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.

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 muscle spasticity can cause gait patterns to be awkward and jerky. The constant spastic state of the muscle can lead to bone and tendon deformation, further complicating the patient's mobility. Many patients with spastic hemiplegia are subjected to canes, walkers and even wheelchairs. Due to the decrease in weight bearing, patients are at a higher risk of developing osteoporosis. An unhealthy weight can further complicate mobility. Patients with spastic hemiplegia are a high risk for experiencing seizures. Oromotor dysfunction puts patients at risk for aspiration pneumonia. Visual field deficits can cause impaired two-point discrimination. Many patients experience the loss of sensation in the arms and legs on the affected side of the body. Nutrition is essential for the proper growth and development for a child with spastic hemiplegia.

There are many different brain dysfunctions that can account for the cause for spastic hemiplegia. Spastic hemiplegia occurs either at birth or in the womb. The cause can be all types of strokes, head injuries, hereditary diseases, brain injuries and infections. Malformations of the veins or arteries in any part of the body can lead to spastic hemiplegia. The artery most commonly affected is the middle cerebral artery. Unborn and newborn babies are susceptible to strokes. Leukodystrophies are a group of hereditary diseases that are known to cause spastic hemiplegia. Brain infections that cause spastic hemiplegia are meningitis, multiple sclerosis, and encephalitis. The spasticity occurs when the afferent pathways in the brain are compromised and the communication between the brain to the motor fibers is lost. When the inhibitory signals to deactivate the stretch reflex is lost the muscle remains in a constant contracted state. With spastic hemiplegia, one upper extremity and one lower extremity is affected, so cervical, lumbar and sacral segments of the spinal column can be affected.

Spastic quadriplegia is generally caused by brain damage or disruptions in normal brain development preceding birth. According to the National Institutes of Health, there are four types of brain damage that can cause spastic quadriplegia. These include, damage to the white matter (periventricular leukomalacia), abnormal brain development (cerebral dysgenesis), bleeding in the brain (intracranial hemorrhage), and brain damage due to lack of oxygen (hypoxic-ischemic encephalopathy or intrapartum asphyxia).

The white matter of the brain is especially vulnerable between the 26th and 34th weeks of maturation, and damage to the white matter can interfere with the brain’s ability to transmit signals to the rest of the body. Spastic quadriplegia can be caused by a condition known as periventricular leukomalacia which results in the formation of lesions and holes in the white matter of the brain.

Prior to the 26th week of maturation, the fetal brain is particularly susceptible to various toxins whose effects can ultimately hinder normal development. Exposure of the brain to infectious agents is especially dangerous because they can trigger immune responses that activate cytokines and lead to inflammation of the brain. Some infections that have been linked to the development of spastic quadriplegia include meningitis, herpes, rubella, and encephalitis. A difference in blood types between the mother and the fetus can also initiate a problematic immune response and cause brain damage. Severe jaundice, can also lead to brain damage and spastic quadriplegia due to a buildup of bilirubin in the blood.

Bleeding in the brain caused by fetal strokes, blood clots, weak and malformed blood vessels, or high maternal blood pressure may also lead to brain damage causing spastic quadriplegia. Maternal infection, most specifically pelvic inflammatory disease, has been shown to increase the risk of fetal stroke.

Hypoxia, lack of oxygen to the brain, can also cause damage in the cerebral motor cortex and other brain regions. This lack of oxygen can be the result of placenta malfunction, womb rupture, umbilical cord damage, low maternal blood pressure or asphyxia during labor and delivery.

Children who experienced many complications during birth, such as, prematurity, insufficient oxygen, low birthweight, aspiration, head injury, or bleeding in the brain have a greater risk of developing spastic quadriplegia. Children whose mothers were ill during the pregnancy or did not receive adequate nutrition are also more likely to develop the disease.

In some cases, spastic cerebral palsy is caused by genetic factors.

The genetic factors for spastic cerebral palsy include:

Although it has its origins in a brain injury, spastic CP can largely be thought of as a collection of orthopaedic and neuromuscular issues because of how it manifests symptomatically over the course of the person's lifespan. It is therefore not the same as "brain damage" and it need not be thought of as such. Spastic quadriplegia in particular, especially if it is combined with verbal speech challenges and strabismus, may be misinterpreted by the general population as alluding to cognitive dimensions to the disability atop the physical ones, but this is false; the intelligence of a person with any type of spastic CP is unaffected by the condition "of the spasticity itself".

In spastic cerebral palsy in children with low birth weights, 25% of children had hemiplegia, 37.5% had quadriplegia, and 37.5% had diplegia.

Many children affected by alternating hemiplegia also suffer from epilepsy. Seizures may occur during an attack but more often occur between attacks. Anti-epilepsy drugs are given to prevent or lessen the seizures, but the drugs often don’t work and have severe side effects that require the patient to discontinue use. Flunarizine, which blocks calcium channels, is an antiepilepsy drugs used in 50% of patients, and has been shown to shorten the duration of attacks as well as reducing the severity of the attacks. While Flunarizine does not stop the attacks, it is most common drug prescribed to treat those suffering from alternating hemiplegia.

The treatment for facial diplegia depends on the underlying cause. Some causes are usually treatable such as infectious, toxic, and vascular by treating the main problem first. After the underlying problem is cured, the facial paralysis usually will go away.

There are several ways of getting diplegia in the arms. It is very common for people with Cerebral Palsy to have diplegia of the arms. Although most people with Cerebral Palsy have diplegia in their legs, some people have diplegia in their arms. Other ways of getting paralysis of both arms is through a traumatic event or injury.

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.

Spastic cerebral palsy is the type of cerebral palsy wherein spasticity is the exclusive impairment present. Itself an umbrella term encompassing spastic hemiplegia, spastic diplegia, spastic quadriplegia and — where solely one limb or one specific area of the body is affected— spastic monoplegia. Spastic cerebral palsy affects the cerebral cortex it is overwhelmingly the most common type of overall cerebral palsy.

The Society for Cerebral Palsy in Europe (SCPE) estimates that the spasticity-only cerebral palsy classification sweeps in 90% of global cerebral palsy cases. But even if the 90% assertion is an exaggeration, more conservative scientific estimates still place the prevalence of spasticity-dominant or spasticity-only cerebral palsy at anywhere from 70–80% of all cases, leaving cases dominated by ataxic cerebral palsy, dyskinetic cerebral palsy and athetoid cerebral palsy trailing at 20–30%.

Spastic quadriplegia, also known as spastic tetraplegia, is a subset of spastic cerebral palsy that affects all four limbs (both arms and legs).

Compared to quadriplegia, spastic tetraplegia is defined by spasticity of the limbs as opposed to strict paralysis. It is distinguishable from other forms of cerebral palsy in that those afflicted with the condition display stiff, jerky movements stemming from hypertonia of the muscles.

Spastic quadriplegia, while affecting all four limbs more or less equally, can still present parts of the body as stiffer than others, such as one arm being tighter than another arm, and so forth. Spastic triplegia, meanwhile, involves three limbs (such as one arm and two legs, or one leg and two arms, etc.); spastic diplegia affects two limbs (commonly just the legs), spastic hemiplegia affects one or another entire side of the body (left or right); and spastic monoplegia involves a single limb.

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.

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.

An occurrence of Todd's paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects of the seizure, not the occurrence of the paralysis.

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.

Bruns apraxia, or frontal ataxia is a gait apraxia found in patients with bilateral frontal lobe disorders. It is characterised by an inability to initiate the process of walking, despite the power and coordination of the legs being normal when tested in the seated or lying position. The gait is broad-based with short steps with a tendency to fall backwards. It was originally described in patients with frontal lobe tumours, but is now more commonly seen in patients with cerebrovascular disease.

It is named after Ludwig Bruns.

Brown-Séquard syndrome (also known as Brown-Séquard's hemiplegia, Brown-Séquard's paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.

Dysdiadochokinesia, dysdiadochokinesis, dysdiadokokinesia, dysdiadokokinesis (from Greek "δυς" "dys" "bad", "διάδοχος" "diadochos" "succeeding", "κίνησις" "kinesis" "movement"), often abbreviated as DDK, is the medical term for an impaired ability to perform rapid, alternating movements (i.e., diadochokinesia). Complete inability is called adiadochokinesia.

Unlike ataxias of cerebellar origin, Bruns apraxia exhibits many frontal lobe ataxia characteristics, with some or all present.

- Difficulty in initiating movement

- Poor truncal mobility

- Falls due to minor balance disturbances

- Greatly hindered postural responses

- Characteristic magnetic gait, the inability to raise one's foot off of the floor.

- Wide base, poor balance control when in stance

- Short stride

- En bloc turns

Often patients with frontal lobe ataxia may experience minute cognitive changes that accompany the gait disturbances, such as frontal dementia and presentation of frontal release signs (Plantar reflex). Urinary incontinence may also be present.

Bruns apraxia can be distinguished from Parkinsonian ataxia and cerebellar ataxia in a number of ways. Patients typically afflicted with Parkinsonian ataxia typically have irregular arm swing, a symptom not typically present in frontal ataxia. Walking stride in cerebellar ataxia varies dramatically, accompanied by erratic foot placement and sudden, uncontrolled lurching, not generally characteristic of Bruns apraxia.

Dysdiadochokinesia is a feature of cerebellar ataxia and may be the result of lesions to either the cerebellar hemispheres or the frontal lobe (of the cerebrum), it can also be a combination of both. It is thought to be caused by the inability to switch on and switch off antagonising muscle groups in a coordinated fashion due to hypotonia, secondary to the central lesion.

Dysdiadochokinesia is also seen in Friedreich's ataxia and multiple sclerosis, as a cerebellar symptom (including ataxia, intention tremor and dysarthria). It is also a feature of ataxic dysarthria. Dysdiadochokinesia often presents in motor speech disorders (dysarthria), therefore testing for dysdiadochokinesia can be used for a differential diagnosis.

Dysdiadochokinesia has been linked to a mutation in "SLC18A2", which encodes vesicular monoamine transporter 2 (VMAT2).

Benedikt syndrome, also called Benedikt's syndrome or paramedian midbrain syndrome, is a rare type of posterior circulation stroke of the brain, with a range of neurological symptoms affecting the midbrain, cerebellum and other related structures.

It is characterized by the presence of an oculomotor nerve (CN III) palsy and cerebellar ataxia including tremor and involuntary choreoathetotic movements. Neuroanatomical structures affected include CNIII nucleus, Red nucleus, corticospinal tracts, brachium conjunctivum, and the superior cerebellar peduncle decussation. It has a very similar cause, morphology and signs and symptoms to Weber's syndrome; the main difference between the two being that Weber's is more associated with hemiplegia (i.e. paralysis), and Benedikt's with hemiataxia (i.e. disturbed coordination of movements). It is also similar to Claude's syndrome, but is distinguishable in that Benedikt's has more predominant tremor and choreoathetotic movements while Claude's is more marked by the ataxia.

Besides complications of surgery and anesthesia in general, there may be drainage, swelling, or redness of the incision, gagging or coughing during eating or drinking, or pneumonia due to aspiration of food or liquids. Undesirable complications are estimated to occur in 10-30% of cases. If medical therapy is unsuccessful and surgery cannot be performed due to concurrent disease (such as heart or lung problems) or cost, euthanasia may be necessary if the animal's quality of life is considered unacceptable due to the disease.

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.