CP and Mobility Limitations

Cerebral palsy, which is occasionally referred to by the shortened term of “CP,” consists of a neurological acquired traumatic brain injury ultimately manifesting as the neurologic disorder spectrum of symptoms most commonly associated with a cerebral palsy diagnosis. Characteristic of cerebral palsy symptoms have a latent onset in infants with most medical professionals declining to provide a formal diagnosis prior to the neonate patient reaching mid to late infant development stages during twelve (12) to thirty-six (36) months postpartum. During these critical development years for infants, substantial and rapid physical and cognitive growth typically occurs, in which among other things, an infant gradually learns to walk, or facilitate bipedal locomotion, as well as deploy fine tactile motor skills as well. In the case of cerebral palsy, the damages to the neonate’s brain, commonly suspected as part of the birth process involving hypoxia at a given point, circumvent the possibility of many cerebral palsy patients ever meeting these developmental goals in their lifetime, with most others overcoming substantially delayed developmental growth vis a vis their non-afflicted peers.

In short, mobility limitations exhibit the following high degrees of prevalence in CP patient populations, including:

  • Of the nearly 700,000 CP patients living in the US today, over 33% are completely dependent upon a wheelchair for mobility, or a total impairment of gross motor function and mobility at Stage 4 or Stage 5 per the Gross Motor Function Classification System used to gauge the relative degree of mobility impairment in CP patients and others
  • Of the expected 10,000 new annual cases of cerebral palsy in the United States, it is also anticipated that virtually all will exhibit some degree of Level 2 or Level 3 mobility impairment, with only a small minority of cerebral palsy patients categorized as capable of mobility without complications, per Level 1 of the GMFCS in CP patient cases
  • However, cerebral palsy is not universal in the manifestation of symptomology, or a broad spectrum of comorbidities, associated conditions, and primary complications emerge unpredictably from patient to patient. Certain vague complications, such as pain that are experienced by over 80% of CP patients, only exaggerate the difficulties of mobility as well over 50% of CP patients must endure some degree of cognitive deficits as well
  • Moreover, mobility impairment is such a defining feature of cerebral palsy that medical subtypes of CP are delineated based on the type of motor skill impairment exhibited by a patient
  • Commonly seen movement issues in cerebral palsy patients include awkward gait, unsustainable muscle atrophy for mobility, cervical and spinal malformations impeding mobility, and in many cases, a chronic barrage of neurological impulses perceived as muscle spasms are endured by patients, whose mobility is greatly hampered by the misfiring of these motor axons.

The degree to which of the sub-types of the cerebral palsy impairs aspects of the individual patient’s motor movements is presumably predicated on the extent of the neurological deficits incurred during a hypoxic or anoxic event. Thought to be caused by a hypoxic or anoxic event in utero, intrapartum, or postpartum, medical researchers have historically posited that cerebral palsy is directly attributable to only oxygen deprivation in an infant, which ultimately causes relatively quick and permanent brain damage in the neonate. Growing bodies of cases of cerebral palsy emerging with patients not sustaining any known hypoxic or anoxic event have stymied researchers’ original theory and left the medical community unsure as to a definitive cause or cause of cerebral palsy.

Classifications of Cerebral Palsy by Degree and Type of Mobility Limitations Occurring

Physicians classify cerebral palsy by how it affects movement. There are three types of cerebral palsy, each presenting particular variations on the types of mobility limitations faced by the average patient, including:

  • Spastic cerebral palsy: By far the most prevalent form of CP with 80% of patients manifesting symptoms, spastic cerebral palsy causes significant impediments by way of spastic neuronal charges to the muscle groups chronically. The predominant three (3) subtypes of spastic cerebral palsy include diplegia, hemiplegia, and quadriplegia, which impede mobility the legs, one side of the patient, and the entire body, respectively.
  • Dyskinetic cerebral palsy: Causing extensive muscle atrophy over time, dyskinetic cp causes involuntary neurological motor neurons to incorrectly stimulate muscle groups despite the patient’s intentions to do so otherwise. The chronic tensing of the muscles groups, while relative immobility of others, causing disjointed movement and ultimately immobility due to muscle atrophy as patients age
  • Ataxic cerebral palsy: Causing impairment in balance and coordination of muscle movements, ataxic CP greatly impedes bipedal coordination and fine motor skill hand movements
  • A noticeable minority of cerebral palsy patients exhibit what is known as mixed cerebral palsy, or the patient expresses symptoms covering more than one cerebral palsy diagnosis concurrently.

Problematically while extensive research and new therapeutic techniques are showing incredible breakthroughs annually, the medical reality that patients, parents, and doctors known today is that the symptomology of cerebral palsy remains progressively worsening, with co-morbidities and primary symptoms frequently overwhelming patients’ medically. From a legal perspective as well, it must be considered that future mobility, and clearly the future quality of life and capacity to garner an income, will be highly unlikely in the majority, but not all, cerebral palsy patients. Addressing cerebral palsy for its limiting nature on mobility, as well as a monolithic number of other complications, requires extensive coordination and collaboration between patients, parents, legal counsel, physicians, and therapists.

References:

http://www.aafp.org/afp/2006/0101/p91.html

http://www.ncbi.nlm.nih.gov/pubmed/12578237

http://www.cdc.gov/ncbddd/cp/data.html

https://www.opm.gov/forms/pdf_fill/sf256.pdf

http://www.ada.gov/taman2.html

 

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