Dyskinetic cerebral palsy

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Dyskinetic cerebral palsy (DCP) is a subtype of cerebral palsy (CP) and is characterized by impaired muscle tone regulation, coordination and movement control. Dystonia and choreoathetosis are the two most dominant movement disorders in patients with DCP. [1] [2]

Contents

Presentation

In dyskinetic cerebral palsy, both motor and non-motor impairments are present. Motor impairments, such as impaired muscle tone regulations, lack of muscle control and bone deformations are often more severe compared to the other subtypes of CP. [3] Non-motor impairments increase with motor severity. Half of the DCP group shows severe learning disabilities, 51% has epilepsy. Hearing and visual impairments occur frequently, respectively 11% and 45%. Dysarthria or anarthria are also common, so alternative and augmentative communication tools are needed. [3] [4]

Dystonia and choreoathetosis

Dystonia and choreoathetosis mostly occur concurrently in DCP, [5] but they are two independent motor disorders with their own characteristics. Dystonia predominates in most patients.

Dystonia (DYS) is defined by twisting and repetitive movements, abnormal postures due to sustained muscle contractions, and hypertonia. Dystonia is aggravated by voluntary movements and postures, or with stress, emotion or pain. [6] [7] A video of dystonia in a patient with dyskinetic cerebral palsy can be seen here: Dyskinetic cerebral palsy: dystonia on YouTube. [7]

Choreoathetosis (CA) is characterized by hyperkinesia (chorea i.e. rapid involuntary, jerky, often fragmented movements) and hypokinesia (athetosis i.e. slower, constantly changing, writhing or contorting movements). [8] [5] A video of choreoathetosis in a patient with dyskinetic cerebral palsy can be seen here: Dyskinetic cerebral palsy: choreoathetosis on YouTube. [7]

Clinical patterns

Patients with DCP are more likely to obtain a high level of functional disability. Respectively 12,7% and 49% of the patients were assigned in level IV and V of the Gross Motor Function Classification System (GMFCS). The same trend appeared in manual ability with 21,8% in level IV and 43,6% in level V of the Manual Ability Classification System (MACS). A good correlation between the functional classification scales and the total dystonia level was found, meaning that a higher level of functional disability correlates with a higher dystonia level. The same study showed no associations with choreoathetosis. These results suggest that dystonia typically has a bigger impact on functionality and a larger effect on activity, participation and quality of life than choreoathetosis. [9] [2]

As previously mentioned, dystonia predominates in most patients, partly because dystonia is often more noticeable and severe than choreoathetosis. Both increase with activity and are generalized over all body regions with a higher severity in the upper limbs than in the lower limbs. Dystonia has a significantly higher level of severity in the distal parts of the extremities, whereas choreoathetosis is more equally distributed. [2]

Causes

Dyskinetic cerebral palsy could have multiple causes. The majority of the children are born at term and experience perinatal adverse events which can be supported by neuroimaging. Possible causes are perinatal hypoxic-ischaemia and neonatal shock in children born at term or near term. Hyperbilirubinaemia used to be a common contributing factor, [10] but is now rare in high-income countries due to preventive actions. Other aetiological factors are growth retardation, [11] brain maldevelopment, intracranial haemorrhage, stroke or cerebral infections. [3]

Diagnosis

Multiple classification systems using Magnetic Resonance Imaging (MRI) have been developed, linking brain lesions to time of birth, cerebral palsy subtype and functional ability. [12] [13] [14] [15] The overall goal of these studies is to elucidate etiology, timing of injury and pathogenesis of cerebral palsy. [12]

Around 70% of patients with DCP show lesions in the cortical and deep grey matter of the brain, more specifically in the basal ganglia and thalamus. However, other brain lesions and even normal-appearing MRI findings can occur, for example white matter lesions and brain maldevelopments. [2] [14] [16] [17] Patients with pure basal ganglia and thalamus lesions are more likely to show more severe choreoathetosis whereas dystonia may be associated with other brain lesions, such as the cerebellum. [2] These lesions occur mostly during the peri- and postnatal period since these regions have a high vulnerability during the late third trimester of the pregnancy. [18] Unfortunately, contemporary imaging is not sophisticated enough to detect all subtle brain deformities and network disorders in dystonia. Research with more refined imaging techniques including diffusion tensor imaging and functional MRI is required. [7] [19]

Prevention

Prevention strategies have been developed for the different risk factors of the specific cerebral palsy subtypes. Primary prevention consists of reducing the possible risk factors. However, when multiple risk factors cluster together, prevention is much more difficult. Secondary preventions may be more appropriate at that time, e.g. prevention of prematurity. Studies showed a reduced risk of cerebral palsy when administering magnesium sulfate to women at risk of preterm delivery. [20] [21]

Cooling or therapeutic hypothermia for 72 hours immediately after birth has a significant clinical effect on reducing mortality and severity of neurodevelopmental disabilities in neonates with birth asphyxia. This has been documented for newborns with hypoxic-ischemic encephalopathy. [22] [23]

Management

Measurement

Measuring dystonia and choreoathetosis can be very challenging. It is however crucial to have reliable measurements for the evaluation and effects of targeted management. So far, measurements involved the usage of clinical qualitative assessment scales judged by video observation. The Barry-Albright Dystonia Rating Scale (BADS), the Burke-Fahn-Marsden Dystonia Rating Scale (BFMS) and the Dyskinesia Impairment Scale (DIS) are most commonly used. [24] [25] [26]

The BADS was developed and validated to assess secondary dystonia in patients with CP. [24] The BFMS has been validated for use in primary dystonia and is clinically the most used scale in both primary and secondary dystonia. [25] Both the BADS and BFMS do not include scoring for choreoathetosis. The DIS is currently stated as the most sensitive, valid and reliable scale. It has been validated for use in secondary dystonia, as it occurs in patients with DCP. The value lays in its detailed full-body consideration and the differentiation action-rest, proximal-distal limb and duration-amplitude. Moreover, the DIS includes both the evaluation of dystonia and choreoathetosis. Although this scale is currently seen as the gold standard to evaluate patients with DCP in research, substantial time and experience with the current CA and DYS definitions is needed from the rater in scoring dystonia and choreoathetosis. [26] [27] [28]

Both the DIS and BFMS can be used as outcome measure in intervention studies such as deep brain stimulation (DBS) [29] [30] or intrathecal baclofen. [31]

Aim of treatment interventions

Dyskinetic cerebral palsy is a non-progressive, non-reversible disease. The current management is symptomatic, since there is no cure. The main goal is to improve daily activity, quality of life and autonomy of the children by creating a timed and targeted management.

The many management options for patients with DCP are not appropriate as standalone treatment but must be seen within an individualized multidisciplinary rehabilitation program.

Medical and rehabilitation interventions

Management options can be subdivided into medical treatment and rehabilitation interventions.

Medical treatment consists of oral medication and surgery. Before using oral drugs, it is important to differentiate between spasticity, dystonia and choreoathetosis since each motor disorder has a specific approach. In general, many oral drugs have low efficacy, unwanted side-effects and variable effects. [32] Oral baclofen and trihexyphenidyl are commonly used to decrease dystonia, although its efficacy is relatively low in most patients. Adverse effects of the latter can include worsening of choreoathetosis. [7] Since dystonia predominates over choreoathetosis in most patients, reducing dystonia allows the possibility of a full expression of choreoathetosis. This suggests that the discrimination of dystonia and choreoathetosis is crucial, since misinterpretations in diagnosing can contribute to the administration of inappropriate medication, causing unwanted effects. [7] [33] Intrathecal baclofen pump (ITB) is often used as an alternative to reduce side-effects of the oral dystonic medication over the whole body and botulinum toxin injections are applied to decrease dystonia in specific muscles or muscle groups. [7] [34] [35] Research on the effects of ITB and botulinum toxin on choreoathetosis is lacking.

Regarding surgical treatment in patients with DCP, deep brain stimulation (DBS) has shown to decrease dystonia. [36] However, the responsiveness is less beneficial and the effects are more variable than in patients with inherited or primary dystonia. [37] The effects on choreoathetosis have not been investigated.

Orthopedic surgery is performed to correct musculoskeletal deformities, but it is recommended that all other alternatives are considered first. [7]

The previous management options need to be combined with rehabilitation programs, adapted to the specific needs of each individual. Unfortunately, evidence for rehabilitation strategies is scarce and is based on clinical expertise. The team of caregivers can consist of physiotherapists, occupational therapists and speech/communication therapists. The therapy mainly focusses on the motor problems by using principles of neuroplasticity, patterning, postural balance, muscle strengthening and stretching. [34] Non-motor impairments such as epilepsy require specific treatment.

Prevalence

Dyskinetic cerebral palsy is the second most common subtype of cerebral palsy, after spastic CP. A European Cerebral Palsy study reported a rate of 14,4% of patients with DCP [38] which is similar to the rate of 15% reported in Sweden. [39] The rate appeared lower in Australia, where data from states with full population-based ascertainment listed DCP as the predominant motor type in only 7% of the cases. [40] The differences reported from various registers and countries may relate to under-identification of dyskinetic CP due to a lack of standardization in definition and classification based on predominant type. [41] [8]

Related Research Articles

<span class="mw-page-title-main">Cerebral palsy</span> Group of movement disorders that appear in early childhood

Cerebral palsy (CP) is a group of movement disorders that appear in early childhood. Signs and symptoms vary among people and over time, but include poor coordination, stiff muscles, weak muscles, and tremors. There may be problems with sensation, vision, hearing, and speaking.

<span class="mw-page-title-main">Athetosis</span> Medical condition

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 physical disability. Treatments for athetosis are not very effective, and in most cases are simply aimed at managing the uncontrollable movement, rather than the cause itself.

Worster-Drought syndrome is a form of congenital suprabulbar paresis that occurs in some children with cerebral palsy. It is caused by inadequate development of the corticobulbar tracts and causes problems with the mouth and tongue including impaired swallowing. A similar syndrome in adults is called anterior opercular syndrome.

The Bobath concept is an approach to neurological rehabilitation that is applied in patient assessment and treatment. The goal of applying the Bobath concept is to promote motor learning for efficient motor control in various environments, thereby improving participation and function. This is done through specific patient handling skills to guide patients through the initiation and completing of intended tasks. This approach to neurological rehabilitation is multidisciplinary, primarily involving physiotherapists, occupational therapists, and speech and language therapists. In the United States, the Bobath concept is also known as 'neuro-developmental treatment' (NDT).

<span class="mw-page-title-main">Progressive supranuclear palsy</span> Medical condition

Progressive supranuclear palsy (PSP) is a late-onset neurodegenerative disease involving the gradual deterioration and death of specific volumes of the brain. The condition leads to symptoms including loss of balance, slowing of movement, difficulty moving the eyes, and cognitive impairment. PSP may be mistaken for other types of neurodegeneration such as Parkinson's disease, frontotemporal dementia and Alzheimer's disease. The cause of the condition is uncertain, but involves the accumulation of tau protein within the brain. Medications such as levodopa and amantadine may be useful in some cases.

Hypokinesia is one of the classifications of movement disorders, and refers to decreased bodily movement. Hypokinesia is characterized by a partial or complete loss of muscle movement due to a disruption in the basal ganglia. Hypokinesia is a symptom of Parkinson's disease shown as muscle rigidity and an inability to produce movement. It is also associated with mental health disorders and prolonged inactivity due to illness, amongst other diseases.

<span class="mw-page-title-main">Periventricular leukomalacia</span> Degeneration of white matter near the lateral ventricles of the brain

Periventricular leukomalacia (PVL) is a form of white-matter brain injury, characterized by the necrosis of white matter near the lateral ventricles. It can affect newborns and fetuses; premature infants are at the greatest risk of neonatal encephalopathy which may lead to this condition. Affected individuals generally exhibit motor control problems or other developmental delays, and they often develop cerebral palsy or epilepsy later in life. The white matter in preterm born children is particularly vulnerable during the third trimester of pregnancy when white matter developing takes place and the myelination process starts around 30 weeks of gestational age.

Hypertonia is a term sometimes used synonymously with spasticity and rigidity in the literature surrounding damage to the central nervous system, namely upper motor neuron lesions. Impaired ability of damaged motor neurons to regulate descending pathways gives rise to disordered spinal reflexes, increased excitability of muscle spindles, and decreased synaptic inhibition. These consequences result in abnormally increased muscle tone of symptomatic muscles. Some authors suggest that the current definition for spasticity, the velocity-dependent over-activity of the stretch reflex, is not sufficient as it fails to take into account patients exhibiting increased muscle tone in the absence of stretch reflex over-activity. They instead suggest that "reversible hypertonia" is more appropriate and represents a treatable condition that is responsive to various therapy modalities like drug or physical therapy.

<span class="mw-page-title-main">ATP1A3</span> Protein-coding gene in the species Homo sapiens

Sodium/potassium-transporting ATPase subunit alpha-3 is an enzyme that in humans is encoded by the ATP1A3 gene.

Benedikt syndrome, also called Benedikt's syndrome or paramedian midbrain syndrome, is a rare type of posterior circulation stroke of the brain, with a range of neurological symptoms affecting the midbrain, cerebellum and other related structures.

<span class="mw-page-title-main">Paroxysmal kinesigenic choreoathetosis</span> Medical condition

Paroxysmal kinesigenic choreoathetosis (PKC) also called paroxysmal kinesigenic dyskinesia (PKD) is a hyperkinetic movement disorder characterized by attacks of involuntary movements, which are triggered by sudden voluntary movements. The number of attacks can increase during puberty and decrease in a person's 20s to 30s. Involuntary movements can take many forms such as ballism, chorea or dystonia and usually only affect one side of the body or one limb in particular. This rare disorder only affects about 1 in 150,000 people, with PKD accounting for 86.8% of all the types of paroxysmal dyskinesias, and occurs more often in males than females. There are two types of PKD, primary and secondary. Primary PKD can be further broken down into familial and sporadic. Familial PKD, which means the individual has a family history of the disorder, is more common, but sporadic cases are also seen. Secondary PKD can be caused by many other medical conditions such as multiple sclerosis (MS), stroke, pseudohypoparathyroidism, hypocalcemia, hypoglycemia, hyperglycemia, central nervous system trauma, or peripheral nervous system trauma. PKD has also been linked with infantile convulsions and choreoathetosis (ICCA) syndrome, in which patients have afebrile seizures during infancy and then develop paroxysmal choreoathetosis later in life. This phenomenon is actually quite common, with about 42% of individuals with PKD reporting a history of afebrile seizures as a child.

<span class="mw-page-title-main">Basal ganglia disease</span> Group of physical problems resulting from basal ganglia dysfunction

Basal ganglia disease is a group of physical problems that occur when the group of nuclei in the brain known as the basal ganglia fail to properly suppress unwanted movements or to properly prime upper motor neuron circuits to initiate motor function. Research indicates that increased output of the basal ganglia inhibits thalamocortical projection neurons. Proper activation or deactivation of these neurons is an integral component for proper movement. If something causes too much basal ganglia output, then the ventral anterior (VA) and ventral lateral (VL) thalamocortical projection neurons become too inhibited, and one cannot initiate voluntary movement. These disorders are known as hypokinetic disorders. However, a disorder leading to abnormally low output of the basal ganglia leads to reduced inhibition, and thus excitation, of the thalamocortical projection neurons which synapse onto the cortex. This situation leads to an inability to suppress unwanted movements. These disorders are known as hyperkinetic disorders.

<span class="mw-page-title-main">Management of cerebral palsy</span>

Over time, the approach to cerebral palsy management has shifted away from narrow attempts to fix individual physical problems – such as spasticity in a particular limb – to making such treatments part of a larger goal of maximizing the person's independence and community engagement. Much of childhood therapy is aimed at improving gait and walking. Approximately 60% of people with CP are able to walk independently or with aids at adulthood. However, the evidence base for the effectiveness of intervention programs reflecting the philosophy of independence has not yet caught up: effective interventions for body structures and functions have a strong evidence base, but evidence is lacking for effective interventions targeted toward participation, environment, or personal factors. There is also no good evidence to show that an intervention that is effective at the body-specific level will result in an improvement at the activity level, or vice versa. Although such cross-over benefit might happen, not enough high-quality studies have been done to demonstrate it.

The Gross Motor Function Classification System or GMFCS is a 5 level clinical classification system that describes the gross motor function of people with cerebral palsy on the basis of self-initiated movement abilities. Particular emphasis in creating and maintaining the GMFCS scale rests on evaluating sitting, walking, and wheeled mobility. Distinctions between levels are based on functional abilities; the need for walkers, crutches, wheelchairs, or canes / walking sticks; and to a much lesser extent, the actual quality of movement.

<span class="mw-page-title-main">Athetoid cerebral palsy</span> Type of cerebral palsy associated with basal ganglia damage

Athetoid cerebral palsy, or dyskinetic cerebral palsy, 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.

<span class="mw-page-title-main">Ataxic cerebral palsy</span> Medical condition

Ataxic cerebral palsy is clinically 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 and dyskinetic cerebral palsy.

<span class="mw-page-title-main">Ulegyria</span> Type of cortical scarring deep in the sulci

Ulegyria is a diagnosis used to describe a specific type of cortical scarring in the deep regions of the sulcus that leads to distortion of the gyri. Ulegyria is identified by its characteristic "mushroom-shaped" gyri, in which scarring causes shrinkage and atrophy in the deep sulcal regions while the surface gyri are spared. This condition is most often caused by hypoxic-ischemic brain injury in the perinatal period. The effects of ulegyria can range in severity, although it is most commonly associated with cerebral palsy, mental retardation and epilepsy. N.C. Bresler was the first to view ulegyria in 1899 and described this abnormal morphology in the brain as “mushroom-gyri." Although ulegyria was first identified in 1899, there is still limited information known or reported about the condition.

Sepiapterin reductase deficiency is an inherited pediatric disorder characterized by movement problems, and most commonly displayed as a pattern of involuntary sustained muscle contractions known as dystonia. Symptoms are usually present within the first year of age, but diagnosis is delayed due to physicians lack of awareness and the specialized diagnostic procedures. Individuals with this disorder also have delayed motor skills development including sitting, crawling, and need assistance when walking. Additional symptoms of this disorder include intellectual disability, excessive sleeping, mood swings, and an abnormally small head size. SR deficiency is a very rare condition. The first case was diagnosed in 2001, and since then there have been approximately 30 reported cases. At this time, the condition seems to be treatable, but the lack of overall awareness and the need for a series of atypical procedures used to diagnose this condition pose a dilemma.

<span class="mw-page-title-main">General movements assessment</span>

A general movements assessment is a type of medical assessment used in the diagnosis of cerebral palsy, and is particularly used to follow up high-risk neonatal cases. The general movements assessment involves measuring movements that occur spontaneously among those less than four months of age and appears to be most accurate test for the condition.

<span class="mw-page-title-main">Diane Damiano</span> American biomedical scientist and physical therapist

Diane Louise Damiano is an American biomedical scientist and physical therapist specializing in physical medicine and rehabilitation approaches in children with cerebral palsy. She is chief of the functional and applied biomechanics section at the National Institutes of Health Clinical Center. Damiano has served as president of the Clinical Gait and Movement Analysis Society and the American Academy for Cerebral Palsy and Developmental Medicine.

References

  1. ↑ Rosenbaum, P.; Paneth, N.; Leviton, A.; Goldstein, M.; Bax, M.; Damiano, D.; Dan, B.; Jacobsson, B. (February 2007). "A report: the definition and classification of cerebral palsy April 2006". Developmental Medicine & Child Neurology. 49 (6): 8–14. doi: 10.1111/j.1469-8749.2007.tb12610.x .
  2. 1 2 3 4 5 Monbaliu, E.; de Cock, P.; Ortibus, E.; Heyrman, L.; Klingels, K.; Feys, H. (February 2016). "Clinical patterns of dystonia and choreoathetosis in participants with dyskinetic cerebral palsy". Developmental Medicine & Child Neurology. 58 (2): 138–144. doi: 10.1111/dmcn.12846 . PMID   26173923.
  3. 1 2 3 Himmelmann, K.; Hagberg, G.; Wiklund, L. M.; Eek, M. N.; Uvebrant, P. (April 2007). "Dyskinetic cerebral palsy: a population-based study of children born between 1991 and 1998". Developmental Medicine & Child Neurology. 49 (4): 246–251. doi: 10.1111/j.1469-8749.2007.00246.x . PMID   17376133.
  4. ↑ Himmelmann, K.; McManus, V.; Hagberg, G.; Uvebrant, P.; Krägeloh-Mann, I.; Cans, C. (May 2009). "Dyskinetic cerebral palsy in Europe: trends in prevalence and severity". Archives of Disease in Childhood. 94 (12): 921–926. doi:10.1136/adc.2008.144014. PMID   19465585. S2CID   25093584.
  5. 1 2 Sanger, T. D.; Delgado, M. R.; Gaebler-Spira, D.; Hallett, M.; Mink, J. W. (January 2003). "Classification and Definition of Disorders Causing Hypertonia in Childhood". Pediatrics. 111 (1): e89–e97. doi:10.1542/peds.111.1.e89. PMID   12509602.
  6. ↑ Sanger, T. D.; Chen, D.; Fehlings, D. L.; Hallett, M.; Lang, A. E.; Mink, J. W.; Singer, H. S.; Alter, K.; Ben-Pazi, H.; Butler, E. E.; Chen, R.; Collins, A.; Dayanidhi, S.; Forssberg, H.; Fowler, E.; Gilbert, D. L.; Gorman, S. L.; Gormley, M. E.; Jinnah, H. A.; Kornblau, B.; Krosschell, K. J.; Lehman, R. K.; MacKinnon, C.; Malanga, C. J.; Mesterman, R.; Michaels, M. B.; Pearson, T. S.; Rose, J.; Russman, B. S.; Sternad, D.; Swoboda, K. J.; Valero-Cuevas, F. (August 2010). "Definition and classification of hyperkinetic movements in childhood". Movement Disorders. 25 (11): 1538–1549. doi:10.1002/mds.23088. PMC   2929378 . PMID   20589866.
  7. 1 2 3 4 5 6 7 8 Monbaliu, E.; Himmelmann, K.; Lin, J. P.; Ortibus, E.; Bonouvrié, L.; Feys, H.; Vermeulen, R. J.; Dan, B. (September 2017). "Clinical presentation and management of dyskinetic cerebral palsy". Lancet Neurology. 16 (9): 741–749. doi:10.1016/S1474-4422(17)30252-1. PMID   28816119. S2CID   22841349.
  8. 1 2 Cans, C.; Dolk, H.; Platt, M.; Colver, A.; Prasauskiene, A.; Krägeloh-Mann, I (February 2007). "Recommendations from the SCPE collaborative group for defining and classifying cerebral palsy". Developmental Medicine & Child Neurology. 49 (s109): 35–38. doi: 10.1111/j.1469-8749.2007.tb12626.x . PMID   17370480.
  9. ↑ Monbaliu, E.; De Cock, P.; Mailleux, L.; Dan, B.; Feys, H. (March 2017). "The relationship of dystonia and choreoathetosis with activity, participation and quality of life in children and youth with dyskinetic cerebral palsy". European Journal of Paediatric Neurology. 21 (2): 327–335. doi:10.1016/j.ejpn.2016.09.003. PMID   27707657.
  10. ↑ Kyllerman, M.; Bager, B.; Bensch, J.; Bille, B.; Olow, I.; Voss, H. (July 1982). "Dyskinetic cerebral palsy. I. Clinical categories, associated neurological abnormalities and incidences". Acta Paediatrica. 71 (4): 543–550. doi:10.1111/j.1651-2227.1982.tb09472.x. PMID   7136669. S2CID   40382546.
  11. ↑ Jarvis, S.; Glinianaia, S.; Torrioli, M. G.; Platt, M. J.; Miceli, M.; Jouk, P. S.; Johnson, A.; Hutton, J.; Hemming, K.; Hagberg, G.; Dolk, H.; Chalmers, J. (October 2003). "Cerebral palsy and intrauterine growth in single births: European collaborative study". Lancet. 362 (9390): 1106–1111. doi:10.1016/S0140-6736(03)14466-2. PMID   14550698. S2CID   21236988.
  12. 1 2 Krägeloh-Mann, I.; Horber, V. (February 2007). "The role of magnetic resonance imaging in elucidating the pathogenesis of cerebral palsy: a systematic review". Developmental Medicine & Child Neurology. 49 (2): 144–151. doi:10.1111/j.1469-8749.2007.00144.x. PMID   17254004.
  13. ↑ Himmelmann, K.; Horber, V.; De La Cruz, J.; Horridge, K.; Mejaski-Bosnjak, V.; Hollody, K.; Krägeloh-Mann, I. (January 2017). "MRI classification system (MRICS) for children with cerebral palsy: development, reliability, and recommendations". Developmental Medicine & Child Neurology. 59 (1): 57–64. doi: 10.1111/dmcn.13166 . PMID   27325153.
  14. 1 2 Benini, R.; Dagenais, L.; Shevell, M. I. (February 2013). "Normal Imaging in Patients with Cerebral Palsy: What Does It Tell Us?". The Journal of Pediatrics. 162 (2): 369–374.e1. doi:10.1016/j.jpeds.2012.07.044. PMID   22944004.
  15. ↑ Reid, S. M.; Dagia, C. D.; Ditchfield, M. R.; Carlin, J. B; Reddihough, D. S. (March 2014). "Population-based studies of brain imaging patterns in cerebral palsy". Developmental Medicine & Child Neurology. 56 (3): 222–232. doi: 10.1111/dmcn.12228 . PMID   23937113.
  16. ↑ Horber, V.; Sellier, E.; Horridge, K.; Rackauskaite, G.; Andersen, G. L.; Virella, D.; Ortibus, E.; Dakovic, I.; Hensey, O.; Radsel, A.; Papavasiliou, A.; Cruz De la, J.; Arnaud, C.; Krägeloh-Mann, I.; Himmelmann, K. (March 2020). "The Origin of the Cerebral Palsies: Contribution of Population-Based Neuroimaging Data". Neuropediatrics. 51 (2): 113–119. doi:10.1055/s-0039-3402007. PMID   32120429. S2CID   211835380.
  17. ↑ Krägeloh-Mann, I.; Cans, C. (August 2009). "Cerebral palsy update". Brain and Development. 31 (7): 537–544. doi:10.1016/j.braindev.2009.03.009. PMID   19386453. S2CID   8374616.
  18. ↑ Krägeloh-Mann, I. (November 2004). "Imaging of early brain injury and cortical plasticity". Experimental Neurology. 190 (Suppl 1): 84–90. doi:10.1016/j.expneurol.2004.05.037. PMID   15498546. S2CID   9500238.
  19. ↑ Korzeniewski, S. J.; Birbeck, G.; DeLano, M. C.; Potchen, M. J.; Paneth, N. (February 2008). "A Systematic Review of Neuroimaging for Cerebral Palsy". Journal of Child Neurology. 23 (2): 216–227. doi:10.1177/0883073807307983. PMID   18263759. S2CID   11724552.
  20. ↑ Conde-Agudelo, A.; Romero, R. (June 2009). "Antenatal magnesium sulfate for the prevention of cerebral palsy in preterm infants less than 34 weeks' gestation: a systematic review and metaanalysis". American Journal of Obstetrics and Gynecology. 200 (6): 595–609. doi:10.1016/j.ajog.2009.04.005. PMC   3459676 . PMID   19482113.
  21. ↑ Graham, H. K.; Rosenbaum, P.; Paneth, N.; Dan, B.; Lin, J. P.; Damiano, D. L.; Becher, J. G.; Gaebler-Spira, D.; Colver, A.; Reddihough, D. S.; Crompton, K. E.; Lieber, R. L. (January 2016). "Cerebral palsy". Nature Reviews Disease Primers. 2: 15082. doi:10.1038/nrdp.2015.82. PMC   9619297 . PMID   27188686. S2CID   4037636.
  22. ↑ Jacobs, S. E.; Hunt, R.; Tarnow-Mordi, W. O.; Inder, T. E.; Davis, P. G. (December 2008). "Cochrane Review: Cooling for newborns with hypoxic-ischaemic encephalopathy". Evidence-Based Child Health: A Cochrane Review Journal. 3 (4): 1049–1115. doi:10.1002/ebch.293.
  23. ↑ Azzopardi, D. V.; Strohm, B.; Edwards, A. D.; Dyet, L.; Halliday, H. L.; Juszczak, E.; Kapellou, O.; Levene, M.; Marlow, N.; Porter, E.; Thoresen, M.; Whitelaw, A.; Brocklehurst, P. (October 2009). "Moderate Hypothermia to Treat Perinatal Asphyxial Encephalopathy". New England Journal of Medicine. 361 (14): 1349–1358. doi: 10.1056/NEJMoa0900854 . PMID   19797281. S2CID   27308372.
  24. 1 2 Barry, M. J; VanSwearingen, J. M; Albright, A L. (June 1999). "Reliability and responsiveness of the Barry–Albright Dystonia Scale". Developmental Medicine & Child Neurology. 41 (6): 404–411. doi:10.1017/s0012162299000870. PMID   10400175.
  25. 1 2 Burke, R. E.; Fahn, S.; Marsden, C. D.; Bressman, S. B.; Moskowitz, C.; Friedman, J. (January 1985). "Validity and reliability of a rating scale for the primary torsion dystonias". Neurology. 35 (1): 73–77. doi:10.1212/wnl.35.1.73. PMID   3966004. S2CID   40488467.
  26. 1 2 Monbaliu, E.; Ortibus, E.; De Cat, J.; Dan, B.; Heyrman, L.; Prinzie, P.; De Cock, P.; Feys, H. (March 2012). "The Dyskinesia Impairment Scale: a new instrument to measure dystonia and choreoathetosis in dyskinetic cerebral palsy". Developmental Medicine & Child Neurology. 54 (3): 278–283. doi: 10.1111/j.1469-8749.2011.04209.x . PMID   22428172.
  27. ↑ Stewart, Ki.; Harvey, A.; Johnston, L. M (August 2017). "A systematic review of scales to measure dystonia and choreoathetosis in children with dyskinetic cerebral palsy". Developmental Medicine & Child Neurology. 59 (8): 786–795. doi: 10.1111/dmcn.13452 . hdl: 11343/292881 . PMID   28485494.
  28. ↑ Vanmechelen, I.; Dan, B.; Feys, H.; Monbaliu, E. (December 2019). "Test–retest reliability of the Dyskinesia Impairment Scale: measuring dystonia and choreoathetosis in dyskinetic cerebral palsy". Developmental Medicine & Child Neurology. 62 (4): 489–493. doi: 10.1111/dmcn.14424 . PMID   31833574. S2CID   209341122.
  29. ↑ Gimeno, H.; Lin, J. P. (January 2017). "The International Classification of Functioning (ICF) to evaluate deep brain stimulation neuromodulation in childhood dystonia-hyperkinesia informs future clinical & research priorities in a multidisciplinary model of care". European Journal of Paediatric Neurology. 21 (1): 147–167. doi: 10.1016/j.ejpn.2016.08.016 . PMID   27707656.
  30. ↑ Koy, A.; Timmermann, L. (January 2017). "Deep brain stimulation in cerebral palsy: Challenges and opportunities". European Journal of Paediatric Neurology. 21 (1): 118–121. doi:10.1016/j.ejpn.2016.05.015. PMID   27289260.
  31. ↑ Bonouvrié, L. A; Becher, J. G; Vles, J. S.H.; Boeschoten, K.; Soudant, D.; de Groot, V.; van Ouwerkerk, W. J.R.; Strijers, R. L.M.; Foncke, E.; Geytenbeek, J.; van de Ven, P. M.; Teernstra, O.; Vermeulen, R. J. (October 2013). "Intrathecal baclofen treatment in dystonic cerebral palsy: a randomized clinical trial: the IDYS trial". BMC Pediatrics. 13: 175. doi: 10.1186/1471-2431-13-175 . PMC   3840690 . PMID   24165282.
  32. ↑ Lumsden, D. E.; Kaminska, M.; Tomlin, S.; Lin, J. P. (July 2016). "Medication use in childhood dystonia". European Journal of Paediatric Neurology. 20 (4): 625–629. doi:10.1016/j.ejpn.2016.02.003. PMID   26924167.
  33. ↑ Termsarasab, P. (December 2017). "Medical treatment of dyskinetic cerebral palsy: translation into practice". Developmental Medicine & Child Neurology. 59 (12): 1210. doi: 10.1111/dmcn.13549 . PMID   28892137.
  34. 1 2 Colver, A.; Fairhurst, C.; Pharoah, P. O. D. (April 2014). "Cerebral palsy". Lancet. 383 (9924): 1240–1249. doi:10.1016/S0140-6736(13)61835-8. PMID   24268104. S2CID   24655659.
  35. ↑ Elkamil, A. I.; Andersen, G. L.; Skranes, J.; Lamvik, T.; Vik, T. (September 2012). "Botulinum neurotoxin treatment in children with cerebral palsy: A population-based study in Norway". European Journal of Paediatric Neurology. 16 (5): 522–527. doi:10.1016/j.ejpn.2012.01.008. PMID   22325829.
  36. ↑ Coubes, P.; Roubertie, A.; Vayssiere, N.; Hemm, S.; Echenne, B. (June 2000). "Treatment of DYT1-generalised dystonia by stimulation of the internal globus pallidus". Lancet. 355 (9222): 2220–2221. doi:10.1016/S0140-6736(00)02410-7. PMID   10881900. S2CID   12077880.
  37. ↑ Vidailhet, M.; Yelnik, J.; Lagrange, C.; Fraix, V.; Grabli, D.; Thobois, S.; Burbaud, P.; Welter, M. L.; Xie-Brustolin, J.; Braga, M. C. C.; Ardouin, C.; Czernecki, V.; Klinger, H.; Chabardes, S.; Seigneuret, E.; Mertens, P.; Cuny, E.; Navarro, S.; Cornu, P.; Benabid, A. L.; LeBas, J. F.; Dormont, D.; Hermier, M.; Dujardin, K.; Blond, S.; Krystkowiak, P.; Destée, A.; Bardinet, E.; Agid, Y.; Krack, P.; Broussolle, E.; Pollak, P. (August 2009). "Bilateral pallidal deep brain stimulation for the treatment of patients with dystonia-choreoathetosis cerebral palsy: a prospective pilot study". Lancet Neurology. 8 (8): 709–717. doi:10.1016/S1474-4422(09)70151-6. PMID   19576854. S2CID   24345609.
  38. ↑ Bax, M.; Tydeman, C.; Flodmark, O. (October 2006). "Clinical and MRI Correlates of Cerebral Palsy". JAMA. 296 (13): 1602–1608. doi:10.1001/jama.296.13.1602. PMID   17018805.
  39. ↑ Himmelmann, K.; Hagberg, G.; Beckung, E.; Hageberg, B.; Uvebrant, P. (March 2005). "The changing panorama of cerebral palsy in Sweden. IX. Prevalence and origin in the birth-year period 1995-1998". Acta Paediatrica. 94 (3): 287–294. doi:10.1111/j.1651-2227.2005.tb03071.x. PMID   16028646. S2CID   8322621.
  40. ↑ Report of the Australian Cerebral Palsy Register Birth years 1995-2012 (Report). The Australian Cerebral Palsy Register Group. November 2018.
  41. ↑ Cans, C. (February 2007). "Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers". Developmental Medicine & Child Neurology. 42 (12): 816–824. doi: 10.1111/j.1469-8749.2000.tb00695.x .
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