Acute primary HIV TM is mediated by immune dysregulation from HIV virion CNS penetration and occurs with primary infection and seroconversion ​(61)​. Classical features include back pain, urinary retention, lower extremity paraesthesia, spastic paraparesis, a band-like sensory level, hyperreflexia, and abnormal plantar responses in addition to constitutional signs of primary HIV or seroconversion (fevers, malaise, lymphadenopathy). CD4 counts are classically preserved (> 500 cell/mm3). Exclusion of other aetiologies of TM is essential, including other viral aetiolgies and immune mediated disorders, with MRI and CSF examination. HIV associated TM is associated with a normal MRI or longitudinal T2 hyperintensity, and CSF shows a lymphocytic pleocytosis with normal or elevated protein and elevated CSF viral load. This disorder is often responsive to effective cART and reduction of CSF viral load with consideration of adjunctive pulsed steroids ​(61)​.  

Notably, a separate phenomenon of immune-mediated TM associated with HIV infection manifests as a central demyelinating disorder mimetic of multiple sclerosis (MS) or neuromyelitis optica (NMO). This disorder has been found to be present in early, controlled and uncontrolled disease. It remains unclear if this is a separate entity to MS/NMO, with similar clinical course including prodromal optic neuritis followed by paraesthesias, paraparesis and bladder dysfunction. Investigations demonstrate longitudinal T2 enhancement on MR imaging with or without T1 gadolinium enhancement, and CSF reveals a normal cell count or mild lymphocytic pleocytosis, elevated protein, oligoclonal bands and negative JC virus PCR. There is no consensus on treatment with variable response to cART, modest outcomes with steroids and steroid sparing immunomodulators and a paucity of data on MS immunotherapy.