Irritable Bowel Syndrome (IBS),

Fibromyalgia (FMS),

Chronic Fatigue Syndrome (CFS),

Chronic Pelvic Pain (CPP),

Interstitial Cystitis (IC),

Temporomandibular Joint Pain (TMJ), Functional Neurological Symptom Disorder (FNsD),

Non-Cardiac Chest Pain (NCCP),

Post-Traumatic Stress Disorder (PTSD),

Dysuria (Pain On Urination),

and Multiple Chemical Sensitivity

Whether a given medical condition is termed a "functional disorder" depends in part on the state of knowledge. Some diseases, including epilepsy, schizophrenia, and migraine headaches were once considered functional disorders, but are no longer generally classified that way.

Fibrinogen disorders are set of hereditary or acquired abnormalities in the quantity and/or quality of circulating fibrinogens. The disorders may lead to pathological bleeding and/or blood clotting or the deposition of fibrinogen in the liver, kidneys, or other organs and tissues. These disorders include:

- Congenital afibrinogenemia, an inherited blood disorder in which blood does not clot normally due to the lack of fibrinogen; the disorder causes abnormal bleeding and thrombosis.

- Congenital hypofibrinogenemia, an inherited disorder in which blood may not clot normally due to reduced levels of fibrinogen; the disorder may cause abnormal bleeding and thrombosis.

- Fibringogen storage disease, a form of congenital hypofibrinogenemia in which specific hereditary mutations in fibrinogen cause it to accumulate in, and damage, liver cells. The disorder may lead to abnormal bleeding and thrombosis but also to cirrhosis.

- Congenital dysfibrinogenemia, an inherited disorder in which normal levels of fibrinogen composed at least in part of a dysfunctional fibrinogen may cause abnormal bleeding and thrombosis.

- Hereditary fibrinogen Aα-Chain amyloidosis, a form of dysfibrinogenemia in which certain fibrinogen mutations cause blood fibrinogen to accumulate in the kidney and cause one type of familial renal amyloidosis; the disorder is not associated with abnormal bleeding or thrombosis.

- Acquired dysfibrinogenemia, a disorder in which normal levels of fibrinogen are composed at least in part of a dysfunctional fibrinogen due to an acquired disorder (e.g. liver disease) that leads to the synthesis of an incorrectly glycosylated (i.e. wrong amount of sugar residues) added to an otherwise normal fibrinogen. The incorrectly glycosalated fibrinogen is dysfunctional and may cause pathological episodes of bleeding and/or blood clotting.

- Congenital hypodysfibrinogenemia, an inherited disorder in which low levels of fibrinogen composed at least in part of a dysfunctional fibrinogen may cause pathological episodes of bleeding or blood clotting.

- Cryofibrinogenemia, an acquired disorder in which fibrinogen precipitates at cold temperatures and may lead to the intravascular precipitation of fibrinogen, fibrin, and other circulating proteins thereby causing the infarction of various tissues and bodily extremities.

The mutated gene responsible for the disorder is the FGFR3 gene, more specifically; a Lys650Met missense mutation of the FGFR3 gene is what causes SADDAN. This gene codes for the instructions of a protein that is integral in the development and maintenance of bone and brain tissue. Mutations of this gene cause the protein to be overly active, causing many characteristics of this disorder.

SADDAN is an autosomal dominant genetic disorder. Autosomal means that the gene responsible for the mutation and disorder is found on a non-sex chromosome and that either the mother or father can pass on the gene, while dominant means that only one copy of the gene is required for the individual to have the disorder.

Fortunately the disorder is very rare and has only been described in a few number of cases worldwide. While the disorder can be genetically inherited, no instances of inheritance have been recorded as of yet. Rather, of the few cases documented, the individual affected by the disorder is affected as a product of a random mutation, also called a de novo mutation, of the FGFR3 gene only, not by inheritance of the mutated gene.

Opsismodysplasia is a type of skeletal dysplasia (a bone disease that interferes with bone development) first described by Zonana and associates in 1977, and designated under its current name by Maroteaux (1984). Derived from the Greek "opsismos" ("late"), the name "opsismodysplasia" describes a delay in bone maturation. In addition to this delay, the disorder is characterized by (short or undersized bones), particularly of the hands and feet, delay of ossification (bone cell formation), platyspondyly (flattened vertebrae), irregular metaphyses, an array of facial aberrations and respiratory distress related to chronic infection. Opsismodysplasia is congenital, being apparent at birth. It has a variable mortality, with some affected individuals living to adulthood. The disorder is rare, with an incidence of less than 1 per 1,000,000 worldwide. It is inherited in an autosomal recessive pattern, which means the defective (mutated) gene that causes the disorder is located on an autosome, and the disorder occurs when two copies of this defective gene are inherited. No specific gene has been found to be associated with the disorder. It is similar to spondylometaphyseal dysplasia, Sedaghatian type.

The prevalence of excoriation disorder is not well understood.

Estimates of prevalence of the condition range from 1.4 to 5.4% in the general population. One U.S. telephone survey found that 16.6% of respondents "picked their skin to the point of noticeable tissue damage" and that 1.4% would qualify as meeting the requirements of excoriation disorder. Another community survey found a rate of 5.4% had excoriation disorder. A survey of college students found a rate of 4%. One study found that among non-disabled adults, 63% of individuals engaged in some form of skin picking and 5.4% engaged in serious skin picking. Lastly, a survey of dermatology patients found that 2% suffered from excoriation disorder.

In some patients excoriation disorder begins with the onset of acne in adolescence, but the compulsion continues even after the acne has gone away. Skin conditions such as keratosis pilaris, psoriasis, and eczema can also provoke the behavior. In patients with acne, the grooming of the skin is disproportionate to the severity of the acne. Certain stressful events including marital conflicts, deaths of friends or family, and unwanted pregnancies have been linked to the onset of the condition. If excoriation disorder does not occur during adolescence another common age of onset is between the ages of 30 to 45. Additionally, many cases of excoriation disorder have been documented to begin in children under the age of 10. One small survey of patients with excoriation disorder found that 47.5% of them had an early onset of excoriation disorder that began before age 10. Traumatic childhood events may initiate the behavior.

Excoriation disorder is statistically more common in females than in males.

Excoriation disorder has a high rate of comorbidity with other psychiatric conditions, especially with mood and anxiety disorders . One survey of patients with excoriation disorder found that 56.7% also had a DSM-IV Axis-I disorder and 38% had alcohol- or drug-abuse problems. Studies have shown the following rates of psychiatric conditions found in patients with excoriation disorder: trichotillomania (38.3%), substance abuse (38%), major depressive disorder (approximately 31.7% to 58.1%), anxiety disorders (approximately 23% to 56%), obsessive-compulsive disorder (approximately 16.7% to 68%), and body dysmorphic disorder (approximately 26.8% to 44.9%). There are also higher rates of excoriation disorder in patients in psychiatric facilities; a study of adolescent psychiatric inpatients found that excoriation disorder was present in 11.8% of patients. It is also present at high rates with some other conditions: 44.9% of patients with body dysmorphic disorder also have excoriation disorder; 8.9% of patients with OCD have excoriation disorder; and 8.3% of patients with trichotillomania have excoriation disorder.

Skin picking is also common in those with certain developmental disabilities; for example, Prader–Willi syndrome and Smith–Magenis syndrome. Studies have shown that 85% of people with Prader–Willi syndrome also engage in skin-picking. Children with developmental disabilities are also at an increased risk for excoriation disorder.

Excoriation disorder also correlates with "social, occupational, and academic impairments, increased medical and mental health concerns (including anxiety, depression, obsessive–compulsive disorder) ... and financial burden". Excoriation disorder also has a high degree of comorbidity with occupational and marital difficulties.

Substance abuse is often present, and individuals with excoriation disorder are twice as likely to have first-degree relatives who have substance abuse disorders than those without the condition.

Some cases of body-focused repetitive behaviors also suggest a hereditary factor.

Severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN), is a very rare genetic disorder. This disorder is one that affects bone growth and is characterized by skeletal, brain, and skin abnormalities. Those affected by the disorder are severely short in height and commonly possess shorter arms and legs. In addition, the bones of the legs are often bowed and the affected have smaller chests with shorter rib bones, along with curved collarbones. Other symptoms of the disorder include broad fingers and extra folds of skin on the arms and legs. Developmentally, many individuals who suffer from the disorder show a higher level in delays and disability. Seizures are also common due to structural abnormalities of the brain. Those affected may also suffer with apnea, the slowing or loss of breath for short periods of time.

Many of the features of SADDAN are similar to those seen in other skeletal disorders, specifically achondroplasia and thanatophoric dysplasia.

Achondroplasia is a form of short-limbed dwarfism. This type of dwarfism is caused by the inability of the cartilage of the skeleton to ossify and turn to bone. Acanthosis nigricans is a skin condition in which areas of the skin is of a dark and velvety discoloration, often seen in the body folds and creases such as the armpits, groin, and neck. Within those affected by SADDAN, acanthosis nigricans develops early on, usually in infancy or early childhood.

Gillespie syndrome, also called aniridia, cerebellar ataxia and mental deficiency. is a rare genetic disorder. The disorder is characterized by partial aniridia (meaning that part of the iris is missing), ataxia (motor and coordination problems), and, in most cases, intellectual disability. It is heterogeneous, inherited in either an autosomal dominant or autosomal recessive manner. Gillespie syndrome was first described by American ophthalmologist Fredrick Gillespie in 1965.

Isobutyryl-coenzyme A dehydrogenase deficiency, commonly known as IBD deficiency, is a rare metabolic disorder in which the body is unable to process certain amino acids properly.

People with this disorder have inadequate levels of an enzyme that helps break down the amino acid valine, resulting in a buildup of valine in the urine, a symptom called valinuria.

Opsismodysplasia is inherited in an autosomal recessive manner. This means the defective gene(s) responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Currently, no specific mutation in any gene has been found to cause the disorder.

It appears that the gene inositol polyphosphate phosphatase-like 1 is the cause of this condition in at least some cases.

Giant axonal neuropathy is a rare, autosomal recessive neurological disorder that causes disorganization of neurofilaments. Neurofilaments form a structural framework that helps to define the shape and size of neurons and are essential for normal nerve function.

Babies with this disorder are usually healthy at birth. The signs and symptoms may not appear until later in infancy or childhood and can include poor feeding and growth (failure to thrive), a weakened and enlarged heart (dilated cardiomyopathy), seizures, and low numbers of red blood cells (anemia). Another feature of this disorder may be very low blood levels of carnitine (a natural substance that helps convert certain foods into energy).

Isobutyryl-CoA dehydrogenase deficiency may be worsened by long periods without food (fasting) or infections that increase the body's demand for energy. Some individuals with gene mutations that can cause isobutyryl-CoA dehydrogenase deficiency may never experience any signs and symptoms of the disorder.

Atelosteogenesis, type II is a severe disorder of cartilage and bone development. It is rare, and infants with the disorder are usually stillborn; however, those who survive birth die soon after

There have been many different theories regarding the causes of excoriation disorder including biological and environmental factors.

A common hypothesis is that excoriation disorder is often a coping mechanism to deal with elevated levels of turmoil, arousal or stress within the individual, and that the individual has an impaired stress response. A review of behavioral studies found support in this hypothesis in that skin-picking appears to be maintained by automatic reinforcement within the individual.

In contrast to neurological theories, there are some psychologists who believe that picking behavior can be a result of repressed rage felt toward authoritarian parents. A similar theory holds that overbearing parents can cause the behavior to develop in their children.

Autosomal recessive multiple epiphyseal dysplasia (ARMED), also called epiphyseal dysplasia, multiple, 4 (EDM4), multiple epiphyseal dysplasia with clubfoot or –with bilayered patellae, is an autosomal recessive congenital disorder affecting cartilage and bone development. The disorder has relatively mild signs and symptoms, including joint pain, scoliosis, and malformations of the hands, feet, and knees.

Some affected individuals are born with an inward- and downward-turning foot (a clubfoot). An abnormality of the kneecap called a double-layered patella is also relatively common. Although some people with recessive multiple epiphyseal dysplasia have short stature as adults, most are of normal height. The incidence is unknown as many cases are not diagnosed due to mild symptoms.

Atelosteogenesis, type 2 is one of a spectrum of skeletal disorders caused by mutations in the SLC26A2 gene. The protein made by this gene is essential for the normal development of cartilage and for its conversion to bone. Mutations in the SLC26A2 gene disrupt the structure of developing cartilage, preventing bones from forming properly and resulting in the skeletal problems characteristic of atelosteogenesis, type 2.

This condition is an autosomal recessive disorder, which means the defective gene is located on an autosome, and two copies of the gene—one from each parent—must be inherited for a child to be born with the disorder. The parents of a child with an autosomal recessive disorder are not affected by disorder, but are carriers of one copy of the altered gene.

At least once a week, 10-30% of those under 18 years of age suffer from unexplainable headaches and abdominal pains in the United States, and the number is rising. People from collectivistic countries such as Japan, China, and Mexico are more likely to suffer from pain disorder than individualistic countries such as the US and Sweden.

Brain MRI shows vermis atrophy or hypoplasic. Cerebral and cerebellar atrophy with white matter changes in some cases.

Mutations in the SLC26A2 (DTDST) gene, located at human chromosome 5q32-33.1, are the cause of ARMED. It is considered a milder disorder within a spectrum of skeletal disorders caused by mutations in the gene, which encodes a protein that is essential for the normal development of cartilage and its conversion to bone. Mutations in the SLC26A2 gene alter the structure of developing cartilage, preventing bones from forming properly and resulting in associated skeletal maldevelopment.

The disorder is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome (chromosome 5 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder.

Although not necessary for the diagnosis, individuals with intellectual disability are at higher risk for SMD. It is more common in boys, and can occur at any age.

Giant axonal neuropathy results from mutations in the "GAN" gene, which codes for the protein gigaxonin. This alters the shape of the protein, changing how it interacts with other proteins when organizing the structure of the neuron.

Neurons affected by the altered protein accumulate excess neurofilaments in the axon, the long extension from the nerve cell that transmits its signal to other nerve cells and to muscles. These enlarged or 'giant' axons cannot transmit signals properly, and eventually deteriorate, resulting in the range of neurological anomalies associated with the disorder.

This disease is an autosomal recessive disorder, which means the defective gene is located on an autosome, and both parents must have one copy of the defective gene in order to have a child born with the disorder. The parents of a child with an autosomal recessive disorder are carriers, but are usually not affected by the disorder.

Pain disorder is chronic pain experienced by a patient in one or more areas, and is thought to be caused by psychological stress. The pain is often so severe that it disables the patient from proper functioning. Duration may be as short as a few days or as long as many years. The disorder may begin at any age, and occurs more frequently in girls than boys. This disorder often occurs after an accident or during an illness that has caused pain, which then takes on a 'life' of its own.

Prognosis depends on the severity of the disorder. Recognizing symptoms early can help reduce the risk of self-injury, which can be lessened with meditations. Stereotypic movement disorder due to head trauma may be permanent.

Idiopathic generalized epilepsy (IGE) is a group of epileptic disorders that are believed to have a strong underlying genetic basis. Patients with an IGE subtype are typically otherwise normal and have no structural brain abnormalities. People also often have a family history of epilepsy and seem to have a genetically predisposed risk of seizures. IGE tends to manifest itself between early childhood and adolescence although it can be eventually diagnosed later. The genetic cause of some IGE types is known, though inheritance does not always follow a simple monogenic mechanism.

This form of epilepsy is very rare, representing less than 1% of cases, and is twice as prevalent in boys compared to girls. Age of seizure onset is between 5 months and 5 years of age. Children with this disorder often present with head drops and brief arm jerks. Although there is believed to be a genetic basis for this disorder, no genetic linkage has been shown.