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.

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.

Diagnosis of ataxic cerebral palsy is based on clinical assessment using standardized assessment tools. Diagnosis begins with the observation of slow motor development, abnormal muscle tone, and unusual posture in children that fail to reach developmental milestones. Diagnosis differs in adults and children because a child’s brain is still developing and acquiring new motor, linguistic, adaptive, and social skills. The testing strategy is based on the pattern of development of symptoms, the patient’s family history, and any factors that might influence the diagnosis, such as injury or trauma. Associated disabilities such as those previously described under symptoms associated with ataxic cerebral palsy, i.e., sensory impairment and cognitive dysfunction, are also helpful in diagnosing the disease.

In children, assessment of infantile reflexes is also a diagnostic tool, such as the Moro reflex and the Romberg Test. The Moro reflex is rarely present in infants after 6 months of age and is characterized as a response to a sudden loss of support that causes the infant to feel like it is falling. The infant will respond by abduction and adduction (or spreading and unspreading) of the arms, as well as crying. The Moro reflex is significant in evaluating the integration of the central nervous system and patients with ataxic cerebral palsy will show a persistence and exacerbation of the reflex. In addition, patients with ataxic cerebral palsy will rarely show a positive Romberg test, which indicates that there is localized cerebellar dysfunction.

Physical diagnostic tests, such as cerebral imaging using Computerized Tomography (CT), Magnetic Resonance Imaging (MRI), and ultrasound are also useful, but not preferred to clinical assessments. These neuroimaging techniques can show brain abnormalities that have been found in previous patients with cerebral palsy, i.e., focal infarction and various brain malformations, however in a study of 273 children who were born after 35 weeks of gestation and underwent neuroimaging studies, one-third of the infants showed normal studies. In addition, infants undergo neuroimaging studies once the infant has neurological findings suggestive of cerebral palsy.

For developmental diagnosis in children and infants, there are a number of milestones of motor, linguistic, adaptive, and social behavior, such as.

1. When the child could sit up on their own with or without support

2. Say their first words

3. Feed themselves

4. Play successfully with children of same age

MRI is often done to diagnose PSP. MRI may show atrophy in the midbrain with preservation of the pons giving a "hummingbird" sign appearance.

PBP is aggressive and relentless, and there were no treatments for the disease as of 2005. However, early detection of PBP is the optimal scenario in which doctors can map out a plan for management of the disease. This typically involves symptomatic treatments that are frequently used in many lower motor disorders.

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.

Current forms of prevention are focused during pregnancy, while others are focused immediately after birth. Some methods that have been used include prolonging the pregnancy using interventions such as 17-alpha progesterone, limiting the number of gestations during pregnancy (for pregnancies induced by assistive reproductive technology), antenatal steroid for mothers likely to deliver prematurely, high caffeine for premature births with extremely low birth weights.

PSP is frequently misdiagnosed as Parkinson's disease because of the slowed movements and gait difficulty, or as Alzheimer's disease because of the behavioral changes. It is one of a number of diseases collectively referred to as Parkinson plus syndromes. A poor response to levodopa along with symmetrical onset can help differentiate this disease from PD. Also, patients with the Richardson variant tend to have an upright or arched-back posture as opposed to the stooped-forward posture of other Parkinsonian disorders, although PSP-Parkinsonism (see below) may show the stooped posture. Early falls are characteristic, especially with Richardson-syndrome.

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.

Progressive Bulbar Palsy is slow in onset, with symptoms starting in most patients around 50–70 years of age. PBP has a life expectancy typically between 6 months and 3 years from onset of first symptoms. It is subtype of the Motor Neurone Diseases (MND) accounting for around 1 in 4 cases. Amyotrophic lateral sclerosis (ALS) is another sub-type. Pure PBP without any EMG or clinical evidence of abnormalities in the legs or arms is possible, albeit extremely rare. Moreover, about twenty-five percent of patients with PBP eventually develop the widespread symptoms common to ALS.

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).

There is no known cure for cerebral palsy, however there is a large array of treatments proven effective at improving quality of life and relieving some of the symptoms associated with CP, especially SHCP. Some treatments are aimed at improving mobility, strengthening muscle and improving coordination. Although CP is due to permanent damage and is not progressive in nature, without treatment the symptoms can become worse, intensifying in pain and severity, and create complications that were not initially present. Some treatments are preventative measures to help prevent further complications, such as complete paralysis of the arm due to non-use and subsequent worsening hypertonia and joint contracture. Others forms of treatment are corrective in nature. Many treatments target symptoms that are indirectly related to or caused by the SHCP. Many of these treatments are common for other forms of CP as well. Treatment is individualized based on each case and the specific needs of the patient. Treatments are often combined with other forms of treatment and a long term treatment plan is created and continuously evaluated. Treatment can include the following:

- "Physical therapy" – Physical therapy is the most common form of treatment (source needed). It may include sensory stimulation, stretching, strengthening and positioning. Constraint-induced movement therapy is a newer form of physical therapy for SHCP that involves casting or splinting the unaffected arm to promote use of the affected arm (Taub). The theory behind constraint-induced movement therapy is that new neural pathways are created. Alternative forms of physical therapy include yoga and dance. Physical therapy may also include the use of braces while not actively involved with the therapist.

- "Occupational therapy" – Occupational therapy evaluates and treats patients through selected activities in order to enable people to function as effectively and independently as possible in daily life. Occupational therapy is geared toward the individual to achieve optimal results and performance while learning to cope with their disability.

- "Speech therapy" – Due to difficulties in speech, speech therapy is often necessary. Aside from helping with understanding language and increasing communication skills, speech therapists can also assist children that have difficulty eating and drinking.

- "Behavioral therapy" — Psychotherapy and counseling are heavily used in treatment of individuals with SHPD to help them cope emotionally with their needs and frustrations. Counseling through social work can be very beneficial for social issues and adjustments to society. Psychotherapy becomes a more important aspect of therapy when more serious issues such as depression become problematic. Play therapy is a common treatment for all young children with or without disabilities, but can be very useful helping children with SHCP. This therapy again is individualized geared to improve emotional and social development; reduce aggression; improve cooperation with others; assist a child in processing a traumatic event or prepare for an upcoming event such as surgery.

- "Surgery" – Although surgery may become necessary in some cases, physical therapy and the consistent use of braces can help mitigate the need for surgery. Surgical procedures are painful with long and difficult recoveries and do not cure the condition. Most common, is surgery that effectively lengthens the muscle. This type of surgery is usually performed on the legs, but can be performed on the arms as well. Surgeries also may be necessary to realign joints. Other, less popular surgical techniques try to reduce spasticity by severing selected overactive nerves that control muscles. This procedure, known as selective dorsal root rhizotomy, is still somewhat controversial, and is generally used only on the lower extremities of severe cases. Other experimental surgical techniques are also being investigated. The benefits of surgery can also be negated or reversed if the patient does not participate in physical therapy and braces (or casts) are not worn regularly.

- "Medicinal" – Medication targeting symptoms associated with spasticity is also a relatively new treatment that is utilized, but is still in the early stages of development. Drugs such as baclofen, benzodiazepines (e.g., diazepam), tizanidin, and sometimes dantrolene have shown promise in the effort to diminish spasticity. Botulinum toxin ("Botox") type A may reduce spasticity a few months at a time and has frequently been considered a beneficial treatment for children with SHCP and other forms of CP. Botox has been shown to be especially beneficial to reducing spasticity in the gastrocnemius (calf) muscle. This therapy can improve range of motion, reduce deformity, improve response to occupational and physical therapy, and delay the need for surgery. Botox injections have also shown advantages for upper extremities. There is still some doubt for the effectiveness, and some side effects to the relaxed muscles have been a loss of strength for patients with some muscle control. Casting, in conjunction with Botox injections may be an additional option for better results. Research is constantly investing in new improvements and more experimental therapy and treatment.

Bell's palsy is a diagnosis of exclusion, meaning it is diagnosed by elimination of other reasonable possibilities. By definition, no specific cause can be determined. There are no routine lab or imaging tests required to make the diagnosis. The degree of nerve damage can be assessed using the House-Brackmann score.

One study found that 45% of patients are not referred to a specialist, which suggests that Bell’s palsy is considered by physicians to be a straightforward diagnosis that is easy to manage.

Other conditions that can cause similar symptoms include: herpes zoster, Lyme disease, sarcoidosis, stroke, and brain tumors.

As athetosis is relatively difficult to treat, efforts are being made to help those with the condition live and perform tasks more effectively and more efficiently. One such example of work that has been recently undertaken is a project to help those affected with athetosis to use a computer with more ease. Software for the control of the computer uses joysticks that perform linear filtering to aid in control.

An additional possible treatment option for those afflicted with the symptom is neurostimulation. Studies have begun, and in cerebral palsy patients affected with dystonia-choreoathetosis, it has been demonstrated that neurostimulation has been an effective treatment in lessening symptoms in patients. There has not been a tremendous amount of experimentation, though, in this as a possible treatment option.

There are several different treatment approaches to dealing with athetosis. The most common methods are the use of drugs, surgical intervention, and retraining movements of the afflicted person. It is suggested that training a person to relearn movements can be helpful in select situations. Though, generally, this type of treatment will not work, in certain cases it can be found to be very helpful in treating the symptom of athetosis.

Drugs can also be used in the treatment of athetosis, however their collective effectiveness is not very convincing. There is not a single drug that is a standard among treatment. Many different medicines can be used, including:

- Artane

- Cogentin

- Curare, though not practical due to respiratory paralysis

- Tetrabenazine

- Haloperidol

- Thiopropazate

- Diazepam

Most instances of drug use where the symptoms seem to be lessened tend to be in more mild cases of athetosis.

Treatment by surgical intervention can obviously have the most immediate impact, again however, it is not a cure-all. In patients that have cerebral palsy as the cause of their athetosis, it has been demonstrated that a subthalamotomy tends to help relieve the extent of athetosis in approximately half of patients. Additionally, late 19th and early 20th century surgical accounts state that athetosis can be relieved by the removal of a part of the cerebral motor cortex or by cutting a part of the posterior spinal roots. Patients who undergo surgical treatment to relieve the athetosis often see significant improvement in the control of their limbs and digits. While surgery is often very beneficial in the short term and can produce near immediate results, in the long term it has been seen that its effects are not incredibly long lasting.

Scanning techniques include EEG, SPECT, MRI, and CT brain scanning. These additional techniques are useful in determining what type of lesion the patient has, and allows physicians to determine more effective ways in treating the patient.

Neuropsychology is the study of neurobiology and psychology. Neuropsychological tests are utilized for the purpose of observing an individuals’ abilities in cognitive functioning, reasoning, and memories. The tests most commonly used for neuropsychological testing include WAIS-III, Stroop test, Bourdon Wiersma test, and the Rey-Osterrieth complex figure test. These tests allow physicians to evaluate the degree to which the bilateral lesions in the operculum have been affected, and allow for the determination of proper treatment.

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.

A thorough medical history and physical examination, including a neurological examination, are the first steps in making a diagnosis. This alone may be sufficient to diagnose Bell's Palsy, in the absence of other findings. Additional investigations may be pursued, including blood tests such as ESR for inflammation, and blood sugar levels for diabetes. If other specific causes, such as sarcoidosis or Lyme disease are suspected, specific tests such as angiotensin converting enzyme levels, chest x-ray or Lyme titer may be pursued. If there is a history of trauma, or a tumour is suspected, a CT scan may be used.

In the industrialized world, the incidence of overall cerebral palsy, which includes but is not limited to spastic diplegia, is about 2 per 1000 live births. Thus far, there is no known study recording the incidence of CP in the overall nonindustrialized world. Therefore, it is safe to assume that not all spastic CP individuals are known to science and medicine, especially in areas of the world where healthcare systems are less advanced. Many such individuals may simply live out their lives in their local communities without any medical or orthopedic oversight at all, or with extremely minimal such treatment, so that they are never able to be incorporated into any empirical data that orthopedic surgeons or neurosurgeons might seek to collect. It is shocking to note that—as with people with physical disability overall—some may even find themselves in situations of institutionalization, and thus barely see the outside world at all.

From what "is" known, the incidence of spastic diplegia is higher in males than in females; the Surveillance of Cerebral Palsy in Europe (SCPE), for example, reports a M:F ratio of 1.33:1. Variances in reported rates of incidence across different geographical areas in industrialized countries are thought to be caused primarily by discrepancies in the criteria used for inclusion and exclusion.

When such discrepancies are taken into account in comparing two or more registers of patients with cerebral palsy and also the extent to which children with mild cerebral palsy are included, the incidence rates still converge toward the average rate of 2:1000.

In the United States, approximately 10,000 infants and babies are born with CP each year, and 1200–1500 are diagnosed at preschool age when symptoms become more obvious. It is interesting to note that those with extremely mild spastic CP may not even be aware of their condition until much later in life: Internet chat forums have recorded men and women as old as 30 who were diagnosed only recently with their spastic CP.

Overall, advances in care of pregnant mothers and their babies has not resulted in a noticeable decrease in CP; in fact, because medical advances in areas related to the care of premature babies has resulted in a greater survival rate in recent years, it is actually "more" likely for infants with cerebral palsy to be born into the world now than it would have been in the past. Only the introduction of quality medical care to locations with less-than-adequate medical care has shown any decreases in the incidences of CP; the rest either have shown no change or have actually shown an increase. The incidence of CP increases with premature or very low-weight babies regardless of the quality of care.

EMG &NCV can help to treatment with the diagnosis of the location and severity of the lesion.

As a matter of everyday maintenance, muscle stretching, range of motion exercises, yoga, contact improvisation, modern dance, resistance training, and other physical activity regimens are often utilized by those with spastic CP to help prevent contractures and reduce the severity of symptoms.

Major clinical treatments for spastic diplegia are:

- Baclofen (and its derivatives), a gamma amino butyric acid (GABA) substitute in oral (pill-based) or intrathecal form. Baclofen is essentially chemically identical to the GABA that the damaged, over-firing nerves cannot absorb, except that it has an extra chemical 'marker' on it that makes the damaged nerves 'think' it is a different compound, and thus those nerves will absorb it. Baclofen is noted for being the sole medication available for GABA-deficiency-based spasticity which acts on the actual cause of the spasticity rather than simply reducing symptomatology as muscle relaxants and painkillers do. The intrathecal solution is a liquid injected into the spinal fluid for trial, and if successful in reducing spasticity, thereafter administered via an intrathecal pump, which has variously been proven potentially very dangerous on one or another level with long-term use (see article), including sudden and potentially lethal baclofen overdose, whereas the oral route, which comes in 10- or 20-milligram tablets and the dosage of which can be gently titrated either upward or downward, as well as safely ceased entirely, has not.

- Antispasmodic muscle relaxant chemicals such as tizanidine and botulinum toxin (Botox), injected directly into the spastic muscles; Botox wears off every three months.

- Phenol and similar chemical 'nerve deadeners', injected selectively into the over-firing nerves in the legs on the muscle end to reduce spasticity in their corresponding muscles by preventing the spasticity signals from reaching the legs; Phenol wears off every six months.

- Orthopedic surgery to release the spastic muscles from their hypertonic state, a usually temporary result because the spasticity source is the nerves, not the muscles; spasticity can fully reassert itself as little as one year post-surgery.

- Selective dorsal rhizotomy, a neurosurgery directly targeting and eliminating ("cutting" or "lesioning") the over-firing nerve rootlets and leaving the properly firing ones intact, thereby permanently eliminating the spasticity but compelling the person to spend months re-strengthening muscles that will have been severely weakened by the loss of the spasticity, due to the fact of those muscles not really having had actual strength to begin with.

Because the causes of CP are varied, a broad range of preventative interventions have been investigated.

Electronic fetal monitoring has not helped to prevent CP, and in 2014 the American College of Obstetricians and Gynecologists, the Royal Australian and New Zealand College of Obstetricians and Gynaecologists, and the Society of Obstetricians and Gynaecologists of Canada have acknowledged that there are no long-term benefits of electronic fetal monitoring. Prior to this, electronic fetal monitoring was widely used to prop up obstetric litigation.

In those at risk of an early delivery, magnesium sulphate appears to decrease the risk of cerebral palsy. It is unclear if it helps those who are born at term. In those at high risk of preterm labor a review found that moderate to severe CP was reduced by the administration of magnesium sulphate, and that adverse effects on the babies from the magnesium sulphate were not significant. Mothers who received magnesium sulphate could experience side effects such as respiratory depression and nausea. Caffeine is used to treat apnea of prematurity and reduces the risk of cerebral palsy in premature babies, but there are also concerns of long term negative effects. A moderate level of evidence has been shown for giving women antibiotics during preterm labour when their waters had not broken was associated with an increased risk of cerebral palsy in the child. Additionally, allowing a preterm birth to proceed rather than trying to delay the birth also had a moderate level of evidence for increased risk of cerebral palsy in the child.

Cooling high-risk full-term babies shortly after birth may reduce disability, but this may only be useful for some forms of the brain damage that causes CP.

Facial nerve paralysis may be divided into supranuclear and infranuclear lesions.