Spastic cerebral palsy

Spastic cerebral palsy
Classification and external resources
ICD-10	Xxx.x
ICD-9-CM	xxx
Patient UK	Spastic cerebral palsy

Spastic cerebral palsy, sometimes also termed bilateral spasticity, is the type of cerebral palsy wherein spasticity (also known in some versions of colloquial English as "muscle tightness") is either the dominant or exclusive impairment present.

It is by far the most common type of overall cerebral palsy, occurring in 90% of all cases according to the Society for Cerebral Palsy in Europe (SCPE); even if the 90% assertion is an exaggeration, however, more conservative scientific estimates still place the prevalence of spasticity-dominant 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%.

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, and there is apparent weakness of their antagonists leading to abnormal positions of the joints on which they act. 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 fixed contractures with time. Changes in spasticity and postures may occur with excitement, fear or anxiety and pain which increase muscle tension.

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.

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.

• Spastic hemiplegia is one side being affected. Generally, injury to muscle-nerves controlled by the brain's left side will cause a right body deficit, and vice versa. Typically, people that have spastic hemiplegia are the most ambulatory of all the forms, although they generally have dynamic equinus (a limping instability) on the affected side and are primarily prescribed ankle-foot orthoses to prevent said equinus.
• Spastic diplegia is the lower extremities affected, with little to no upper-body spasticity. The most common form of the spastic forms (70–80% of known cases), most people with spastic diplegia are fully ambulatory, but are "tight" and have a scissors gait. Flexed knees and hips to varying degrees, and moderate to severe adduction (stemming from tight adductor muscles and comparatively weak abductor muscles), are present. Gait analysis is often done in early life on a semi-regular basis, and assistive devices are often provided like walkers, crutches or canes; any ankle-foot orthotics provided usually go on both legs rather than just one. In addition, these individuals are often nearsighted. Over time, the effects of the spasticity sometimes produce hip problems and dislocations (see the main article and spasticity for more on spasticity effects). In three-quarters of spastic diplegics, also strabismus (crossed eyes) can be present as well.
• Spastic monoplegia is one single limb being affected.
• Spastic triplegia is three limbs being affected.
• Spastic quadriplegia is all four limbs more or less equally affected. People with spastic quadriplegia are the least likely to be able to walk, or if they can, to desire to walk, because their muscles are too tight and it is too much of an effort to do so. Some children with spastic quadriplegia also have hemiparetic tremors, an uncontrollable shaking that affects the limbs on one side of the body and impairs normal movement. (This is not the same as clonus; see below.)

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).

Difficulty in tracking CP progression through the later years

Unusually, cerebral palsy, including spastic cerebral palsy, is notable for a glaring overall research deficiency—the fact that it is one of the very few major groups of conditions on the planet in human beings for which medical science has not yet (as of 2011) collected wide-ranging empirical data on the development and experiences of young adults, the middle aged and older adults. An especially puzzling aspect of this lies in the fact that cerebral palsy as defined by modern science was first "discovered" and specifically addressed well over 100 years ago and that it would therefore be reasonable to expect by now that at least some empirical data on the adult populations with these conditions would have long since been collected, especially over the second half of the 20th century when existing treatment technologies rapidly improved and new ones came into being. The vast majority of empirical data on the various forms of cerebral palsy is concerned near-exclusively with children (birth to about 10 years of age) and sometimes pre-teens and early teens (11–13). Some doctors attempt to provide their own personal justifications for keeping their CP specialities purely paediatric, but there is no objectively apparent set of reasons backed by any scientific consensus as to why medical science has made a point of researching adult cases of multiple sclerosis, muscular dystrophy and the various forms of cancer in young and older adults, but has failed to do so with CP. There are a few orthopaedic surgeons and neurosurgeons who claim to be gathering pace with various studies as of the past few years, but these claims do not yet seem to have been matched by real-world actualisation in terms of easily accessible and objectively verifiable resources available to the general public on the internet and in-person, where many, including medical-science researchers and doctors themselves, would more than likely agree such resources would ideally belong.

Scientific classifications

The scientific classifications for these types include:

Type	OMIM	Gene	Locus
CPSQ1	603513	GAD1	2q31
CPSQ2	612900	ANKRD15	9p24.3
CPSQ3	612936	AP4M1	7q22.1