HIV associated VM is a well described complication of AIDS with a historical prevalence estimated between 7 – 55% (61). Current epidemiology is unknown but it is uncommon in the post cART era. VM is characterised by white matter spinal cord vacuolisation. Pathologically VM closely resembles subacute combined spinal cord degeneration and is associated with vitamin B12-dependent transmethylation and reduced levels of s-adenosyl-methionine (62). VM often presents subacutely with indolent progression with spastic paraparesis with associated bladder and bowel dysfunction, although rapidly progressive courses have been described. Investigations are non-specific with spinal cord atrophy followed by normal or T2 hyperintensity on MRI and a normal or mild lymphocytic pleocytosis and elevated protein on CSF examination. Treatment is limited, with variable response to cART, modest and diminishing response to intravenous immunoglobulin (IVIG) and no benefit demonstrated with B12 or L-methionine administration (61,63). VM is frequently associated with HAD, and in cART responsive cases the dominant pathology is a multinucleated giant cell myelitis similar to the pathology in the brain.
Infectious radioculomyelitis
Radioculomyelitis in PLWH can be caused by multiple infectious aetiologies including Cytomegalovirus (CMV), Herpes zoster virus (HSV), Varicella zoster virus (VZV), spinal cord neurosyphilis and spinal cord Tuberculosis (TB). These have distinct clinical features, pre-disposing degree of immunosuppression, investigation findings and treatment which are detailed in the table 4.
| Aetiology of infectious myelitis | CMV | HSV | VZV | Spinal cord neurosyphilis | Spinal cord TB |
| Clinical features | Distinct sensory level, urinary retention, paraesthesias, asymmetric UMN weakness +/- polyradiculitis | Prodromal vesicular rash, perirectal pain, urinary retention, loss of rectal tone, ascending flaccid paraplegia | Progressive asymmetric motor and sensory impairment ipsilateral to dermatomal rash | Back pain, slowly progressive lower limb weakness, paraesthesias, urinary incontinence, hyperreflexia, sensory level extensor plantars | Subacute flaccid paralysis, lower extremity, bladder and bowel dysfunction |
| CD4 count | < 100 | All stages, Increased severity < 200 | < 300 | All stages, increased risk < 350 | All stages, increased risk < 200 |
| MRI | Increased T2 and gadolinium enhancement on MRI of spinal cord | Increased T2 and gadolinium enhancement on MRI of conus medullaris and adjacent nerve roots | Extensive Increased T2 and gadolinium enhancement on MRI of spinal cord (extensive) | Extensive Increased T2 with discrete and irregular superficial enhancement | Variable based on syndrome: meningeal enhancement, loculated CSF, mass lesions, syringomyelia, Increased T2 spinal cord lesions |
| CSF | Neutrophilic pleocytosis, elevated protein, low glucose, high quantitative CMV DNA PCR | Lymphocytic pleocytosis, elevated protein, positive HSV PCR | Lymphocytic pleocytosis, elevated protein, positive VZV PCR (can be negative), antiVZV IgM/IgG | CSF VDRL, elevated protein, lymphocytic pleocytosis | Highly elevated protein, lymphocytic pleocytosis, low glucose, AFB, Mycobacterial cultures (low sensitivity), TB PCR (low sensitivity) |
| Treatment | IV Ganciclovir and/or IV Foscarnet | IV Aciclovir 14 – 21 days | IV Aciclovir 14 – 21 days | IV Benzylpenicillin 10.8g q24hourly for 15 days | TB therapy with CNS penetrating agents +/- steroid therapy, Delay cART initiation but commence within 2 months |
| Table 4: Clinical features, diagnosis and management of infectious aetiologies of radiculomyelitis in PLWH (54,61) | |||||