ADCP is often characterized by slow, uncontrolled movements of the extremities and trunk. Small, rapid, random and repetitive, uncontrolled movements known as chorea may also occur. Involuntary movements often increase during periods of emotional stress or excitement and disappear when the patient is sleeping or distracted. Patients experience difficulty in maintaining posture and balance when sitting, standing, and walking due to these involuntary movements and fluctuations in muscle tone. Coordinated activities such as reaching and grasping may also be challenging. Muscles of the face and tongue can be affected, causing involuntary facial grimaces, expressions, and drooling. Speech and language disorders, known as dysarthria, are common in athetoid CP patients. In addition, ADCP patients may have trouble eating. Hearing loss is a common co-occurring condition, and visual disabilities can be associated with Athetoid Cerebral Palsy. Squinting and uncontrollable eye movements may be initial signs and symptoms. Children with these disabilities rely heavily on visual stimulation, especially those who are also affected by sensory deafness.

Cognitive impairment occur in 30% of cases.

Epilepsy occur in 25% of cases.

Due to impaired balance, patients suffering from ataxic cerebral palsy often walk with their feet unusually far apart (a wide gait). In addition, the low muscle tone caused by ataxic cerebral palsy causes people suffering from the disease to appear very unsteady, as their body is constantly trying to counterbalance itself. Infants with the disease often take a significantly longer amount of time to be able to walk without support, and over 50% of all children with ataxic cerebral palsy experience some form of a learning disability or speech impediment.

The condition, whether resulting from cerebellar malformation or injury, results in incomplete cerebral development and no two people are affected in the same way. In general, cerebral palsy is a physical impairment that affects posture and the development of movement. Ataxic cerebral palsy in particular, is manifested in the performance of movements with abnormal force, rhythm, and accuracy. Patients have hypotonia (decreased muscle tone), signs of ataxia (loss of full control of bodily movement), impaired balance and coordination, intention tremors, and a wide-based gait (in walking patients).

Cerebral development normally occurs in the first two years of life when the infant is acquiring new motor and adaptive skills, consequently signs and symptoms of ataxic cerebral palsy begin to manifest during this time period. Typically patients fail to reach motor milestones and show a qualitative difference in motor development. During the neonatal period (first 28 days of life), children are noted to be lethargic, relatively immobile, and floppy. Moreover, hypotonia is greatest during this period, even though muscle tone increases with age, it never reaches normal levels. The limbs show weakness, incoordination in voluntary movement, dysdiadochokinesis (in inability to perform rapidly alternating movements), and titubation.

Athetoid cerebral palsy or dyskinetic cerebral palsy (sometimes abbreviated ADCP) is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic-ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

Classification of cerebral palsy can be based on severity, topographic distribution, or motor function. Severity is typically assessed via the Gross Motor Function Classification System (GMFCS) or the International Classification of Functioning, Disability and Health (described further below). Classification based on motor characteristics classifies CP as occurring from damage to either the corticospinal pathway or extrapyramidal regions. Athetoid dyskinetic cerebral palsy is a non-spastic, extrapyramidal form of cerebral palsy (spastic cerebral palsy, in contrast, results from damage to the brain’s corticospinal pathways). Non-spastic cerebral palsy is divided into two groups, ataxic and dyskinetic. Dyskinetic cerebral palsy is separated further into two different groups; choreoathetoid and dystonic. Choreo-athetotic CP is characterized by involuntary movements most predominantly found in the face and extremities. Dystonic ADCP is characterized by slow, strong contractions, which may occur locally or encompass the whole body.

Clinically, physicians have also classified cerebral palsy according to the topographic distribution of muscle spasticity. This method classifies children as diplegic, (bilateral involvement with leg involvement greater than arm involvement), hemiplegic (unilateral involvement), or quadriplegic (bilateral involvement with arm involvement equal to or greater than leg involvement).

Ataxic cerebral palsy is clinically observed in approximately 5-10% of all cases of cerebral palsy, making it the least frequent form of cerebral palsy diagnosed. Ataxic cerebral palsy is caused by damage to cerebellar structures, differentiating it from the other two forms of cerebral palsy, which are spastic cerebral palsy (damage to cortical motor areas and underlying white matter) and athetoid cerebral palsy (damage to basal ganglia).

Because of the damage to the cerebellum, which is essential for coordinating muscle movements and balance, patients with ataxic cerebral palsy experience problems in coordination, specifically in their arms, legs, and trunk. Ataxic cerebral palsy is known to decrease muscle tone.

The most common manifestation of ataxic cerebral palsy is intention (action) tremor, which is especially apparent when carrying out precise movements, such as tying shoe laces or writing with a pencil. This symptom gets progressively worse as the movement persists, causing the hand to shake. As the hand gets closer to accomplishing the intended task, the trembling intensifies which makes it even more difficult to complete.

Like all forms of CP, there is no "cure" for ataxic cerebral palsy. However, there are a number of diverse treatments which together have been used to limit the negative effects of the condition. Like all forms of CP it is most common for ataxic cerebral palsy to be congenital, resulting from errors in the development of the cerebellum and connexins during pregnancy. However it is also possible to be acquired via meningitis or even by head trauma, although the latter more often leads to one of the many forms of traumatic brain injury, which is categorically separate from cerebral palsy as a class.

People with the spastic/spasticity type of CP are hypertonic—i.e., they present with very stiff and tight muscle groups, far greater than typical humans—and have what is essentially a neuromuscular mobility impairment (rather than hypotonia or paralysis) which stems from an upper motor neuron lesion in the brain. The corticospinal tract or the motor cortex may be secondarily affected.

Spastic muscles are continuously contracting, or "tight", because the corresponding nerves permanently over-fire the command to tighten. This is caused by their inability to properly absorb GABA, or gamma amino butyric acid. The tightness, in addition to restricting movement, also acts as an overwhelming opposing force to neighbouring muscles and joints, eventually leaving the entire skeleton deformed compared to normal skeletal, bone, and joint structure in people without spasticity. Abnormal postures are usually associated with the antigravity muscles, which are extensors in the leg and the flexors in the arm. Deformities of joints develop which may become joint contractures, or "fixed contractures", with time.

Changes in spasticity and corresponding postures may also occur with other brain activity, such as excitement, fear or anxiety, or even pain, which increase muscle tension.

A person with spastic CP will commonly show, in addition to higher muscle tone, persistent primitive reflexes, greater stretch reflexes, plantar reflex, and ankle clonus.

A third of people with cerebral palsy have seizures - this is most common in spastic CP.

Spastic quadriplegia can be detected by the abnormal development of motor skills in children. Symptoms can present themselves as early as three months but are generally seen before the child reaches two years of age. Some warning signs include: a child of more than two months who has stiff legs that scissor and is unable to control his or her head, and a child of more than twelve months who has not developed the ability to crawl or stand.

Spastic quadriplegia also presents a range of symptoms that affect the musculature. Many experience contractures, which are defined as joints that cannot be stretched or moved. Clonus is another symptom that is characterized by alternating, rapid muscle contraction and relaxation. This presents itself as tremors and scissoring of the limbs. Distonia, or lasting muscle contractions and tightness, is also often experienced by those affected by spastic quadriplegia. These involuntary muscle contractions may affect the development of structural muscle around the hip and lead to hip dysplasia and dislocation, making it difficult to sit. The combination of these symptoms often makes it difficult for the patients to walk as well. Although the arms and legs of patients are often stiff, the neck is usually limp due to the lack of voluntary muscle control. Some adults have issues with sexual organs such as the ones that control the sphincter (anus) as well and bladder control. These can sometimes be treated with training and stimulation even if the problems have presented for years, some issues can be corrected in many cases with nutrition modification in 90 percent of cases, especially B12. Stimulation of the muscles involved can treat some forms of nerve damage, depending on what the issue is. Sexual issues can be difficult for those with this, and sexual acts and stimulation can correct most of the sexual issues.

Spastic cerebral palsy, or cerebral palsy where spasticity (muscle tightness) is the exclusive or almost exclusive impairment present, is by far the most common type of overall cerebral palsy, occurring in upwards of 70% of all cases. People with this type of CP are hypertonic and have what is essentially a neuromuscular mobility impairment (rather than hypotonia or paralysis) stemming from an upper motor neuron lesion in the brain as well as the corticospinal tract or the motor cortex. This damage impairs the ability of some nerve receptors in the spine to receive "gamma"-Aminobutyric acid properly, leading to hypertonia in the muscles signaled by those damaged nerves.

As compared to other types of CP, and especially as compared to hypotonic or paralytic mobility disabilities, spastic CP is typically more easily manageable by the person affected, and medical treatment can be pursued on a multitude of orthopedic and neurological fronts throughout life. In any form of spastic CP, clonus of the affected limb(s) may sometimes result, as well as muscle spasms resulting from the pain or stress of the tightness experienced. The spasticity can and usually does lead to a very early onset of muscle stress symptoms like arthritis and tendinitis, especially in ambulatory individuals in their mid-20s and early-30s. Occupational therapy and physical therapy regimens of assisted stretching, strengthening, functional tasks, or targeted physical activity and exercise are usually the chief ways to keep spastic CP well-managed. If the spasticity is too much for the person to handle, other remedies may be considered, such as antispasmodic medications, botulinum toxin, baclofen, or even a neurosurgery known as a selective dorsal rhizotomy (which eliminates the spasticity by reducing the excitatory neural response in the nerves causing it).

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%.

Athetoid cerebral palsy or dyskinetic cerebral palsy (sometimes abbreviated ADCP) is primarily associated with damage to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic-ischemic brain injury. ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques.

Athetoid dyskinetic cerebral palsy is a non-spastic, extrapyramidal form of cerebral palsy. Dyskinetic cerebral palsy can be divided into two different groups; choreoathetoid and dystonic. Choreo-athetotic CP is characterized by involuntary movements most predominantly found in the face and extremities. Dystonic ADCP is characterized by slow, strong contractions, which may occur locally or encompass the whole body.

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.

Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction. It is the "one-sided version" of spastic diplegia. It falls under the mobility impairment umbrella of cerebral palsy. About 20–30% of people with cerebral palsy have spastic hemiplegia. Due to brain or nerve damage, the brain is constantly sending action potentials to the neuromuscular junctions on the affected side of the body. Similar to strokes, damage on the left side of the brain affects the right side of the body and damage on the right side of the brain affects the left side of the body.

The affected side of the body is rigid, weak and has low functional abilities. In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. If both arms are affected, the condition is referred to as double hemiplegia. Some patients with spastic hemiplegia only suffer minor impairments, where in severe cases one side of the body could be completely paralyzed. The severity of spastic hemiplegia is dependent upon the degree of the brain or nerve damage.

Diplegia, when used singularly, refers to paralysis affecting symmetrical parts of the body. This should not be confused with hemiplegia which refers to spasticity restricted to one side of the body, or quadriplegia which requires the involvement of all four limbs but not necessarily symmetrical. Diplegia is the most common cause of crippling in children, specifically in children with Cerebral Palsy. Other causes may be due to injury of the spinal cord. There is no set course of progression for people with diplegia. Symptoms may get worse but the neurological part does not change. The primary parts of the brain that are affected by diplegia are the ventricles, fluid filled sacs in the brain, and the wiring from the center of the brain to the cerebral cortex. There is also usually some degeneration of the cerebral neurons, as well as problems in the upper motor neuron system.

The term diplegia can refer to any bodily area, such as the face, arms, or legs.

Facial diplegia refers to people with paralysis of both sides of their face. Bilateral occurs when the onset of the second side occurs within one month of the onset of the first side. Facial diplegia occurs in 50% of patients with Guillain–Barré syndrome. Facioscapulohumeral muscular dystrophy (FSHD) is the second most common adult-onset muscular dystrophy with facial weakness being a distinct feature of FSHD in over 90% of cases.

Spastic diplegia, historically known as Little's Disease, is a form of cerebral palsy (CP) that is a chronic neuromuscular condition of hypertonia and spasticity—manifested as an especially high and constant "tightness" or "stiffness"—in the muscles of the lower extremities of the human body, usually those of the legs, hips and pelvis. Doctor William John Little's first recorded encounter with cerebral palsy is reported to have been among children who displayed signs of spastic diplegia.

Spastic diplegia accounts for about 22% of all diagnoses of cerebral palsy, and together with spastic quadriplegia and spastic triplegia make up the broad classification spastic cerebral palsy, which accounts for 70% of all cerebral palsy diagnoses.

Individuals with spastic diplegia are very tight and stiff and must work very hard to successfully resist and "push through" the extra tightness they perpetually experience. Other than this, however, these individuals are almost always normal in every significant clinical sense. When they are younger, spastic diplegic individuals typically undergo gait analysis so that their clinicians can determine the best assistive devices for them, if any are necessary, such as a walker or crutches. The main difference between spastic diplegia and a normal gait pattern is its signature "scissor gait"—a style that some able-bodied people might tend to confuse with the effects of drunkenness, multiple sclerosis, or another nerve disease. The degree of spasticity in spastic diplegia (and, for that matter, other types of spastic CP) varies widely from person to person. No two people with spastic diplegia are exactly alike. Balance problems and/or stiffness in gait can range from barely noticeable all the way to misalignments so pronounced that the person needs crutches (typically forearm crutches/lofstrand crutches) or a cane / walking stick to assist in ambulation. Less often, spasticity is severe enough to compel the person to use a wheelchair. In general, however, lower-extremity spasticity in spastic diplegia is rarely so great as to totally prevent ambulation—most people with the condition can walk, and can do so with at least a basic amount of overall stability. Regardless, it should be noted that from case to case, steeply varying degrees of imbalance, potential tripping over uneven terrain while walking, or needing to hold on to various surfaces or walls in certain circumstances to keep upright, are typically ever-present potential issues and are much more common occurrences amongst those with spastic diplegia than among those with a normal or near-normal gait pattern. Among some of the people with spastic diplegia who choose to be ambulatory on either an exclusive or predominant basis, one of the seemingly common lifestyle choices is for the person to ambulate within his or her home without an assistive device, and then to use the assistive device, if any, once outdoors. Others may use no assistive device in any "indoor" situation at all, while always using one when outdoors. Above the hips, persons with spastic diplegia typically retain normal or near-normal muscle tone and range of motion, though some lesser spasticity may also affect the upper body, such as the trunk and arms, depending on the severity of the condition in the individual (the spasticity condition affecting the whole body equally, rather than just the legs, is spastic quadriplegia, a slightly different classification). In addition, because leg tightness often leads to instability in ambulation, extra muscle tension usually develops in the shoulders, chest, and arms due to compensatory stabilisation movements, regardless of the fact that the upper body itself is not directly affected by the condition.

Athetosis can vary from mild to severe motor dysfunction; it is generally characterized by unbalanced, involuntary movements of muscle and a difficulty maintaining a symmetrical posture. The associated motor dysfunction can be restricted to a part of body or present throughout the body, depending on the individual and the severity of the symptom. One of the pronounced signs can be observed in the extremities in particular, as the writhing, convoluted movement of the digits. Athetosis can appear as early as 18 months from birth with first signs including difficulty feeding, hypotonia, spasm, and involuntary writhing movements of the hands, feet, and face, which progressively worsen through adolescence and at times of emotional distress. Athetosis is caused by lesions in several brain areas such as the hippocampus and the motor thalamus, as well as the corpus striatum; therefore children during the developmental age could possibly suffer from cognitive deficits such as speech impairment, hearing loss, and failed or delayed acquirement of sitting balance.

Prognosis for PBP patients is poor. Progressive bulbar palsy symptoms can include progressive difficulty with chewing, talking, and swallowing. Patients can also exhibit reduced gag reflexes, weak palatal movements, fasciculations, and weak movement of the facial muscles and tongue. In advanced cases of PBP, the patient may be unable to protrude their tongue or manipulate food in their mouth.

Patients with early cases of PBP have difficulty with pronunciations, particularly lateral consonants (linguals) and velars, and may show problems with drooling saliva. If the corticobulbar tract is affected a pseudobulbar affect with emotional changes may occur. Because PBP patients have such difficulty swallowing, food and saliva can be inhaled into the lungs. This can cause gagging and choking, and it increases the risk of pneumonia. Death, which is often from pneumonia, usually occurs 1 to 3 years after the start of the disorder.

Athetosis is a symptom characterized by slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases, arms, legs, neck and tongue. Movements typical of athetosis are sometimes called "athetoid" movements. Lesions to the brain are most often the direct cause of the symptoms, particularly to the

corpus striatum. This symptom does not occur alone and is often accompanied by the symptoms of cerebral palsy, as it is often a result of this disease. Treatments for athetosis are not very effective, and in most cases are simply aimed at the uncontrollable movement, rather than the cause itself.

Infants with spastic hemiplegia may develop a hand preference earlier than is typical.

Signs and symptoms of pseudobulbar palsy include:

- Slow and indistinct speech

- Dysphagia (difficulty in swallowing)

- Small, stiff and spastic tongue

- Brisk jaw jerk

- Dysarthria

- Labile affect

- Gag reflex may be normal, exaggerated or absent

- Examination may reveal upper motor neuron lesion of the limbs

Premature infants often exhibit visual impairment and motor deficits in eye control immediately after birth. However, the correction of these deficits occurs "in a predictable pattern" in healthy premature infants, and infants have vision comparable to full-term infants by 36 to 40 weeks after conception. Infants with PVL often exhibit decreased abilities to maintain a steady gaze on a fixed object and create coordinated eye movements. Additionally, children with PVL often exhibit nystagmus, strabismus, and refractive error.

Occurrence of seizures is often reported in children with PVL. In an Israel-based study of infants born between 1995 and 2002, seizures occurred in 102 of 541, or 18.7%, of PVL patients. Seizures are typically seen in more severe cases of PVL, affecting patients with greater amounts of lesions and those born at lower gestational ages and birth weights.

The initial symptoms in two-thirds of cases are loss of balance, lunging forward when mobilizing, fast walking, bumping into objects or people, and falls.

Other common early symptoms are changes in personality, general slowing of movement, and visual symptoms.

Later symptoms and signs are dementia (typically including loss of inhibition and ability to organize information), slurring of speech, difficulty swallowing, and difficulty moving the eyes, particularly in the vertical direction. The latter accounts for some of the falls experienced by these patients as they are unable to look up or down.

Some of the other signs are poor eyelid function, contracture of the facial muscles, a backward tilt of the head with stiffening of the , sleep disruption, urinary incontinence and constipation.

The visual symptoms are of particular importance in the diagnosis of this disorder. Patients typically complain of difficulty reading due to the inability to look down well. Notably, the ophthalmoparesis experienced by these patients mainly concerns voluntary eye movement and the inability to make vertical saccades, which is often worse with downward saccades. Patients tend to have difficulty looking down (a downgaze ) followed by the addition of an upgaze palsy. This vertical gaze paresis will correct when the examiner passively rolls the patient's head up and down as part of a test for the oculocephalic reflex. Involuntary eye movement, as elicited by Bell's phenomenon, for instance, may be closer to normal. On close inspection, eye movements called "square-wave jerks" may be visible when the patient fixes at distance. These are fine movements, that can be mistaken for nystagmus, except that they are saccadic in nature, with no smooth phase. Difficulties with convergence (convergence insufficiency), where the eyes come closer together while focusing on something near, like the pages of a book, is typical. Because the eyes have trouble coming together to focus at short distances, the patient may complain of diplopia (double vision) when reading.

Cardinal manifestations:

- Supranuclear ophthalmoplegia

- Neck dystonia

- Parkinsonism

- Pseudobulbar palsy

- Behavioral and cognitive impairment

- Imbalance and walking difficulty

- Frequent falls

Pseudobulbar palsy is a medical condition characterized by the inability to control facial movements (such as chewing and speaking) and caused by a variety of neurological disorders. Patients experience difficulty chewing and swallowing, have increased reflexes and spasticity in tongue and the bulbar region, and demonstrate slurred speech (which is often the initial presentation of the disorder), sometimes also demonstrating uncontrolled emotional outbursts.

The condition is usually caused by the damage (bilateral degeneration) to the neurons of the brain stem, specifically to the corticobulbar tract (upper motor neuron tract to cranial nerve motor nuclei).

Clonus (i.e. involuntary, rhythmic, muscular contractions and relaxations) tends to co-exist with spasticity in many cases of stroke and spinal cord injury likely due to their common physiological origins. Some consider clonus as simply an extended outcome of spasticity. Although closely linked, clonus is not seen in all patients with spasticity. Clonus tends to not be present with spasticity in patients with significantly increased muscle tone, as the muscles are constantly active and therefore not engaging in the characteristic on/off cycle of clonus. Clonus results due to an increased motor neuron excitation (decreased action potential threshold) and is common in muscles with long conduction delays, such as the long reflex tracts found in distal muscle groups. Clonus is commonly seen in the ankle but may exist in other distal structures as well, such as the knee or spine.