Title : Insulin neuritis presenting as thoracic pseudo-sensory level neuropathy: A rare manifestation of Treatment-Induced Neuropathy of Diabetes (TIND)
Abstract:
Background: Treatment-induced neuropathy of diabetes (TIND), or insulin neuritis, is a painful neuropathy following rapid glycemic improvement. It commonly presents as diffuse burning pain, paresthesia, and allodynia. A sharply demarcated sensory level mimicking spinal pathology is exceedingly rare and can lead to misdiagnosis and unnecessary interventions.
Case Description: A 22-year-old man with longstanding poorly controlled type 1 diabetes initially presented with HbA1c of 12.2%. After switching to insulin degludec and intensive monitoring, his HbA1c fell to 9.4% within three months (reduction of 2.8%).
Six weeks after improved glycemic control, he experienced severe bilateral lower limb pain with marked brush-evoked allodynia and a distinct sensory boundary below the T2 dermatome. Sensations below this level were notably intensified. Examination showed mildly reduced vibration sense and proprioception at toes, diminished patellar and ankle reflexes, but normal motor strength.
Extensive imaging, including brain and spinal MRI, showed no lesions. Cerebrospinal fluid (CSF) had mildly elevated protein (116 mg/dL), slight lymphocytic pleocytosis (16 leukocytes/mm³), and no oligoclonal bands. Hematologic, metabolic, autoimmune, and infectious workups were normal.
Management and Outcome: The clinical diagnosis of TIND presenting as pseudo-sensory-level neuropathy was made. Treatment with gabapentin (300 mg three times daily) and duloxetine (initially 30 mg three times daily, adjusted to 60 mg twice daily) effectively managed pain, facilitating discharge by day four.
Outpatient nerve conduction studies (NCS) and electromyography (EMG) performed one week later were normal, consistent with small-fiber neuropathy. At three-month follow-up, pain scores improved dramatically from 9/10 to 2/10, with complete resolution of allodynia. HbA1c was stabilized at 8.8%, using slower individualized glycemic targets.
Discussion: TIND arises from ischemic injury to vasa nervorum due to rapid glycemic normalization, causing acute axonal damage. While typically diffuse, rare cases can mimic thoracic myelopathy through segmental hyperexcitability of dorsal root ganglia or small nerve fibers, manifesting a sharply defined sensory boundary. Severe allodynia suggests central sensitization involving altered ion-channel dynamics. Prompt recognition prevented unnecessary invasive procedures.
Clinical Implications: HbA1c reductions exceeding 2% within months significantly elevate TIND risk.
Acute neuropathy with normal spinal imaging strongly suggests TIND.
Gabapentin and serotonin-norepinephrine reuptake inhibitors (SNRIs) are effective first-line treatments.
Gradual glycemic improvement mitigates risk.
Patient education facilitates timely intervention.
Conclusion: This unique case broadens TIND's clinical spectrum, demonstrating pronounced allodynia and pseudo-sensory levels without spinal cord pathology. Increased awareness aids timely diagnosis and appropriate management.
