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.