Coexistence of Metabolic Neuropathy and Cervical Myelopathy
Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine
A 63-year-old man with extensive multilevel degenerative cervical and thoracic spine disease, class 1 obesity, essential hypertension, mixed hyperlipidemia, and a history of type 2 diabetes mellitus presented with progressive bilateral upper and lower extremity paresthesias, burning pain in the hands and feet, gait instability, and a history of a fall with transient loss of consciousness. Initial workup revealed a hemoglobin A1c (HbA1c) of 5.4%, and an extensive neuropathy panel was unrevealing. Imaging demonstrated ossification of the posterior longitudinal ligament (OPLL) with multilevel central canal stenosis and cord deformity without cord signal change. The clinical picture was attributed primarily to cervical myelopathy, and the patient underwent anterior cervical discectomy and fusion (ACDF) at C3-C4 and C6-C7. Postoperatively, symptoms failed to improve and progressively worsened, with new-onset dense numbness involving the face and oral mucosa. Serial HbA1c measurements revealed a dramatic rise from 5.4% at initial presentation to 5.9% two months later and ultimately to 13.8% approximately seven months after initial presentation, unmasking poorly controlled type 2 diabetes as a likely major contributor to the patient's length-dependent sensorimotor polyneuropathy. This case underscores that diabetic peripheral neuropathy (DPN) can present and progress even when HbA1c is within the non-diabetic range, particularly in patients with metabolic syndrome, and that structur
Abstract
A 63-year-old man with extensive multilevel degenerative cervical and thoracic spine disease, class 1 obesity, essential hypertension, mixed hyperlipidemia, and a history of type 2 diabetes mellitus presented with progressive bilateral upper and lower extremity paresthesias, burning pain in the hands and feet, gait instability, and a history of a fall with transient loss of consciousness. Initial workup revealed a hemoglobin A1c (HbA1c) of 5.4%, and an extensive neuropathy panel was unrevealing. Imaging demonstrated ossification of the posterior longitudinal ligament (OPLL) with multilevel central canal stenosis and cord deformity without cord signal change. The clinical picture was attributed primarily to cervical myelopathy, and the patient underwent anterior cervical discectomy and fusion (ACDF) at C3-C4 and C6-C7. Postoperatively, symptoms failed to improve and progressively worsened, with new-onset dense numbness involving the face and oral mucosa. Serial HbA1c measurements revealed a dramatic rise from 5.4% at initial presentation to 5.9% two months later and ultimately to 13.8% approximately seven months after initial presentation, unmasking poorly controlled type 2 diabetes as a likely major contributor to the patient's length-dependent sensorimotor polyneuropathy. This case underscores that diabetic peripheral neuropathy (DPN) can present and progress even when HbA1c is within the non-diabetic range, particularly in patients with metabolic syndrome, and that structural spinal pathology may coexist with, but not fully explain, progressive neurological symptoms.