Spondylodiscitis and Multilevel Radiculopathy

Pathophysiological Mechanisms

Spondylodiscitis causes multilevel radiculopathy through direct extension of infection to the epidural space, paravertebral soft tissues, and posterior spinal elements, resulting in nerve root compression at multiple levels, a pattern that occurs in approximately 20% of cases with contiguous multilevel involvement and 10% with non-contiguous multilevel disease 1, 2
Infection spreads from the initial vertebral endplate focus into the adjacent disc space and then to the opposing vertebral body, creating a classic pattern of two adjacent vertebral bodies with intervening disc involvement 1

Infection extends posteriorly into the epidural space, creating epidural abscesses that directly compress nerve roots and the spinal cord, with the epidural abscess spanning multiple vertebral levels, causing compression of nerve roots at each affected level 1
Infection spreads laterally into paravertebral soft tissues and can form paravertebral abscesses, compressing exiting nerve roots in the neural foramina at multiple levels 1

Approximately 20% of spondylodiscitis cases involve contiguous multilevel infection, where the infectious process spreads sequentially from one disc-vertebral unit to adjacent levels, creating a continuous column of inflammation and abscess formation affecting multiple nerve root levels 1, 2
About 10% of cases present with non-contiguous multilevel infections, where separate foci of infection occur at distant spinal levels, resulting from multiple septic emboli during bacteremia, creating independent sites of nerve root compression 1, 2, 3, 4

MRI with contrast is essential to assess the full extent of epidural and soft tissue involvement causing nerve root compression, and sagittal imaging views are critical to identify all levels of involvement and epidural extension 1, 4
[18F]FDG PET/CT is particularly valuable for detecting multilevel disease and is recommended for evaluation of multilevel spondylodiscitis 1

Surgical intervention is indicated when neurological deficits with spinal cord compression are present, as this represents direct mechanical compression from epidural abscess or soft tissue extension 2

The valveless nature of the Batson plexus allows bidirectional blood flow, enabling bacteria from distant infection sites to reach vertebral structures directly without pulmonary or hepatic filtering, particularly in immunocompromised patients and those with recent spinal surgery 5
The low-pressure environment in the Batson plexus facilitates bacterial seeding and colonization of the highly vascularized vertebral endplates, which are the initial site of infection in adult spondylodiscitis 5
Adults develop infection at the vertebral endplate first via arterial end-arteries that communicate with the Batson plexus, and the infection then spreads to the adjacent disc 5

Immunocompromised patients, such as those with HIV, diabetes mellitus, or hepatic or renal failure, are at increased susceptibility to bacteremia and subsequent vertebral seeding via the Batson plexus 5
Post-spinal surgery patients are at risk for multilevel disease due to surgical manipulation introducing bacteria directly into the vertebral structures or creating conditions for hematogenous seeding via the Batson plexus 5
IV drug users are at risk for multilevel or multifocal spine infection due to repeated bacteremia episodes providing multiple opportunities for bacterial seeding through the Batson plexus 5