The condition usually consists of:

Sensation to the face is preserved, due to the sparing of the trigeminal nucleus.

The syndrome is said to be "alternating" because the lesion causes symptoms both contralaterally and ipsilaterally. Sensation of pain and temperature is preserved, because the spinothalamic tract is located more laterally in the brainstem and is also not supplied by the anterior spinal artery (instead supplied by the posterior inferior cerebellar arteries and the vertebral arteries).

Medial inferior pontine syndrome is a condition associated with a contralateral hemiplegia.

"Medial inferior pontine syndrome" has been described as equivalent to Foville's syndrome.

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

Damage to the following areas produces symptoms (from medial to lateral):

This produces ipsilateral horizontal gaze palsy and facial nerve palsy and contralateral hemiparesis, hemisensory loss, and internuclear ophthalmoplegia.

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.

Foville's syndrome is caused by the blockage of the perforating branches of the basilar artery in the region of the brainstem known as the pons. Most frequently caused by vascular disease or tumors involving the dorsal pons.[3]

Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus. There's involvement of the fifth to eighth cranial nerves, central sympathetic fibres (Horner syndrome) and horizontal gaze palsy.[3]

Locked-in syndrome usually results from quadriplegia and the inability to speak in otherwise cognitively intact individuals. Those with locked-in syndrome may be able to communicate with others through coded messages by blinking or moving their eyes, which are often not affected by the paralysis. The symptoms are similar to those of sleep paralysis. Patients who have locked-in syndrome are conscious and aware, with no loss of cognitive function. They can sometimes retain proprioception and sensation throughout their bodies. Some patients may have the ability to move certain facial muscles, and most often some or all of the extraocular muscles. Individuals with the syndrome lack coordination between breathing and voice. This prevents them producing voluntary sounds, though the vocal cords are not paralysed.

Anterior cerebral artery syndrome is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum.

Depending upon the area and severity of the occlusion, signs and symptoms may vary within the population affected with ACA syndrome. Blockages to the proximal (A1) segment of the vessel produce only minor deficits due to the collateral blood flow from the opposite hemisphere via the anterior communicating artery. Occlusions distal to this segment will result in more severe presentation of ACA syndrome. Contralateral hemiparesis and hemisensory loss of the lower extremity is the most common symptom associated with ACA syndrome.

Locked-in syndrome (LIS), also known as pseudocoma, is a condition in which a patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for vertical eye movements and blinking. The individual is conscious and sufficiently intact cognitively to be able to communicate with eye movements.

The EEG is "normal" in locked-in syndrome.

Total locked-in syndrome, or completely locked-in state (CLIS), is a version of locked-in syndrome wherein the eyes are paralyzed as well. Fred Plum and Jerome Posner coined the term for this disorder in 1966.

Clinical presentation of CPM is heterogeneous and depend on the regions of the brain involved. Prior to its onset, patients may present with the neurological signs and symptoms of hyponatraemic encephalopathy such as nausea and vomiting, confusion, headache and seizures. These symptoms may resolve with normalisation of the serum sodium concentration. Three to five days later, a second phase of neurological manifestations occurs correlating with the onset of myelinolysis. Observable immediate precursors may include seizures, disturbed consciousness, gait changes, and decrease or cessation of respiratory function.

The classical clinical presentation is the progressive development of spastic quadriparesis, pseudobulbar palsy, and emotional lability (pseudobulbar affect), with other more variable neurological features associated with brainstem damage. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem.

Causes of the one and a half syndrome include pontine hemorrhage, ischemia, tumors, infective mass lesions such as tuberculomas, and demyelinating conditions like multiple sclerosis.

Central pontine myelinolysis (CPM) is a neurological disorder caused by severe damage of the myelin sheath of nerve cells in the area of the brainstem termed the "pons", predominately of iatrogenic, treatment-induced cause. It is characterized by acute paralysis, dysphagia (difficulty swallowing), and dysarthria (difficulty speaking), and other neurological symptoms.

Central pontine myelinolysis was first described by Adams et al. in 1959 as a clinicopathological entity. The original paper described four cases with fatal outcomes, and the findings on autopsy. The cause was not known then but the authors suspected either a toxin or a nutritional deficiency. ‘Central pontine’ indicated the site of the lesion and ‘myelinolysis’ was used to emphasise that myelin was affected preferentially compared to the other neuronal elements. The authors intentionally avoided the term ‘demyelination’ to describe the condition, in order to differentiate this condition from multiple sclerosis and other neuroinflammatory disorders.

Since this original description, demyelination in other areas of the central nervous system associated with osmotic stress has been described outside the pons. The more general term "osmotic demyelination syndrome" is now preferred to the original more restrictive term "central pontine myelinolysis".

Central pontine myelinolysis presents most commonly as a complication of treatment of patients with profound hyponatremia (low sodium), which can result from a varied spectrum of conditions, based on different mechanisms. It occurs as a consequence of a rapid rise in serum tonicity following treatment in individuals with chronic, severe hyponatremia who have made intracellular adaptations to the prevailing hypotonicity.

The one and a half syndrome is a rare weakness in eye movement affecting both eyes, in which one cannot move laterally at all, and the other can move in only one lateral direction (inward or outward). More formally, it is characterized by ""a conjugate horizontal gaze palsy in one direction and an internuclear ophthalmoplegia in the other"". The most common manifestation of this unusual syndrome is limitation of horizontal eye movement to abduction (moving away from the midline) of one eye (e.g. right eye in the diagram on the right) with no horizontal movement of the other eye (e.g. left eye in the diagram on the right). Nystagmus is also present when the eye on the opposite side of the lesion is abducted. Convergence is classically spared as cranial nerve III (oculomotor nerve) and its nucleus is spared bilaterally.

King–Kopetzky syndrome is an auditory disability characterised by difficulty in hearing speech in the presence of background noise in conjunction with the finding of normal hearing test results.

It is an example of auditory processing disorder (APD) or "auditory disability with normal hearing (ADN)".

King–Kopetzky syndrome patients have a worse Social Hearing Handicap index (SHHI) than others, indicating they suffer a significant degree of speech-hearing disability.

The condition is named after Samuel J. Kopetzky, who first described the condition in 1948, and P. F. King, who first discussed the aetiological factors behind it in 1954.

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 characteristic features of the syndrome are:

- Limitation of abduction (outward movement) of the affected eye.

- Less marked limitation of adduction (inward movement) of the same eye.

- Retraction of the eyeball into the socket on adduction, with associated narrowing of the palpebral fissure (eye closing).

- Widening of the palpebral fissure on attempted abduction. (N. B. Mein and Trimble point out that this is "probably of no significance" as the phenomenon also occurs in other conditions in which abduction is limited.)

- Poor convergence.

- A head turn to the side of the affected eye to compensate for the movement limitations of the eye(s) and to maintain binocular vision.

While usually isolated to the eye abnormalities, Duane syndrome can be associated with other problems including cervical spine abnormalities Klippel-Feil syndrome, Goldenhar syndrome, heterochromia, and congenital deafness.

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.

Magnetic resonance imaging (MRI) is the imaging of choice in spinal cord lesions.

Brown-Séquard syndrome is an incomplete spinal cord lesion characterized by findings on clinical examination which reflect hemisection of the spinal cord (cutting the spinal cord in half on one or the other side). It is diagnosed by finding motor (muscle) paralysis on the same (ipsilateral) side as the lesion and deficits in pain and temperature sensation on the opposite (contralateral) side. This is called ipsilateral hemiplegia and contralateral pain and temperature sensation deficits. The loss of sensation on the opposite side of the lesion is because the nerve fibers of the spinothalamic tract (which carry information about pain and temperature) crossover once they meet the spinal cord from the peripheries.

A patient may be diagnosed with a conjugate gaze palsy by a physician performing a number of tests to examine the patient's eye movement abilities. In most cases, the gaze palsy can simply be seen by inability to move both eyes in one direction. However, sometimes a patient exhibits an abduction nystagmus in both eyes, indicating evidence of a conjugate gaze palsy. A nystagmus is a back and forth "jerk" of the eye when attempting to hold a gaze in one direction.

Horizontal gaze palsies affect gaze of both eyes either toward or away from the midline of the body. Horizontal gaze palsies are generally caused by a lesion in the brain stem and connecting nerves, normally in the pons.

In the clinical setting, the principal difficulties in differential diagnosis arise as a consequence of the very early age at which patients with this condition first present. The clinician must be persistent in examining abduction and adduction, and in looking for any associated palpebral fissure changes or head postures, when attempting to determine whether what often presents as a common childhood squint (note-"squint" is a British term for two eyes not looking in the same direction) is in fact Duane syndrome. Fissure changes, and the other associated characteristics of Duane's such as up or down shoots and globe retraction, are also vital when deciding whether any abduction limitation is the result of Duane's and not a consequence of VI or abducens cranial nerve palsy.

Acquired Duane's syndrome is a rare event occurring after peripheral nerve palsy.

Facial nerve paralysis is characterised by unilateral facial weakness, with other symptoms including loss of taste, , and decreased salivation and tear secretion. Other signs may be linked to the cause of the paralysis, such as s in the ear, which may occur if the facial palsy is due to shingles. Symptoms may develop over several hours. Acute facial pain radiating from the ear may precede the onset of other symptoms.

Sixth nerve palsy, or abducens nerve palsy, is a disorder associated with dysfunction of cranial nerve VI (the abducens nerve), which is responsible for causing contraction of the lateral rectus muscle to abduct (i.e., turn out) the eye. The inability of an eye to turn outward results in a convergent strabismus or esotropia of which the primary symptom is diplopia (commonly known as double vision) in which the two images appear side-by-side. The condition is commonly unilateral but can also occur bilaterally.

The unilateral abducens nerve palsy is the most common of the isolated ocular motor nerve palsies.