Abstract

Background:Treatment-induced neuropathy of diabetes (TIND), also termed insulin neuritis, is a
painful neuropathic complication occurring after rapid improvement in glycemic control. It typically manifests as diffuse, symmetric neuropathic pain with burning sensations, paresthesias, and allodynia. The presence of a sharply demarcated sensory level mimicking spinal pathology is exceedingly rare, leading to potential misdiagnosis and unnecessary invasive interventions.
Case Description:A 22-year-old male with longstanding poorly controlled type 1 diabetes presented to our tertiary-care center. At initial presentation, his HbA1c was markedly elevated at 12.2%.
 Following a change to insulin degludec therapy and intensified outpatient monitoring, his HbA1c significantly improved to 9.4% within three months, an absolute reduction of 2.8%.
Six weeks after achieving improved glycemic control, the patient developed severe, debilitating bilateral lower limb pain associated with marked brush-evoked allodynia. Additionally, he reported a distinct sensory boundary below the T2 dermatome, with sensations below this level notably heightened, estimated at 150% intensity relative to facial sensation. Examination revealed mildly reduced vibration sense and proprioception at the toes, diminished patellar and ankle reflexes, but full motor strength.
Extensive imaging including magnetic resonance imaging (MRI) of the brain and entire spinal cord showed no compressive, inflammatory, or demyelinating lesions.
Cerebrospinal fluid (CSF) analysis revealed a mild elevation in protein (116 mg/dL), a modest lymphocytic pleocytosis (16 leukocytes/mm³), and absence of oligoclonal bands. Comprehensive hematologic, metabolic, autoimmune, and infectious evaluations yielded unremarkable results.
Management and Outcome:Given the clinical picture, a diagnosis of TIND manifesting as pseudo-sensory-level neuropathy was made. The patient was initiated on gabapentin (300 mg three times daily) and duloxetine (30 mg three times daily, subsequently adjusted to 60 mg twice daily). These medications rapidly alleviated pain, facilitating hospital discharge by day four.
Outpatient nerve conduction studies (NCS) and electromyography (EMG), performed one week post-discharge, were entirely normal, supporting the clinical impression of predominantly small-fiber neuropathic involvement. At three-month follow-up, the patient reported substantial symptomatic improvement, with pain scores decreasing dramatically from 9/10 to 2/10 and complete resolution of allodynia. His HbA1c was further stabilized at 8.8%, employing a slower, individualized glycemic target of ≤1% reduction per quarter.
Discussion:TIND results from ischemic injury to the vasa nervorum following rapid glycemic normalization, precipitating acute axonal degeneration. While typically presenting as diffuse neuropathy, unusual cases such as ours illustrate that segmental hyperexcitability of dorsal root ganglia or small nerve fibers can mimic thoracic myelopathy by creating a clearly defined sensory boundary. Severe allodynia highlights possible central sensitization involving altered sodium and calcium channel dynamics. Prompt clinical recognition of this atypical presentation prevented unnecessary invasive spinal procedures and guided effective pharmacologic therapy.
Clinical Implications:HbA1c reductions exceeding 2% within months significantly increase TIND risk.
Normal spinal imaging with acute neuropathic symptoms following rapid glycemic improvement strongly suggests TIND after exclusion of other etiologies.
Effective first-line treatment includes gabapentin and serotonin-norepinephrine reuptake inhibitors (SNRIs).
Gradual and individualized glycemic targets can mitigate TIND risk.
Patient education regarding potential neuropathic symptoms enables timely clinical intervention.
Conclusion:This unique case expands the recognized clinical spectrum of TIND by demonstrating that profound allodynia and thoracic pseudo-sensory levels can occur without spinal cord involvement. Increased clinical awareness facilitates early recognition, prevents unnecessary diagnostic procedures, and informs safer, patient-centered glycemic management strategies.