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.

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.

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%.

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.

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.

Bell's palsy is characterized by a one-sided facial droop that comes on within 72 hours. In rare cases (<1%), it can occur on both sides resulting in total facial paralysis.

The facial nerve controls a number of functions, such as blinking and closing the eyes, smiling, frowning, lacrimation, salivation, flaring nostrils and raising eyebrows. It also carries taste sensations from the anterior two-thirds of the tongue, via the chorda tympani nerve (a branch of the facial nerve). Because of this, people with Bell's palsy may present with loss of taste sensation in the anterior 2/3 of the tongue on the affected side.

Although the facial nerve innervates the stapedial muscles of the middle ear (via the tympanic branch), sound sensitivity and dysacusis are hardly ever clinically evident.

Although defined as a mononeuritis (involving only one nerve), people diagnosed with Bell’s palsy may have "myriad neurological symptoms" including "facial tingling, moderate or severe headache/neck pain, memory problems, balance problems, ipsilateral limb paresthesias, ipsilateral limb weakness, and a sense of clumsiness" that are "unexplained by facial nerve dysfunction".

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.

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.

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.

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.

People with diplegia in their arms experience difficulties in reaching, pointing, grasping, releasing, manipulating objects and many other motor functions performed by the hands and arms.

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.

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

Bell's palsy is a type of facial paralysis that results in an inability to control the facial muscles on the affected side. Symptoms can vary from mild to severe. They may include muscle twitching, weakness, or total loss of the ability to move one or rarely both sides of the face. Other symptoms include drooping of the eyelid, a change in taste, pain around the ear, and increased sensitivity to sound. Typically symptoms come on over 48 hours.

The cause of Bell's palsy is unknown. Risk factors include diabetes and a recent upper respiratory tract infection. It results from a dysfunction of cranial nerve VII (the facial nerve). Many believe that this is due to a viral infection that results in swelling. Diagnosis is based on a person's appearance and ruling out other possible causes. Other conditions that can cause facial weakness include brain tumor, stroke, Ramsay Hunt syndrome, and Lyme disease.

The condition normally gets better by itself with most achieving normal or near-normal function. Corticosteroids have been found to improve outcomes, while antiviral medications may be of a small additional benefit. The eye should be protected from drying up with the use of eye drops or an eyepatch. Surgery is generally not recommended. Often signs of improvement begin within 14 days, with complete recovery within six months. A few may not recover completely or have a recurrence of symptoms.

Bell's palsy is the most common cause of one sided facial nerve paralysis (70%). It occurs in 1 to 4 per 10,000 people per year. About 1.5% of people are affected at some point in their life. It most commonly occurs in people between ages 15 and 60. Males and females are affected equally. It is named after Scottish surgeon Charles Bell (1774–1842), who first described the connection of the facial nerve to the condition.

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.

Cerebral palsy is defined as "a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain." While movement problems are the central feature of CP, difficulties with thinking, learning, feeling, communication and behavior often co-occur, with 28% having epilepsy, 58% having difficulties with communication, at least 42% having problems with their vision, and 2356% having learning disabilities. Muscle contractions in people with cerebral palsy is commonly thought to arise from overactivation.

Cerebral palsy is characterized by abnormal muscle tone, reflexes, or motor development and coordination. There can be joint and bone deformities and contractures (permanently fixed, tight muscles and joints). The classical symptoms are spasticity, spasms, other involuntary movements (e.g., facial gestures), unsteady gait, problems with balance, or soft tissue findings consisting largely of decreased muscle mass. Scissor walking (where the knees come in and cross) and toe walking (which can contribute to a gait reminiscent of a marionette) are common among people with CP who are able to walk, but taken on the whole, CP symptomatology is very diverse. The effects of cerebral palsy fall on a continuum of motor dysfunction, which may range from slight clumsiness at the mild end of the spectrum to impairments so severe that they render coordinated movement virtually impossible at the other end of the spectrum. Although most people with CP have problems with increased muscle tone, some have normal or low muscle tone. High muscle tone can either be due to spasticity or dystonia.

Babies born with severe CP often have an irregular posture; their bodies may be either very floppy or very stiff. Birth defects, such as spinal curvature, a small jawbone, or a small head sometimes occur along with CP. Symptoms may appear or change as a child gets older. Some babies born with CP do not show obvious signs right away. Classically, CP becomes evident when the baby reaches the developmental stage at 6 to 9 months and is starting to mobilise, where preferential use of limbs, asymmetry, or gross motor developmental delay is seen.

Drooling is common among children with cerebral palsy, which can have a variety of impacts including social rejection, impaired speaking, damage to clothing and books, and mouth infections. It can additionally cause choking.

An average of 55.5% of people with cerebral palsy experience lower urinary tract symptoms, more commonly excessive storage issues than voiding issues. Those with voiding issues and pelvic floor overactivity can deteriorate as adults and experience upper urinary tract dysfunction.

Children with CP may also have sensory processing issues.`

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).

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).

Facial nerve paralysis is characterised by unilateral facial weakness, with other symptoms including loss of taste, , and decreased salivation and tear secretion. Other signs may be linked to the cause of the paralysis, such as s in the ear, which may occur if the facial palsy is due to shingles. Symptoms may develop over several hours. Acute facial pain radiating from the ear may precede the onset of other symptoms.

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.

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.

Facial nerve paralysis is a common problem that involves the paralysis of any structures innervated by the facial nerve. The pathway of the facial nerve is long and relatively convoluted, and so there are a number of causes that may result in facial nerve paralysis. The most common is Bell's palsy, a disease of unknown cause that may only be diagnosed by exclusion.

Klumpke's paralysis (or Klumpke's palsy or Dejerine–Klumpke palsy) is a variety of partial of the lower roots of the brachial plexus. The brachial plexus is a network of spinal nerves that originates in the back of the neck, extends through the axilla (armpit), and gives rise to nerves to the upper limb. (see picture - click to enlarge). It is named after Augusta Déjerine-Klumpke.

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

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

Symptoms include intrinsic minus hand deformity, paralysis of intrinsic hand muscles, and C8/T1 Dermatome distribution numbness. Involvement of T1 may result in Horner's syndrome, with ptosis, and miosis. Weakness or lack of ability to use specific muscles of the shoulder or arm.It can be contrasted to Erb-Duchenne's palsy, which affects C5 and C6.