Athetoid cerebral palsy
Dyskinetic cerebral palsy | |
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Other names | Dyskinetic cerebral palsy |
The basal ganglia are instrumental in motor function. Damage to these areas may results in athetoid/ dyskinetic cerebral palsy (ADCP), or subtle movement disorders. | |
Specialty | Neurology |
Athetoid cerebral palsy, or dyskinetic cerebral palsy (sometimes abbreviated ADCP), is a type of
Classification of cerebral palsy can be based on severity, topographic distribution, or motor function. Severity is typically assessed via the
Signs and symptoms
ADCP is often characterized by slow, uncontrolled movements of the extremities and trunk.[3] Small, rapid, random and repetitive, uncontrolled movements known as chorea may also occur.[1] Involuntary movements often increase during periods of emotional stress or excitement and disappear when the patient is sleeping or distracted.[1] Patients experience difficulty in maintaining posture and balance when sitting, standing, and walking due to these involuntary movements and fluctuations in muscle tone.[3] Coordinated activities such as reaching and grasping may also be challenging.[3] Muscles of the face and tongue can be affected, causing involuntary facial grimaces, expressions, and drooling.[3] Speech and language disorders, known as dysarthria, are common in athetoid CP patients.[5] In addition, ADCP patients may have trouble eating.[3] Hearing loss is a common co-occurring condition,[2] 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.[6] Cognitive impairment occur in 30% of cases. Epilepsy occur in 25% of cases.[citation needed]
Cause
CP in general is a
Hypoxic-ischemic brain injury
Hypoxic-ischemic brain injury is a form of cerebral hypoxia in which oxygen cannot perfuse to cells in the brain. Lesions in the putamen and thalamus caused by this type of brain injury are primary causes of ADCP and can occur during the prenatal period and shortly after.[1] Lesions that arise after this period typically occur as a result of injury or infections of the brain.[7] Cerebral cortex and white matters are often relative spared, so intelligence is often normal.[citation needed]
Bilirubin encephalopathy
Bilirubin encephalopathy, also known as
Diagnosis
Motor function
Movement and posture limitations are aspects of all CP types and as a result, CP has historically been diagnosed based on parental reporting of developmental motor delays such as failure to sit upright, reach for objects, crawl, stand, or walk at the appropriate age.[3] Diagnosis of ADCP is also based on clinical assessment used in conjunction with milestone reporting.[2] The majority of ADCP assessments now use the Gross Motor Function Classification System (GMFCS) or the International Classification of Functioning, Disability and Health (formerly the International Classification of Impairments Disease, and Handicaps), measures of motor impairment that are effective in assessing severe CP.[1][2] ADCP is typically characterized by an individual's inability to control their muscle tone, which is readily assessed via these classification systems.[1][2]
Neuroimaging
Magnetic resonance imaging (MRI) is used to detect morphological brain abnormalities associated with ADCP in patients that are either at risk for ADCP or have shown symptoms thereof.[4] The abnormalities chiefly associated with ADCP are lesions that appear in the basal ganglia.[4] The severity of the disease is proportional to the severity and extent of these abnormalities, and is typically greater when additional lesions appear elsewhere in the deep grey matter or white matter.[4] MRI also has the ability to detect brain malformation, periventricular leukomalacia (PVL), and areas affected by hypoxia-ischemia, all of which may play a role in the development of ADCP.[2] The MRI detection rate for ADCP is approximately 54.5%, however this statistic varies depending on the patient's age and the cause of the disease and has been reported to be significantly higher.[1]
Treatment
Physical and occupational therapy
Speech therapy
Speech impairment is common in ADCP patients.[2][5] Speech therapy is the treatment of communication diseases, including disorders in speech production, pitch, intonation, respiration and respiratory disorders. Exercises advised by a speech therapist or speech-language pathologist help patients to improve oral motor skills, restore speech, improve listening skills, and use communication aids or sign language if necessary.[9]
Drug therapy
Medications that impede the release of excitatory neurotransmitters have been used to control or prevent spasms.
Deep brain stimulation
Prognosis
The severity of impairment and related prognosis is dependent on the location and severity of brain lesions.[1] Up to 75% of patients will achieve some degree of ambulation.[5] Speech problems, such as dysarthria, are common to these patients.[5]
References
- ^ a b c d e f g h i j k l m n o p q Hou, M; Zhao, J; Yu, R (2006). "Recent advances in dyskinetic cerebral palsy" (PDF). World J Pediatr. 2 (1): 23–28.
- ^ PMID 18981805.
- ^ a b c d e f g "Athetoid Dyskinetic". Swope, Rodante P.A. Retrieved 31 October 2012.
- ^ S2CID 6967370.
- ^ PMID 17478303.
- PMID 7055543.
- ^ Facts about cerebral palsy. Centers for Disease Control and Prevention. (2012).
- ISBN 9780199398911. Retrieved 1 August 2017.
- ^ a b "Cerebral Palsy Treatments". Education That Works. Archived from the original on 22 January 2013. Retrieved 31 October 2012.
- ^ PMID 19907680.
- PMID 26706479.