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.

The incidence of cerebral palsy has increased in the past 40 years. It has been estimated that in the United States cerebral palsy occurs in 4 out every 1000 births. Of these births about 20–30% of them have spastic hemiplegia. Spasticity overall, is the more common type of cerebral palsy, whereas as non-spastic cerebral palsy is less common. Studies show that spastic type cerebral palsy is on the rise, and the occurrence of diplegia type is decreasing. The prevalence of cerebral palsy is higher in areas of low socioeconomic status. This could potentially be because cerebral palsy incidence increases as birth weight decreases.

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.

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.

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.

The most common cause of diplegia in the legs is Cerebral Palsy. Paralysis of the legs may also be caused by trauma, injury, or genetics but this is very rare

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.

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.

In any manifestation of spastic CP, clonus of the affected limb(s) may intermittently result, as well as muscle spasms, each of which results from the pain and/or stress of the tightness experienced, indicating especially hard-working and/or exhausted musculature. The spasticity itself can and usually does also lead to very early onset of muscle-stress symptoms like arthritis and tendinitis, especially in ambulatory individuals in their mid-20s and early-30s. As compared to other types of CP, however, and especially as compared to hypotonic CP or more general paralytic mobility disabilities, spastic CP is typically more easily manageable by the person affected, and medical treatment can be pursued on a multitude of orthopaedic and neurological fronts throughout life.

Physical therapy and occupational therapy regimens of assisted stretching, strengthening, functional tasks, and/or targeted physical activity and exercise are usually the chief ways to keep spastic CP well-managed, although if the spasticity is too much for the person to handle, other remedies may be considered, such as various antispasmodic medications, botox, baclofen, or even a neurosurgery known as a selective dorsal rhizotomy (which eliminates the spasticity by eliminating the nerves causing it).

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 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.

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.

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.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.

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.

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.

Claude's syndrome is a form of brainstem stroke syndrome characterized by the presence of an ipsilateral oculomotor nerve palsy, contralateral hemiparesis, contralateral ataxia, and contralateral hemiplegia of the lower face, tongue, and shoulder.

Claude's syndrome affects oculomotor nerve, red nucleus and brachium conjunctivum

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.

Claude's syndrome is caused by midbrain infarction as a result of occlusion of a branch of the posterior cerebral artery. This lesion is usually a unilateral infarction of the red nucleus and cerebral peduncle, affecting several structures in the midbrain including:

It is very similar to Benedikt's syndrome.

In most cases, the cause of laryngeal paralysis is unknown or idiopathic. However, the disorder may arise secondary to general neuropathies, generalized neuromuscular diseases, muscular diseases, neoplasia either in the cervical (neck) region or the cranial mediastinum, or trauma. This acquired form occurs predominantly in middle-aged to old large breed or giant breed dogs such as the Labrador Retriever, golden retriever, Siberian Husky, Newfoundland, and St. Bernard. Usually these dogs are born with a normal larynx, but over time the nerves and muscles that control the laryngeal cartilages lose function.

Laryngeal paralysis may also be congenital in some breeds (e.g. Bouvier des Flandres, Dalmatians, Siberian huskies, and bulldogs), appearing in dogs between two and six months of age. Affected puppies may have difficulty swallowing and breathing, they may gag frequently, and their bark often sounds abnormal. In Dalmatians it is part of another condition called 'laryngeal paralysis-polyneuropathy complex.' Affected puppies should not be used for breeding.

Choke collars are not thought to be a significant risk factor for this disorder. However, after LP is diagnosed it is usually recommended to stop using a collar or anything else around the dog's neck and to switch to a harness instead.

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.

Posterior cerebral artery syndrome is a condition whereby the blood supply from the posterior cerebral artery (PCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the occipital lobe, the inferomedial temporal lobe, a large portion of the thalamus, and the upper brainstem and midbrain.

This event restricts the flow of blood to the brain in a near-immediate fashion. The blood hammer is analogous to the water hammer in hydrology and it consists of a sudden increase of the upstream blood pressure in a blood vessel when the bloodstream is abruptly blocked by vessel obstruction. Complete understanding of the relationship between mechanical parameters in vascular occlusions is a critical issue, which can play an important role in the future diagnosis, understanding and treatment of vascular diseases.

Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with PCA syndrome. Blockages of the proximal portion of the vessel produce only minor deficits due to the collateral blood flow from the opposite hemisphere via the posterior communicating artery. In contrast, distal occlusions result in more serious complications. Visual deficits, such as agnosia, prosopagnosia or cortical blindness (with bilateral infarcts) may be a product of ischemic damage to occipital lobe. Occlusions of the branches of the PCA that supply the thalamus can result in central post-stroke pain and lesions to the subthalamic branches can produce “a wide variety of deficits”.

Left posterior cerebral artery syndrome presents alexia without agraphia; the lesion is in the splenium of the corpus callosum.