Chewing: Horses may develop choke if they do not chew their food properly. Therefore, horses with dental problems (e.g. acquired or congenital malocclusion, loose or missing teeth, or excessively sharp dental ridges) that do not allow them to completely grind their food are particularly at risk. In addition, horses that bolt their feed and do not take the time to chew properly are more likely to suffer from choke.

Dry Food: Dry foods may cause choke, especially if the horse does not have free access to water, or if the horse has other risk factors linked to choking. While pelleted or cubed feeds in general fall in this category, horse owners sometimes express particular concerns about beet pulp. However, while horses have choked on beet pulp, a university study did not document that beet pulp is a particular problem. It is believed that choke related to beet pulp is linked to the particle size and the horse's aggressive feeding behaviour, rather than the actual feed itself. Research suggests that horses that bolt their feed without sufficient chewing, or who do not have adequate access to water, are far more likely to choke, regardless of the type of feed, compared to horses that eat at a more leisurely rate. The risk of choke associated with any dry feed can be reduced by soaking the ration prior to feeding.

Foreign Objects: Horse may ingest non-edible materials such as pieces of wood. Cribbers may be more prone to this type of choke, if they happen to swallow a piece of wood or other material while cribbing.

Choking horses should be deprived of food and drink pending veterinary attention, so as not to increase the obstructive load within the esophagus. The veterinarian will often sedate the horse and administer spasmolytics, such as butylscopolamine, to help the esophagus to relax. Once the muscles of the esophagus no longer force the food down the throat (active peristalsis), it may slip down on its own accord. If spasmolytics do not solve the problem, the veterinarian will usually pass a stomach tube through one of the nostrils and direct it into the esophagus until the material is reached, at which point "gentle" pressure is applied to manually push the material down. Gentle warm water lavage (water sent through the stomach tube, to soften the food material) may be required to help the obstructing matter pass more easily, but caution should be exercised to prevent further aspiration of fluid into the trachea.

Refractory cases are sometimes anesthetised, with an orotracheal tube placed to prevent further aspiration and to allow for more vigorous lavage. Disruption of the impacted material can sometimes be achieved via endoscopy. If these methods still do not lead to results, the horse may require surgery to remove the material.

Some workers have advocated the use of oxytocin in choke, on the grounds that it decreases the esophageal muscular tone. However, this technique is not suitable in pregnant mares, as it may lead to abortion.

Besides complications of surgery and anesthesia in general, there may be drainage, swelling, or redness of the incision, gagging or coughing during eating or drinking, or pneumonia due to aspiration of food or liquids. Undesirable complications are estimated to occur in 10-30% of cases. If medical therapy is unsuccessful and surgery cannot be performed due to concurrent disease (such as heart or lung problems) or cost, euthanasia may be necessary if the animal's quality of life is considered unacceptable due to the disease.

Mild cases are managed by limiting activity, keeping a healthy body weight, and avoiding exposure to high ambient temperatures. Mild sedatives can be used to decrease anxiety and panting and therefore improve respiration. Corticosteroids may also be administered in acute cases to decrease inflammation and edema of the larynx.

Severe acute symptoms, such as difficulty breathing, hyperthermia, or aspiration pneumonia, must be stabilized with sedatives and oxygen therapy and may require steroid or antibiotic medications. Sometimes a tracheotomy is required to allow delivery of oxygen. Once the patient is stabilized, surgical treatment may be beneficial especially when paralysis occurs in both aretynoid cartilages (bilateral paralysis). The surgery (aretynoid lateralization, or a "laryngeal tieback") consists of suturing one of the aretynoid cartilages in a maximally abducted (open) position. This reduces the signs associated with inadequate ventilation (such as exercise intolerance or overheating) but may exacerbate the risk of aspiration and consequent pneumonia. Tying back only one of the aretynoid cartilages instead of both helps reduce the risk of aspiration. Afterwards the dog will still sound hoarse, and will need to be managed in the same way as those with mild cases of LP.

Recent studies have found that many dogs with laryngeal paralysis have decreased motility of their esophagus. Animals with a history of regurgitation or vomiting should be fully evaluated for esophageal or other gastrointestinal disorders. Dogs with megaesophagus or other conditions causing frequent vomiting or regurgitation are at high risk for aspiration pneumonia after laryngeal tie-back. Permanent tracheostomy is an alternative surgical option for these dogs to palliate their clincical signs.

Some 25% to 40% of young children are reported to have feeding problems—mainly colic, vomiting, slow feeding, and refusal to eat. It has been reported that up to 80% of infants with developmental handicaps also demonstrate feeding problems while 1 to 2% of infants aged less than one year show severe food refusal and poor growth. Among infants born prematurely, 40% to 70% experience some form of feeding problem.

A feeding disorder in infancy or early childhood is a child's refusal to eat certain food groups, textures, solids or liquids for a period of at least one month, which causes the child to not gain enough weight, grow naturally, or cause any developmental delays. Feeding disorders resemble failure to thrive, except that at times in feeding disorder there is no medical or physiological condition that can explain the very small amount of food the children consume or their lack of growth. Some of the times a previous medical condition that has been resolved is causing the issue.

Around 75% of cases are caused by alcohol and tobacco use.

Tobacco smoke is one of the main risk factors for head and neck cancer and one of the most carcinogenic compounds in tobacco smoke is acrylonitrile. (See Tobacco smoking). Acrylonitrile appears to indirectly cause DNA damage by increasing oxidative stress, leading to increased levels of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and formamidopyrimidine in DNA (see image). Both 8-oxo-dG and formamidopyrimidine are mutagenic. DNA glycosylase NEIL1 prevents mutagenesis by 8-oxo-dG and removes formamidopyrimidines from DNA.

However, cigarette smokers have a lifetime increased risk for head and neck cancers that is 5- to 25-fold increased over the general population.

The ex-smoker's risk for squamous cell cancer of the head and neck begins to approach the risk in the general population twenty years after smoking cessation. The high prevalence of tobacco and alcohol use worldwide and the high association of these cancers with these substances makes them ideal targets for enhanced cancer prevention.

Smokeless tobacco is cause of oral and pharyngeal cancers (oropharyngeal cancer). Cigar smoking is an important risk factor for oral cancers as well.

Other environmental carcinogens suspected of being potential causes of head and neck cancer include occupational exposures such as nickel refining, exposure to textile fibers, and woodworking. Use of marijuana, especially while younger, is linked to an increase in squamous-cell carcinoma cases while other studies suggest use is not shown to be associated with oral squamous cell carcinoma, or associated with decreased squamous cell carcinoma.

Excessive consumption of processed meats and red meat were associated with increased rates of cancer of the head and neck in one study, while consumption of raw and cooked vegetables seemed to be protective.

Vitamin E was not found to prevent the development of leukoplakia, the white plaques that are the precursor for carcinomas of the mucosal surfaces, in adult smokers.

Another study examined a combination of Vitamin E and beta carotene in smokers with early-stage cancer of the oropharynx, and found a worse prognosis in the vitamin users.

Some herbaceous hosts naturally have the Cherry X Disease. Once the spreads to the cherry hosts, with the help of the mountain leafhoppers, the cherry leafhoppers can spread the disease around to other woody hosts. Here are some approaches at management with each host type:

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

Sleep paralysis is equally experienced in both males and females. Lifetime prevalence rates derived from 35 aggregated studies indicate that approximately 8% of the general population, 28% of students, and 32% of psychiatric patients experience at least one episode of sleep paralysis at some point in their lives. Rates of recurrent sleep paralysis are not as well known, but 15%-45% of those with a lifetime history of sleep paralysis may meet diagnostic criteria for Recurrent Isolated Sleep Paralysis. In surveys from Canada, China, England, Japan and Nigeria, 20% to 60% of individuals reported having experienced sleep paralysis at least once in their lifetime. In general, non-whites appear to experience sleep paralysis at higher rates than whites, but the magnitude of the difference is rather small. Approximately 36% of the general population that experiences isolated sleep paralysis is likely to develop it between 25 and 44 years of age.

Isolated sleep paralysis is commonly seen in patients that have been diagnosed with narcolepsy. Approximately 30–50% of people that have been diagnosed with narcolepsy have experienced sleep paralysis as an auxiliary symptom. A majority of the individuals who have experienced sleep paralysis have sporadic episodes that occur once a month to once a year. Only 3% of individuals experiencing sleep paralysis that is not associated with a neuromuscular disorder have nightly episodes.

Sleep paralysis could lead the individual to acquire conditioned fear of the experience ("worry attacks"), resulting in more nighttime awakening and fragmented sleep (because of nocturnal arousal and hyper-alertness to symptoms of paralysis), making the person more likely to have sleep paralysis in the future.

While moderate to severe traumatic brain injury is a risk for ALS, it is unclear if mild traumatic brain injury increases rates.

In 1994 the National Institute for Occupational Safety and Health (NIOSH) reported a nonsignificant increase in nervous system disorders due to four cases of ALS among National Football League (NFL) players. It was unclear if this was due to chance or not. Another study from 2012 also found a possible increase in ALS in NFL football players. An older study did not find an increased risk among high school football players. A 2007 review found an increased risk among soccer players. ALS may also occur more often among the US military veterans however the reason is unknown. This may be due to head injury.

After the 2012 report was released, some NFL players involved in the legal settlement with the NFL complained that the NFL, which initially agreed to pay $765 million, was not doing enough to help players. The judge in the case concurred, and the NFL then agreed to pay an unlimited amount of damages for players found to have ALS, Parkinson's disease, Alzheimer's disease and dementia.

Sleep paralysis is when, during awakening or falling asleep, one is aware but unable to move. During an episode, one may hear, feel, or see things that are not there. It often results in fear. Episodes generally last less than a couple of minutes. It may occur as a single episode or be recurrent.

The condition may occur in those who are otherwise healthy, those with narcolepsy, or may run in families as a result of specific genetic changes. The condition can be triggered by sleep deprivation, psychological stress, or abnormal sleep cycles. The underlying mechanism is believed to involve a dysfunction in REM sleep. Diagnosis is based on a person's description. Other conditions that can present similarly include narcolepsy, atonic seizure, and hypokalemic periodic paralysis.

Treatment options for sleep paralysis have been poorly studied. People should generally be reassured that the condition is common and not serious. Other efforts that may be tried include sleep hygiene, cognitive behavioral therapy, and antidepressants.

Between 8% and 50% of people experience sleep paralysis at some time. About 5% of people have regular episodes. Males and females are affected equally. Sleep paralysis has been described throughout history. It is believed to have played a role in the creation of stories about alien abduction and other paranormal events.

About 5–10% of cases are directly inherited from a person's parents. Overall, first-degree relatives of an individual with ALS have a 1% risk of developing ALS.

A defect on chromosome 21, which codes for superoxide dismutase, is associated with about 20% of familial cases of ALS, or about 2% of ALS cases overall. This mutation is believed to be transmitted in an autosomal dominant manner, and has over a hundred different forms of mutation. The most common ALS-causing mutation is a mutant "SOD1" gene, seen in North America; this is characterized by an exceptionally rapid progression from onset to death. The most common mutation found in Scandinavian countries, D90A-SOD1, is more slowly progressive than typical ALS, and people with this form of the disorder survive for an average of 11 years.

In 2011, a genetic abnormality known as a hexanucleotide repeat was found in a region called C9orf72, which is associated with ALS combined with frontotemporal dementia ALS-FTD, and accounts for some 6% of cases of ALS among white Europeans.

Alien hand syndrome (AHS) is a condition in which a person experiences their limbs acting seemingly on their own, without control over the actions. The term is used for a variety of clinical conditions and most commonly affects the left hand. There are many similar names used to describe the various forms of the condition but they are often used inappropriately. The afflicted person may sometimes reach for objects and manipulate them without wanting to do so, even to the point of having to use the controllable hand to restrain the alien hand. While under normal circumstances, thought, as intent, and action can be assumed to be deeply mutually entangled, the occurrence of alien hand syndrome can be usefully conceptualized as a phenomenon reflecting a functional "disentanglement" between thought and action.

Alien hand syndrome is best documented in cases where a person has had the two hemispheres of their brain surgically separated, a procedure sometimes used to relieve the symptoms of extreme cases of epilepsy and epileptic psychosis, e.g., temporal lobe epilepsy. It also occurs in some cases after brain surgery, stroke, infection, tumor, aneurysm, migraine and specific degenerative brain conditions such as Alzheimer's disease and Creutzfeldt–Jakob disease. Other areas of the brain that are associated with alien hand syndrome are the frontal, occipital, and parietal lobes.

"Alien behavior" can be distinguished from reflexive behavior in that the former is flexibly purposive while the latter is obligatory. Sometimes the sufferer will not be aware of what the alien hand is doing until it is brought to his or her attention, or until the hand does something that draws their attention to its behavior. There is a clear distinction between the behaviors of the two hands in which the affected hand is viewed as "wayward" and sometimes "disobedient" and generally out of the realm of their own voluntary control, while the unaffected hand is under normal volitional control. At times, particularly in patients who have sustained damage to the corpus callosum that connects the two cerebral hemispheres (see also split-brain), the hands appear to be acting in opposition to each other.

A related syndrome described by the French neurologist François Lhermitte involves the release through disinhibition of a tendency to compulsively utilize objects that present themselves in the surrounding environment around the patient. The behavior of the patient is, in a sense, obligatorily linked to the "affordances" (using terminology introduced by the American ecological psychologist, James J. Gibson) presented by objects that are located within the immediate peri-personal environment.

This condition, termed "utilization behavior", is most often associated with extensive bilateral frontal lobe damage and might actually be thought of as "bilateral" alien hand syndrome in which the patient is compulsively directed by external environmental contingencies (e.g. the presence of a hairbrush on the table in front of them elicits the act of brushing the hair) and has no capacity to "hold back" and inhibit pre-potent motor programs that are obligatorily linked to the presence of specific external objects in the peri-personal space of the patient. When the frontal lobe damage is bilateral and generally more extensive, the patient completely loses the ability to act in a self-directed manner and becomes totally dependent upon the surrounding environmental indicators to guide his behavior in a general social context, a condition referred to as "environmental dependency syndrome".

In order to deal with the alien hand, some patients engage in personification of the affected hand. Usually these names are negative in nature, from mild such as "cheeky" to malicious "monster from the moon". For example, Doody and Jankovic described a patient who named her alien hand "baby Joseph". When the hand engaged in playful, troublesome activities such as pinching her nipples (akin to biting while nursing), she would experience amusement and would instruct baby Joseph to "stop being naughty". Furthermore, Bogen suggested that certain personality characteristics, such as a flamboyant personality, contribute to frequent personification of the affected hand.

Neuroimaging and pathological research shows that the frontal lobe (in the frontal variant) and corpus callosum (in the callosal variant) are the most common anatomical lesions responsible for the alien hand syndrome. These areas are closely linked in terms of motor planning and its final pathways.

The callosal variant includes advanced willed motor acts by the non-dominant hand, where patients frequently exhibit "intermanual conflict" in which one hand acts at cross-purposes with the other "good hand". For example, one patient was observed putting a cigarette into her mouth with her intact, "controlled" hand (her right, dominant hand), following which her alien, non-dominant, left hand came up to grasp the cigarette, pull the cigarette out of her mouth, and toss it away before it could be lit by the controlled, dominant, right hand. The patient then surmised that "I guess 'he' doesn't want me to smoke that cigarette." Another patient was observed to be buttoning up her blouse with her controlled dominant hand while the alien non-dominant hand, at the same time, was unbuttoning her blouse. The frontal variant most often affects the dominant hand, but can affect either hand depending on the lateralization of the damage to medial frontal cortex, and includes grasp reflex, impulsive groping toward objects or/and tonic grasping (i.e. difficulty in releasing grip).

In most cases, classic alien-hand signs derive from damage to the medial frontal cortex, accompanying damage to the corpus callosum. In these patients the main cause of damage is unilateral or bilateral infarction of cortex in the territory supplied by the anterior cerebral artery or associated arteries. Oxygenated blood is supplied by the anterior cerebral artery to most medial portions of the frontal lobes and to the anterior two-thirds of the corpus callosum, and infarction may consequently result in damage to multiple adjacent locations in the brain in the supplied territory. As the medial frontal lobe damage is often linked to lesions of the corpus callosum, frontal variant cases may also present with callosal form signs. Cases of damage restricted to the callosum however, tend not to show frontal alien-hand signs.

According to a systematic review from 2014, prevalence rates of sexual addiction and related sexual disorders ranges from 3% to 6%.

Sexual addiction, also known as sex addiction, is a state characterized by [[compulsive]] participation or engagement in [[Human sexual activity|sexual activity]], particularly [[sexual intercourse]], despite negative consequences. Proponents of a [[diagnostic model]] for sexual addiction, as defined here, consider it to be one of several sex-related disorders within an umbrella concept known as [[hypersexual disorder]]. The term "sexual dependence" is also used to refer to people who report being unable to control their [[sexual urges]], behaviors, or thoughts. Related models of pathological sexual behavior include [[hypersexuality]] (nymphomania and satyriasis), [[erotomania]], [[Don Juanism]] (or Don Juanitaism), and [[paraphilia]]-related disorders.

The concept of sexual addiction is contentious. There is considerable debate amongst [[psychiatrists]], psychologists, [[sexologist]]s, and other specialists whether compulsive sexual behavior constitutes an addiction, and therefore its classification and possible diagnosis. , sexual addiction is not a clinical diagnosis in either the [[Diagnostic and Statistical Manual of Mental Disorders|DSM]] or [[International Statistical Classification of Diseases and Related Health Problems|ICD]] medical classifications of diseases and medical disorders. Some argue that applying such concepts to normal behaviors such as sex, can be problematic, and suggest that applying medical models such as addiction to human sexuality can serve to [[Slut-shaming|pathologise normal behavior]] and cause harm

Neuroscientists, pharmacologists, molecular biologists, and other researchers in related fields have identified the [[transcription factor|transcriptional]] and [[epigenetic]] mechanisms of addiction [[pathophysiology]]. Diagnostic models, which use the pharmacological model of addiction (this model associates addiction with drug-related concepts, particularly [[physical dependence]], [[drug withdrawal]], and [[drug tolerance]]), do not currently include diagnostic criteria to identify sexual addictions in a clinical setting. In the brain disease model of addiction, which uses neuropsychological concepts to characterize addictions, sexual addictions are identifiable and well-characterized. In this model, [[addictive drugs]] are characterized as those which are both [[reinforcing]] and [[reward system|rewarding]]. Addictive behaviors (those which can induce a compulsive state) are similarly identified and characterized by their rewarding and reinforcing properties.

In "Sexual Addiction and Compulsivity", authors Taylor and Francis argue that: "Obsessive sexual behavior illness is defined by a continual pattern of failure to control intense, repetitive sexual impulses or urges."