The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown.

Avellis syndrome is a neurological disorder characterized by a peculiar form of alternating paralysis. There is paralysis of the soft palate and vocal cords on one side and loss of pain sensation and temperature sense on the other side, including the extremities, trunk, and neck. It usually results from occlusion of the vertebral artery in lesions of the nucleus ambiguous and pyramidal tract. Horner's syndrome may be associated. In the original description, the vagus and glossopharyngeal nerves were involved; concomitant involvement of the neighbouring cranial nerves was observed later.

Möbius syndrome results from the underdevelopment of the VI and VII cranial nerves. The VI cranial nerve controls lateral eye movement, and the VII cranial nerve controls facial expression.

The causes of Möbius syndrome are poorly understood. Möbius syndrome is thought to result from a vascular disruption (temporary loss of bloodflow) in the brain during prenatal development. There could be many reasons that a vascular disruption leading to Möbius syndrome might occur. Most cases do not appear to be genetic. However, genetic links have been found in a few families. Some maternal trauma may result in impaired or interrupted blood flow (ischemia) or lack of oxygen (hypoxia) to a developing fetus. Some cases are associated with reciprocal translocation between chromosomes or maternal illness. In the majority of cases of Möbius syndrome in which autosomal dominant inheritance is suspected, sixth and seventh cranial nerve paralysis (palsy) occurs without associated limb abnormalities.

The use of drugs and a traumatic pregnancy may also be linked to the development of Möbius syndrome. The use of the drugs misoprostol or thalidomide by women during pregnancy has been linked to the development of Möbius syndrome in some cases. Misoprostol is used to induce abortions in Brazil and Argentina as well as in the United States. Misoprostol abortions are successful 90% of the time, meaning that 10% of the time the pregnancy continues. Studies show that the use of misoprostal during pregnancy increases the risk of developing Möbius syndrome by a factor of 30. While this is a dramatic increase in risk, the incidence of Möbius syndrome without misoprostal use is estimated at one in 50000 to 100000 births (making the incidence of Möbius syndrome with misoprostol use, less than one in 1000 births). The use of cocaine (which also has vascular effects) has been implicated in Möbius syndrome.

Some researchers have suggested that the underlying problem of this disorder could be congenital hypoplasia or agenesis of the cranial nerve nuclei. Certain symptoms associated with Möbius syndrome may be caused by incomplete development of facial nerves, other cranial nerves, and other parts of the central nervous system.

Harlequin syndrome is not debilitating so treatment is not normally necessary. In cases where the individual may feel socially embarrassed, contralateral sympathectomy may be considered, although compensatory flushing and sweating of other parts of the body may occur. In contralateral sympathectomy, the nerve bundles that cause the flushing in the face are interrupted. This procedure causes both sides of the face to no longer flush or sweat. Since symptoms of Harlequin syndrome do not typically impair a person’s daily life, this treatment is only recommended if a person is very uncomfortable with the flushing and sweating associated with the syndrome.

One possible cause of Harlequin syndrome is a lesion to the preganglionic or postganglionic cervical sympathetic fibers and parasympathetic neurons of the ciliary ganglion. It is also believed that torsion (twisting) of the thoracic spine can cause blockage of the anterior radicular artery leading to Harlequin syndrome. The sympathetic deficit on the denervated side causes the flushing of the opposite side to appear more pronounced. It is unclear whether or not the response of the undamaged side was normal or excessive, but it is believed that it could be a result of the body attempting to compensate for the damaged side and maintain homeostasis.

Since the cause and mechanism of Harlequin syndrome is still unknown, there is no way to prevent this syndrome.

Foix–Alajouanine syndrome is a disorder caused by an arteriovenous malformation of the spinal cord. The patients present with symptoms indicating spinal cord involvement (paralysis of arms and legs, numbness and loss of sensation and sphincter dysfunction), and pathological examination reveals disseminated nerve cell death in the spinal cord and abnormally dilated and tortuous vessels situated on the surface of the spinal cord. Surgical treatment can be tried in some cases. If surgical intervention is contraindicated, corticosteroids may be used.

The condition is named after Charles Foix and Théophile Alajouanine.

BPES is very rare: only 50-100 cases have been described. It affects slightly more males than females.

Smoking is the number one cause of Reinke's edema. Other factors include gastroesophageal reflux, hypothyroidism and chronic overuse of the voice. Smoking is the only risk factor that may lead to cancer. Additionally, the combination of several risk factors increase the likelihood of an individual developing Reinke's edema. For example, an individual who smokes and also has gastric reflux would have an increased susceptibility for developing Reinke's edema over time.

Reinke's edema is commonly diagnosed in middle-aged females with a history of smoking (aged 50 years or older). Because males have lower pitched voices than females, males are less likely to observe a significant changes in the voice, and are therefore less likely to seek treatment. Females also report more physical discomfort due to Reinke's edema. The risk of Reinke's edema increases with age and also with prolonged exposure to smoking. Additionally, individuals in professions that require constant use of the voice, such as singers, teachers, and radio hosts, may be at an increased risk for developing the disease.

Because the disease is heavily linked to smoking, there is no established way to screen for Reinke's edema. Similarly, the only way to prevent Reinke's edema is to avoid smoking. By adopting a non-smoking lifestyle after being diagnosed with Reinke's edema, it is possible to stop the disease's progression, although it is not possible to reverse it. Therefore, it is critical to maintain a non-smoking lifestyle even after surgery, because the fluid can re-emerge. In fact, in many cases surgeons will not perform surgery without the guarantee that the individual will stop smoking.

Seaver Cassidy syndrome is a very rare disorder characterized by certain facial, genital, and skeletal deformities, as well as an unusual susceptibility to bleeding. Seaver Cassidy syndrome was first described in 1991 by Laurie Seaver and Suzanne Cassidy.

Cobb syndrome is a rare congenital disorder characterized by visible skin lesions with underlying spinal angiomas or arteriovenous malformations (AVMs). The skin lesions of Cobb syndrome typically are present as port wine stains or angiomas, but reports exist of angiokeratomas, angiolipomas, and lymphangioma circumscriptum. The intraspinal lesions may be angiomas or AVMs and occur at levels of the spinal cord corresponding to the affected skin dermatomes. They may in turn produce spinal cord dysfunction and weakness or paralysis.

The disorder was first described by Berenbruch in 1890, but became widely known only after Cobb's report in 1915. Cobb syndrome is thought to be more common in males and have no racial predilection, but only a few dozen cases are known. It is believed to be due to a sporadic mutation, since parents of affected children usually have no evidence of the disease.

Somatic mutations in the PIK3CA have been identified as a cause of CLOVES syndrome. PIK3CA is a protein involved in the PI3K-AKT signalling pathway. Mutations in other parts of this pathway cause other overgrowth syndromes including proteus syndrome and hemimegaencephaly.

Signs of Seaver Cassidy syndrome include several facial disorders, including hypertelorism and telecanthus, epicanthal folds, downslanting palpebral fissures, ptosis, a broad nasal bridge, malar hypoplasia, a thin upper lip, a smooth philtrum, and low-set, prominent ears. Males with Seaver Cassidy syndrome may also experience an underdeveloped shawl scrotum and cryptorchidism. Skeletal anomalies, such genu valgum, hyperextended joints, or cubitus valgus, may also be present.

Horner's syndrome is acquired as a result of disease, but may also be congenital (inborn, associated with heterochromatic iris) or iatrogenic (caused by medical treatment). Although most causes are relatively benign, Horner syndrome may reflect serious disease in the neck or chest (such as a Pancoast tumor (tumor in the apex of the lung) or thyrocervical venous dilatation).

Causes can be divided according to the presence and location of anhidrosis:

- Central (anhidrosis of face, arm and trunk)

- Syringomyelia

- Multiple sclerosis

- Encephalitis

- Brain tumors

- Lateral medullary syndrome

- Preganglionic (anhidrosis of face)

- Cervical rib traction on stellate ganglion

- Thyroid carcinoma

- Thyroidectomy

- Goiter

- Bronchogenic carcinoma of the superior fissure (Pancoast tumor) on apex of lung

- Klumpke paralysis

- Trauma - base of neck, usually blunt trauma, sometimes surgery.

- As a complication of tube thoracostomy

- Thoracic aortic aneurysm

- Postganglionic (no anhidrosis)

- Cluster headache - combination termed Horton's headache

- An episode of Horner's syndrome may occur during a migraine attack and be relieved afterwards

- Carotid artery dissection/carotid artery aneurysm

- Cavernous sinus thrombosis

- Middle ear infection

- Sympathectomy

- Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene block

CLOVES syndrome is an extremely rare overgrowth syndrome, with complex vascular anomalies. CLOVES syndrome affects people with various symptoms, ranging from mild fatty soft-tissue tumors to vascular malformations encompassing the spine or internal organs. CLOVES syndrome is closely linked to other overgrowth disorders like proteus syndrome, Klippel–Trénaunay syndrome, Sturge–Weber syndrome, and hemihypertrophy, to name a few.

'CLOVES' is an acronym for:

- C is for congenital.

- L is for lipomatous, which means pertaining to or resembling a benign tumor made up of mature fat cells. Most CLOVES patients present with a soft fatty mass at birth, often visible on one or both sides of the back, legs and/or abdomen.

- O is for overgrowth, because there is an abnormal increase in the size of the body or a body part that is often noted at birth. Patients with CLOVES may have affected areas of their bodies that grow faster than in other people. Overgrowth of extremities (usually arms or legs) is seen, with large wide hands or feet, large fingers or toes, wide space between fingers, and asymmetry of body parts.

- V is for vascular malformations, which are blood vessel abnormalies. Patients with CLOVES have different venous, capillary, and lymphatic channels - typically capillary, venous and lymphatic malformations are known as "slow flow" lesions. Some patients with CLOVES have combined lesions (which are fast flow) and some have aggressive vascular malformation known as arteriovenous malformations (AVM). The effect of a vascular malformation varies per patient based on the type, size, and location of the malformation, and symptoms can vary.

- E is for Epidermal naevi, which are sharply-circumscribed chronic lesions of the skin, and benign. These are often flesh-colored, raised or warty.

- S is for Spinal/Skeletal Anomalies or scoliosis. Some patients with CLOVES have tethered spinal cord, vascular malformations in or around their spines, and other spinal differences. High-flow aggressive spinal lesions (like AVM) can cause serious neurological deficits/paralysis.

The syndrome was first recognised by Saap and colleagues who recognised the spectrum of symptoms from a set of seven patients. In this initial description the syndrome is named CLOVE syndrome. It is believed that the first description of a case of CLOVES syndrome was written by Hermann Friedberg, a German physician, in 1867.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

After the last primary tooth is lost, usually around the age of twelve, final orthodontic treatment can be initiated. A patient that has not been able to close or swallow well probably will have an open bite, deficient lower-jaw growth, a narrow archform with crowded teeth, and upper anterior flaring of teeth. Orthognathic (jaw) surgery may be indicated. This should be completed in most situations before the smile surgery where the gracilis muscle is grafted to the face.

Genetic links to 13q12.2 and 1p22 have been suggested.

Blepharophimosis, ptosis, epicanthus inversus syndrome or BPES is a rare disease characterized by the conditions it is named after: blepharophimosis, ptosis, and epicanthus inversus.

Michels syndrome is a syndrome characterised by intellectual disability, craniosynostosis, blepharophimosis, ptosis, epicanthus inversus, highly arched eyebrows, and hypertelorism. And vary in other symptoms such as asymmetry of the skull, eyelid, and anterior chamber anomalies, cleft lip and palate, umbilical anomalies, and growth and cognitive development.

THS is uncommon in both the United States and internationally. In New Zealand, there is only one recorded case, there is also one recorded case in New South Wales, Australia. Both genders, male and female, are affected equally, and it typically occurs around the age of 60.

Fazio–Londe disease is linked to a genetic mutation in the "SLC52A3" gene on chromosome 20 (locus: 20p13). It is allelic and phenotypically similar to Brown–Vialetto–Van Laere syndrome.

The condition is inherited in an autosomal recessive manner.

The gene encodes the intestinal riboflavin transporter (hRFT2).

Brown-Séquard syndrome may be caused by a spinal cord tumour, trauma [such as a gunshot wound or puncture wound to the cervical (neck) or thoracic spine (back)], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place.

The disease is present at birth, but clinical manifestations are often not seen until later in life. Patients typically experience the sudden onset of pain, numbness, or weakness in their extremities as children or young adults. These symptoms may remit or remain stable and often can be localized below a specific dermatome. Symptoms tend to worsen over time either by discrete steps or continuously. Early development of weakness may portend a more aggressive course. Less commonly, weakness or bowel and bladder dysfunction may be presenting symptoms.

The major debility from Cobb syndrome is the onset of weakness, paresis, sensory loss, and loss of bowel and bladder control. A possible complication if treatment is delayed is Foix-Alajouanine disease or subacute necrotic myelopathy due to thrombosis in the spinal angioma.

Cutaneous lesions may be distributed anywhere in the dermatome, from midline back to abdomen. Midline back lesions may be associated with spina bifida. The cutaneous lesion may be very faint and may be more pronounced when the patient performs a Valsalva maneuver which increases abdominal pressure and causes preferential filling of the cutaneous angioma. Neurological examination will reveal weakness or paralysis and numbness or decreased sensation with a sharp upper cutoff.

The prognosis of THS is usually considered good. Patients usually respond to corticosteroids, and spontaneous remission can occur, although movement of ocular muscles may remain damaged. Roughly 30–40% of patients who are treated for THS experience a relapse.

The cause of alternating hemiplegia is the mutation of ATP1A3 gene. In a study of fifteen females and nine males’ patient with alternating hemiplegia, a mutation in ATP1A3 gene was present. Three patients showed heterozygous de-novo missense mutation. Six patients were found with de-novo missense mutation and one patient was identified with de-novo splice site mutation. De novo mutation is a mutation that occurs in the germ cell of one parent. Neither parent has the mutation, but it is passed to the child through the sperm or egg.

Minor's disease, a syndrome involving the sudden onset of back pain and paralysis caused by haemorrhage into the spinal cord substance, was named after the Russian neurologist, Lazar Salomowitch Minor (1855–1942).

The term "Minor's syndrome" is now only rarely used in connection with his work and is increasingly being used, both inside and outside the medical profession, to refer to superior canal dehiscence syndrome (SCDS), first described in 1998 by Dr. Lloyd B. Minor of The Johns Hopkins University, Baltimore, USA.