Atonic seizures (also called drop seizures, akinetic seizures or drop attacks), are a type of seizure that consist of a brief lapse in muscle tone that are caused by temporary alterations in brain function. The seizures are brief – usually less than fifteen seconds. They begin in childhood and may persist into adulthood. The seizure itself causes no injury, but the loss of muscle control can result in direct injury from falling. Electroencephalography can be used to confirm diagnosis. It is rare and can be indicative of Lennox-Gastaut syndrome ("see" Henri Gastaut).

Atonic seizures can occur while standing, walking or sitting, and are often noticeable by a head drop (the neck muscles relaxing) and injury may result from hitting the face or head. As with common epileptic occurrences, no first aid is needed post-seizure, except in the instances where falling injuries have occurred. In some cases, a person may become temporarily paralyzed in part of his or her body. This usually does not last longer than 3 minutes.

There is no general treatment for patients with a seizure disorder. Each treatment plan is specifically tailored to the individual patient based on their diagnosis and symptoms. Treatment options may include medical therapy, nerve stimulation, dietary therapy, or surgery, as appropriate. Clinical trials may also be a valuable treatment alternative.

Usually, anticonvulsants are given based on other symptoms and / or associated problems.

Because the areas of the cerebellum which determine increases and decreases in muscular tonus are close together, people experiencing atonic seizures are most likely experiencing myoclonic ones too, at some point. This may play a role in therapy and diagnostic.

A differential diagnosis should include:

- Thrombosis of the basilar artery

- Cardioembolic stroke

- Complex partial seizures

- Frontal lobe epilepsy

- Lacunar syndromes

- Migraine variants

- Posterior cerebral artery stroke

- Syncope and related paroxysmal spells

- Temporal lobe epilepsy

If the event lasts less than one hour, transient epileptic amnesia (TEA) might be implicated.

If the condition lasts longer than 24 hours, it is not considered TGA by definition. A diagnostic investigation would then probably focus on some form of undetected ischemic attack or cranial bleed.

The underlying cause of TGA remains enigmatic.

The leading hypotheses are some form of epileptic event, a problem with blood circulation around, to or from the brain, or some kind of migraine-like phenomenon.

The differences are sufficiently meaningful that transient amnesia may be considered a heterogeneous clinical syndrome with multiple etiologies, corresponding mechanisms, and differing prognoses.

Cataplexy manifests itself as muscular weakness which may range from a barely perceptible slackening of the facial muscles to complete muscle paralysis with postural collapse. Attacks are brief, most lasting from a few seconds to a couple of minutes, and typically involve dropping of the jaw, neck weakness, and/or buckling of the knees. Even in a full-blown collapse, people are usually able to avoid injury because they learn to notice the feeling of the cataplectic attack approaching and the fall is usually slow and progressive. Speech may be slurred and vision may be impaired (double vision, inability to focus), but hearing and awareness remain normal.

Cataplexy attacks are self-limiting and resolve without the need for medical intervention. If the person is reclining comfortably, he or she may transition into sleepiness, hypnagogic hallucinations, or a sleep-onset REM period. While cataplexy worsens with fatigue, it is different from narcoleptic sleep attacks and is usually, but not always, triggered by strong emotional reactions such as laughter, anger, surprise, awe, and embarrassment, or by sudden physical effort, especially if the person is caught off guard. One well known example of this was the reaction of 1968 Olympic long jump medalist Bob Beamon on understanding that he had broken the previous world record by over 0.5 meters (2 feet). Cataplectic attacks may occasionally occur spontaneously, with no identifiable emotional trigger.

The diagnosis of narcolepsy and cataplexy is usually made by symptom presentation. Presenting with the tetrad of symptoms (Excessive daytime sleepiness, sleep onset paralysis, hypnogogic hallucinations, cataplexy symptoms) is strong evidence of the diagnosis of narcolepsy. A Multiple Sleep Latency Test (MSLT) is often conducted in order to quantify daytime sleepiness.

A drop attack is a sudden fall without loss of consciousness. Drop attacks stem from diverse mechanisms, including orthopedic causes (for example, leg weakness and knee instability), hemodynamic causes (for example, transient vertebrobasilar insufficiency, a type of interruption of blood flow to the brain), and neurologic causes (such as epileptic seizures or unstable vestibular function), among other reasons. Those afflicted typically experience abrupt leg weakness, sometimes after sudden movement of the head. The weakness may persist for hours.

The term "drop attack" is used to categorize otherwise unexplained falls from a wide variety of causes and is considered ambiguous medical terminology; drop attacks are currently reported much less often than in the past, possibly as a result of better diagnostic precision. By definition, drop attacks exclude syncopal falls (fainting), which involve short loss of consciousness. In neurology, the term "drop attack" is used to describe certain types of seizure which occur in epilepsy. Drop attacks that have a vestibular origin within the inner ear may be experienced by some people in the later stages of Ménière's disease (these may be referred to as Tumarkin [drop] attacks, or as Tumarkin's otolithic crisis).

Drop attacks often occur in elderly people. Falls in older adults happen for many reasons, and the goals of health care include preventing any preventable falls and correctly diagnosing any falls that do happen.

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.

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.

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.

The typical symptoms of cluster headache include grouped occurrence and recurrence (cluster) of headache attack, severe unilateral orbital, supraorbital and/or temporal pain. If left untreated, attack frequency may range from one attack every two days to eight attacks per day. Cluster headache attack is accompanied by at least one of the following autonomic symptoms: drooping eyelid, pupil constriction, redness of the conjunctiva, tearing, runny nose, and less commonly, facial blushing, swelling, or sweating, typically appearing on the same side of the head as the pain.

Restlessness (for example, pacing or rocking back and forth), photosensitivity, aversion to light (photophobia) or sensitivity to noise (phonophobia) may occur during a CH. Nausea is a rare symptom, although it has been reported. Secondary effects may include inability to organize thoughts and plans, physical exhaustion, confusion, agitation, aggressiveness, depression and anxiety.

People with CH may dread facing another headache and adjust their physical or social activities around a possible future occurrence. Likewise they may seek assistance to accomplish what would otherwise be normal tasks. They may hesitate to make plans because of the regularity, or conversely, the unpredictability of the pain schedule. These factors can lead to generalized anxiety disorders, panic disorder, serious depressive disorders, social withdrawal and isolation.

Cluster headaches may occasionally be referred to as "alarm clock headache" because of the regularity of their recurrence. CH attacks often awaken individuals from sleep. Both individual attacks and the cluster grouping can have a metronomic regularity; attacks typically striking at a precise time of day each morning or night. The recurrence of headache cluster grouping may occur more often around solstices, or seasonal changes, sometimes showing circannual periodicity. Conversely, attack frequency may be highly unpredictable, showing no periodicity at all. These observations have prompted researchers to speculate an involvement, or dysfunction of the hypothalamus. The Hypothalamus controls the body's "biological clock" and circadian rhythm.

In episodic cluster headache, attacks occur once or more daily, often at the same time each day for a period of several weeks, followed by a headache-free period lasting weeks, months, or years. Approximately 10–15% of cluster headaches are chronic, with multiple headaches occurring every day for years, sometimes without any remission.

In accordance with the International Headache Society (IHS) diagnostic criteria, cluster headaches occurring in two or more cluster periods, lasting from 7 to 365 days with a pain-free remission of one month or longer between the headache attacks, may be classified as episodic. If headache attacks occur for more than a year without pain-free remission of at least one month, the condition is classified as chronic.

Chronic CH both occurs and recurs without any remission periods between cycles; there may be variation in cycles, meaning the frequency and severity of attacks may change without predictability for a period of time. The frequency, severity and duration of headache attacks experienced by people during these cycles varies between individuals and does not demonstrate complete remission of the episodic form. The condition may change unpredictably, from chronic to episodic and from episodic to chronic.

Hyperkalemic periodic paralysis (HYPP, HyperKPP) is a genetic disorder. It occurs in humans, horses (where it is also known as Impressive syndrome, after an index case in a horse named Impressive, or possibly one of his ancestors), and perhaps other animals. It is an inherited autosomal dominant disorder that affects sodium channels in muscle cells and the ability to regulate potassium levels in the blood. It is most commonly associated with horses, but occurs in humans, where it may be called Gamstorp episodic adynamy. It is characterized by muscle hyperexcitability or weakness which, exacerbated by potassium, heat or cold, can lead to uncontrolled shaking followed by paralysis. Onset in humans usually occurs in early childhood, but still occurs with adults.

The mutation which causes this disorder is dominant on SCN4A with linkage to the sodium channel expressed in muscle. The mutation causes single amino acid changes in parts of the channel which are important for inactivation. In the presence of high potassium levels, including those induced by diet, sodium channels fail to inactivate properly.

Equine hyperkalemic periodic paralysis occurs in 1 in 50 Quarter Horses and can be traced to a single ancestor, a stallion named Impressive.

Horner syndrome is due to a deficiency of sympathetic activity.

The site of lesion to the sympathetic outflow is on the ipsilateral side of the symptoms.

The following are examples of conditions that cause the clinical appearance of Horner's syndrome:

- "First-order neuron disorder:" Central lesions that involve the hypothalamospinal tract (e.g. transection of the cervical spinal cord).

- "Second-order neuron disorder:" Preganglionic lesions (e.g. compression of the sympathetic chain by a lung tumor) that releases acetylcholine.

- "Third-order neuron disorder:" Postganglionic lesions at the level of the internal carotid artery (e.g. a tumor in the cavernous sinus or a carotid artery dissection) that releases norepinephrine.

- "Partial Horner's syndrome": In case of a third-neuron disorder, anhidrosis is limited to the middle part of the forehead or can be absent, resulting in a partial Horner's syndrome.

If someone has impaired sweating above the waist affecting only one side of the body, yet they do not have a clinically apparent Horner's syndrome, then the lesion is just below the stellate ganglion in the sympathetic chain.

Signs that are found in patients on the affected side of the face include

- partial ptosis

- upside-down ptosis (slight elevation of the lower lid)

- anhidrosis

- miosis

- pseudoenophthalmos (the impression that the eye is sunken, caused by a narrow palpebral aperture)

- pupillary dilation lag

- loss of ciliospinal reflex

- bloodshot conjunctiva, depending on the site of lesion.

- unilateral straight hair (in congenital Horner's syndrome); the hair on the affected side may be straight in some cases.

- heterochromia iridum (in congenital Horner's syndrome)

Interruption of sympathetic pathways leads to several implications. It inactivates the dilator muscle and thereby produces miosis. It inactivates the superior tarsal muscle which produces ptosis. It inactivates the orbitalis muscle which produces the effect of enophthalmos. It also reduces sweat secretion in the face.

Sometimes there is flushing on the affected side of the face due to dilation of blood vessels under the skin. The pupil's light reflex is maintained as this is controlled via the parasympathetic nervous system.

In children, Horner's syndrome sometimes leads to heterochromia, a difference in eye color between the two eyes. This happens because a lack of sympathetic stimulation in childhood interferes with melanin pigmentation of the melanocytes in the superficial stroma of the iris.

In veterinary medicine, signs can include partial closure of the third eyelid, or nictitating membrane.

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.

Episodes of vasovagal syncope are typically recurrent and usually occur when the predisposed person is exposed to a specific trigger. Before losing consciousness, the individual frequently experiences early signs or symptoms such as lightheadedness, nausea, the feeling of being extremely hot or cold (accompanied by sweating), ringing in the ears, an uncomfortable feeling in the heart, fuzzy thoughts, confusion, a slight inability to speak or form words (sometimes combined with mild stuttering), weakness and visual disturbances such as lights seeming too bright, fuzzy or tunnel vision, black cloud-like spots in vision, and a feeling of nervousness can occur as well. The symptoms may become more intense over several seconds to several minutes before the loss of consciousness (if it is lost). Onset usually occurs when a person is sitting up or standing.

When people lose consciousness, they fall down (unless prevented from doing so) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness. If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the blood's inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense. Fainting occurs with a loss of oxygen to the brain.

The autonomic nervous system's physiological state (see below) leading to loss of consciousness may persist for several minutes, so

- If sufferers try to sit or stand when they wake up, they may pass out again

- The person may be nauseated, pale, and sweaty for several minutes or hours

Reflex syncope is a brief loss of consciousness due to a neurologically induced drop in blood pressure. Before the person passes out there may be sweating, a decreased ability to see, or ringing in the ears. Occasionally the person may twitch when unconscious. Complications may include injury from a fall.

Reflex syncope is divided into three types: vasovagal, carotid sinus, and situational. Vasovagal syncope is typically triggered by seeing blood, emotional stress, or prolonged standing. Situational syncope is often triggered by urination, swallowing, or coughing. Carotid sinus syncope is due to pressure on the carotid sinus in the neck. The underlying mechanism involves the nervous system slowing the heart rate and dilating blood vessels resulting in low blood pressure and therefore not enough blood flow to the brain. Diagnosis is based on symptoms after ruling out other possible causes.

Recovery happens without specific treatment. Prevention involves avoiding the triggers. Drinking sufficient fluids, salt, and exercise may also be useful. If this is not sufficient in vasovagal syncope medications like midodrine or fludrocortisone may be tried. Occasionally a cardiac pacemaker may be used. Reflex syncope affects at least 1 per 1,000 people a year. It is the most common type of syncope, making up more than 50% of all cases.

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.

This is described as a rare form of severe mental illness, with the following characteristics:

- Sudden onset in a previously asymptomatic person.

- Brief duration, with full recovery.

- Psychotic symptoms that can include confusion or hallucinations, mutism and stupor, delusions, or manic state. These are distinct from premenstrual tension, premenstrual syndrome, premenstrual (late luteal phase) depression or dysphoric disorder or menstrual mood disorder.

- Occurrence in rhythm with the menstrual cycle.

It shares clinical features with, and presents similarly to, postpartum psychosis. Researchers Deuchar and Brockington proposed that a sudden drop in levels of estrogen in the brain could be the trigger for both conditions.

People may vomit or retch six to twelve times an hour, and an episode may last from a few hours to well over three weeks, and in some cases months, with a median episode duration of 41 hours. Acid, bile and (if the vomiting is severe) blood may be vomited. Some sufferers will ingest water to reduce the irritation of bile and acid on the esophagus during emesis. Between episodes the sufferer is usually normal and healthy otherwise but can be in a weak state of fatigue or suffer from muscle pain. In approximately half of cases the attacks, or episodes, occur in a time-related manner. Each attack is stereotypical; that is, in any given individual, the timing, frequency and severity of attacks is similar.

Episodes may happen every few days, every few weeks or every few months. For some there is not a pattern in time that can be recognized. Some sufferers have a warning of an attack. They may experience a prodrome, usually intense nausea and pallor, heightened sensitivity, especially to light, though sensitivity to smell, sound, pressure, and temperature, as well as oncoming muscle pain and fatigue, are also reported by some patients. The majority of sufferers can identify triggers that may precipitate an attack. The most common are various foods, infections (such as colds), menstruation, extreme physical exertion, lack of sleep, and psychological stresses both positive and negative.

A sufferer may also be light-sensitive (photophobic) during an attack, as well as sound-sensitive (phonophobic) and, less frequently, temperature- or pressure-sensitive. Some sufferers also have a strong urge to bathe in warm or cold water. Some sufferers report that they experience a restless sensation or stinging pain along the spine, hands, and feet followed by weakness in both legs. Some of these symptoms may be due to dehydration rather than the underlying cause of CVS.

Usually beginning in one or both hands, MMN is characterized by weakness, muscle atrophy, cramping, and often profuse fasciculations (muscle twitching). The symptoms are progressive over long periods, often in a stepwise fashion, but unlike ALS are often treatable.

Sensory nerves are usually unaffected.

Wrist drop and foot drop (leading to trips and falls) are common symptoms. Other effects can include gradual loss of finger extension, leading to a clawlike appearance. Cold & hot temperatures exacerbates MMN symptoms to such an extent, unlike other neuropathies, that it is being investigated as a diagnostic tool.

Menstrual psychosis is a debated form of psychosis with a brief, sudden onset related to the menstrual cycle. The symptoms associated to it are dramatic and include delirium, mania or mutism. Most psychiatrists do not recognise the condition. Only 80 established cases are reported in medical literature and most of them were described by 19th Century physicians. It is thought to be linked with postpartum psychosis. This journal has been published looking at the 'evidence' for menstrual psychosis'.

Cyclic vomiting syndrome (US English) or cyclical vomiting syndrome (UK English) (CVS) is a chronic functional condition of unknown cause characterised by recurring attacks of intense nausea, vomiting, and sometimes abdominal pain, headaches, or migraines. CVS typically develops during childhood, usually between ages 3 and 7; although it often remits during adolescence, it can persist into adult life.

Symptoms can be as follows. They are periodic, and occur only during an "episode", usually after eating.

- Sinus bradycardia

- Difficulty inhaling

- Angina pectoris

- Left ventricular discomfort

- Fatigue

- Anxiety

- Uncomfortable breathing

- Poor perfusion

- Muscle pain (crampiness)

- Burst or sustained vertigo or dizziness

- Sleep disturbance (particularly when sleeping within a few hours of eating, or lying on the left side)

- Extrasystoles

- Hot flashes