Motivational deficiency disorder is the name of a fake disease imagined for a health campaign to raise awareness of disease mongering.

Aboulia has been known to clinicians since 1838. However, in the time since its inception, the definition of aboulia has been subjected to many different forms, some contradictory. Aboulia has been described as a loss of drive, expression, loss of behavior and speech output, slowing and prolonged speech latency, and reduction of spontaneous thought content and initiative. The clinical features most commonly associated with aboulia are:

- Difficulty in initiating and sustaining purposeful movements

- Lack of spontaneous movement

- Reduced spontaneous speech

- Increased response-time to queries

- Passivity

- Reduced emotional responsiveness and spontaneity

- Reduced social interactions

- Reduced interest in usual pastimes

Especially in patients with progressive dementia, it may affect feeding. Patients may continue to chew or hold food in their mouths for hours without swallowing it. The behavior may be most evident after these patients have eaten part of their meals and no longer have strong appetites.

Aboulia or abulia (from , meaning "will", with the prefix -a), in neurology, refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM). Aboulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than aboulia. A patient with aboulia is unable to act or make decisions independently. It may range in severity from subtle to overwhelming. It is also known as Blocq's disease (which also refers to abasia and astasia-abasia). Aboulia was originally considered to be a disorder of the will.

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Disease mongering is a term for the practice of widening the diagnostic boundaries of illnesses and aggressively promoting their public awareness in order to expand the markets for treatment.

Among the entities benefiting from selling and delivering treatments are pharmaceutical companies, physicians, alternative practitioners and other professional or consumer organizations. It is distinct from the promulgation of bogus or unrecognised diagnoses.

The term “monger” has ancient roots, providing the basis for many common compound forms such as cheesemonger, fishmonger, and fleshmonger for those who peddle such wares respectively. “Disease mongering” as a label for the "invention" or promotion of diseases in order to capitalize on their treatment was first used in 1992 by health writer Lynn Payer, who applied it to the Listerine mouthwash campaign against halitosis (bad breath).

Payer defined disease mongering as a set of practices which include the following:

- Stating that normal human experiences are abnormal and in need of treatment

- Claiming to recognize suffering which is not present

- Defining a disease such that a large number of people have it

- Defining a disease's cause as some ambiguous deficiency or hormonal imbalance

- Associating a disease with a public relations spin campaign

- Directing the framing of public discussion of a disease

- Intentionally misusing statistics to exaggerate treatment benefits

- Setting a dubious clinical endpoint in research

- Advertising a treatment as without side effect

- Advertising a common symptom as a serious disease

The incidence of conditions not previously defined as illness being medicalised as "diseases" is difficult to scientifically assess due to the inherent social and political nature of the definition of what constitutes a disease, and what aspects of the human condition should be managed according to a medical model. For example, halitosis, the condition which prompted Payer to coin the phrase "disease mongering", isn't merely an imagined social stigma but can stem from any of a wide spectrum of conditions spanning from bacterial infection of the gums to kidney failure, and is recognized by the Scientific Council of the American Dental Association as "a recognizable condition which deserves professional attention".

This disorder usually appears in the first few months of life, when development of new motor and cognitive skills becomes delayed or stops. Eventually, affected children may lose previously acquired skills such as head control or the ability to sit unsupported.

This disorder causes neurological problems, including mental retardation, brain atrophy and ventricular dilation, myoclonus, hypotonia, and epilepsy.

It is also associated with growth retardation, megaloblastic anemia, pectus excavatum, scoliosis, vomiting, diarrhea, and hepatosplenomegaly.

Disorder of written expression is a type of learning disability in which a person’s writing ability falls substantially below normally expected range based on the individual’s age, educational background, and measured intelligence. Poor writing skills must interfere significantly with academic progress or daily activities that involves written expression (spelling, grammar, handwriting, punctuation, word usage, etc.). This disorder is also generally concurrent with disorders of reading and/or mathematics, as well as disorders related to behavior. Since it is so often associated with other learning disorders and mental problems, it is uncertain whether it can appear by itself. The prevalence of disorder of written expression is estimated to be of a similar frequency to other learning disorders, between 3 - 5%. A diagnosis can be made based on results of several assessments.

Genes are attributed about a third of general anxiety disorder's variance. Individuals with a genetic predisposition for GAD are more likely to develop GAD, especially in response to a life stressor.

Specific causes of this disorder are unknown. The interaction of physical, psychological, and environmental factors is thought to contribute to the disorder of written expression. In neuropsychological and neurobiological research, some studies show evidence that abnormally high testosterone levels and abnormalities in cognitive processes (visual-motor, linguistic, attentional, and memory) are thought to play a role in learning disorder cases. The impact of brain injuries in both children and adults can impair any of these cognitive processes.

Generalized anxiety disorder (GAD) is an anxiety disorder characterized by excessive, uncontrollable and often irrational worry, that is, apprehensive expectation about events or activities. This excessive worry often interferes with daily functioning, as individuals with GAD typically anticipate disaster, and are overly concerned about everyday matters such as health issues, money, death, family problems, friendship problems, interpersonal relationship problems, or work difficulties. Individuals may exhibit a variety of physical symptoms, including feeling tired, fidgeting, headaches, numbness in hands and feet, muscle tension, difficulty swallowing, upset stomach, vomiting, diarrhea, breathing difficulty, difficulty concentrating, trembling, irritability, sweating, restlessness, sleeping difficulties, hot flashes, rashes, and inability to fully control the anxiety (ICD-10). These symptoms must be consistent and ongoing, persisting at least six months, for a formal diagnosis of GAD.

Standardized rating scales such as GAD-7 can be used to assess severity of GAD symptoms. GAD is the most common cause of disability in the workplace in the United States.

In a given year, approximately two percent of American adults and European adults experience GAD. Globally about 4% are affected at some point in their life. GAD is seen in women twice as much as men. GAD is also common in individuals with a history of substance abuse and a family history of the disorder. Once GAD develops, it may become chronic, but can be managed or eliminated with proper treatment.

In addition to the symptoms associated with immunodeficiency, such as depletion of T-cells, decline of lymphocyte activity, and an abrupt proliferation of both benign and opportunistic infections — PNP-deficiency is often characterized by the development of autoimmune disorders. lupus erythematosus, autoimmune hemolytic anemia, and idiopathic thrombocytopenic purpura have been reported with PNP-deficiency.

Neurological symptoms, such as developmental decline, hypotonia, and mental retardation have also been reported.

Research by governments in Australia led to a universal definition for that country which appears to be the only research-based definition not to use diagnostic criteria: "Problem gambling is characterized by many difficulties in limiting money and/or time spent on gambling which leads to adverse consequences for the gambler, others, or for the community." The University of Maryland Medical Center defines pathological gambling as "being unable to resist impulses to gamble, which can lead to severe personal or social consequences".

Most other definitions of problem gambling can usually be simplified to any gambling that causes harm to the gambler or someone else in any way; however, these definitions are usually coupled with descriptions of the type of harm or the use of diagnostic criteria. The "DSM-V" has since reclassified pathological gambling as "gambling disorder" and has listed the disorder under substance-related and addictive disorders rather than impulse-control disorders. This is due to the symptomatology of the disorder resembling an addiction not dissimilar to that of substance-abuse. There are both environmental and genetic factors that can influence on gambler and cause some type of addiction. In order to be diagnosed, an individual must have at least four of the following symptoms in a 12-month period:

- Needs to gamble with increasing amounts of money in order to achieve the desired excitement

- Is restless or irritable when attempting to cut down or stop gambling

- Has made repeated unsuccessful efforts to control, cut back, or stop gambling

- Is often preoccupied with gambling (e.g., having persistent thoughts of reliving past gambling experiences, handicapping or planning the next venture, thinking of ways to get money with which to gamble)

- Often gambles when feeling distressed (e.g., helpless, guilty, anxious, depressed)

- After losing money gambling, often returns another day to get even ("chasing" one's losses)

- Lies to conceal the extent of involvement with gambling

- Has jeopardized or lost a significant relationship, job, education or career opportunity because of gambling

- Relies on others to provide money to relieve desperate financial situations caused by gambling

The symptoms of SSADH deficiency fall into three primary categories: neurological, psychiatric, and ocular. The most constant features seen are developmental delay, hypotonia and intellectual disability. Nearly half of patients seen manifest ataxia, behavior problems, seizures, and hyporeflexia.

The age of onset ranges from newborn period to 25 years. Problems unique to neonates can include prematurity, lethargy, decreased sucking, respiratory difficulty and hypoglycemia. Gastrointestinal symptoms have been seen primarily in this

population and are usually related to increased feeding.

Ocular problems related to the disorder include strabismus, nystagmus, retinitis, disc pallor, and oculomotor apraxia.

Over half of the patients with SSADH deficiency have seizures. These include absence, tonic clonic, and convulsive status epilepticus. It is unclear whether decreased levels of GABA or elevated levels of GHB are responsible for these seizures but alterations in these neurotransmitters and their receptor binding or neurotransmitter transport is hypothesized to play a role in the pathogenesis of the seizures in this population.

Symptoms associated with SSADH may be mild, moderate or severe and often vary greatly from case to case. The symptoms of SSADH are caused by the accumulation of GHB in the brain and include the following manifestations (Defined as: common, > 70% of patients; frequent 30-70% of patients;unusual, < 30% of patients):

Common manifestations include:

- Delayed gross motor development

- Delayed mental development

- Delayed fine motor skill development

- Delayed speech and language development

- Hypotonia

Frequent manifestations include:

- Seizures

- Hyporeflexia

- Ataxia

- Behavioral problems

- Hyperkinesis

Unusual manifestations include:

- Neonatal problems

- EEG abnormalities

- Psychoses

- MRI or X-ray computed tomography abnormalities

- Oculomotor apraxia

- Microcephaly

- Macrocephaly

- Hyperreflexia

- Somnolence

- Choreoathetosis

- Myopathy

Symptoms of this disorder commonly appear between one and two years of age. Symptoms include mildly coarsened facial features, deafness, ichthyosis and an enlarged liver and spleen (hepatosplenomegaly). Abnormalities of the skeleton, such as a curving of the spine and breast bone may occur. The skin of individuals afflicted with this disorder, is typically dry. Children affected by this disorder develop more slowly than normal and may display delayed speech and walking skills.

The disease is fatal, with symptoms that include neurological damage and severe mental retardation. These sulfatase enzymes are responsible for breaking down and recycling complex sulfate-containing sugars from lipids and mucopolysaccharides within the lysosome. The accumulation of lipids and mucopolysaccharides inside the lysosome results in symptoms associated with this disorder. Worldwide, forty cases of Multiple Sulfatase Deficiency have been reported to date.

Psychological dependence is a form of dependence that involves emotional–motivational withdrawal symptoms (e.g., a state of unease or dissatisfaction, a reduced capacity to experience pleasure, or anxiety) upon cessation of drug use or engagement in certain behaviors. Physical and psychological dependence are sometimes classified as a facet or component of addiction, such as in the DSM-IV-TR; however, some drugs which produce dependence syndromes do not produce addiction, and vice versa, in humans. Addiction and psychological dependence are both mediated through reinforcement, a form of operant conditioning, but are associated with different forms of reinforcement. Addiction is a compulsion for rewarding stimuli that is mediated through positive reinforcement. Psychological dependence, which is mediated through negative reinforcement, involves a desire to use a drug or perform a behavior to avoid the unpleasant withdrawal syndrome that results from cessation of exposure to it.

Psychological dependence develops through consistent and frequent exposure to a stimulus. Behaviors which can produce observable psychological withdrawal symptoms (i.e., cause psychological dependence) include physical exercise, shopping, sex and self-stimulation using pornography, and eating food with high sugar or fat content, among others. Behavioral therapy is typically employed to help individuals overcome psychological dependence upon drugs or maladaptive behaviors that produce psychological dependence.

The oculogyric crises usually occur in the later half of the day and during these episodes patients undergo extreme agitation and irritability along with uncontrolled head and neck movements. Apart from the aforementioned symptoms, patients can also display Parkinsonism, sleep disturbances, small head size (microcephaly), behavioral abnormalities, weakness, drooling, and gastrointestinal symptoms.

Guanidinoacetate methyltransferase deficiency, also called GAMT deficiency, is an autosomal recessive metabolic disorder that primarily affects the nervous system and muscles. It is the first observed disorder of creatine metabolism.

Problem gambling (or ludomania, but usually referred to as "gambling addiction" or "compulsive gambling") is an urge to gamble continuously despite harmful negative consequences or a desire to stop. Problem gambling is often defined by whether harm is experienced by the gambler or others, rather than by the gambler's behaviour. Severe problem gambling may be diagnosed as clinical pathological gambling if the gambler meets certain criteria. Pathological gambling is a common disorder that is associated with both social and family costs.

The "DSM-5" has re-classified the condition as an addictive disorder, with sufferers exhibiting many similarities to those who have substance addictions.

The term "gambling addiction" has long been used in the recovery movement. Pathological gambling was long considered by the American Psychiatric Association to be an impulse control disorder rather than an addiction. However, data suggest a closer relationship between pathological gambling and substance use disorders than exists between PG and obsessive-compulsive disorder, largely because the behaviors in problem gambling and most primary substance use disorders ("i.e.", those not resulting from a desire to "self-medicate" for another condition such as depression) seek to activate the brain's reward mechanisms while the behaviors characterizing obsessive-compulsive disorder are prompted by overactive and misplaced signals from the brain's fear mechanisms.

Problem gambling is an addictive behavior with a high comorbidity with alcohol problems. Comorbidity is the presence of one or more diseases or disorders co-occurring with each other. A common feature shared by people who suffer from gambling addiction is impulsivity.

Symptoms may differ greatly, as apparently modifiers control to some degree the amount of FX that is produced. Some affected individuals have few or no symptoms while others may experience life-threatening bleeding. Typically this bleeding disorder manifests itself as a tendency to easy bruising, nose bleeding, heavy and prolonged menstruation and bleeding during pregnancy and childbirth, and excessive bleeding after dental or surgical interventions. Newborns may bleed in the head, from the umbilicus, or excessively after circumcision. Other bleeding can be encountered in muscles or joints, brain, gut, or urine

While in congenital disease symptoms may be present at birth or show up later, in patients with acquired FX deficiency symptoms typically show up in later life.

Infants with this disorder appear normal at birth but usually develop signs and symptoms during the first year of life or in early childhood. The characteristic features of this condition, which can range from mild to life-threatening, include feeding difficulties, recurrent episodes of vomiting and diarrhea, excessive tiredness (lethargy), and weak muscle tone (hypotonia). If untreated, this disorder can lead to delayed development, seizures, and coma. Early detection and lifelong management (following a low-protein diet and using appropriate supplements) may prevent many of these complications. In some cases, people with gene mutations that cause 3-methylcrotonyl-CoA carboxylase deficiency never experience any signs or symptoms of the disorder.

The characteristic features of this condition are similar to those of Reye syndrome, a severe disorder that develops in children while they appear to be recovering from viral infections such as chicken pox or flu. Most cases of Reye syndrome are associated with the use of aspirin during these viral infections.

Presenting in infancy, symptoms include lack of appetite, vomiting, dehydration, hypotonia and failure to thrive.

Sepiapterin reductase deficiency is an inherited pediatric disorder characterized by movement problems, and most commonly displayed as a pattern of involuntary sustained muscle contractions known as dystonia. Symptoms are usually present within the first year of age, but diagnosis is delayed due to physicians lack of awareness and the specialized diagnostic procedures. Individuals with this disorder also have delayed motor skills development including sitting, crawling, and need assistance when walking. Additional symptoms of this disorder include intellectual disability, excessive sleeping, mood swings, and an abnormally small head size. SR deficiency is a very rare condition. The first case was diagnosed in 2001, and since then there have been approximately 30 reported cases. At this time, the condition seems to be treatable, but due to a lack of overall awareness and a series of atypical procedures used to diagnose this condition pose a dilemma.

Succinic semialdehyde dehydrogenase deficiency (SSADHD), also known as 4-hydroxybutyric aciduria or gamma-hydroxybutyric aciduria, is a rare autosomal recessive disorder of the degradation pathway of the inhibitory neurotransmitter γ-aminobutyric acid, or GABA. The disorder has been identified in approximately 350 families, with a significant proportion being consanguineous families. The first case was identified in 1981 and published in a Dutch clinical chemistry journal that highlighted a person with a number of neurological conditions such as delayed intellectual, motor, speech, and language as the most common manifestations. Later cases reported in the early 1990s began to show that hypotonia, hyporeflexia, seizures, and a nonprogressive ataxia were frequent clinical features as well.

SSADH deficiency is caused by an enzyme deficiency in GABA degradation. Under normal conditions, SSADH works with the enzyme GABA transaminase to convert GABA to succinic acid. Succinic acid can then be utilized for energy production via the Krebs cycle. However, because of the deficiency, the final intermediate of the GABA degradation pathway, succinic semialdehyde, accumulates and cannot be oxidized to succinic acid and is therefore reduced to gamma-hydroxybutyric acid (GHB) by gamma-hydroxybutyric dehydrogenase. This causes elevations in GHB and is believed to be the trademark of this disorder and cause for the neurological manifestations seen.

The main symptoms of ADA deficiency are pneumonia, chronic diarrhea, and widespread skin rashes. Affected children also grow much more slowly than healthy children and some have developmental delay. Most individuals with ADA deficiency are diagnosed with SCID in the first 6 months of life.