title: The phenomenon of disproportionate antecollis in Parkinson's disease and multiple system atrophy.
abstract: We sought to explore the phenomenon of disproportionate antecollis in multiple system atrophy (MSA) and Parkinson's disease (PD). The etiology is much debated and the main issue is whether it represents a primary myopathy or is secondary to the underlying motor disorder. The clinical, electrophysiological, and biopsy data of MSA or PD patients with antecollis were reviewed. We reviewed 16 patients (7 MSA and 9 PD) who developed antecollis during the course of their disease. The interval between onset of motor symptoms and of antecollis was shorter in the MSA group (4.6 +/- 1.7 years vs. 10.5 +/- 7.0 years). In 6 patients, the antecollis developed subacutely, and in 2 the abnormal neck flexion was initially an off-period phenomenon. Two additional patients also showed some dopa-responsiveness. Clinically, the antecollis was characterized by a forward flexion and anterior shift of the neck, with prominent cervical paraspinal and levator scapulae muscles, usually without weakness of residual neck extension. Electromyography of cervical paraspinal muscles showed mixed myopathic, normal, and neurogenic units, without early recruitment. Cervical paraspinal muscle biopsy in 2 patients disclosed fibrosis and nonspecific myopathic changes. We suggest that, in the context of MSA or PD, the initiating event in antecollis could be a disproportionately increased tone in anterior neck muscles that leads to secondary fibrotic and myopathic changes. However, a primary but yet unexplained neck extensor myopathy still remains the alternative possibility and longitudinal studies are necessary to settle this issue.
authors.affiliation: Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, London, United Kingdom. b.vandewarrenburg@neuro.umcn.nl
authors.forename: Bart P C
authors.initials: BP
authors.lastname: van de Warrenburg
authors.forename: Carla
authors.initials: C
authors.lastname: Cordivari
authors.forename: Aisling M
authors.initials: AM
authors.lastname: Ryan
authors.forename: Rahul
authors.initials: R
authors.lastname: Phadke
authors.forename: Janice L
authors.initials: JL
authors.lastname: Holton
authors.forename: Kailash P
authors.initials: KP
authors.lastname: Bhatia
authors.forename: Mike G
authors.initials: MG
authors.lastname: Hanna
authors.forename: Niall P
authors.initials: NP
authors.lastname: Quinn
mesh_terms: D000368:Aged; D000978:Antiparkinson Agents / Q000627:therapeutic use; D019274:Botulinum Toxins, Type A / Q000627:therapeutic use; D004576:Electromyography; D004594:Electrophysiology; D005260:Female; D005355:Fibrosis / Q000473:pathology; D006257:Head; D006801:Humans; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009068:Movement / Q000502:physiology*; D019578:Multiple System Atrophy / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000473:pathology / Q000503:physiopathology; D009333:Neck; D009465:Neuromuscular Agents / Q000627:therapeutic use; D010300:Parkinson Disease / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*
chemical_list: D000978:Antiparkinson Agents; D009465:Neuromuscular Agents; D007980:Levodopa; D019274:Botulinum Toxins, Type A