A 51-year-old female presented with a 3-year history of thoracic back pain. Her medical history included diabetes, rheumatoid arthritis, and Sjögren's syndrome. The pain, when severe, was associated with nausea and vomiting. The patient reported longstanding reduced sensation bilaterally, in the L5 and S1 distribution, secondary to chronic lumbar spondylosis. There was no change in her lower limb neurological symptoms, specifically, no radicular pain or sphincter disturbance. There was no history of spinal trauma. Upon clinical examination, there was mild mid-thoracic tenderness. Lower limb neurological examination was complicated by leg stiffness related to the Sjögren's syndrome. There was global mild weakness Medical Research Council (MRC) grade 4/5 in bilateral lower limbs, and reflexes were normal. There was reduced sensation in the L5 and S1 distribution, which was a longstanding finding. MRI of the thoracic spine demonstrated features consistent with ISCH. T2-weighted images showed anterior deviation and flattening of the spinal cord at the T7 vertebral body level, with a small ventral dural defect and mild cord herniation []. The patient was treated conservatively, and at 4-year follow-up, her neurological condition remained stable.
A 48-year-old female presented with two year history of back pain and progressive difficultly walking. She gradually developed increasing numbness in both lower limbs over one year. She also developed increasing urinary retention. There was no history of trauma/fever or any other systemic disease. She was evaluated by an orthopedic spine surgeon and was referred to a physician following a negative lumbar magnetic resonance imaging (MRI). Neurological examination revealed presence of weakness in bilateral lower extremities (4-/5, Medical Research Council [MRC] grade) and asymmetrical sensory loss from T8 below consistent with a diagnosis of thoracic myelopathy (Nurick grade 4). Persistent symptoms with worsening gait imbalance led us to perform of thoracic spine MRI which surprisingly revealed presence of a focal anterior kink of the thoracic cord at the T7-T8 level (). The spinal cord at T7/8 level was narrow and deformed without any definite T2 signal abnormality with prominence of the dorsal subarachnoid space. The MRI imaging was suspicious of a diagnosis of anterior transdural spinal cord herniation (). Surgical management was planned and a unilateral right paramedian incision was used to perform a transpedicular exposure due to slight eccentric location of the spinal cord herniation to the right (). Intraoperative neuromonitoring was performed recording somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs). T7/T8 pediculotomy was performed with partial costotransversectomy to provide the optimal anterolateral trajectory. A paramedian right dura incision was made, providing exquisite visualization of the anterior dural defect with the herniated spinal cord (). Using a Woodson dissector, the spinal cord was reduced back into the thoracic dura. The SSEP's were normal throughout the procedure. There was transient reduction in MEP amplitude during mobilization of the spinal cord to reduce the herniation. The MEP amplitude returned to baseline status an hour later. A Duragen (Integra Life Sciences Corp., Plainsboro, NJ, USA) patch was used as graft to seal the defect which was reinforced with Tisseel fibrin glue. (Baxter Healthcare Corp., Deerfield, IL, USA) No fusion or instrumentation was performed. Patient experienced improvement in sensory symptoms right after the surgery and had improvement in her pain, motor strength (4+/5, MRC grade) and gait at three months follow-up with improvement in her Nurick myelopathy grade to 2. Postoperative MRI revealed reduction of the spinal cord with no evidence of herniation ().