A papulosquamous disorder is a condition which presents with both papules and scales, or both scaly papules and plaques.

Examples include psoriasis, lichen planus, and pityriasis rosea.

Pustular psoriasis appears as raised bumps filled with noninfectious pus (pustules). The skin under and surrounding the pustules is red and tender.

Seborrheic-like psoriasis is a common form of psoriasis with clinical aspects of psoriasis and seborrheic dermatitis, and it may be difficult to distinguish from the latter. This form of psoriasis typically manifests as red plaques with greasy scales in areas of higher sebum production such as the scalp, forehead, skin folds next to the nose, skin surrounding the mouth, skin on the chest above the sternum, and in skin folds.

The most common type of eruption is a morbilliform (resembling measles) or erythematous rash (approximately 90% of cases). Less commonly, the appearance may also be urticarial, papulosquamous, pustular, purpuric, bullous (with blisters) or lichenoid. Angioedema can also be drug-induced (most notably, by angiotensin converting enzyme inhibitors).

Some of the most severe and life-threatening examples of drug eruptions are erythema multiforme, Stevens–Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), hypersensitivity vasculitis, Drug induced hypersensitivity syndrome (DIHS), erythroderma and acute generalized exanthematous pustulosis (AGEP). These severe cutaneous drug eruptions are categorized as hypersensitivity reactions and are immune-mediated. There are four types of hypersensitivity reactions and many drugs can induce one or more hypersensitivity reactions.

Episodes of skin picking are often preceded or accompanied by tension, anxiety, or stress. In some cases, following picking, the affected person may feel depressed. During these moments, there is commonly a compulsive urge to pick, squeeze, or scratch at a surface or region of the body, often at the location of a perceived skin defect. When picking one may feel a sense of relief or satisfaction.

The region most commonly picked is the face, but other frequent locations include the arms, legs, back, gums, neck, shoulders, scalp, abdomen, chest, and extremities such as the fingernails, cuticles, and toenails. Most patients with excoriation disorder report having a primary area of the body that they focus their picking on, but they will often move to other areas of the body to allow their primary picking area to heal. Individuals with excoriation disorder vary in their picking behaviour; some do it briefly multiple times a day while others can do one picking session that can last for hours. The most common way to pick is to use the fingers although a significant minority of people use tools such as tweezers or needles.

Skin picking often occurs as a result of some other triggering cause. Some common triggers are feeling or examining irregularities on the skin and feeling anxious or other negative feelings.

Complications arising from excoriation disorder include: infection at the site of picking, tissue damage, and septicemia. Damage from picking can be so severe as to require skin grafting. Severe picking can cause epidermal abscesses. Severe cases of excoriation disorder can cause life-threatening injuries. For example, in one reported case a female picked a hole through the bridge of her nose, which required surgery to fix, and a 48-year-old female picked through the skin on her neck exposing the carotid artery. Pain in the neck or back can arise due to prolonged bent-over positions while engaging in the behavior. Besides physical injuries, excoriation disorder can cause severe physical scarring and disfigurement.

Excoriation disorder can cause feelings of intense helplessness, guilt, shame, and embarrassment in individuals, and this greatly increases the risk of self-harm. Studies have shown that excoriation disorder presented suicidal ideation in 12% of individuals with this condition, suicide attempts in 11.5% of individuals with this condition, and psychiatric hospitalizations in 15% of individuals with this condition.

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.

Typically, individuals with excoriation disorder find that the disorder interferes with daily life. Hindered by shame, embarrassment, and humiliation, they may take measures to hide their disorder by not leaving home, wearing long sleeves and pants even in heat, or covering visible damage to skin with cosmetics and/or bandages. Activities such as typing may be painful for those who pick at their fingers or hands, or walking for those who pick at the soles of their feet.

Infants born with this condition have very short arms and legs, a narrow chest, and a prominent, rounded abdomen. This disorder is also characterized by an opening in the roof of the mouth (cleft palate), distinctive facial features, an inward- and downward-turning foot (clubfoot), and unusually positioned thumbs (hitchhiker thumbs).

The signs and symptoms of atelosteogenesis, type 2, are similar to those of another skeletal disorder called diastrophic dysplasia. Atelosteogenesis, type 2 tends to be more severe, however.

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

Opsismodysplasia can be characterized by a delay in bone maturation, which refers to "bone aging", an expected sequence of developmental changes in the skeleton corresponding to the chronological age of a person. Factors such as gender and ethnicity also play a role in bone age assessment. The only indicator of physical development that can be applied from birth through mature adulthood is bone age. Specifically, the age and maturity of bone can be determined by its state of ossification, the age-related process whereby certain cartilaginous and soft tissue structures are transformed into bone. The condition of epiphyseal plates (growth plates) at the ends of the long bones (which includes those of the arms, hands, legs and feet) is another measurement of bone age. The evaluation of both ossification and the state of growth plates in children is often reached through radiography (X-rays) of the carpals (bones of the hand and wrist). In opsismodysplasia, the process of ossification in long bones can be disrupted by a failure of ossification centers (a center of organization in long bones, where cartilage cells designated to await and undergo ossification gather and align in rows) to form. This was observed in a 16-month-old boy with the disorder, who had no apparent ossification centers in the carpals (bones of the hand and wrist) or tarsals (bones of the foot). This was associated with an absence of ossification in these bones, as well as disfigurement of the hands and feet at age two. The boy also had no ossification occurring in the lower femur (thigh bone) and upper tibia (the shin bone).

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.

Medical diagnosis is required. Clinical tests can be performed, as well as molecular genetic testing. The available tests include:

Sequence analysis of the entire coding region

- Severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN) - Sanger Sequencing: Diagnosis, Mutation Confirmation, Pre-symptomatic, Risk Assessment, Screening

- Craniosynostosis: Diagnosis

- Invitae FGFR3-Related Disorders Test: Pre-symptomatic, Diagnosis, Therapeutic management

Mutation scanning of select exons

- Skeletal Dysplasia Panel: Diagnosis, Prognostic

Sequence analysis of select exons

- Severe Achondroplasia with Developmental Delay and Acanthosis Nigricans (SADDAN, FGFR3): Diagnosis, Mutation Confirmation, Risk Assessment

- Severe Achondroplasia, Developmental Delay, Acanthosis Nigricans: Diagnosis, Mutation Confirmation

Deletion/duplication analysis

- Invitae FGFR3-Related Disorders Test: Pre-symptomatic, Diagnosis, Therapeutic management

Life with SADDAN is manageable, although therapy, surgery, and lifelong doctor surveillance may be required.

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

The combination of muscular hypotonia and fixed dilated pupils in infancy is suspicious of Gillespie syndrome. Early onset partial aniridia, cerebellar ataxia, and mental retardation are hallmark of syndrome. The iris abnormality is specific and seems pathognomonic of Gillespie syndrome. The aniridia consisting of a superior coloboma and inferior iris hypoplasia, foveomacular dysplasia.

Atypical Gillespie syndrome associated with bilateral ptosis, exotropia, correctopia, iris hypoplasia, anterior capsular lens opacities, foveal hypoplasia, retinal vascular tortuosity, and retinal hypopigmentation.

Neurological signs ar nystagmus, mild craniofacial asymmetry, axial hypotonia, developmental delay, and mild mental retardation. Mariën P did not support the prevailing view of a global mental retardation as a cardinal feature of Gillespie syndrome but primarily reflect cerebellar induced neurobehavioral dysfunctions following disruption of the cerebrocerebellar anatomical circuitry that closely resembles the "cerebellar cognitive and affective syndrome" (CeCAS).

Congenital pulmonary stenosis and helix dysplasia can be associated.

Giant axonal neuropathy usually appears in infancy or early childhood, and is progressive. Early signs of the disorder often present in the peripheral nervous system, causing individuals with this disorder to have problems walking. Later, normal sensation, coordination, strength, and reflexes become affected. Hearing or vision problems may also occur. Abnormally kinky hair is characteristic of giant axonal neuropathy, appearing in almost all cases. As the disorder progresses, central nervous system becomes involved, which may cause a gradual decline in mental function, loss of control of body movement, and seizures.

Tics should be distinguished from other causes of tourettism, stereotypies, chorea, dyskinesias, myoclonus, and obsessive-compulsive disorder.

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.

Because these are frequently found in cases of autistic disorders, criteria could be met for multiple neurological disorders, or cause severe symptoms.

Some examples include:

1. Learning difficulties symptoms such as dyslexia, dysgraphia, dyscalcula, NVLD, slow learning, poor memory, etc.

2. AD/HD symptoms such as poor concentration, poor decision making, poor judgement, impulsiveness, difficulty sitting still, etc.

3. Synesthesia.

4. Neurological sleep disorders such as narcolepsy, insomnia, circadian rhythm disorder, etc.

5. Conditions affecting perceptions and/or cognition, such as agnosia, aphasia, etc.

6. Tourette syndrome or Tic disorder.

7. Epilepsy or Seizure disorder.

8. Parkinsonian syndrome features such as tremors, stiff movements, etc.

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.

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.

The current diagnostic criteria for MCDD are a matter of debate due to it not being in the DSM-IV or ICD-10. Various websites contain various diagnostic criteria. At least three of the following categories should be present. Co-occurring clusters of symptoms must also not be better explained by being symptoms of another disorder such as experiencing mood swings due to autism, cognitive difficulties due to schizophrenia, and so on. The exact diagnostic criteria for MCDD remain unclear but may be a useful diagnosis for people who do not fall into any specific category. It could also be argued that MCDD is a vague and unhelpful term for these patients.

Other conditions which feature repetitive behaviors in the differential diagnosis include autism spectrum disorders, obsessive–compulsive disorder, tic disorders (e.g., Tourette syndrome), and other conditions including dyskinesias.

Stereotypic movement disorder is often misdiagnosed as tics or Tourette syndrome (TS). Unlike the tics of TS, which tend to appear around age six or seven, repetitive movements typically start before age three, are more bilateral than tics, and consist of intense patterns of movement for longer runs than tics. Tics are less likely to be stimulated by excitement. Children with stereotypic movement disorder do not always report being bothered by the movements as a child with tics might.

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.

The fifth revision of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-5), published in May 2013, classifies Tourette's and tic disorders as motor disorders listed in the neurodevelopmental disorder category.

Tic disorders, in order of severity, are:

- 307.20 Other specified tic disorder (specify reason)

- 307.20 Unspecified tic disorder

- 307.21 Provisional tic disorder

- 307.22 Persistent (chronic) motor or vocal tic disorder (specify motor or vocal)

- 307.23 Tourette's disorder