Acute Paraparesis with Hepatorenal Dysfunction Revealing Aortic Dissection: A Diagnostic Challenge in Neurologic Practice

Dear Editor, Acute aortic dissection (AAD) represents a critical vascular emergency caused by a separation of the aortic wall layers, which allows blood to enter a false lumen due to degeneration of the media. Without prompt diagnosis and intervention, the condition carries a rapidly increasing risk of death, making early identification essential for patient survival. Depending on the dissection’s extent and anatomic involvement, neurologic manifestations can arise, including ischemic stroke, spinal cord infarction, hypoxia-induced encephalopathy, or peripheral neuropathies.1 When classic signs such as chest or back pain are absent, AAD can mimic primary neurologic diseases, delaying appropriate diagnosis. This diagnostic challenge can be further complicated by multiorgan dysfunction, which may obscure the vascular cause. We report a previously healthy middle-aged male who developed sudden painless paraparesis and hepatorenal dysfunction following a syncopal episode, who was ultimately diagnosed with having a DeBakey type I aortic dissection extending to the iliac bifurcation. This case underscores the importance of recognizing atypical neurologic or systemic signs suggestive of AAD, particularly in the absence of pain. A 47-year-old male with no history of chronic illness presented with sudden paraparesis and acute kidney injury after experiencing syncope. His only previous symptom was a syncopal event; he reported no prior medical issues. Initial evaluations at an externalhospital showed elevated serum troponin levels, raising concern for acute coronary syndrome, but coronary angiography was unremarkable. Upon arrival at our emergency department, he was normotensive. A neurologic examination revealed symmetrical paraparesis with lower limb muscle strength graded as 1/5, absent deep-tendon reflexes, reduced sensation in the L1 dermatome, and loss of proprioception in both legs, but no bowel or bladder dysfunction. Laboratory results demonstrated significant liver enzyme elevations (aspartate aminotransferase: 5170 U/L and alanine transaminase: 3465 U/L) and renal dysfunction (urea: 84 mg/dL and creatinine: 3.68 mg/dL). Given the presence of paraparesis, thoracolumbar magnetic resonance imaging (MRI) was obtained approximately 24 h after the onset of clinical symptoms, revealing a T2-hyperintense lesion extending from T12 to the conus medullaris, findings consistent with spinal cord ischemia Figure 1A. In addition, abnormal flow voids in the abdominal aorta raised a suspicion of vascular pathology Figure 1B. Computed tomography angiography (CTA) of the thoracoabdominal aorta confirmed a DeBakey type I dissection involving the aortic valve down to the iliac arteries Figure 1C. The left renal artery originated from the false lumen, while the celiac trunk branched from the true lumen. The patient underwent emergency surgical repair approximately 30 h after the onset of symptoms. Despite timely intervention, neurological recovery was limited, and the degree of paraparesis remained unchanged at the 3-month postoperative evaluation. He continues to receive physiotherapy.Figure 1: Thoracolumbar spinal magnetic resonance imaging computed tomography (CT) angiography findings. (A) Axial and sagittal T2-weighted images demonstrate a hyperintense signal extending from the T12 level to the conus medullars (red arrows), consistent with spinal cord ischemia, (B) Axial T2-weighted turbo spin-echo images shows intimal flap (blue arrows) in descending and torasic aorta, (C) Axial and sagittal multiplanar reconstruction (MPR) of the CT aortogram study showing type A aortic dissection extending to the aortic root (green arrows)This case exemplifies a rare presentation of AAD characterized by painless paraparesis, necessitating emergency surgical intervention. Although AAD typically presents with sudden, intense pain, there are the reports of patients manifesting neurologic deficits such as paraparesis or paraplegia without pain.2 Systemic signs such as syncope, hemodynamic instability, or absent pulses may offer diagnostic clues. In our patient, syncope was the only preceding symptom before the onset of neurologic and systemic findings. Painless dissections can delay a suspicion for AAD, often leading to misdiagnoses including compressive or inflammatory myelopathies. However, spinal cord ischemia, although rare, occurs in up to 8% of AAD cases,1 generally resulting from decreased perfusion of the anterior spinal artery or occlusion of radicular arteries such as the artery of Adamkiewicz. Our patient’s spinal cord MRI findings from T12 to the conus medullaris were consistent with ischemic injury corresponding to the observed paraparesis. Spinal imaging is crucial in patients presenting with paraparesis and a well-defined spinal level of hypoesthesia, as in our case. When paraparesis develops acutely, especially in individuals with risk factors such as anticoagulant therapy, trauma, or vascular pathology, imaging must be performed urgently to ensure prompt the diagnosis and management. Recognizing the anatomic extent of AAD is critical, and classification systems such as DeBakey and Stanford guide management decisions. CTA remains the gold standard imaging modality, providing precise classification and evaluation for complications. Although spinal MRI is typically used to evaluate myelopathies, it can incidentally reveal aortic abnormalities, as it did in our patient, prompting confirmatory CTA. The dissection was categorized as DeBakey type I/Stanford type A, indicating involvement of both the ascending and descending aorta and requiring emergency surgery. Notably, our patient had no hypertension, which is the most frequent risk factor for AAD; nor did he present with other known predispositions such as connective tissue disease or trauma, underscoring the need for clinical vigilance even in individuals at low-risk. In addition, laboratory abnormalities indicating hepatic and renal dysfunction suggested multiorgan ischemia, which imaging confirmed as arising from compromised perfusion: the left renal artery stemmed from the false lumen, likely causing renal hypoperfusion, and hepatic ischemia may have resulted from reduced flow through the celiac trunk despite its origin in the true lumen. Although rare, similar patterns of multisystem involvement have been described.3,4 Therefore, in patients presenting with paraparesis combined with systemic signs of organ dysfunction, prompt vascular imaging should be considered to confirm or exclude AAD and allow timely intervention. Paraparesis due to spinal cord infarction secondary to aortic dissection generally carries a poor prognosis. Outcome depends on the extent of ischemia, timing of diagnosis, and reperfusion. When motor deficits are complete at onset, recovery is rare because of irreversible ischemic necrosis of the anterior horn cells and corticospinal tracts. Even with early aortic repair, persistent paraparesis or paraplegia is common.5 Partial recovery may occur if perfusion is restored early and the lesion is incomplete, typically within the first 3–6 months.6 However, only a minority regain independent ambulation, most have lasting weakness and sphincter dysfunction.7 In our case, no neurologic improvement was observed at 3 months, suggesting irreversible and extensive ischemic injury, consistent with prior reports. In summary, our case emphasizes that AAD should be included in the differential diagnosis of painless paraparesis, particularly when accompanied by syncope or signs of multiorgan failure. The absence of typical pain or risk factors should not lower clinical suspicion. Early vascular imaging and recognition of subtle neurologic and systemic indicators are essential for rapid diagnosis and life-saving treatment. Author contributions ŞA, EA, SA designed and conceptualized the study, and ŞA, BK, CC drafted the manuscript. ŞA revised the manuscript. All authors contributed to the article and approved the submitted version. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.