Neurological Complications in a Patient With Thalassemia Intermedia and Chronic Myeloid Leukemia: A Case of Extramedullary Hematopoiesis-Induced Spinal Cord Compression

Abstract

Extramedullary hematopoiesis (EMH) is a rare but significant compensatory response to chronic ineffective erythropoiesis, frequently seen in hematologic disorders such as thalassemia intermedia (TI) and chronic myeloid leukemia (CML). While EMH is typically asymptomatic, it can manifest as paraspinal masses that cause spinal cord compression, resulting in severe neurological deficits. This case highlights the complexities in managing overlapping hematologic conditions and emphasizes the importance of timely diagnosis and intervention. We present a 50-year-old male with a longstanding history of TI and CML, who developed progressive lower extremity weakness, gait instability, and sensory deficits due to spinal cord compression from EMH. This case underscores the critical need for clinical awareness and early intervention in patients with hematologic disorders who present with neurological symptoms. EMH-induced spinal cord compression, though rare, can lead to significant morbidity if left untreated. Multidisciplinary management involving neurology, hematology, radiology, and rehabilitation is essential to optimize outcomes and prevent permanent neurological deficits in affected patients.

Keywords: chronic myeloid leukemia; extramedullary hematopoiesis; myelopathy; spinal cord compression; thalassemia intermedia.

Figure 1. Magnetic resonance imaging (MRI) of the spine showing (A) thoracic spine and (B) lumbar spine.

(A) Thoracic spine MRI (upper panels) reveals soft tissue signal abnormalities in the paravertebral region at thoracic levels, resulting in significant spinal cord compression from T4 to T8, as observed in T1-weighted, T2-weighted, and T2-weighted fat-suppressed short tau inversion recovery (STIR) sequences (red arrows). (B) Lumbar spine MRI (lower panels) displays lesions occupying the spinal canal from the S1 to S4 vertebral levels, with extension into the presacral area, resulting in notable compression of the dural sac (red arrows).

Figure 2. Axial (A) and sagittal (B) magnetic resonance imaging (MRI) scans of the thoracic spine.

T2-weighted MRI sequences reveal soft tissue signal abnormalities within the paravertebral region at thoracic levels, resulting in severe narrowing of the spinal canal to approximately 5 mm and associated with evidence of myelopathic changes.

Figure 3. Cranial magnetic resonance imaging (MRI).

Cranial MRI demonstrates marked thickening of the diploic space within the calvarial bones, most prominently in the frontal region. This feature, highlighted by a red asterisk (*), is most clearly visualized on the axial section (A), and is also appreciable on the sagittal (B) and coronal (C) planes.

Figure 4. Post-radiotherapy thoracic spine magnetic resonance imaging (MRI).

(A-C) Post-radiotherapy imaging demonstrated a notable reduction in the extent of compressive lesions compared to the prior neuroimaging and radiotherapy-induced thoracic spine distructions from T3 to T9.