classified as a channelopathy. The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant.

Treatment of the hypokalemia, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks. It occurs predominantly in males of Chinese, Japanese, Vietnamese, Filipino, and Korean descent. TPP is one of several conditions that can cause periodic paralysis.

Hypoesthesia (or hypesthesia) refer to a reduced sense of touch or sensation, or a partial loss of sensitivity to sensory stimuli. In everyday speech this is sometimes referred to as "numbness".

Hypoesthesia is one of the negative sensory symptoms associated with cutaneous sensory disorder (CSD). In this condition, patients have abnormal disagreeable skin sensations that can be increased (stinging, itching or burning) or decreased (numbness or hypoesthesia). There are no other apparent medical diagnoses to explain these symptoms.

Cutaneous hyperesthesia has been associated with diagnosis of appendicitis in children but this symptom was not supported by the evidence.

Hypoesthesia originating in (and extending centrally from) the feet, fingers, navel, and/or lips is one of the common symptoms of beriberi, which is a set of symptoms caused by thiamine deficiency.

Hypoesthesia is also one of the more common manifestations of decompression sickness (DCS), along with joint pain, rash and generalized fatigue.

Affected individuals may not have symptoms in some cases. Symptomatic individuals present with symptoms identical to those of patients who are on thiazide diuretics, given that the affected transporter is the exact target of thiazides.

Clinical signs of Gitelman syndrome include a high blood pH in combination with low levels of chloride, potassium, and magnesium in the blood and decreased calcium excretion in the urine. In contrast to people with Gordon's syndrome, those affected by Gitelman's syndrome generally have low or normal blood pressure. Individuals affected by Gitelman's syndrome often complain of severe muscle cramps or weakness, numbness, thirst, waking up at night to urinate, salt cravings, abnormal sensations, chondrocalcinosis, or weakness expressed as extreme fatigue or irritability. More severe symptoms such as seizures, tetany, and paralysis have been reported. Abnormal heart rhythms and a prolonged QT interval can be detected on electrocardiogram and cases of sudden cardiac death have been reported due to low potassium levels. Phenotypic variations observed among patients probably result from differences in their genetic background and may depend on which particular amino acid in the NCCT protein has been mutated.

Ataxia can develop very abruptly or it can develop over time. Some signs and symptoms of ataxia are loss of balance, loss of muscle coordination in an arm, hand, or leg, difficulty walking, slur of speech, or difficulty swallowing. Ataxia is a non-specific condition characterized by a lack of voluntary movements to some degree. Rather than involving damage to the cerebellum, ataxia in EAST syndrome is due to the KCNJ10 mutation. In the brain, KCNJ10 is expressed in glial cells surrounding synapses and blood vessels as a K+ ion buffer. K+ is necessary to maintain a neuronal cell's membrane potential, and these glial cells are responsible for transferring K+ ions from sites of excess K+ to sites with deficient K+. KCNJ10 is a major potassium channel in these glial cells, and when this gene is mutated, these glial cells cannot properly clear K+ from the extracellular space and deliver K+ ions to places that need it. Excess K+ in these areas of synapse disturbs physiological excitability, resulting in symptoms of ataxia.

The treatment of ataxia depends on the cause, and there is not current research for EAST syndrome specific treatment; however, there are some general ways to improve disability from ataxia. The movement disorders associated with ataxia can be managed by pharmacological treatments and through physical therapy and occupational therapy to reduce disability. Physical therapy treatment is highly dependent on each individual and varies. A recent review states that physical therapy is effective, however, there is only moderate evidence to support this.

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

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.

Familial dysautonomia (FD), sometimes called Riley–Day syndrome and hereditary sensory and autonomic neuropathy type III (HSAN-III), is a disorder of the autonomic nervous system which affects the development and survival of sensory, sympathetic and some parasympathetic neurons in the autonomic and sensory nervous system resulting in variable symptoms, including insensitivity to pain, inability to produce tears, poor growth, and labile blood pressure (episodic hypertension and postural hypotension). People with FD have frequent vomiting crises, pneumonia, problems with speech and movement, difficulty swallowing, inappropriate perception of heat, pain, and taste, as well as unstable blood pressure and gastrointestinal dysmotility. FD does not affect intelligence. Originally reported by Drs. Conrad Milton Riley (1913–2005) and Richard Lawrence Day (1905–1989) in 1949, FD is one example of a group of disorders known as hereditary sensory and autonomic neuropathies (HSAN). All HSAN are characterized by widespread sensory dysfunction and variable autonomic dysfunction caused by incomplete development of sensory and autonomic neurons. The disorders are believed to be genetically distinct from each other.

Symptoms most frequently reported include a persistent sensation of motion usually described as rocking, swaying, or bobbing, disequilibrium with difficulty maintaining balance; it is seldom accompanied by a true spinning vertigo. Chronically fatigued, sufferers can become fatigued quickly with minimal exertion and experience neck and back pain. Other common symptoms include difficulty concentrating or inability to multitask, visual intolerance of busy patterns, headaches and/or migraine headaches, and ear pain or fullness.

Fluctuations in weather, in particular barometric pressure, also affect suffers. Many have photo-sensitivity and find it more difficult to walk in the dark as well as other sensitivities to strong smells including chemical smells. Cognitive impairment ("brain fog") includes an inability to recall words, short term memory loss, an inability to multi-task, misspelling and mispronunciation of words. MdDS sufferers report they are unable to use a computer for any length of time due to the visual overstimulation, and some are even unable to watch television.

The condition may be masked by a return to motion such as in a car, train, plane, or boat; however, once the motion ceases, the symptoms rebound or return, often at much higher levels than when the journey first commenced. Symptoms can be increased by stress, lack of sleep, crowds, flickering lights, loud sounds, fast or sudden movements, enclosed areas or busy patterns.

MdDS sufferers can sleep up to 12 or more hours a day, depending on their symptom levels. Research reveals MdDS is not migraine related and many sufferers have never had migraine symptoms prior to the onset of the disorder. However, for some MdDS sufferers there maybe have been a correlation between migraine and some pathophysiological overlap or even some other precipitating illness.

The symptoms of MdDS may be extremely debilitating and fluctuate high and low on a daily basis; it greatly affects the working capacity of sufferers with many having to relinquish work; it also limits most other daily and social activities. Sufferers can have low quality of life in both the physical and emotional realms, comparable to people who have multiple sclerosis.

This condition is distinct and usually episodic, with the people experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. An elevation of 40 mm Hg over baseline systolic should be suspicious for dysreflexia.

In persistent MdDS, the symptoms continue for more than a month, possibly years or indefinitely. The longer the disorder remains, there is a progressively lower likelihood of remission. All medical treatment is palliative for sufferers with persistent MdDS symptoms.

Epilepsy is caused by the mutation KCNJ10 within EAST syndrome. Glial cells express KCNJ10, which establishes the neuronal cells resting membrane potential. Therefore, through repolarization, a neuron constantly takes up sodium, which causes the membrane potential to decrease because potassium is no longer being taken up intracellularly. Seizures occur because the KCNJ10 mutation increases the sodium uptake and decreases the potassium uptake, which means the protective barrier of potassium is no longer there.

Some signs of epilepsy can be temporary confusion, a staring spell, or uncontrollable movements of the arms and legs. A person may also experience a loss of consciousness or psychic symptoms. Someone with epilepsy typically has the same type of seizure each time one occurs and so the symptoms are also similar each time.

The treatments of epilepsy vary depending on the case. Some treatments include medications, surgery, therapies, or a ketogenic diet. Researchers are also looking to develop a new treatment, a pacemaker for epilepsy. This device would sense a seizure before it would occur and then send a drug or electric charge to prevent the seizure. Another potential treatment for epilepsy is stereotactic radiosurgery. For this treatment doctors would direct radiation to a specific area of the brain that is causing the seizures to occur.

Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.

Other visual hallucinations tend to stem from psychological disorders. Whereas a person with a psychological disorder thinks their hallucinations are real, people with peduncular hallucinosis normally know that the visual hallucinations they see are not real. Peduncular hallucinations are independent of seizures, unlike some other visual hallucinations.

Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.

- Difficulty in initiating movement

- Poor truncal mobility

- Falls due to minor balance disturbances

- Greatly hindered postural responses

- Characteristic magnetic gait, the inability to raise one's foot off of the floor.

- Wide base, poor balance control when in stance

- Short stride

- En bloc turns

Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs (Plantar reflex). Urinary incontinence may also be present.

Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia.

Gitelman syndrome is an autosomal recessive kidney disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. The disorder is caused by genetic mutations resulting in improper function of the thiazide-sensitive sodium-chloride symporter (also known as NCC, NCCT, or TSC) located in the distal convoluted tubule of the kidney. This symporter is a channel responsible for the transport of multiple electrolytes such as sodium, chloride, calcium, magnesium, and potassium.

Gitelman syndrome was formerly considered a subset of Bartter syndrome until the distinct genetic and molecular bases of these disorders were identified. Bartter syndrome is also an autosomal recessive hypokalemic metabolic alkalosis, but it derives from a mutation to the NKCC2 found in the thick ascending limb of the loop of Henle.

Sensory-based motor disorder shows motor output that is disorganized as a result of incorrect processing of sensory information affecting postural control challenges, resulting in postural disorder, or developmental coordination disorder.

The SBMD subtypes are:

1. Dyspraxia

2. Postural disorder

They are normally colorful, vivid images and occur during wakefulness, and predominately at night. Lilliputian hallucinations (also called Alice in Wonderland syndrome), hallucinations in which people or animals appear smaller than they would be in real life, are common in cases of peduncular hallucinosis. Most patients exhibit abnormal sleep patterns characterized by insomnia and daytime drowsiness. Peduncular hallucinosis has been described as a “release phenomenon” due to damage to the ascending reticular activating system, which is supported by the sleep disturbance characteristic of this syndrome. In most cases, people are aware that the hallucinations are not real. However, some people experience agitation and delusion and mistake their hallucinations for reality.