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Localization of Basal Ganglia and Thalamic Damage in Dyskinetic Cerebral Palsy
Affiliation:1. Department of Neurology, Boston Children''s Hospital, Boston, Massachusetts;2. Harvard Medical School, Boston, Massachusetts;3. Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts;1. Department of Neurology, Sorbonne Université, Paris, France;2. Institut du Cerveau et de la Moëlle épinière—Inserm U1127, Groupe Hospitalier Pitié-Salpêtrière, France;3. Department of Neurology, Groupe Hospitalier Pitié-Salpêtrière, France;1. Department of Neurology, Universitätsmedizin Mannheim, Medical Faculty Mannheim, University of Heidelberg, Germany;2. Department of Neurosurgery, Hannover Medical School, Germany;3. Department of Neurology, Hannover Medical School, Germany;1. Department of Biomedical Engineering, University of Southern California, Los Angeles, CA, USA;2. Department of Neurology, University of Southern California and Children''s Hospital Los Angeles, Los Angeles, CA, USA;3. Department of Neurosurgery, University of Southern California and Children''s Hospital Los Angeles, Los Angeles, CA, USA;4. Department of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles, CA, USA;1. Division of Pediatric Neurology, Department of Neurology, Washington University School of Medicine and St. Louis Children''s Hospital, St. Louis, Missouri;2. Nationwide Children''s Hospital, Columbus, Ohio
Abstract:BackgroundDyskinetic cerebral palsy affects 15%-20% of patients with cerebral palsy. Basal ganglia injury is associated with dyskinetic cerebral palsy, but the patterns of injury within the basal ganglia predisposing to dyskinetic cerebral palsy are unknown, making treatment difficult. For example, deep brain stimulation of the globus pallidus interna improves dystonia in only 40% of patients with dyskinetic cerebral palsy. Basal ganglia injury heterogeneity may explain this variability.MethodsTo investigate this, we conducted a qualitative systematic review of basal ganglia and thalamic damage in dyskinetic cerebral palsy. Reviews and articles primarily addressing genetic or toxic causes of cerebral palsy were excluded yielding 22 studies (304 subjects).ResultsThirteen studies specified the involved basal ganglia nuclei (subthalamic nucleus, caudate, putamen, globus pallidus, or lentiform nuclei, comprised by the putamen and globus pallidus). Studies investigating the lentiform nuclei (without distinguishing between the putamen and globus pallidus) showed that all subjects (19 of 19) had lentiform nuclei damage. Studies simultaneously but independently investigating the putamen and globus pallidus also showed that all subjects (35 of 35) had lentiform nuclei damage (i.e., putamen or globus pallidus damage); this was followed in frequency by damage to the putamen alone (70 of 101, 69%), the subthalamic nucleus (17 of 25, 68%), the thalamus (88 of 142, 62%), the globus pallidus (7/35, 20%), and the caudate (6 of 47, 13%). Globus pallidus damage was almost always coincident with putaminal damage.ConclusionsNoting consistent involvement of the lentiform nuclei in dyskinetic cerebral palsy, these results could suggest two groups of patients with dyskinetic cerebral palsy: those with putamen-predominant damage and those with panlenticular damage involving both the putamen and the globus pallidus. Differentiating between these groups could help predict response to therapies such as deep brain stimulation.
Keywords:cerebral palsy  basal ganglia  thalamus  dystonia
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