The prognosis for those with spastic muscles depends on multiple factors, including the severity of the spasticity and the associated movement disorder, access to specialised and intensive management, and ability of the affected individual to maintain the management plan (particularly an exercise program). Most people with a significant UMN lesion will have ongoing impairment, but most of these will be able to make progress. The most important factor to indicate ability to progress is seeing improvement, but improvement in many spastic movement disorders may not be seen until the affected individual receives help from a specialised team or health professional.

Doublecortin positive cells, Similar to stem cells, are extremely adaptable and, when extracted from a brain, cultured and then re-injected in a lesioned area of the same brain, they can help repair and rebuild it. The treatment using them would take some time to be available for general public use, as it has to clear regulations and trials.

Assessment of motor control may involve several health professionals depending on the affected individual's situation, and the severity of their condition. This may include physical therapists, physicians (including neurologists and psychiatrists ) and rehabilitation physicians, orthotists, occupational therapists, and speech-language pathologists. Assessment is needed of the affected individual's goals, their function, and any symptoms that may be related to the movement disorder, such as pain. A thorough assessment then uses a clinical reasoning approach to determine why difficulties are occurring. Elements of assessment will include analysis of posture, active movement, muscle strength, movement control and coordination, and endurance, as well as muscle tone and spasticity. Impaired muscles typically demonstrate a loss of selective movement, including a loss of eccentric control (decreased ability to actively lengthen); this decreased active lengthening of a muscle is a key factor that limits motor control. While multiple muscles in a limb are usually affected in the Upper Motor Neuron Syndrome, there is usually an imbalance of muscle activity (muscle tone), such that there is a stronger pull on one side of a joint, such as into elbow flexion. Decreasing the degree of this imbalance is a common focus of muscle strengthening programs. Impaired motor control also typically features a loss of stabilisation of an affected limb or the head from the trunk, so a thorough assessment requires this to be analysed as well, and exercise to improve proximal stability may be indicated.

Secondary effects are likely to impact on assessment of impaired muscles. If muscle tone is assessed with passive muscle lengthening, increased muscle stiffness may affect the feeling of resistance to passive stretch, in addition to neurological resistance to stretch. Other secondary changes such as loss of muscle fibres following acquired muscle weakness are likely to compound the weakness arising from the upper motor neuron lesion. In severely affected muscles, there may be marked secondary changes, such as muscle contracture, particularly if management has been delayed or absent.

Treatment should be based on assessment by the relevant health professionals. For muscles with mild-to-moderate impairment, exercise should be the mainstay of management, and is likely to need to be prescribed by a physical therapist or other health professional skilled in neurological rehabilitation.

Muscles with severe impairment are likely to be more limited in their ability to exercise, and may require help to do this. They may require additional interventions, to manage the greater neurological impairment and also greater secondary complications. These interventions may include serial casting, flexibility exercise such as sustained positioning programs, and medical interventions.

Research has clearly shown that exercise is beneficial for impaired muscles, even though it was previously believed that strength exercise would "increase" muscle tone and impair muscle performance further. Also, in previous decades there has been a strong focus on other interventions for impaired muscles, particularly stretching and splinting, but the evidence does not support these as effective. One of the challenges for health professionals working with UMNS movement disorders is that the degree of muscle weakness makes developing an exercise programme difficult. For muscles that lack any volitional control, such as after complete spinal cord injury, exercise may be assisted, and may require equipment, such as using a standing frame to sustain a standing position. Often, muscles require specific stimulation to achieve small amounts of activity, which is most often achieved by weight-bearing (e.g. positioning and supporting a limb such that it supports body weight) or by stimulation to the muscle belly (such as electrical stimulation or vibration).

Medical interventions may include such medications as baclofen, diazepam, dantrolene, or clonazepam. Phenol injections or botulinum toxin injections into the muscle belly can be used to attempt to dampen the signals between nerve and muscle. The effectiveness of medications varies between individuals, and varies based on location of the upper motor neuron lesion (in the brain or the spinal cord). Medications are commonly used for movement disorders, but research has not shown functional benefit for some drugs. Some studies have shown that medications have been effective in decreasing spasticity, but that this has not been accompanied by functional benefits.

There are a variety of standardized assessment scales available to physiotherapists and other health care professionals for use in the ongoing evaluation of the status of a patient’s hemiplegia. The use of standardized assessment scales may help physiotherapists and other health care professionals during the course of their treatment plant to:

- Prioritize treatment interventions based on specific identifiable motor and sensory deficits

- Create appropriate short- and long-term goals for treatment based on the outcome of the scales, their professional expertise and the desires of the patient

- Evaluate the potential burden of care and monitor any changes based on either improving or declining scores

Some of the most commonly used scales in the assessment of hemiplegia are:

- The Fugl-Meyer Assessment of Physical Performance (FMA)

The FMA is often used as a measure of functional or physical impairment following a cerebrovascular accident (CVA). It measures sensory and motor impairment of the upper and lower extremities, balance in several positions, range of motion, and pain. This test is a reliable and valid measure in measuring post-stroke impairments related to stroke recovery. A lower score in each component of the test indicates higher impairment and a lower functional level for that area. The maximum score for each component is 66 for the upper extremities, 34 for the lower extremities, and 14 for balance. Administration of the FMA should be done after reviewing a training manual.

- The Chedoke-McMaster Stroke Assessment (CMSA)

This test is a reliable measure of two separate components evaluating both motor impairment and disability. The disability component assesses any changes in physical function including gross motor function and walking ability. The disability inventory can have a maximum score of 100 with 70 from the gross motor index and 30 from the walking index. Each task in this inventory has a maximum score of seven except for the 2 minute walk test which is out of two. The impairment component of the test evaluates the upper and lower extremities, postural control and pain. The impairment inventory focuses on the seven stages of recovery from stroke from flaccid paralysis to normal motor functioning. A training workshop is recommended if the measure is being utilized for the purpose of data collection.

- The Stroke Rehabilitation Assessment of Movement (STREAM)

The STREAM consists of 30 test items involving upper-limb movements, lower-limb movements, and basic mobility items. It is a clinical measure of voluntary movements and general mobility (rolling, bridging, sit-to-stand, standing, stepping, walking and stairs) following a stroke. The voluntary movement part of the assessment is measured using a 3-point ordinal scale (unable to perform, partial performance, and complete performance) and the mobility part of the assessment uses a 4-point ordinal scale (unable, partial, complete with aid, complete no aid). The maximum score one can receive on the STREAM is a 70 (20 for each limb score and 30 for mobility score). The higher the score, the better movement and mobility is available for the individual being scored.

Movement and posture limitations are aspects of all CP types and as a result, CP has historically been diagnosed based on parental reporting of developmental motor delays such as failure to sit upright, reach for objects, crawl, stand, or walk at the appropriate age. Diagnosis of ADCP is also based on clinical assessment used in conjunction with milestone reporting. The majority of ADCP assessments now use the Gross Motor Function Classification System (GMFCS) or the International Classification of Functioning, Disability and Health (formerly the International Classification of Impairments Disease, and Handicaps), measures of motor impairment that are effective in assessing severe CP. ADCP is typically characterized by an individual’s inability to control their muscle tone, which is readily assessed via these classification systems.

Magnetic resonance imaging (MRI) is used to detect morphological brain abnormalities associated with ADCP in patients that are either at risk for ADCP or have shown symptoms thereof. The abnormalities chiefly associated with ADCP are lesions that appear in the basal ganglia. The severity of the disease is proportional to the severity and extent of these abnormalities, and is typically greater when additional lesions appear elsewhere in the deep grey matter or white matter. MRI also has the ability to detect brain malformation, periventricular leukomalacia (PVL), and areas affected by hypoxia-ischemia, all of which may play a role in the development of ADCP. The MRI detection rate for ADCP is approximately 54.5%, however this statistic varies depending on the patient’s age and the cause of the disease and has been reported to be significantly higher.

Like ALS, diagnosing PLS is a diagnosis of exclusion, as there is no one test that can confirm a diagnosis of PLS. The Pringle Criteria, proposed by Pringle et al, provides a guideline of nine points that, if confirmed, can suggest a diagnosis of PLS. Due to the fact that a person with ALS may initially present with only upper motor neuron symptoms, indicative of PLS, one key aspect of the Pringle Criteria is requiring a minimum of three years between symptom onset and symptom diagnosis. When these criteria are met, a diagnosis of PLS is highly likely. Other aspects of Pringle Criteria include normal EMG findings, thereby ruling out lower motor neuron involvement that is indicative of ALS, and absence of family history for Hereditary Spastic Paraplegia (HSP) and ALS. Imaging studies to rule out structural or demyelinating lesions may be done as well. Hoffman's sign and Babinski reflex may be present and indicative of upper motor neuron damage.

Hemiplegia is identified by clinical examination by a health professional, such as a physiotherapist or doctor. Radiological studies like a CT scan or magnetic resonance imaging of the brain should be used to confirm injury in the brain and spinal cord, but alone cannot be used to identify movement disorders. Individuals who develop seizures may undergo tests to determine where the focus of excess electrical activity is.

Hemiplegia patients usually show a characteristic gait. The leg on the affected side is extended and internally rotated and is swung in a wide, lateral arc rather than lifted in order to move it forward. The upper limb on the same side is also adducted at the shoulder, flexed at the elbow, and pronated at the wrist with the thumb tucked into the palm and the fingers curled around it.

Hereditary spastic paraplegias can be classified based on the symptoms; mode of inheritance; the patient’s age at onset; the affected genes; and biochemical pathways involved.

Physiotherapy has been shown to be effective in controlling hypertonia through the use of stretching aimed to reduce motor neuron excitability. The aim of a physical therapy session could be to inhibit excessive tone as far as possible, give the patient a sensation of normal position and movement, and to facilitate normal movement patterns. While static stretch has been the classical means to increase range of motion, PNF stretching has been used in many clinical settings to effectively reduce muscle spasticity.

Icing and other topical anesthetics may decrease the reflexive activity for short period of time in order to facilitate motor function. Inhibitory pressure (applying firm pressure over muscle tendon) and promoting body heat retention and rhythmic rotation (slow repeated rotation of affected body part to stimulate relaxation) have also been proposed as potential methods to decrease hypertonia. Aside from static stretch casting, splinting techniques are extremely valuable to extend joint range of motion lost to hypertonicity. A more unconventional method for limiting tone is to deploy quick repeated passive movements to an involved joint in cyclical fashion; this has also been demonstrated to show results on persons without physical disabilities. For a more permanent state of improvement, exercise and patient education is imperative. Isokinetic, aerobic, and strength training exercises should be performed as prescribed by a physiotherapist, and stressful situations that may cause increased tone should be minimized or avoided.

Therapeutic interventions are best individualized to particular patients.

Basic principles of treatment for hypertonia are to avoid noxious stimuli and provide frequent range of motion exercise.

Diagnosis of pseudobulbar palsy is based on observation of the symptoms of the condition. Tests examining jaw jerk and gag reflex can also be performed. It has been suggested that the majority of patients with pathological laughter and crying have pseudobulbar palsy due to bilateral corticobulbar lesions and often a bipyrimidal involvement of arms and legs. To further confirm the condition, MRI can be performed to define the areas of brain abnormality.

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.

Initial diagnosis of HSPs relies upon family history, the presence or absence of additional signs and the exclusion of other nongenetic causes of spasticity, the latter being particular important in sporadic cases.

Cerebral and spinal MRI is an important procedure performed in order to rule out other frequent neurological conditions, such as multiple sclerosis, but also to detect associated abnormalities such as cerebellar or corpus callosum atrophy as well as white matter abnormalities. Differential diagnosis of HSP should also exclude spastic diplegia which presents with nearly identical day-to-day effects and even is treatable with similar medicines such as baclofen and orthopedic surgery; at times, these two conditions may look and feel so similar that the only "perceived" difference may be HSP's hereditary nature versus the explicitly non-hereditary nature of spastic diplegia (however, unlike spastic diplegia and other forms of spastic cerebral palsy, HSP cannot be reliably treated with selective dorsal rhizotomy).

Ultimate confirmation of HSP diagnosis can only be provided by carrying out genetic tests targeted towards known genetic mutations.

Surgery, such as the denervation of selected muscles, may also provide some relief; however, the destruction of nerves in the limbs or brain is not reversible and should be considered only in the most extreme cases. Recently, the procedure of deep brain stimulation (DBS) has proven successful in a number of cases of severe generalised dystonia. DBS as treatment for medication-refractory dystonia, on the other hand, may increase the risk of suicide in patients. However, reference data of patients without DBS therapy are lacking.

Doublecortin positive cells, similar to stem cells, are extremely adaptable and, when extracted from a brain, cultured and then re-injected in a lesioned area of the same brain, they can help repair and rebuild it. The treatment using them would take some time to be available for general public use, as it has to clear regulations and trials.

Spastic quadriplegia can be diagnosed as early as age one after a noticed delay in development, particularly a delay in rolling, crawling, sitting, or walking. However, depending on the severity, signs may not show up until the age of three. Muscle tone is sometimes used to make the diagnosis for spastic quadriplegia as affected children often appear to be either too stiff or too floppy.

Another important diagnostic factor is the persistence of primitive reflexes past the age at which they should have disappeared (6–12 months of age). These reflexes include the rooting reflex, the sucking reflex, and the Moro reflex, among others.

Magnetic resonance imaging (MRI) or a computed tomography scan (CT scan) may be used to locate the cause of the symptoms. Ultrasound may be used for the same function in premature babies.

Because cerebral palsy refers to a group of disorders, it is important to have a clear and systematic naming system. These disorders must be non-progressive, non-transient, and not due to injury to the spinal cord. Disorders within the group are classified based on two characteristics- the main physiological symptom, and the limbs that are affected. For a disorder to be diagnosed as spastic quadriplegia, an individual must show spastic symptoms (as opposed to athetotic, hypertonic, ataxic, or atonic symptoms) and it must be present in all four limbs (as opposed to hemiplegic, diplegic, or triplegic cases).

While a diagnosis may be able to be made shortly after birth based on family history and observation of the infant, it is often postponed until after the child is between 18–24 months old in order to monitor the possible regression or progression of symptoms.

Patients can often live with PLS for many years and very often outlive their neurological disease and succumb to some unrelated condition. There is currently no effective cure, and the progression of symptoms varies. Some people may retain the ability to walk without assistance, but others eventually require wheelchairs, canes, or other assistive devices.

Delayed diagnosis of cervical spine injury has grave consequences for the victim. About one in 20 cervical fractures are missed and about two-thirds of these patients have further spinal-cord damage as a result. About 30% of cases of delayed diagnosis of cervical spine injury develop permanent neurological deficits. In high-level cervical injuries, total paralysis from the neck can result. High-level tetraplegics (C4 and higher) will likely need constant care and assistance in activities of daily living, such as getting dressed, eating and bowel and bladder care. Low-level tetraplegics (C5 to C7) can often live independently.

Even with "complete" injuries, in some rare cases, through intensive rehabilitation, slight movement can be regained through "rewiring" neural connections, as in the case of the late actor Christopher Reeve.

In the case of cerebral palsy, which is caused by damage to the motor cortex either before, during (10%), or after birth, some people with tetraplegia are gradually able to learn to stand or walk through physical therapy.

Quadriplegics can improve muscle strength by performing resistance training at least three times per week. Combining resistance training with proper nutrition intake can greatly reduce co-morbidities such as obesity and type 2 diabetes.

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).

While research in the area of effectiveness of physical therapy intervention for dystonia remains weak, there is reason to believe that rehabilitation will benefit patients with dystonia. Physical therapy can be utilized to manage changes in balance, mobility and overall function that occur as a result of the disorder. A variety of treatment strategies can be employed to address the unique needs of each individual. Potential treatment interventions include splinting, therapeutic exercise, manual stretching, soft tissue and joint mobilization, postural training and bracing, neuromuscular electrical stimulation, constraint-induced movement therapy, activity and environmental modification, and gait training.

A patient with dystonia may have significant challenges in activities of daily living (ADL), an area especially suited for treatment by occupational therapy (OT). An occupational therapist (OT) may perform needed upper extremity splinting, provide movement inhibitory techniques, train fine motor coordination, provide an assistive device, or teach alternative methods of activity performance to achieve a patient's goals for bathing, dressing, toileting, and other valued activities.

Recent research has investigated further into the role of physiotherapy in the treatment of dystonia. A recent study showed that reducing psychological stress, in conjunction with exercise, is beneficial for reducing truncal dystonia in patients with Parkinson’s Disease. Another study emphasized progressive relaxation, isometric muscle endurance, dynamic strength, coordination, balance, and body perception, seeing significant improvements to patients’ quality of life after 4 weeks.

Since the root of the problem is neurological, doctors have explored sensorimotor retraining activities to enable the brain to "rewire" itself and eliminate dystonic movements. The work of several doctors such as Nancy Byl and Joaquin Farias has shown that sensorimotor retraining activities and proprioceptive stimulation can induce neuroplasticity, making it possible for patients to recover substantial function that was lost due to Cervical Dystonia, hand dystonia, blepharospasm, oromandibular dystonia, dysphonia and musicians' dystonia.

Some focal dystonias have been proven treatable through movement retraining in the Taubman approach, particularly in the case of musicians. However other focal dystonias may not respond and may even be made worse by this treatment.

Due to the rare and variable nature of dystonia, research investigating the effectiveness of these treatments is limited. There is no "gold standard" for physiotherapy rehabilitation. To date, focal cervical dystonia has received the most research attention; however, study designs are poorly controlled and limited to small sample sizes.

Incomplete spinal cord injuries result in varied post injury presentations. There are three main syndromes described, depending on the exact site and extent of the lesion.

1. The central cord syndrome: most of the cord lesion is in the gray matter of the spinal cord, sometimes the lesion continues in the white matter.

2. The Brown–Séquard syndrome: hemi section of the spinal cord.

3. The anterior cord syndrome: a lesion of the anterior horns and the anterolateral tracts, with a possible division of the anterior spinal artery.

For most patients with ASIA A (complete) tetraplegia, ASIA B (incomplete) tetraplegia and ASIA C (incomplete) tetraplegia, the International Classification level of the patient can be established without great difficulty. The surgical procedures according to the International Classification level can be performed. In contrast, for patients with ASIA D (incomplete) tetraplegia it is difficult to assign an International Classification other than International Classification level X (others). Therefore, it is more difficult to decide which surgical procedures should be performed. A far more personalized approach is needed for these patients. Decisions must be based more on experience than on texts or journals.

The results of tendon transfers for patients with complete injuries are predictable. On the other hand, it is well known that muscles lacking normal excitation perform unreliably after surgical tendon transfers. Despite the unpredictable aspect in incomplete lesions tendon transfers may be useful. The surgeon should be confident that the muscle to be transferred has enough power and is under good voluntary control. Pre-operative assessment is more difficult to assess in incomplete lesions.

Patients with an incomplete lesion also often need therapy or surgery before the procedure to restore function to correct the consequences of the injury. These consequences are hypertonicity/spasticity, contractures, painful hyperesthesias and paralyzed proximal upper limb muscles with distal muscle sparing. Spasticity is a frequent consequence of incomplete injuries. Spasticity often decreases function, but sometimes a patient can control the spasticity in a way that it is useful to their function. The location and the effect of the spasticity should be analyzed carefully before treatment is planned. An injection of Botulinum toxin (Botox) into spastic muscles is a treatment to reduce spasticity. This can be used to prevent muscle shorting and early contractures.

Over the last ten years an increase in traumatic incomplete lesions is seen, due to the better protection in traffic.

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.

Since pseudobulbar palsy is a syndrome associated with other diseases, treating the underlying disease may eventually reduce the symptoms of pseudobulbar palsy.

Possible pharmacological interventions for pseudobulbar affect include the tricyclic antidepressants, serotonin reuptake inhibitors, and a novel approach utilizing dextromethorphan and quinidine sulfate. Nuedexta is an FDA approved medication for pseudobulbar affect. Dextromethorphan, an N-methyl-D-aspartate receptor antagonist, inhibits glutamatergic transmission in the regions of the brainstem and cerebellum, which are hypothesized to be involved in pseudobulbar symptoms, and acts as a sigma ligand, binding to the sigma-1 receptors that mediate the emotional motor expression.