Journal of Infection (2010) 60, 458e466

www.elsevierhealth.com/journals/jinf

Paradoxical vision loss associated with

optochiasmatic tuberculoma in tuberculous
meningitis: A report of 8 patients
Manish Kumar Sinha a, Ravindra Kumar Garg a,*, H.K. Anuradha a,
Atul Agarwal a, Anit Parihar b, Palavi Aga Mandhani b
a
b

Department of Neurology Chhatrapati Shahuji Maharaj Medical University, Uttar Pradesh, Lucknow, India
Department of Radiodiagnosis Chhatrapati Shahuji Maharaj Medical University, Uttar Pradesh, Lucknow, India

Accepted 19 March 2010

Available online 25 March 2010

KEYWORDS
Tuberculosis;
Tuberculoma;
Tuberculous meningitis;
Vision loss

Summary Background: Paradoxical appearance of new or expansion of existing optochiasmatic tuberculoma, leading to severe vision loss, is a devastating complication in patient with
tuberculous meningitis.
Methods: We report a series of 8 cases of tuberculous meningitis that developed paradoxical vision
loss associated with optochiasmatic tuberculoma. Clinical assessment and magnetic resonance
imaging (MRI) done at presentation, at the time of deterioration, and at 9 months were analyzed.
Results: All patients had good vision acuity and normal visual field at baseline. None of them had
optochiasmatic tuberculoma on magnetic resonance imaging at baseline, though 3 patients had
optochiasmatic arachnoiditis. The mean interval of onset of paradoxical optochiasmatic tuberculoma was 41 days after starting antituberculosis therapy. Paradoxical optochiasmatic tuberculoma
was associated with vision deterioration in all patients, 6 of whom developed severe vision loss
(vision acuity 6/60). Repeat neuroimaging showed new optochiasmatic tuberculoma in all patients. All patients were treated with extended course of dexamethasone for 6 weeks along with
antituberculosis therapy. Two patients died at 62 and 211 days respectively. Repeat neuroimaging
in rest of the patients showed resolution of optochiasmatic tuberculoma. At 9 months follow-up,
vision improved completely in 3 patients and partially in 3 patients.
Conclusion: Prompt recognition of paradoxical optochiasmatic tuberculoma with the help of vision assessment and neuroimaging is vital for patients life and vision. Paradoxical reactions should
not be labeled as a new or resistant infection. The prior treatment schedule should continue, and
dexamethasone may be added or its dose enhanced.
2010 The British Infection Society. Published by Elsevier Ltd. All rights reserved.

* Corresponding author. Tel.: 91 9335901790; fax: 91 522 2258852.

E-mail address: garg50@yahoo.com (R.K. Garg).
0163-4453/$36 2010 The British Infection Society. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.jinf.2010.03.013

Paradoxical vision loss associated with optochiasmatic tuberculoma in tuberculous meningitis

Introduction
Optochiasmatic tuberculoma is an uncommon cause of vision
loss in tuberculous meningitis which is seen in up to 18% of
patients at the time of diagnosis.1 Optochiasmatic tuberculoma may appear paradoxically in patients with tuberculous
meningitis while they receive adequate antituberculosis
treatment. Paradoxical deterioration in tuberculous meningitis is a well recognized entity. The paradoxical deterioration is defined as expansion of an existing tuberculoma or
development of new brain lesions in a patient whose symptoms have initially improved with antituberculosis treatment.2 The paradoxical changes pose serious challenges to
the treating physician, often igniting fear of possible treatment failure and leading to inappropriate dose increment
or addition of more toxic second line antituberculosis drugs.
Moreover, the expanding lesions may cause irreversible neurological deficits and unfavorable outcome if they are located on the structures consisting of dense nerve fiber
tracts such as optic chiasma, internal capsule, or brainstem.3
Information available, so far, on this subject is in form of isolated case reports.4,5 We are reporting a series of 8 cases of
tuberculous meningitis that developed paradoxical vision
loss associated with optochiasmatic tuberculoma.

459

weeks, starting at a total of 4 mg per day and decreasing

by 1 mg each week.8 Patients were followed for 9 months.
Paradoxical optochiasmatic tuberculoma was defined as
development of new optochiasmatic tuberculoma or expansion of a pre-existing optochiasmatic tuberculoma on
post-contrast MRI associated with new-onset vision impairment or deterioration of vision status (decrease in vision
acuity and/or vision field) in patients with tuberculous
meningitis receiving antituberculosis treatment.

Case reports
In this study, we included a series of 8 cases of tuberculous
meningitis that developed paradoxical vision loss associated with optochiasmatic tuberculoma. The mean duration
of illness of 134 patients of tuberculous meningitis admitted during the study duration was 51 days (range: 9e240
days). The mean duration of illness in patients with
optochiasmatic tuberculoma (prior to presentation) was
57 days (range: 20e118 days). The patients other characteristics, clinical features, cerebrospinal fluid parameters,
radiological findings, treatments administered, and outcome are summarized in Table 1.

Patient 1

Patients and methods

This study was conducted in the Department of Neurology
of Chhatrapati Shahuji Maharaj Medical University, Lucknow. Our university is a large tertiary care medical center
of North India. We retrospectively reviewed the clinical
records of all patients of tuberculous meningitis admitted
between December, 2007 and May, 2009. Eight cases of
paradoxical optochiasmatic tuberculoma and paradoxical
vision loss were identified among 134 patients meeting the
criteria of tuberculous meningitis. Tuberculous meningitis
was defined as definite if acid-fast bacilli were seen in
cerebrospinal fluid (CSF) or mycobacterial polymerase
chain reaction (PCR) was positive in CSF. Tuberculous
meningitis was defined as probable in patients with
one or more of the following: active pulmonary tuberculosis
on chest radiography, acid-fast bacilli found in any specimen other than the CSF, and clinical evidence of other
extrapulmonary tuberculosis. It was defined as possible
in patients with at least four of the following: duration of
illness of more than five days, history of tuberculosis,
altered consciousness, focal neurologic signs, turbid CSF,
predominance of lymphocytes in the cerebrospinal fluid, or
a ratio of CSF glucose to plasma glucose of less than 0.5.6
As per the antituberculosis treatment schedule for
tuberculous meningitis followed in our hospital, all patients
received two months of daily oral rifampicin (10 mg per
kilogram), isoniazid (5 mg per kilogram of body weight),
pyrazinamide (25 mg per kilogram), and intramuscular
streptomycin (20 mg per kilogram; maximum, 1 g per
day), followed by seven months of rifampicin and isoniazid
at the same daily doses.7 None of the patients received ethambutol. All patients also received intravenous dexamethasone for four weeks (0.4 mg per kilogram body weight
per day during first week and then tapered off deceasing
0.1 mg/kg every week) and then oral treatment for four

A 14-year-old male was admitted with fever, headache and

vomiting of 4 months duration. At admission, patient was
febrile. Neurological examination revealed only signs of
meningeal irritation. Vision acuity, visual field and fundii
were normal. Chest radiography showed bilateral miliary
shadows. Cerebrospinal fluid examination was suggestive of
tuberculous meningitis. (Table 1) MRI of brain at the time of admission showed basal and optochiasmal exudates along with
multiple small parenchymal tuberculoma. Patient was diagnosed as probable tuberculous meningitis (stage I). Antituberculosis treatment along with dexamethasone was started.
Patient improved and was discharged after 1 month. After 1
month of discharge, he returned with acute diminution of vision. This episode was not associated with fever, headache
or drug default. His vision acuity were 6/36 and 6/60 in right
and left eye respectively. Pupils were dilated and lacked response to light. Fundii were normal. A repeat MRI revealed
multiple coalescing optochiasmatic tuberculoma and increase
in size of parenchymal tuberculoma. (Fig. 1A) At that time, patient was receiving 1 mg of oral dexamethasone per day. The
dose was increased to 16 mg through intravenous route, and
tapered over next 6 weeks. The antituberculosis treatment
schedule was unchanged. His vision acuity improved to 6/9 in
both eyes by second week. A repeat MRI, at 6 months, showed
resolution of optochiasmatic and parenchymal tuberculoma.
Patient was asymptomatic after 9 months of follow-up.

Patient 2
A 35-year-old man presented with fever, headache, mild
confusion and signs of meningeal irritation. Polymerase
chain reaction for Mycobacterium tuberculosis was positive
in CSF. MRI showed basal meningeal enhancement and
multiple parenchymal tuberculoma. He received a diagnosis
of definite tuberculous meningitis (stage II). With

460

Table 1

Summary of tuberculous meningitis patients with optochiasmatic tuberculoma.

Case No.

Age/sex
Duration of
illness (days)
Clinical
features

14/M
118

35/M
32

20/M
90

45/F
68

32/M
20

29/M
30

21/F
81

14/F
20

Fever,
headache,
vomiting

Fever,
headache,
mild confusion

Fever,
headache,
confusion

Fever,
headache

Fever,
headache,
diplopia

Fever,
headache,
seizures

Fever,
headache,
confusion,
paraparesis

Fever,
headache,
diplopia,
ataxia

6/6
6/6
normal
normal
Nil

6/9
6/6
normal
normal
nil

6/6
6/6
normal
normal
Left
hemiparesis

6/6
6/6
normal
papilledema
Left 6th cranial
nerve palsy

6/6
6/6
normal
normal
Left upper
limb weakness

I
160

II
60

III
90

6/6
6/6
normal
normal
Bilateral
6th cranial
nerves palsy
II
224

II
278

III
86

6/9
6/9
normal
normal
Bilateral 6th
cranial nerves
palsy
III
106

6/6
6/6
normal
normal
Right 3rd and
bilateral 6th cranial
nerves palsy
III
422

2.20
0.46

2.12
0.42

0.78
0.18

3.78
0.23

2.51
0.31

0.91
0.33

1.91
0.22

4.78
0.18

No
No
No
Miliary
shadows
Basal
meningeal
enhancement,
optochiasmatic
arachnoiditis,
multiple
parenchymal
tuberculoma.
Probable

No
Positive
No
Normal

Positive
Positive
No
Normal

Positive
Positive
No
Bilateral
pleural effusion
Basal meningeal
enhancement,
non-communicating
hydrocephalous.

No
No
No
Normal

No
Positive
No
Bilateral upper
zone opacities
Basal meningeal
enhancement,
optochiasmatic
arachnoiditis

No
No
No
Normal

Basal meningeal
enhancement,
multiple
parenchymal
tuberculoma.

No
No
No
Left apical
opacities
Basal
meningeal
enhancement,
right frontal
tuberculoma

Definite

Probable

Definite

Definite

Possible

Definite

Possible

RHZS + Dexa
53

RHZS + Dexa
38

RHZS + Dexa
30

RHZS + Dexa
42

RHZS + Dexa
60

RHZS + Dexa
46

RHZS + Dexa
28

RHZS + Dexa
34

Vision at baseline
Right eye
Left eye
Vision field
Fundus
Other neurologic
deficits
BMRC stage
CSF Total
counts (/mL)
Protein (g/L)
Glucose/blood
glucose
AFB culture
PCR
HIV
Chest X-ray
MRI (baseline)

Basal meningeal
enhancement,
optochiasmatic
arachnoiditis,
right frontal
tuberculoma

Basal
meningeal
enhancement

M.K. Sinha et al.

TBM diagnostic
category
Treatment
Onset interval of
paradoxical
tuberculoma
(days)

Basal
meningeal
enhancement.

Fundus

Normal

6/60
6/60
Right
hemianopia
Normal

MRI at time of
deterioration

Multiple
optochiasmatic
tuberculoma,
increase in
size of
parenchymal
tuberculoma
Dexa extended
for 6 weeks
more

Multiple
optochiasmatic
tuberculoma,
increase in
size of
parenchymal
tuberculoma
Dexa extended
for 8 weeks
more

Solitary
optochiasmatic
tuberculoma,
no change in
size of frontal
tuberculoma
Dexa extended
for 6 weeks
more

Dexa
continued

Optochiasmatic
tuberculoma
resolved, size
of parenchymal
tuberculoma
decreased, no
meningeal
enhancement

Size of
optochiasmatic
and
parenchymal
tuberculoma
decreased, no
meningeal
enhancement

Optochiasmatic
tuberculoma
resolved, size
of frontal
tuberculoma
decreased, no
meningeal
enhancement

6/9
6/9
normal

6/36
6/60
Right
hemianopia
Independent

6/9
6/9
normal

Treatment
modifications

MRI at 6
months

Vision at 9 months
Right eye
Left eye
Vision field
Physical
disability
status at
9 months

6/36
6/9
Normal

HM
HM
e

Normal

Bilateral
optic atrophy
Multiple
optochiasmatic
and
parenchymal
tuberculoma

Independent

Independent

Died at 62
days

6/60
6/60
Bitemporal field
defects
Papilledema

6/18
6/18
Normal

HM
LP
e

HM
HM
e

Normal

Left optic
atrophy
Multiple
optochiasmatic
tuberculoma,
non-communicating
hydrocephalous

Normal
Multiple
optochiasmatic
tuberculoma,
non-communicating
hydrocephalous,
left basal ganglia
and thalamic infarct
Dexa extended
for 8 weeks
more

Multiple
optochiasmatic
tuberculoma,
hydrocephalous
increased

Multiple
optochiasmatic
and parenchymal
tuberculoma

Levofloxacin
750 mg +
Ethionamide
250 mg twice
daily added,
Dexa extended
for 8 weeks more
Ventriculoperitoneal
shunt surgery
Size of
optochiasmatic
and parenchymal
tuberculoma
decreased,
hydrocephalous
decreased

Dexa extended
for 6 weeks
more

Dexa extended
for 8 weeks
more

Optochiasmatic
tuberculoma
resolved, size
of parenchymal
tuberculoma
decreased

Size of
optochiasmatic
and parenchymal
tuberculoma
decreased,
hydrocephalous
decreased

Optochiasmatic
tuberculoma
resolved,
hydrocephalous
decreased

6/6
6/6
normal

6/60
6/12
Right temporal
field constricted
Independent

6/60
6/18
Right
hemianopia
Partially
dependent

Died at 211 days

Independent

Paradoxical vision loss associated with optochiasmatic tuberculoma in tuberculous meningitis

Vision at time of deterioration

Right eye
6/36
Left eye
3/60
Vision field
e

AFB Z acid-fast bacillus; BMRC Z British Medical Research Council; CSF Z cerebrospinal fluid; TBM Z Tuberculous meningitis; HIV Z human immunodeficiency virus; MRI Z magnetic
resonance imaging; RHZS Z Rifampicin, isoniazid, pyrazinamide and streptomycin; HM Z hand movement; LP Z light perception; Dexa Z dexamethasone.

461

462

M.K. Sinha et al.

Figure 1 Contrast-enhanced cranial magnetic resonance imaging shows multiple paradoxical optochiasmatic tuberculoma in patients 1 (A), 3 (B), 5 (C), and 6 (D). Multiple parenchymal tuberculoma can be seen in cerebellum and left temporal lobe of patient 6 (D).

antituberculosis therapy and dexamethasone therapy his

sensorium improved within 1 week. Vision acuity and field
were evaluated when he became alert. His vision acuity
was 6/9 and 6/6 in right and left eye respectively. Fundii
were normal. He was discharged after 1 month. After 7
days, he needed to be rehospitalized with acute vision
loss (acuity 6/60 in both eyes). He had right hemianopia
as well. Pupils were dilated and unreactive. Fundus examination revealed mild disc pallor in left eye. MRI brain
showed multiple optochiasmatic tuberculoma and increase
in size of parenchymal tuberculoma. The dose of dexamethasone was enhanced to 16 mg per day through intravenous route and tapered over 8 weeks thereafter. His vision
improved to 6/36 in right eye, while left eye vision remained unchanged. MRI, at 6 months, showed decrease in
size of optochiasmatic and parenchymal tuberculoma. His
vision impairment remained unchanged after 9 months of
follow-up.

Patient 3
A 20-year-old man presented with fever, headache, delirium, nuchal rigidity, and left hemiparesis. His chest

radiograph showed left apical opacities. MRI showed basal

exudates and right frontal tuberculoma. He was diagnosed
as probable tuberculous meningitis (stage III). His vision
acuity and field were normal. With antituberculosis therapy
and dexamethasone therapy, fever and sensorium improved. After 1 month, he developed vision impairment
(vision acuity 6/36) in right eye along with left focal
seizures. MRI revealed an optochiasmatic tuberculoma
apart from right frontal tuberculoma. (Fig. 1B) The dose
of dexamethasone was enhanced. Patients vision improved
to 6/9 in both eyes over 2 weeks. MRI, at 6 months, showed
resolution of optochiasmatic and parenchymal tuberculoma. After 9 month of follow-up, patient had good vision
and mild residual hemiparesis with spasticity.

Patient 4
A 45-year-old female was admitted with fever, headache,
nuchal rigidity, and bilateral sixth cranial nerve palsies. Her
vision acuity and field were normal. Polymerase chain
reaction and culture for M. tuberculosis was positive in
CSF. MRI showed extensive basal exudates. She was diagnosed as having definite tuberculous meningitis (stage II).

Paradoxical vision loss associated with optochiasmatic tuberculoma in tuberculous meningitis

She showed favorable signs of recovery with antituberculosis therapy and dexamethasone therapy and was discharged
after 2 weeks. One month later, she was readmitted with
acute vision loss. She could perceive hand movement with
both eyes. Pupils were dilated and unreactive and discs
were pale. MRI showed multiple optochiasmatic and parenchymal tuberculoma. Despite enhancement of dexamethasone dose, she continued to deteriorate. She had recurrent
episodes of secondary generalized seizures. She aspirated
during one of the episodes and developed pneumonitis.
She was treated with oxcarbazepine 600 mg per day and intravenous antibiotics. She died on 20th day of readmission.

Patient 5
A 32-year-old male was admitted with fever, headache, and
diplopia. He had nuchal rigidity and left 6th cranial nerve
palsy. His visual acuity was normal. He had bilateral
papilledema. X-ray chest showed presence of bilateral
pleural effusion. Polymerase chain reaction and culture
for M. tuberculosis was positive in CSF. His cranial MRI
showed basal exudates and non-communicating hydrocephalous. He received a diagnosis of definite tuberculous meningitis (stage II). Antituberculosis treatment along with
dexamethasone was started. Patient improved remarkably
and was discharged after 1 month. After 1 month of discharge, he returned with acute diminution of vision, fever,
headache, and cough. His vision acuity was 6/60 in both
eyes with bilateral temporal field defects. Pupils were dilated with sluggish reaction. Fundus examination revealed
persistence of bilateral papilledema. MRI showed multiple
optochiasmatic tuberculoma and increase in hydrocephalous. (Fig. 1C) Dexamethasone, intravenous mannitol and
furosemide were added to the treatment. A repeat computerized tomographic scan of brain done after 1 week showed
further increase in ventricular size. A ventriculo-peritoneal
shunt was placed, following which hydrocephalous improved. However, he continued to have fever and cough.
A repeat CSF examination showed 180 lymphocytes/mL,
protein 2.82 g/L and glucose 2.01 mmol/L. Culture for M.
tuberculosis was positive in CSF, though drug sensitivity
could not be done. Levofloxacin 750 mg per day and ethionamide 250 mg twice daily were added to the antituberculosis treatment schedule suspecting drug resistance. After
few weeks, his fever and cough subsided, but vision did
not recover. Following discharge, he did not turn up for
follow-up. Later on, it came to our knowledge that he
had expired on 211th day of his first admission.

Patient 6
A 29-year-old man presented with fever, headache, seizures, left arm weakness and signs of meningeal irritation.
His vision was normal. MRI showed basal and optochiasmatic exudates and right frontal tuberculoma. He was
diagnosed as possible tuberculous meningitis (stage III).
With antituberculous, dexamethasone and antiepileptic
therapy, his symptoms improved within 1 week. He was
discharged after 2 weeks. After 1 month, he needed to be
re-hospitalized with diminution of vision (acuity 6/18 in
both eyes). Pupils were mid-size and reactive. Fundus

463

examination was normal. MRI showed optochiasmatic tuberculoma and increase in size of parenchymal tuberculoma. (Fig. 1D) The dose of dexamethasone was
enhanced and tapered over 6 weeks thereafter. His vision
improved to 6/6 in both eyes within 1 week. MRI, at 6
months, showed resolution of optochiasmatic and parenchymal tuberculoma. He was asymptomatic after 9 months.

Patient 7
A 21-year-old female presented with fever, headache,
confusion, signs of meningeal irritation, and spastic paraparesis. Her vision was 6/9 in both eyes. Polymerase chain
reaction for M. tuberculosis was positive in CSF. MRI of
brain showed basal and optochiasmatic enhancement. MRI
of spinal cord showed destruction of 3rd and 4th thoracic
vertebrae with cord compression suggestive of Potts spine.
She received a diagnosis of definite tuberculous meningitis
(stage III). She improved with antituberculosis treatment
and dexamethasone therapy. Potts spine was managed
conservatively with immobilization for 3 months. On 28th
day, she developed blindness and delirium. Pupils were dilated and unreactive. Fundus examination revealed left optic atrophy. A repeat MRI showed multiple optochiasmatic
tuberculoma and non-communicating hydrocephalous. She
was treated with intravenous dexamethasone and mannitol. Her sensorium improved after 1 week but vision improved after 6 months to 6/60 in right eye and 6/12 in
left eye. MRI, at 6 months, showed resolution of optochiasmatic tuberculoma and hydrocephalous. After 9 months of
follow-up she could walk independently though vision impairment in right eye persisted.

Patient 8
A 14-year-old girl was admitted with fever, headache,
diplopia, and ataxia. Her vision acuity was normal. She
had right 3rd and bilateral 6th cranial nerve palsies along
with asymmetrical cerebellar signs. MRI showed basal
exudates. She was diagnosed as having possible tuberculous
meningitis (stage III). She showed favorable signs of recovery with antituberculosis therapy and dexamethasone
therapy and was discharged after 2 weeks. Two weeks
later, she was readmitted with acute vision loss and right
hemiparesis. She could only perceive hand movement with
both eyes. Pupils were dilated and unreactive and discs
were normal. A repeat MRI showed multiple optochiasmatic
tuberculoma, non-communicating hydrocephalous and left
basal ganglia and internal capsule infarcts. A computerized
tomographic angiography showed intermittent stenosis of
left internal carotid and middle cerebral arteries, suggestive of arteritis. (Fig. 2) Her vision improved gradually with
prolonged dexamethasone therapy.

Discussion
The present study, to our knowledge, is the first case series
of paradoxical optochiasmatic tuberculoma associated with
vision loss in patients with tuberculous meningitis. Appearance of new tuberculoma or expansion of pre-existing
tuberculoma while the patient is receiving antituberculosis

464

M.K. Sinha et al.

Figure 2 Baseline cranial magnetic resonance imaging of patient 8 showing normal perichiasmal region (A); contrast-enhanced
magnetic resonance imaging done on day 34 showing multiple paradoxical optochiasmatic tuberculoma (white arrows), thick basal
exudates and ventricular dilatation in axial (B) and coronal (C) images; computerized tomographic angiography done on same day
showing spasm of internal carotid, anterior and middle cerebral arteries (black arrows) (D).

therapy is a well recognized paradoxical reaction in

patients with tuberculous meningitis. There are several
case reports of paradoxical enlargement of intracranial
parenchymal tuberculoma (Table 2).3,9e11 However, there
are only two case reports of paradoxical development of
optochiasmatic tuberculoma.4,5
Paradoxical response is considered to represent a delayed type of hypersensitivity reaction secondary to the
massive release of mycobacterial proteins into the core of
tuberculoma and subarachnoid space (following administration of antituberculosis treatment) leading to intense
inflammation, expansion of tuberculoma, edema, vasculitis, and infarction.3 In perichiasmal region, pia matter and
dura matter are not closely adhered. With enhancement of
inflammation, the subarachnoid tubercles (Richs foci) in
meninges at this location expand readily and become large
and multilobulated. This may be associated with an increase in CSF lymphocytic pleocytosis or transient shift towards polymorphonuclear predominance, a phenomenon
known as the therapeutic paradox and regarded as highly
suggestive of tuberculous meningitis.12 In HIV positive patients of tuberculous meningitis, paradoxical response
may manifest as tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS), a potentially lifethreatening condition that occurs within 3 months after
starting combination antiretroviral therapy.13

Usually, paradoxical response and associated clinical

deterioration occur several weeks after commencement
of antituberculosis therapy. In our cases, the interval
between the institution of antituberculosis therapy and
appearance of paradoxical response ranged from 4 weeks to
8 weeks, which is similar to that reported by other case
series of paradoxical parenchymal tuberculoma in the
literature.3,4,14 Onset of paradoxical response has been reported as early as 2 weeks and as late as 18 months by various authors.3,4,12,13
Six out of 8 of our patients experienced severe vision loss
following development of paradoxical optochiasmatic tuberculoma. Vision loss in them might be due to ischemia of
optic nerve and optic chiasma due to vasculitis of vasa
nervosum supplying these nerves. We found evidence of
vasculitis of internal carotid artery in one patient with the
help of computerized tomographic angiography. (Fig. 2D)
Optic chiasma is supplied by a pial network of arteries fed
by anterior hypophyseal artery (branch of internal carotid
artery), internal carotid artery and posterior communicating artery. Optic nerve is supplied by anterior hypophyseal
artery and ophthalmic artery, both of which are branches of
internal carotid artery.15 Therefore, vasculitis of internal
carotid artery and its aforementioned branches might cause
ischemia of optic nerve and chiasma. Mechanical compression or traction of optic nerve and chiasma by expanding

Paradoxical vision loss associated with optochiasmatic tuberculoma in tuberculous meningitis

Table 2
S. No.
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15

465

Optochiasmatic tuberculoma: treatment and outcome of cases reported in the literature and our case series.
Author, year
19

Mooney, 1959
Schlernitzauer, 197120
Iraci, 198021
Lesoin, 198422
Teoh, 198823
Poon, 199310
Beneggi, 199524
Kadioglu, 199625
Akhaddar, 200126
Aversa, 200316
Sharma, 200311
a
Tsai, 20045
a
Kalkan, 20064
Yeh, 200918
Present series, 2010

Modification in therapy

Vision outcome

Surgery
Surgery
Biopsy
Surgery
Surgery
Corticosteroids
Corticosteroids
Corticosteroids Surgery
Corticosteroids
Prolonged ATT
Corticosteroids
Corticosteroids
Corticosteroids
Methylprednisolone
Dexamethasone

Good recovery
Good recovery
Good recovery
Good recovery
Good recovery
Good recovery
Good recovery
Good recovery
Good recovery
Blindness
Blindness
Good recovery
Good recovery
Blindness
Good in 3 patients, incomplete
recovery in 3 patients,
death in 2 patients

ATT Z antituberculosis therapy.

a
Paradoxical response.

tuberculoma may be another cause of vision loss, though vision loss may occur even when there is no compression such
as in patients with optochiasmatic arachnoiditis. One study
found optochiasmatic arachnoiditis in 41% of patients with
tuberculous meningitis having vision loss.1 Hydrocephalous,
which has been found to be associated with vision loss, was
present in three of our patients. Other possible causes of vision loss such as ethambutol toxicity, occipital lobe tuberculoma or infarct, optic nerve tuberculoma, and choroid
tubercle were not present in any of our patients.
Recognizing onset of paradoxical optochiasmatic tuberculoma has important therapeutic and prognostic implications. A careful vision assessment at the time of initial
presentation and at regular intervals may be of great value
in detecting this condition early. Patients experiencing
new-onset or progressive vision loss should be subjected
to neuroimaging, preferably contrast MRI. Though predictors of paradoxical optochiasmatic tuberculoma have not
been studied, we observed that three of our patients had
optochiasmatic arachnoiditis at baseline. High cerebrospinal fluid protein (>1 g/L) was another consistent abnormality observed in 6 out of 8 patients. Raised protein in
cerebrospinal fluid probably indicates severe meningeal inflammation in these patients, resulting in increased exudates formation around optochiasma and optic nerve
leading to vision impairment.
Management of paradoxical optochiasmatic tuberculoma
is controversial. Some authors prefer medical treatment
while others have preferred neurosurgery. (Table 2) We
managed all of our patients by extending the course dexamethasone for 6e8 weeks. Following extended dexamethasone therapy optochiasmatic tuberculoma resolved in 7 out
of 8 patients. Several authors, in past, have also advocated
addition or enhancement of corticosteroids.3,12,14 The rationale behind the use of adjuvant corticosteroids lies in reducing the harmful effects of pro-inflammatory molecules
released following destruction of the tuberculosis bacilli.

The improvement seen with corticosteroid therapy may

be due to reduction in cerebral edema and/or vasculitis.2
It is difficult to differentiate a paradoxical reaction from
a drug resistance or relapse of the disease. The culture positivity rate of M. tuberculosis is low and drug susceptibility
tests are expensive. The physicians, especially in resourcepoor countries, often add second line antituberculosis drugs
in patients with paradoxical response without confirming
drug resistance. However, the current consensus is that appearance of new intracranial tuberculomas or the expansion of older existing lesions does not indicate the need
to change the antituberculosis drug schedule.3 In one patient, however, we added 2 second line antituberculosis
drugs (levofloxacin and ethionamide) suspecting drug resistance as he had disseminated intracranial and pulmonary
tuberculosis and continued to have positive culture for
M. tuberculosis in CSF despite two months of four first
line antituberculosis drugs.
Surgical intervention may be necessary in situations with
acute complications, such as shunting procedures for the
treatment of hydrocephalus. When the diagnosis is not
confirmed and there is no response to medical therapy
within 8 weeks, a stereotactic biopsy on a suspected
tuberculoma could be performed.3 Few authors suggest
role of neurosurgical decompression of optic chiasma by excision of optochiasmatic tuberculoma if corticosteroids
have failed to provide vision improvement.12,16,17
The outcome of optochiasmatic tuberculoma is variable.
After completion of 9 months of follow-up, vision improvement was complete in 3 patients and partial in 3 patients.
Two patients died at 2 months and 7 months respectively
despite enhanced medical therapy. Other authors have
observed similar vision and physical outcome (Table 2).4,18
Late detection of paradoxical response, advanced disease,
severe vision loss, raised cerebrospinal fluid protein (>1 g/
L), hydrocephalous, and pre-existing optochiasmatic arachnoiditis may be associated with poor outcome.1

466
In conclusion, physicians and ophthalmologists must
recognize this devastating complication of tuberculous
meningitis. Prompt recognition of paradoxical optochiasmatic tuberculoma with the help of regular vision assessment
and timely neuroimaging may be life saving and prevent
further vision loss. Paradoxical reactions should not be
labeled as a new or resistant infection. The prior treatment
schedule should continue, and dexamethasone may be
added or its dose be enhanced. It is not advisable to add
second line antituberculosis drugs unless drug resistance is
proved. Neurosurgical intervention may be considered if the
medical therapy fails to provide improvement.

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