Atul Goel1, Arjun Dhar2, Abhidha Shah3, Dikpal Jadhav3, Nilesh Bakale3, Tejas Vaja3, Neha Jadhav3. 1. Department of Neurosurgery, K.E.M. Hospital and Seth G.S. Medical College, Parel, Mumbai, India; Department of Neurosurgery, Lilavati Hospital and Research Centre, Bandra (E), Mumbai, India. Electronic address: atulgoel62@hotmail.com. 2. Department of Neurosurgery, Lilavati Hospital and Research Centre, Bandra (E), Mumbai, India. 3. Department of Neurosurgery, K.E.M. Hospital and Seth G.S. Medical College, Parel, Mumbai, India.
Abstract
OBJECTIVE: The implications of diagnosis and treatment of central or axial atlantoaxial dislocation (CAAD) as a cause of symptoms of cervical myelopathy are evaluated. METHODS: This is a report of a series of 5 patients who presented with the primary symptoms of spasticity and motor weakness and paresthesias in all the limbs. There was no evidence of any significant compression of the dural tube or neural structures at the craniovertebral junction. There was no craniovertebral junction instability when assessed by classically described radiologic parameters. CAAD was diagnosed based on our recently discussed parameter of facetal alignment, corroborative clinical and radiologic evidence, and direct observation of atlantoaxial instability by manual manipulation of the bones of the region. All patients underwent atlantoaxial fixation. RESULTS: There was remarkable improvement in the clinical symptoms in the immediate postoperative period and during the follow-up period of 12-24 months (average, 16 months). All patients have continued to have progressive clinical recovery. Clinical assessments were done using Goel clinical evaluation scale, Japanese Orthopedic Association score, and visual analog scale. CONCLUSIONS: Identification and treatment of CAAD can have a significant management impact on patients where the cause of spastic quadriparesis is otherwise undiagnosed.
OBJECTIVE: The implications of diagnosis and treatment of central or axial atlantoaxial dislocation (CAAD) as a cause of symptoms of cervical myelopathy are evaluated. METHODS: This is a report of a series of 5 patients who presented with the primary symptoms of spasticity and motor weakness and paresthesias in all the limbs. There was no evidence of any significant compression of the dural tube or neural structures at the craniovertebral junction. There was no craniovertebral junction instability when assessed by classically described radiologic parameters. CAAD was diagnosed based on our recently discussed parameter of facetal alignment, corroborative clinical and radiologic evidence, and direct observation of atlantoaxial instability by manual manipulation of the bones of the region. All patients underwent atlantoaxial fixation. RESULTS: There was remarkable improvement in the clinical symptoms in the immediate postoperative period and during the follow-up period of 12-24 months (average, 16 months). All patients have continued to have progressive clinical recovery. Clinical assessments were done using Goel clinical evaluation scale, Japanese Orthopedic Association score, and visual analog scale. CONCLUSIONS: Identification and treatment of CAAD can have a significant management impact on patients where the cause of spastic quadriparesis is otherwise undiagnosed.