Those at the overall highest risk for lateral medullary syndrome are men at an average age of 55.06. Having a history of hypertension, diabetes and smoking all increase the risk of large artery atherosclerosis. Large artery atherosclerosis is thought to be the greatest risk factor for lateral medullary syndrome due to the deposits of cholesterol, fatty substances, cellular waste products, calcium and fibrin. Otherwise known as plaque build up in the arteries.

The outlook for someone with lateral medullary syndrome depends upon the size and location of the area of the brain stem damaged by the stroke. Some individuals may see a decrease in their symptoms within weeks or months. Others may be left with significant neurological disabilities for years after the initial symptoms appeared. However, more than 85% of patients have seen minimal symptoms present at six months from the time of the originatl stroke, and have been able to independently accomplish average daily within a year.

It can be caused by an interruption to the blood supply of the anterior inferior cerebellar artery or circumferential arteries.

A lateral pontine syndrome is a lesion which is similar to the lateral medullary syndrome, but because it occurs in the pons, it also involves the cranial nerve nuclei of the pons.

Medial medullary syndrome, also known as inferior alternating syndrome, hypoglossal alternating hemiplegia, lower alternating hemiplegia, or Dejerine syndrome, is a type of alternating hemiplegia characterized by a set of clinical features resulting from occlusion of the anterior spinal artery. This results in the infarction of medial part of the medulla oblongata.

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.

The infarction (which arises in the paramedian branches of the anterior spinal artery and/or the vertebral arteries) leads to death of the ipsilateral medullary pyramid, the medial leminiscus, and the hypoglossal nerve fibers that pass through the medulla. The spinothalamic tract is spared because it is located more laterally in the brainstem and is not supplied by the anterior spinal artery, but rather by the vertebral and posterior inferior cerebellar arteries. The trigeminal nucleus is also spared, since most of it is higher up in the pons, and the spinal part of it found in the medulla is lateral to the infarct.

Medial pontine syndrome results from occlusion of paramedian branches of the basilar artery.

Although medial pontine syndrome has many similarities to medial medullary syndrome, because it is located higher up the brainstem in the pons, it affects a different set of cranial nuclei.

Depending upon the size of the infarct, it can also involve the facial nerve.

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

Babinski–Nageotte syndrome, sometimes called Babinski syndrome or hemimedullary syndrome, is an alternating brainstem syndrome. It occurs when there is damage to the dorsolateral or posterior lateral medulla oblongata, likely syphilitic in origin. Hence it is also called the alternating medulla oblongata syndrome.

The rare disorder is caused by damage to a part of the brain (medullobulbar transitional area) which causes a variety of neurological symptoms, some of which affect only one side of the body. Symptoms include ipsilateral (same side) cerebellar ataxia, sensory deficits of the face, and Horner's syndrome, along with weakness and loss of sensation on the contralateral (opposite side) of the body.

It was first described in 1902 and later named after the neurologists who initially investigated it, Joseph Babinski and Jean Nageotte.

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.

Pheochromocytoma is seen in between two and eight in 1,000,000, with approximately 1000 cases diagnosed in United States yearly. It mostly occurs in young or middle age adults, though it presents earlier in hereditary cases.

- About 10% of adrenal cases are bilateral (suggesting hereditary disease)

- About 10% of adrenal cases occur in children (also suggesting hereditary disease)

- About 15% are extra-adrenal (located in any orthosympathetic tissue): Of these 9% are in the abdomen, and 1% are located elsewhere. Some extra-adrenal pheochromocytomas are probably actually paragangliomas, but the distinction can only be drawn after surgical resection.

- About 11.1% of adrenal cases are malignant, but this rises to 30% for extra-adrenal cases

- About 15–20% are hereditary

- About 5% are caused by VHL disease

- About 3% recur after being resected

- About 14% of affected individuals do not have arterial hypertension (Campbell's Urology)

The lateral meningocele syndrome is a very rare skeletal disorder with facial anomalies, hypotonia and meningocele-related neurologic dysfunction.

Alternating hemiplegia is a form of hemiplegia that has an ipsilateral and contralateral presentation in different parts of the body. The disorder is characterized by recurrent episodes of paralysis on one side of the body. There are multiple forms of alternating hemiplegia, Weber's syndrome, middle alternating hemiplegia, and inferior alternating hemiplegia. This type of syndrome can result from a unilateral lesion in the brainstem affecting both upper motor neurons and lower motor neurons. The muscles that would receive signals from these damaged upper motor neurons result in spastic paralysis. With a lesion in the brainstem, this affects the majority of limb and trunk muscles on the contralateral side due to the upper motor neurons decussation after the brainstem. The cranial nerves and cranial nerve nuclei are also located in the brainstem making them susceptible to damage from a brainstem lesion. Cranial nerves III (Oculomotor), VI (Abducens), and XII (Hypoglossal) are most often associated with this syndrome given their close proximity with the pyramidal tract, the location which upper motor neurons are in on their way to the spinal cord. Damages to these structures produce the ipsilateral presentation of paralysis or palsy due to the lack of cranial nerve decussation (aside from the trochlear nerve) before innervating their target muscles. The paralysis may be brief or it may last for several days, many times the episodes will resolve after sleep. Some common symptoms of alternating hemiplegia are mental impairment, gait and balance difficulties, excessive sweating and changes in body temperature.

The massive release of catecholamines in pheochromocytoma can cause damage to heart cells. This damage may be due to either compromising the coronary microcirculation or by direct toxic effects on the heart cells.

Brain related causes are less commonly associated with isolated vertigo and nystagmus but can still produce signs and symptoms, which mimic peripheral causes. Disequilibrium is often a prominent feature.

- Degenerative: age related decline in balance function

- Infectious: meningitis, encephalitis, epidural abscess, syphilis

- Circulatory: cerebral or cerebellar ischemia or hypoperfusion, stroke, lateral medullary syndrome (Wallenberg's syndrome)

- Autoimmune: Cogan syndrome

- Structural: Arnold-Chiari malformation, hydrocephalus

- Systemic: multiple sclerosis, Parkinson's disease

- Vitamin deficiency: Vitamin B12 deficiency

- CNS or posterior neoplasms, benign or malignant

- Neurological: Vertiginous epilepsy, abasia

- Other – There are a host of other causes of dizziness not related to the ear.

- Mal de debarquement is rare disorder of imbalance caused by being on board a ship. Patients suffering from this condition experience disequilibrium even when they get off the ship. Typically treatments for seasickness are ineffective for this syndrome.

- Motion sickness – a conflict between the input from the various systems involved in balance causes an unpleasant sensation. For this reason, looking out of the window of a moving car is much more pleasant than looking inside the vehicle.

- Migraine-associated vertigo

- Toxins, drugs, medications; it is also a known symptom of carbon monoxide poisoning.

Dissociated sensory loss is a pattern of neurological damage caused by a lesion to a single tract in the spinal cord which involves "selective" loss of fine touch and proprioception "without" loss of pain and temperature, or vice versa.

Understanding the mechanisms behind these selective lesions requires a brief discussion of the anatomy involved.

Loss of pain and temperature are due to damage to the lateral spinothalamic tracts, which cross the central part of the cord close to the level where they enter it and travel up the spinal column on the opposite side to the one they innervate (i.e. they "ascend contralaterally"). Note that a lesion of the lateral spinothalamic tract at a given level will not result in sensory loss for the dermatome of the same level; this is due to the fibers of the tract of Lissauer which transmit the neuron one or two levels above the affected segment (thus bypassing the segmental lesion on the contralateral side).

Loss of fine touch and proprioception are due to damage to the dorsal columns, which do not cross the cord until the brainstem, and so travel up the column on the same side to the one they innervate (i.e. they "ascend ipsilaterally").

This means that a lesion of the dorsal columns will cause loss of touch and proprioception below the lesion and on the same side as it, while a lesion of the spinothalamic tracts will cause loss of pain and temperature below the lesion and on the opposite side to it.

Dissociated sensory loss always suggests a focal lesion within the spinal cord or brainstem.

The location of cord lesions affects presentation—for instance, a central lesion (such as that of syringomyelia) will knock out second order neurons of the spinothalamic tract as they cross the centre of the cord, and will cause loss of pain and temperature without loss of fine touch or proprioception.

Other causes of dissociated sensory loss include:

- Diabetes mellitus

- Syringomyelia

- Brown-Séquard syndrome

- Lateral medullary syndrome aka Wallenberg's syndrome

- Anterior spinal artery thrombosis

- Tangier disease

- Subacute combined degeneration

- Multiple sclerosis

- Tabes dorsalis

- Friedreich's ataxia (or other spinocerebellar degeneration)

Singleton Merten Syndrome is an autosomal dominate genetic disorder with variable expression with an onset of symptoms during childhood.

A typical patient with severe McLeod syndrome that begins in adulthood lives for an additional 5 to 10 years. Patients with cardiomyopathy have elevated risk for congestive heart failure and sudden cardiac death. The prognosis for a normal life span is often good in some patients with mild neurological or cardiac sequelae.

In terms of treatment/management one should observe what signs or symptoms are present and therefore treat those as there is no other current guideline. The affected individual should be monitored for cancer of:

- Thyroid

- Breast

- Renal

McLeod syndrome is present in 0.5 to 1 per 100,000 of the population. McLeod males have variable acanthocytosis due to a defect in the inner leaflet bilayer of the red blood cell, as well as mild hemolysis. McLeod females have only occasional acanthocytes and very mild hemolysis; the lesser severity is thought to be due to X chromosome inactivation via the Lyon effect. Some individuals with McLeod phenotype develop myopathy, neuropathy, or psychiatric symptoms, producing a syndrome that may mimic chorea.

McLeod syndrome can cause an increase in the enzymes creatine kinase (CK) and lactate dehydrogenase (LDH) found in routine blood screening.

In medicine, split hand syndrome is a neurological syndrome in which the hand muscles on the side of the thumb (lateral, thenar eminence) appear wasted, whereas the muscles on the side of the little finger (medial, hypothenar eminence) are spared. Anatomically, the abductor pollicis brevis and first dorsal interosseous muscle are more wasted than the abductor digiti minimi.

If lesions affecting the branches of the ulnar nerve that run to the wasted muscles are excluded, the lesion is almost sure to be located in the anterior horn of the spinal cord at the C8-T1 level. It has been proposed as a relatively specific sign for amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease). It can also occur in other disorders affecting the anterior horn, such as spinal muscular atrophy, Charcot-Marie-Tooth disease, poliomyelitis and progressive muscular atrophy. A slow onset and a lack of pain or sensorial symptoms are arguments against a lesion of the spinal root or plexus brachialis. To an extent, these features can also be seen in normal aging (although technically, the apparent muscle wasting is sarcopenia rather than atrophy).

The term split hand syndrome was first coined in 1994 by a researcher from the Cleveland Clinic called Asa J. Wilbourn.

This syndrome appears to be inherited in an autosomal dominant fashion.

Molecular analyses suggest that the causative mutations cause a truncation of the protein. These mutations result in the loss of PEST sequence in the protein. This loss is associated with a prolonged half life of the protein.

Mutations in Notch 3 were found to be associated with this syndrome.

An initial clinical report of this syndrome describes a 6-month-old boy with rhizomelic shortening, particularly in the arms, and protuberances over the lateral aspects of the clavicles. On radiographs the lateral third of the clavicles had a appearance resulting from an abnormal process or protuberance arising from the fusion center. His 22-year-old mother also had a height of 142 cm with an arm span of 136 cm and rhizomelic shortness of the limbs, maximal in the arms, and abnormalities of the acromioclavicular joints. Both the mother and the son had marked bilateral clinodactyly of the fifth fingers associated with hypoplastic middle phalanx.