Hemiplegia is not a progressive disorder, except in progressive conditions like a growing brain tumour. Once the injury has occurred, the symptoms should not worsen. However, because of lack of mobility, other complications can occur. Complications may include muscle and joint stiffness, loss of aerobic fitness, muscle spasms, bed sores, pressure ulcers and blood clots.

Sudden recovery from hemiplegia is very rare. Many of the individuals will have limited recovery, but the majority will improve from intensive, specialised rehabilitation. Potential to progress may differ in cerebral palsy, compared to adult acquired brain injury. It is vital to integrate the hemiplegic child into society and encourage them in their daily living activities. With time, some individuals may make remarkable progress.

The most common cause of hemiparesis and hemiplegia is stroke. Strokes can cause a variety of movement disorders, depending on the location and severity of the lesion. Hemiplegia is common when the stroke affects the corticospinal tract. Other causes of hemiplegia include spinal cord injury, specifically Brown-Séquard syndrome, traumatic brain injury, or disease affecting the brain. As a lesion that results in hemiplegia occurs in the brain or spinal cord, hemiplegic muscles display features of the upper motor neuron syndrome. Features other than weakness include decreased movement control, clonus (a series of involuntary rapid muscle contractions), spasticity, exaggerated deep tendon reflexes and decreased endurance.

The incidence of hemiplegia is much higher in premature babies than term babies. There is also a high incidence of hemiplegia during pregnancy and experts believe that this may be related to either a traumatic delivery, use of forceps or some event which causes brain injury.

Other causes of hemiplegia in adults include trauma, bleeding, brain infections and cancers. Individuals who have uncontrolled diabetes, hypertension or those who smoke have a higher chance of developing a stroke. Weakness on one side of the face may occur and may be due to a viral infection, stroke or a cancer.

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.

Most common causes of lower motor neuron injuries are trauma to peripheral nerves that serve the axons – a virus that selectively attacks ventral horn cells.

Disuse atrophy of the muscle occurs i.e., shrinkage of muscle fibre finally replaced by fibrous tissue (fibrous muscle)

Other causes include Guillain–Barré syndrome, "C. botulism", polio, and cauda equina syndrome; another common cause of lower motor neuron degeneration is amyotrophic lateral sclerosis.

Because the nerve emerges near the bottom of the brain, it is often the first nerve compressed when there is any rise in intracranial pressure. Different presentations of the condition, or associations with other conditions, can help to localize the site of the lesion along the VIth cranial nerve pathway.

The most common causes of VIth nerve palsy in adults are:

- More common: Vasculopathic (diabetes, hypertension, atherosclerosis), trauma, idiopathic.

- Less common: Increased intracranial pressure, giant cell arteritis, cavernous sinus mass (e.g. meningioma, Brain stem Glioblastoma aneurysm, metastasis), multiple sclerosis, sarcoidosis/vasculitis, postmyelography, lumbar puncture, stroke (usually not isolated), Chiari Malformation, hydrocephalus, intracranial hypertension, tuberculosis meningitis.

In children, Harley reports typical causes as traumatic, neoplastic (most commonly brainstem glioma), as well as idiopathic. Sixth nerve palsy causes the eyes to deviate inward (see: Pathophysiology of strabismus). Vallee et al. report that benign and rapidly recovering isolated VIth nerve palsy can occur in childhood, sometimes precipitated by ear, nose and throat infections.

Recent population-based studies have estimated the prevalence of NPH to be about 0.5% in those over 65 years old, with an incidence of about 5.5 patients per 100,000 of people per year. This is in accordance with comparable findings stating that although normal pressure hydrocephalus can occur in both men and women of any age, it is found more often in the elderly population, with a peak onset generally in the sixth to seventh decades.

Paresis () is a condition typified by a weakness of voluntary movement, or partial loss of voluntary movement or by impaired movement. When used without qualifiers, it usually refers to the limbs, but it can also be used to describe the muscles of the eyes (ophthalmoparesis), the stomach (gastroparesis), and also the vocal cords (Vocal cord paresis). Neurologists use the term "paresis" to describe weakness, and "plegia" to describe paralysis in which all voluntary movement is lost. The term "paresis" comes from the "letting go" from παρίημι "to let go, to let fall".

Todd's paresis, Todd's paralysis, or Todd's palsy (or postictal paresis/paralysis, "after seizure") is focal weakness in a part of the body after a seizure. This weakness typically affects appendages and is localized to either the left or right side of the body. It usually subsides completely within 48 hours. Todd's paresis may also affect speech, eye position (gaze), or vision.

The condition is named after Robert Bentley Todd (1809–1860), an Irish-born London physiologist who first described the phenomenon in 1849. It may occur in up to 13% of seizure cases. It is most common after a focal motor seizure affecting one limb or one side of the body. The generally postulated cause is the exhaustion of the primary motor cortex, although no conclusive evidence is available to support this.

The cause of Todd's paresis been attributed to the affected cortex being ‘exhausted’ or silenced due to increased inhibition, but these conjectures are not supported. It has been observed that the impairments that follow seizures are similar to those that follow strokes, where for a period of time blood flow to certain areas of the brain is restricted and these areas are starved of oxygen.

About 2% of all CP cases are inherited, with glutamate decarboxylase-1 being one of the possible enzymes involved. Most inherited cases are autosomal recessive.

A lower motor neuron lesion is a lesion which affects nerve fibers traveling from the ventral horn or anterior grey column of the spinal cord to the relevant muscle(s) – the lower motor neuron.

One major characteristic used to identify a lower motor neuron lesion is flaccid paralysis – paralysis accompanied by loss of muscle tone. This is in contrast to an upper motor neuron lesion, which often presents with spastic paralysis – paralysis accompanied by severe hypertonia.

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.

In babies that are born at term risk factors include problems with the placenta, birth defects, low birth weight, breathing meconium into the lungs, a delivery requiring either the use of instruments or an emergency Caesarean section, birth asphyxia, seizures just after birth, respiratory distress syndrome, low blood sugar, and infections in the baby.

Patients with dementia who are confined to a nursing home and may have undiagnosed NPH can possibly become independent again once treated. So far only one study was able to evaluate the prevalence of NPH, both diagnosed and undiagnosed, among residents of assisted-living facilities, showing a prevalence in 9 to 14% of the residents.

NPH may be relieved by surgically implanting a ventriculoperitoneal shunt to drain excess cerebrospinal fluid to the abdomen where it is absorbed. Once the shunt is in place, the ventricles usually diminish in size in 3 to 4 days, regardless of the duration of the hydrocephalus. Even though the ventricular swelling diminishes, only 21% of patients show a marked improvement in symptoms. The most likely patients to show improvement are those that show only gait disturbance, mild or no incontinence, and mild dementia. A more recent study (2004) found better outcomes, concluding that if patients with idiopathic normal pressure hydrocephalus are correctly identified, shunt insertion yielded beneficial outcomes in 86% of patients, in either gait disturbance (81%), improved continence (70%), or both. They also observed that measurements in the diagnostic clinical triad, the cortical sulci size, and periventricular lucencies were related to outcome. However, other factors such as age of the patient, symptom duration, dilation of ventricles, and the degree of presurgical dementia were unrelated to outcome.

Ophthalmoparesis can result from disorders of various parts of the eye and nervous system:

- Infection around the eye. Ophthalmoplegia is an important finding in orbital cellulitis.

- The orbit of the eye, including mechanical restrictions of eye movement, as in Graves disease.

- The muscle, as in progressive external ophthalmoplegia or Kearns-Sayre syndrome.

- The neuromuscular junction, as in myasthenia gravis.

- The relevant cranial nerves (specifically the oculomotor, trochlear, and abducens), as in cavernous sinus syndrome or raised intracranial pressure.

- The brainstem nuclei of these nerves, as in certain patterns of brainstem stroke such as Foville's syndrome.

- White matter tracts connecting these nuclei, as in internuclear ophthalmoplegia, an occasional finding in multiple sclerosis.

- Dorsal midbrain structures, as in Parinaud's syndrome.

- Certain parts of the cerebral cortex (including the frontal eye fields), as in stroke.

- Toxic envenomation by mambas, taipans, and kraits.

Thiamine deficiency can cause ophthalmoparesis in susceptible persons; this is part of the syndrome called Wernicke encephalopathy. The causal pathway by which this occurs is unknown. Intoxication with certain substances, such as phenytoin, can also cause ophthalmoparesis.

Treatment and prognosis depend on the underlying condition. For example, in thiamine deficiency, treatment would be the immediate administration of vitamin B1.

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

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.

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.

Synkinesis is the result from miswiring of nerves after trauma. This result is manifested through involuntary muscular movements accompanying voluntary movements. For example, voluntary smiling will induce an involuntary contraction of the eye muscles causing the eye to squint when smiling. Most commonly involved are facial muscles and the extraocular muscles, rarely the hands are performing mirror movements.

Causes are diverse and include nerve trauma with improper healing, or nerve degeneration, as in the course of Parkinson´s disease. In congenital cases, mutations of genes involved in nerve growth, specifically axonal growth have been found. Rarely, it is part of syndromes with neuroendocrine problems such as Kallman syndrome.

The prognosis is usually good with normal intelligence and lifespan. Treatment depends on the cause, but is largely conservative with facial retraining or mime therapy, if needed, while Botox and surgery are used as last resort.

Parinaud's syndrome, also known as dorsal midbrain syndrome, vertical gaze palsy, and Sunset Sign, is an inability to move the eyes up and down. It is caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF). The eyes lose the ability to move upward and down .

It is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology.

A gaze palsy is the paresis of conjugate eye movements.

Horizontal gaze palsy may be caused by lesions in the cerebral hemispheres, which cause paresis of gaze away from the side of the lesion, or from brain stem lesions, which, if they occur below the crossing of the fibers from the frontal eye fields in the caudal midbrain, will cause weakness of gaze toward the side of the lesion. These will result in horizontal gaze deviations from unopposed action of the unaffected extraocular muscles. Another way to remember this is that patients with hemisphere lesions look towards their lesion, while patients with pontine gaze palsies look away from their lesions. Note that patients with gaze palsy still have conjugate eye movements and therefore do not complain of diplopia.

The human Robo gene acts as a receptor for a midline repulsive cue. When Robo is mutated, the longitudinal tract formation is disrupted and therefore normal neuronal connections cannot form. This leads to the reduced hindbrain volume and scoliosis, which are common symptoms of horizontal gaze palsy.

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.

Adie syndrome is a neurological disorder characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation). It is frequently seen in females with absent knee or ankle jerks and impaired sweating. It is named after the British neurologist William John Adie. It is caused by damage to the postganglionic fibers of the parasympathetic innervation of the eye, usually by a viral or bacterial infection which causes inflammation, and affects the pupil of the eye and the autonomic nervous system.

The cause of PSP is unknown. Fewer than 1% of those with PSP have a family member with the same disorder. A variant in the gene for tau protein called the H1 haplotype, located on chromosome 17, has been linked to PSP. Nearly all people with PSP received a copy of that variant from each parent, but this is true of about two-thirds of the general population. Therefore, the H1 haplotype appears to be necessary but not sufficient to cause PSP. Other genes, as well as environmental toxins, are being investigated as other possible contributors to the cause of PSP.