Discussion
Brucella species are intracellular pathogens causing systemic infection
in humans and livestock. Brucellosis can involve the central nervous
system through direct damage or indirect induction of immune
neuroinflammation (7). Neurobrucellosis usually presents with classic
meningoencephalitis syndrome. However, we should consider the diagnosis
in any patient presenting with chronic headache or neuropsychiatric
symptoms, even without signs of meningeal irritation or fever (8).
Neurobrucellosis is also suspected in patients with chronic neurological
symptoms accompanied by CSF lymphocytosis or compatible neuroimaging
findings. Nevertheless, it is confirmed by positive serum brucella
agglutination test, positive serological tests (increased brucella
antibody in the CSF), positive CSF Wright test, and isolation of
Brucella species or detection of brucella DNA in the CSF with polymerase
chain reaction (PCR) test (9). Our patient had been previously diagnosed
with idiopathic PTC. Nonetheless, her aggravating symptoms and the
addition of systemic manifestations like fever and myalgia suspected us
of the diagnosis of brucellosis. In addition, the CSF lymphocytosis made
our suspicion to neurobrucellosis stronger.
PTC has been a rare presentation of brucellosis. PTC is characterized by
elevated ICP with normal CSF cell count, biochemistries, and normal
brain imaging findings. It has been more commonly reported in females of
childbearing age and obese individuals(10, 11). PTC may be primary or
secondary to traumatic brain injuries, collagen vascular disorders like
systemic lupus erythematosus (SLE), medications like tetracyclines,
isotretinoin, phenytoin, and other medical conditions (12-15). Our
patient was initially diagnosed as being involved with primary or
idiopathic PTC. However, brucellosis was later identified as the
causative condition for her problem. Previously, rarely reported
infections as the underlying causes of PTC included measles, varicella,
Lyme disease, human immunodeficiency virus (HIV), and tuberculosis
(16-21). However, brucellosis has been more commonly reported recently
as the trigger for PTC, compared with other mentioned infections (6,
22-26). As aforementioned, neuroimaging usually offers normal findings
in PTC.
Nonetheless, flattening of the globe, empty sella, enlarged prelaminar
optic nerve or optic nerve sheath (ONS), enhanced optic nerve head,
increased tortuosity of the optic nerve, distension of the perioptic
subarachnoid space, narrowing of Meckel’s cave and sinovenous stenosis
may be identified as indicators of PTC (27-29). Treatment of PTC is
based on controlling the underlying condition, medical management,
repeated lumbar punctures, and surgical interventions(11). However, PTC
in the settings of brucellosis can readily be controlled by antibiotic
therapy with favorable results if timely diagnosed and not led to
sequels.
On the other hand, delayed diagnosis and management of PTC may result in
poor visual outcomes (30). The best therapeutic regimen has not been
determined for neurobrucellosis. Nevertheless, at least a dual- or
triple therapy with a combination of streptomycin, ceftriaxone,
doxycycline, rifampicin, and trimethoprim-sulfamethoxazole for at least
6 months is recommended. Ceftriaxone-based therapeutic regimens have
yielded the highest cure rates for neurobrucellosis(31). Our patient was
initially responsive to CSF volume-decreasing pharmaceuticals but was
later found to require surgical management. Nevertheless, she was
promptly started on combination antimicrobial therapy after brucellosis
was recognized as the underlying cause of her condition. Fortunately,
she responded favorably to medical treatment and was deprived of the
need to undergo surgical shunt implantation.