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.

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

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.

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).

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).

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.

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.

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

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 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.

Progressive bulbar palsy (PBP) is a medical condition. It belongs to a group of disorders known as motor neuron diseases. PBP is a disease that attacks the nerves supplying the bulbar muscles. These disorders are characterized by the degeneration of motor neurons in the cerebral cortex, spinal cord, brain stem, and pyramidal tracts. This specifically involves the glossopharyngeal nerve (IX), vagus nerve (X), and hypoglossal nerve (XII).

This disorder should not be confused with pseudobulbar palsy or progressive spinal muscular atrophy. The term Infantile progressive bulbar palsy is used to describe progressive bulbar palsy in children. Some neurologists consider this disorder to be a subset of amyotrophic lateral sclerosis (ALS), but others disagree with that classification.

The upper motor neuron lesion in the brain impairs the ability of some nerve receptors in the spine to properly receive gamma amino butyric acid (GABA). That leads to hypertonia in the muscles signaled by those damaged nerves. The limbs and body areas in which hypertonia manifests can be any or even all of them, depending which specific nerve groupings within the spine are rendered unable to receive GABA. Thus, spastic CP is often designated by body topography.

Progressive supranuclear palsy (PSP; or the Steele–Richardson–Olszewski syndrome, after the doctors who described it in 1963) is a degenerative disease involving the gradual deterioration and death of specific volumes of the brain.

Males and females are affected approximately equally and there is no racial, geographical or occupational predilection. Approximately six people per 100,000 population have PSP.

It has been described as a tauopathy.

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.

Spastic diplegia's particular type of brain damage inhibits the proper development of upper motor neuron function, impacting the motor cortex, the basal ganglia and the corticospinal tract. Nerve receptors in the spine leading to affected muscles become unable to properly absorb gamma amino butyric acid (GABA), the amino acid that regulates muscle tone in humans. Without GABA absorption to those particular nerve rootlets (usually centred, in this case, around the sectors L1-S1 and L2-S2), affected nerves (here, the ones controlling the legs) perpetually fire the message for their corresponding muscles to permanently, rigidly contract, and the muscles become permanently hypertonic (spastic).

The abnormally high muscle tone that results creates lifelong difficulty with all voluntary and passive movement in the legs, and in general creates stress over time—depending on the severity of the condition in the individual, the constant spasticity ultimately produces pain, muscle/joint breakdown including tendinitis and arthritis, premature physical exhaustion (i.e., becoming physically exhausted even when you internally know that you have more energy than you are able to use), contractures, spasms, and progressively worse deformities/mis-alignments of bone structure around areas of the tightened musculature as the person's years progress. Severe arthritis, tendinitis, and similar breakdown can start as early as the spastic diplegic person's mid-20s (as a comparison, typical people with normal muscle tone are not at risk of arthritis, tendinitis, and similar breakdown until well into their 50s or 60s, if even then).

No type of CP is officially a progressive condition, and indeed spastic diplegia does not clinically "get worse" given the nerves, damaged permanently at birth, neither recover nor degrade. This aspect is clinically significant because other neuromuscular conditions with similar surface characteristics in their presentations, like most forms of multiple sclerosis, indeed do degrade the body over time and do involve actual progressive worsening of the condition, including the spasticity often seen in MS. However, spastic diplegia is indeed a chronic condition; the symptoms themselves cause compounded effects on the body that are typically just as stressful on the human body as a progressive condition is. Despite this reality and the fact that muscle tightness is the symptom of spastic diplegia and not the cause, symptoms rather than cause are typically seen as the primary area of focus for treatment, especially surgical treatment, except when a selective dorsal rhizotomy is brought into consideration, or when an oral baclofen regimen is attempted.

Unlike any other condition that may present with similar effects, spastic diplegia is entirely congenital in origin—that is, it is almost always acquired shortly before or during a baby's birth process. Things like exposure to toxins, traumatic brain injury, encephalitis, meningitis, drowning, or suffocation do not tend to lead to spastic diplegia in particular or even cerebral palsy generally. Overall, the most common cause of spastic diplegia is Periventricular leukomalacia, more commonly known as neonatal asphyxia or infant hypoxia—a sudden in-womb shortage of oxygen-delivery through the umbilical cord. This sudden lack of oxygen is also almost always combined with premature birth, a phenomenon that, even by itself, would inherently risk the infant developing some type of CP. On the other hand, the presence of certain maternal infections during pregnancy such as congenital rubella syndrome can also lead to spastic diplegia, since such infections can have similar end results to infant hypoxia.

Motor neuron diseases affect either upper motor neurons (UMN) or lower motor neurons (LMN), or both:

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

Facial paralysis is usually caused by traumatic, infectious, neurological, metabolic, toxic, vascular, and idiopathic conditions. While over 50% of the cases of unilateral facial paralysis are caused by idiopathic conditions, less than 20% of bilateral cases are idiopathic. The most common infectious cause of facial diplegia is Lyme disease.

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.

A motor neuron disease (MND) is any of several neurological disorders that selectively affect motor neurons, the cells that control voluntary muscles of the body. They include amyotrophic lateral sclerosis (ALS), hereditary spastic paraplegia (HSP), primary lateral sclerosis (PLS), progressive muscular atrophy (PMA), progressive bulbar palsy (PBP) and pseudobulbar palsy. Spinal muscular atrophies (SMA) are sometimes included in the group by some neurologists but it is different disease with clear genetic cause. They are neurodegenerative in nature and cause increasing disability and eventually, death.

In addition, there may be lower motor neuron lesions of the limbs.

The ocular muscles are spared and this differentiates it from myasthenia gravis.

Bulbar palsy refers to a range of different signs and symptoms linked to impairment of function of the cranial nerves IX, X, XI and XII, which occurs due to a lower motor neuron lesion in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem.

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).