The problem of spinal cord lesions resulting from HIV infection is growing increasingly prominent. Its etiology and mechanism are intricate, and diagnosis and treatment are extremely challenging. HIV-related spinal cord lesions not only inflict great pain on patients but also pose a formidable challenge to medical workers. The etiology and mechanism of it involve multiple aspects [13]. On one hand, the HIV virus itself has neurotropism and can directly damage the nervous system, including the spinal cord [14,15,16,17]. On the other hand, the immune deficiency caused by HIV infection makes patients susceptible to various opportunistic infections and tumors [2, 3, 8], and these factors may also indirectly lead to spinal cord lesions (Table 4 [13]).

HIV indirectly mediates spinal cord injury through immune regulation, degeneration, or related infections and tumors. The pathological manifestations are diverse, ranging from cytotoxic necrosis to demyelination and vasculitis. Clinically, HIV vacuolar myelopathy and opportunistic infections dominate in uncontrolled diseases [13].

HIV infection-related vacuolar myelopathy (HIV-VM) is the most common and typical spinal cord lesion. In fact, this belongs to a pathological diagnosis. It mainly presents as slowly progressive spastic paraplegia, bladder and rectal dysfunction, and sensory disturbances [18, 19]. The pathophysiological mechanism of HIV myelopathy is currently unclear. The neurotoxic factors secreted by HIV-infected monocytes and the impaired utilization of B12 as a source of methionine in transmethylation metabolism are currently popular pathological hypotheses [20]. These factors can lead to multifocal vacuolization of the spinal cord tracts and histologically related pallor of the myelin sheath, so it is called vacuolar myelopathy [21, 22]. Before the introduction of antiretroviral therapy (ART), HIV-related myelopathy (HIV-VM) was extremely common and was mostly diagnosed only after the patient’s death. Postmortem autopsy studies on AIDS patients reported that the proportion of pathological evidence of HIV-VM ranged from 22–55% [21, 23]. However, due to the difficulty and often delay in diagnosis, the actual prevalence is likely to be underestimated.

In the time course of HIV infection, HIV-VM usually appears at a relatively late stage, but in a few cases, it may also occur in the early stage of the disease [11, 24, 25]. There are reports that HIV vacuolar myelopathy may serve as the initial manifestation of newly diagnosed HIV [23, 26, 27]. In the literature on HIV infection-related myelitis, there are also two reports of transverse myelitis as the first manifestation of acute HIV infection [10, 17].

In terms of imaging, HIV myelopathy often shows high T2 signal on spinal cord MRI, commonly seen in the thoracic spinal cord. The lateral and posterior cords of the common spinal cord are involved, and the cervical spinal cord may also appear [23, 28]. Spinal cord atrophy is another common feature of long-term myelopathy [22, 28]. There are also reports that magnetic resonance imaging of patients with HIV myelopathy may show a normal-appearing spinal cord and has no obvious correlation with the severity of the patient’s clinical symptoms [28]. Ernst F et al. [29]reported a case of a patient who had been previously diagnosed with HIV and presented with progressive weakness and difficulty walking. However, there was no abnormal signal on thoracic spinal cord magnetic resonance. After excluding other opportunistic infections, due to the significantly increased HIV load in the cerebrospinal fluid (CSF), HIV-related vacuolar myelopathy was diagnosed. HIV-VM is an exclusionary diagnosis. Negative or non-specific MRI results cannot rule out HIV-VM. In this case, the possible structural and functional damage of spinal cord cells must not be ignored.

The main treatment methods for HIV-related myelopathy are still initiating highly active antiretroviral therapy (HAART) and symptomatic and supportive treatment. Other authors also claim that after receiving highly active antiretroviral therapy, the symptoms and signs of HIV-VM have completely recovered [30,31,32,33]. It has been reported that the symptoms of HIV-related acute transverse myelitis completely resolved and the imaging results turned negative after initiating HAART treatment [10]. However, the impact of HAART on specific neurological complications of HIVM is still controversial and may not be able to stop the progression of the disease [20, 26, 31, 34, 35]. Some studies have shown that patients with HIV-VM may benefit from immunoglobulin treatment, but this still requires further research [36]. In a phase II, double-blind, placebo-controlled study, L-methionine was used to treat AIDS-related myelopathy. The results showed that L-methionine is safe and well tolerated, but there is no significant benefit in any clinical indicators [20].

Given the common latency between initial HIV infection and symptom appearance or diagnosis, along with the fact that HIV can impact patients’ spinal cord function, when coming across patients showing distinct spinal cord symptoms yet having a normal spinal cord MRI, one should stay alert and conduct HIV screening.