Discussion
OND is characterized by the association of optic damage and myelopathy due to acute demyelination of optic nerves and spinal cord caused by a dysimmunitary mechanism (2).
During OND, the immune system produces autoantibodies that target a protein called AQP4. It is a protein of the central nervous system expressed by astrocytes. Thereafter a cascade of reactions leading to the damage of the entire nervous tissue is triggered.
These reactions cause an inflammation leading to the destruction of the myelin sheath covering the neurons but also the neuron itself. This process explains the neurological symptoms of the disease.
Although the association of OND to active pulmonary tuberculosis has been reported and is not a simple coincidence, a definite affiliation between the two conditions has not been demonstrated (3).
This association only can be established after having excluded a pulmonary and neurological localisation of the TB. The pathophysiological mechanism is still uncertain.
The study of the spinal cord injuries of autopsied patients has demonstrated the role of humoral immunity dysregulation, triggered by an infectious disease. Indeed, Mycobacterium tuberculosis surface antigens might initiate the production of reactive antibodies against aquaporin-4 proteins. This process would lead to an acute demyelination induced by BK in our case.
The onset of demyelination clusters far from infectious clusters in tuberculous encephalitis and experimental studies of demyelination after intracisternal injection of antigenic BK or tuberculin extracts are also arguments supporting the dysimmunitary mechanism.
However, since the immunitary response against active TB infection is commonly set towards cell-mediated immune response rather than a humoral response, the involvement of this mechanism is still not proven (4).
Another hypothesis that has been discussed is the anti-bacillary treatment toxicity, but this remains inconclusive considering the possibility of neuro-ophthalmological damage before the initiation of TB treatment.
Moreover, a clinical trial carried in China in patients suffering from OND have concluded to a beneficial impact of anti-TB treatment in patients suffering from steroid-refractory OND, even if the tuberculosis was not patent (4).
The prevailing of pulmonary localization is due to its bacillary population richness compared to other sites. Nevertheless, other localizations of TB have been reported such as abdominal localization (5).
Also, the first case of NMO associated to TB was a tuberculous nephritis reported in a 41-year-old woman in Nigeria (6).
As neurologic deficits are mainly due to an inflammatory process, these injuries respond to medical therapy alone without any surgical intervention if diagnosed promptly (7).
The treatment is based on corticosteroids and antituberculous therapy. A partial recovery of motor symptoms and sphincter control with permanent blindness has been reported in the majority of the cases (8).
The long-term clinical efficiency of ATT in patients with steroid-refractory NMO has been proved. This treatment can reduce disease’s activity and progression resulting in a significant recovery of neurological deficits (9).
We insist on the fact that NMO like disorders are an important diagnosis to consider in patients treated for active TB who present with acute neurological disorders such as transverse myelitis and/or optic neuritis. Thus, Serum anti-Aqp-4 antibodies should be part of the diagnostic tests in these patients (3).
An immune dysfunction caused by Mycobacterium tuberculosis seems to be the most likely hypothesis explaining the association of pulmonary TB to OND in terms of pathophysiology.
Whenever demyelinating spinal cord injury in combination with optic pathways damage is diagnosed in a case of tuberculosis we must first rule out brain injuries by direct mechanism before concluding to Devic’s syndrome.