Hepatic myelopathy (HM) is a rare neurological complication of decompensated chronic liver disease that profoundly impairs quality of life. Liver transplantation is the only curative treatment. However, this case report describes a patient with cirrhosis and post-TIPS HM in whom progressive severe spastic paraparesis markedly improved following embolisation of a previously unrecognised paraspinal vein shunt (PVS), suggesting a novel interventional approach for HM.
Introduction
Hepatic myelopathy, also known as portosystemic shunt myelopathy, is a rare neurological complication of chronic liver disease, characterised by progressive spastic paraparesis of the lower limbs without significant sensory impairment. Its pathogenesis remains poorly understood. Apart from early liver transplantation, HM is considered incurable. Accumulating evidence links HM to spontaneous or iatrogenic portosystemic shunting, but the specific shunt responsible remains unclear. This case report highlights the potential role of a paraspinal vein shunt in HM pathogenesis.
Case Presentation
A 42-year-old man with alcoholic and hepatitis B-related cirrhosis presented with progressive lower limb weakness and recurrent hepatic encephalopathy (HE). Four years earlier, he had undergone TIPS placement for recurrent variceal bleeding (PPG reduced from 25 to 9 mmHg). Four years post-TIPS, he developed progressive spastic paraplegia, unable to ambulate independently, with preserved sensory and sphincter function. He had sustained alcohol abstinence for four years.
Laboratory findings: pancytopenia, hypoalbuminaemia, hyperbilirubinaemia, INR 1.4, hyperammonaemia (122 mcg/dL). Vitamin B12, ceruloplasmin, and 24-hour urinary copper were normal, excluding Wilson disease and B12 deficiency. Cranial MRI showed metabolic encephalopathy changes; spinal MRI showed only degenerative changes without cord compression or intrinsic abnormalities. Abdominal imaging confirmed patent TIPS and multiple collaterals, notably a 1.18-cm gastro-renal shunt (GRS).
Lactulose and rifaximin normalised ammonia but did not improve gait. A diagnosis of HM was established. Attempted GRS embolisation for recurrent HE incidentally identified a PVS connecting the left renal vein to the paraspinal vein and ascending lumbar vein. GRS embolisation alone (residual PPG 10 mmHg) produced no gait improvement. The PVS was then embolised (PPG remained 10 mmHg). Post-embolisation angiography showed significant reduction in venous varicosities.
Outcome: At 1 month, lower limb strength improved. At 2, 3, 6, and 12 months, sustained recovery was observed. The patient now walks independently 3–4 miles daily. MRC grades improved from 0–1 (flaccid paralysis) to 4–5; MAS spasticity from 3–4 to 1+; FAC from 0 (non-ambulatory) to 5 (independent ambulation on all surfaces).
Discussion
HM is associated with portosystemic shunting, allowing toxins to bypass hepatic metabolism. Liver transplantation is the only curative option by restoring hepatic function. Interventional radiology offers alternatives: previous reports showed HM improvement after inferior mesenteric vein shunt embolisation or paraumbilical vein embolisation, presumably by reducing toxin delivery and portal hypertension.
In this case, GRS embolisation alone failed to improve gait, whereas PVS embolisation led to substantial recovery. This suggests the GRS may not be the sole feeder to the PVS, and that venous hypertension—not toxicity—may be the predominant pathogenic mechanism. PVS embolisation likely relieved mechanical compression of the spinal cord by the varicose paraspinal vein, providing empirical support for this hypothesis. The PVS may represent a critical final common pathway in HM pathogenesis.
Limitations: This is a single-case report, limiting generalisability. The outcome may reflect patient-specific factors. Ongoing prospective studies are needed to validate these findings and assess long-term durability.
Conclusions
Embolisation of the PVS may interrupt the pathway through which venous compression mediates spinal cord injury. These findings offer novel insights into HM pathogenesis and suggest a promising interventional alternative for patients who are not candidates for liver transplantation.
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The study was recently published in the Journal of Clinical and Translational Hepatology .
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Journal of Clinical and Translational Hepatology
Occlusion of Paraspinal Vein Shunt Alleviated Post-TIPS Hepatic Myelopathy in a Patient with Cirrhosis