Worster-Drought syndrome is a form of congenital suprabulbar paresis that occurs in some children with cerebral palsy. It is caused by inadequate development of the corticobulbar tracts and causes problems with the mouth and tongue including impaired swallowing. A similar syndrome in adults is called anterior opercular syndrome.

A 1986 study of a family in which multiple members had Worster-Drought Syndrome suggested it might be hereditary.

A 2000 review of cases classified Worster-Drought Syndrome as a form of cerebral palsy, caused by early damage to the brain, but identified no obvious causes during gestation or birth and found some families with a history of the condition.

The syndrome was named after Cecil Charles Worster-Drought, the doctor who discovered it in 1956.

Prevalence is estimated to be 0.005%. The age of onset has been found to be under 15 years in 40% of cases while it is between 10 and 14 years in one third of the cases. Females outnumber males, 4 to 1. Only 3% have attacks after age 52.

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.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

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.

The actual incidence of this disease is not known, but only 243 cases have been reported in the scientific literature, suggesting an incidence of on the order of one affected person in ten million people.

Asymmetric crying facies (ACF), also called Cayler cardiofacial syndrome, partial unilateral facial paresis and hypoplasia of depressor angula oris muscle, is a minor congenital anomaly caused by agenesis or hypoplasia of the depressor anguli oris muscle, one of the muscles that control the movements of the lower lip. This unilateral facial weakness is first noticed when the infant cries or smiles, affecting only one corner of the mouth and occurs on the left side in nearly 80% of cases. It is associated with other birth defects in more than 50% of cases.

When the hypoplasia of the depressor anguli oris muscle is associated with congenital cardiac defects, the term 'Cayler cardiofacial syndrome' is used.

Cayler syndrome is part of 22q11.2 deletion syndrome.

It was characterized by Cayler in 1969.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

Adie's syndrome is not life-threatening or disabling. As such, there is no mortality rate relating to the condition; however, loss of deep tendon reflexes is permanent and may progress over time.

Almost all cases of synkinesis develop as a sequel to nerve trauma (the exception is when it is congenitally acquired as in Duane-Retraction Syndrome and Marcus Gunn phenomenon). Trauma to the nerve can be induced in cases such as surgical procedures, nerve inflammation, neuroma

, and physical injury.

Jugular foramen syndrome, or Vernet's syndrome is characterized by the paresis of 9th–11th (with or without 12th) cranial nerves together.

Symptoms of this syndrome are consequences of this paresis. As such, in an affected patient, you may find:

- dysphonia/hoarseness

- soft palate dropping

- deviation of the uvula towards the normal side

- dysphagia

- loss of sensory function from the posterior 1/3 of the tongue

- decrease in the parotid gland secretion

- loss of gag reflex

- sternocleidomastoid and trapezius muscles paresis

ODD is typically an autosomal dominant condition, but can be inherited as a recessive trait. It is generally believed to be caused by a mutation in the gene GJA1, which codes for the gap junction protein connexin 43. Slightly different mutations in this gene may explain the different way the condition manifests in different families. Most people inherit this condition from one of their parents, but new cases do arise through novel mutations. The mutation has high penetrance and variable expression, which means that nearly all people with the gene show signs of the condition, but these signs can range from very mild to very obvious.

There is currently no effective treatment or cure for PSP, although some of the symptoms can respond to nonspecific measures. The average age at symptoms onset is 63 and survival from onset averages 7 years with a wide variance. Pneumonia is a frequent cause of death.

Sporadic hemiplegic migraine (SHM) is a form of hemiplegic migraine headache isolated cases of which are observed. It is a rare disease. It is considered to be a separate type of migraine.

It most commonly affects younger women (2.6:1 female preponderance) and is unilateral in 80% of cases. Average age of onset is 32 years.

Progressive supranuclear palsy (PSP; or the Steele–Richardson–Olszewski syndrome, after the doctors who described it in 1963) is a degenerative disease involving the gradual deterioration and death of specific volumes of the brain.

Males and females are affected approximately equally and there is no racial, geographical or occupational predilection. Approximately six people per 100,000 population have PSP.

It has been described as a tauopathy.

In Brown's original series there was a 3:2 predominance of women to men and nearly twice as many cases involved the right eye as the left. 10% of cases showed bilaterality. Familial occurrence of Brown's syndrome has been reported.

Synkinesis is an interaction of nerves with muscles (although glands can also be involved). Most cases involve the cranial nerves which innervate many small cranial muscles, such as the facial muscles and the extraocular muscles. This is in contrast to areas of body where miswiring of the larger muscles is less evident due the size of the muscles. Synkinesis can also involve the upper limbs, especially hands which is quite rare, at 1 case in 1 million.

The cause of polymicrogyria is unclear. It is currently classified as resulting from abnormalities during late neuronal migration or early cortical organization of fetal development. Evidence for both genetic and non-genetic causes exists. Polymicrogyria appears to occur around the time of neuronal migration or early cortical development. Non-genetic causes include defects in placental oxygenation and in association with congenital infections, particularly cytomegalovirus.

An association with the gene WDR62 has been identified.

Triplegia is a medical condition characterized by the paralysis of three limbs (Triplegia Muscle Anatomy) . A person with triplegia can be referred to as triplegic. While there is no typical pattern of involvement, it is usually associated with paralysis of both legs and one arm — but can also involve both arms and one leg. Triplegia can sometimes by considered a combination of hemiplegia (paralysis of arm and leg of one side of the body) overlaying diplegia (paralysis of both legs), or as quadriplegia (paralysis of four limbs) with less involvement in one extremity.

The condition is commonly associated with cerebral palsy, although conditions such as stroke can also lead to it. Triplegia has also been found to be due to an increase in intracranial pressure associated with hydrocephalus resulting from traumatic brain injury.

A similar condition is triparesis, in which the patient suffers from paresis in three limbs, meaning that the limbs are very weak, but not completely paralyzed.

In a case reported only due to its rarity, triplegia was reported following a tonsillectomy (surgical removal of the tonsils). An eight-year-old male patient was sent to Willard Parker Hospital on August 12, 1929 and had been diagnosed with poliomyelitis. After an unrelated, and routine, tonsillectomy there was complete flaccid paralysis and loss of feeling in both the legs, right arm, and muscles in the trunk.

Postoperative residual curarization (PORC) is a residual paresis after emergence from general anesthesia with neuromuscular-blocking drugs.

Brown's syndrome is a rare form of strabismus characterized by limited elevation of the affected eye. The disorder may be congenital (existing at or before birth), or acquired. Brown syndrome is caused by a malfunction of the Superior oblique muscle, causing the eye to have difficulty moving up, particularly during adduction (when eye turns towards the nose). Harold W. Brown first described the disorder in 1950 and initially named it the "superior oblique tendon sheath syndrome".

Most commonly affected is the Vertebral Basilar Artery (Vertebral Basilar Dolichoectasia or Vertebrobasillar Dolichoectasia). The Internal Carotid Artery is also at high risk to be affected. Patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) are more likely to be subject to dolichoectasias. Dolichoectasias are most common in elderly males.

In cases involving the basilar artery (VBD), the pathogenesis arises from direct compression of different cranial nerves. Additionally, ischemic effects on the brain stem and cerebellar hemispheres as well as symptoms related to hydrocephalus are common. Direct cranial nerve compression can lead to isolated cranial nerve dysfunction, usually associated with a normal-sized basilar artery that is tortuous and elongated. Cranial nerve dysfunction most commonly involves the VII cranial nerve and the V cranial nerve. Multiple cranial nerve dysfunction is far more likely to occur if there is dilation (ectasia) associated with a tortuous and elongated basilar artery. Cranial nerves affected in descending order of frequency include: VII, V, III, VIII, and VI.

Internal Carotid Artery dolichoectasia is particularly interesting because the artery normally already contains one hairpin turn. Seen in an MRI as two individual arteries at this hairpin, a carotid artery dolichoectasia can progress so far as to produce a second hairpin turn and appear as three individual arteries on an MRI. In the case of a dolichoectasia of the Internal Carotid Artery (ICD), the pathogenesis is primarily related to compression of the Optic Nerves at the Optic Chiasma (see Fig. 1 and 2).

A combination of lifestyle modifications and medications can be used for the treatment of dolichoectasias.

- Antihypertensive medications such as Thiazides, Beta Blocker, ACE Inhibitor

- Trental or other Pentoxifylline drugs

- Dietary changes

- Weight loss

- Regular exercise