Dr. Amit Palkar, P17547, Dr. Chhaya A Shinde, Dr. Akshay Nair, Dr. Roshani
Desai
Abstract
Purpose: To highlight the clinical features of Ocular Motility Disorders (OMD) among patients of microbiologically confirmed cases of Central Nervous System Tuberculosis (CNS-TB) and to study the effect of treatment on OMD.
Design: Prospective clinical study
Participants: Twenty-two consecutive patients of CNS-TB who manifested OMD.
Methods: Ophthalmic features and ocular motility were recorded at the time of diagnosis. All patients received combination of anti-tuberculous therapy with adjunctive corticosteroids. They were followed up subsequently, during the course of the treatment for resolution of the OMD after administration. The data was analyzed. The main outcome measures were clinical features of OMD in CNS-TB and the resolution after initiation of anti-tuberculous drugs with adjunctive corticosteroids.
Results: Of the 22 patients presenting with OMD, nystagmus was observed in 16/22 (72.7%) patients, cranial nerve palsy in 13/22 (59%) and conjugate gaze deficit in 2/22 (9%) patients. Pathologic gazed evoked nystagmus and Bruns nystagmus was found in 59% patients. Sixth nerve palsy (45.4%) was the most common ocular motor cranial nerve palsy. The difference in the proportion of OMD at presentation and at 3 months follow up on treatment was statistically significant, p<0.001.
Conclusions: Ocular Motility Disorders are significant manifestations in CNS-TB that are often overlooked. They render localizing value to a tuberculous lesion. Anti-tuberculous therapy with systemic corticosteroids can reverse OMD and reduce ophthalmic morbidity as well.
Keywords: Ocular motility disorders, CNS-TB, nystagmus, cranial nerve palsy, resolution.
Introduction
Central Nervous System Tuberculosis (CNS-TB) is estimated to account for 10% of the tuberculosis, predominantly affecting the young population in developing countries.[1]The common systemic manifestations include headache, fever, vomiting, seizures, altered sensorium and focal neurological deficit. Cranial nerve palsies and optic neuropathies have been described as associated ophthalmic features.[2] The neuro-ophthalmic manifestations of CNS-TB, their onset, duration, course and the effect of treatment are often overlooked amidst the systemic morbidity. These patients seldom receive referrals, nor present primarily to an ophthalmologist and therefore the ophthalmic manifestations remain under reported in literature. The efficacy of anti-tuberculous therapy (ATT) with combination drugs and adjunctive corticosteroids has promised reduction in mortality.[2] There is however scarce literature on the effect that ATT has on the reversibility and eventual outcome of ocular motility disorders encountered in CNS-TB. Therefore, given the paucity of evidence, this study was envisaged primarily with the aim of documenting the spectrum of OMD among patients of microbiologically confirmed cases of Central Nervous System Tuberculosis (CNS-TB) and secondarily, to study the effect of treatment on OMD.
Methods
A prospective clinical study was conducted at the ophthalmology services of an urban General Hospital in Western India. A prior Institutional Review Board approval was obtained. The study adhered to the tenets of the Declaration of Helsinki. Consecutive cases of CNS TB, diagnosed microbiologically by CSF analysis between April 2013 and March 2015, were included in the study. Patients with pre-existing ocular conditions and immunocompromised (HIV/AIDS) status were excluded from the study. At presentation, patient age, gender, severity of the CNS disease, ophthalmic findings with thorough ocular motility examination and neuroimaging findings were recorded. Severity of the systemic disease was staged according to the British Medical Research Council (BMRC) criteria.[3] In our study, ocular motility disorders were defined as impairment of eye movements as a direct manifestation of a CNS disease. The parameters measured at every contact from presentation to subsequent follow-ups were ocular motor nerve palsy, gaze deficits and nystagmus, if present. The motility patterns were used as clinical pointers to localize the CNS lesions on neuroimaging.
All patients received a institutionally approved regime using daily four drug combination of isoniazid (H) (10-20mg/kg in children; 300mg in adult), rifampicin (R) (10-20mg/kg in children; 450mg in adult <50kg; 600 mg in adult >50kg), pyrazinamide (Z) (15-30mg/kg in children; 1.5g <50kg adult; 2g >50kg adult) and ethambutol (E) (15-20 mg/kg in children; 15mg/kg in adult) as intensive phase of minimum two months (2HRZE). This was followed by isoniazid and rifampicin in continuation phase for at least six months. They also received adjunctive corticosteroids in the form of dexamethasone (0.4mg/kg/day) or prednisolone (4mg/kg/day) in children (<12 years) for at least 4 weeks. The steroids were tapered over 6 to 8 weeks thereafter. The decision to institute steroids was taken by the treating neurophysician and the neurology team monitored the subsequent systemic treatment. Patients with seizure activity secondary to the CNS disease also received anti-convulsants in addition. The patients were followed until a primary outcome of resolution of OMD was achieved. Resolution of OMD was defined as absence of subjective symptoms and improvement in ocular deviation or abnormal movements.
The demographic variables, frequency of OMD, neuroimaging characteristics and resolution were analyzed. The McNemar test was used to test the group differences, before and after treatment, in order to study the primary outcome of resolution. The statistical analysis was performed with the use of Statistical Package for Social Sciences, Version 21.0 (SPSS, Chicago, IL, USA).
Results
A total of 22 patients with CNS TB and ocular motility disorder were included in the study over the duration of 24 months. They were under follow up for a mean duration of 5 months (Range:1-12 months, SD: ±3 months) to look for resolution of OMD, after treatment with ATT and adjunctive corticosteroids. There were 13/22 (59%) male and 9/22 (41%) female patients with a mean age 22.2 years (Range: 6-55 years, SD: ±12.3 years). Twelve patients (54.5%) were in stage II, 5 each (22.7%) in stage III and I, as per BMRC criteria. (Table 1)
Of all the patients, nystagmus was observed in 16/22 (72.7%) patients, cranial nerve palsy in 13/22 (59%) and conjugate gaze deficit in 2/22 (9%) patients. (Table 2) Pathologic gazed evoked nystagmus (PGEN) (8/22) and Bruns’ nystagmus (5/22) were observed in total 59% patients.(Clip 1,2) Ataxic nystagmus was observed in one case and was found to be associated with internuclear ophthalmoplegia (INO). The most common cranial nerve palsy found was sixth nerve (CN VI) palsy in 10/22 (45.4%) patients, of which four had bilateral involvement(Figure 1) and rest six cases unilateral. One patient had concurrent seventh nerve (CN VII) palsy with ipsilateral CN VI palsy(Figure 2). Third nerve (CN III) palsy was identified in two patients (9%), one with fascicular lesion along with contralateral hemiparesis (Figure 3) and other with suspected nuclear lesion.The conjugate gaze deficit noticed was horizontal gaze palsy (Clip 3) and INO(Figure 4).The clinical diagnoses were confirmed with Computed Tomography (CT) and/or Magnetic Resonance Imaging (MRI) as tuberculous meningitis (TBM) in 9/22(40.9%) patients, tuberculoma in 6/22(27.2%) and combined CNS tuberculopathy in 6/22(27.2%). Six patients with TBM and CN VI palsy (all bilateral and two unilateral cases:16,17) were found to be false localizing signs on neuroimaging. Also six patients were noted to have hydrocephalus, two of them (Case 2, 3) underwent ventriculo-peritoneal CSF shunt for obstructive hydrocephalus.
At three months on treatment, out of the 22 patients, four patients (18.1%) succumbed to the CNS disease. 6 patients (27.2%) had persistent OMD, but 12 patients (54.5%) showed resolution of ocular motility dysfunction. (Table 3) (Figure 5)An exact McNemar’s test determined that the difference in the proportion of OMD at presentation and at 3 months follow up was statistically significant, p<0.001.This resolution of OMD was found to be consequent to the treatment received. At six months, out of the six patients with persistent OMD, one patient showed resolution, but 3/6(50%) patients continued to show signs of OMD and 2/6 (33.3%) did not follow up. The resolution persisted in 3/12(25%) previous OMD resolved patients. However, rest of the 9 patients failed to follow up. A total of 11/22 (50%) patients were lost to follow up at variable length in the study.
Discussion
We describe a study of CNS TB patients with ocular motility disorders, who received a combination treatment of ATT and adjunctive corticosteroids. These motility deficits were observed as neuro-ophthalmic manifestation localizing to the lesions of CNS TB. A significant resolution rate was found in response to the treatment, however a high dropout rate was evident.
Sinha et al., [4]in their series of 101 patients, have documented the ocular features of CNS-TB patients. Their study, however was primarily aimed at studying visual impairment and its relevance in prognosticating the disease. In our cohort, CNS TB was observed at younger age (Mean±SD; 22.2 ±12.3vs 30±13), male preponderance (63.6% vs 59%) presenting at BMRC Stage II (54.5% vs 38.6%) in comparison to Sinha et al. Nystagmus, ocular motor cranial nerve palsies and conjugate gaze deficit were found as the ocular motility disorders. All patients completed a follow up of atleast three months on treatment. The primary outcome of resolution of OMD, at three months follow up, with antituberculous therapy and adjunctive corticosteroids, was found to be statistically significant, (p<0.001).
Nystagmus is not a classical finding that is routinely looked for in cases of CNS-TB and this possibly accounts for it being under-reported.[5] We found nystagmus in 72.7% patients, compelling to delve into its pathogenesis and prognosis. The characteristics and type of nystagmus has diagnostic value for the clinician as it helps to localize the lesion.[6] PGEN is a jerk nystagmus with large amplitude and asymmetry, occurring at less eccentricity of gaze. It manifests from a defect in the neural integrators in the brainstem and cerebellar flocculus with close proximity to the fourth ventricle. Usually it indicates either an inflammatory and/or compressive lesion localizing near the fourth ventricle.[7,8]Multiple mechanisms are described disturbing the dynamics of cerebrospinal fluid (CSF) circulation that leads to either communicating and/or obstructive hydrocephalus.[9] On neuroimaging, patients manifesting PGEN were identified with pathologies that directly caused raised intracranial tension (ICT) in our study. This implies that presence of PGEN indicates a disease process either secondary to raised intracranial tension or one that culminates into it. Moreover, patients with PGEN and hydrocephalus showed a poor response to the medical treatment and required surgical shunts, when followed for 3 months. PGEN is also commonly encountered as drug induced nystagmus following use of anti-convulsants or sedative drugs viz. (phenytoin, barbiturates or alcohol),[6] that are prescribed to control seizure activity in CNS TB. This may have confounded the persistence of PGEN in our patients, during follow up.
Bruns’ nystagmus is a variant of gaze evoked nystagmus, with a coarse, high amplitude cerebellar horizontal jerk nystagmus seen when looking in the direction of the lesion and fine high frequency vestibular nystagmus seen when looking away from the lesion.[8] Two different neural integrators: the cerebellar flocculus and peripheral vestibular components are responsible, localizing the lesion to the cerebellopontine angle.[10]Bruns’ nystagmus was observed to be associated with lateral rectus palsy (Case 10-13), of which one patient exhibited ipsilateral lower motor neuron facial paresis. The clinical picture pointed to a lesion antero-laterally at the exit of the CN VI & VII at the ponto-medullary junction extending posteriorly to the flocullus of the cerebellum at the caudal cerebellopontine cistern. Downbeat nystagmus is attributed to a central vestibular pathway affected in lesions of the vestibulocerebellum, cranio-cervical junction or by drug intoxication.[6] Neither of the findings in the two patients in our cohort was supported on neuroimaging.
Ocular motor cranial nerve palsy was found comparable (59% vs 60.8%)to the results presented by Aaron et al.[11],among the various non-uniform studies with CNS TB patients.[11-15](Figure 6)Cranial nerve palsy is frequently seen in children with CNS-TB. [16,17] In our study, acquired CN VI palsy (10/12) was the most common ocular motor cranial involved, affecting children and young adults as well. Its significance is emphasized, as cranial nerve involvement in TBM has been reported as one of the predictor of death or severe disability at 6 months, (p=0.001). [18] Although 70% experienced resolution of lateral rectus paresis in our study, two patients were deceased by the third month follow up. The causal association did not reach statistically significant levels, but warrants investigation.
CN VI palsy can disguise as a false localizing sign of raised ICT causing stretching of the nerve in the subarachnoid space.[19] However, unilateral CN VI palsy may not always misguide [20], usually when accompanied with nystagmus, adjacent CN VII, VIII involvement or absence of disc edema or pallor. And thus, it becomes imperative to actively look for these accompanied manifestations in addition to the sixth nerve palsy.[21]
Acquired third nerve palsy was found in two patients, one with concurrent contralateral hemiplegia (Weber syndrome) localizing lesion to the cerebral peduncle (Case 20, Figure 3). A child was diagnosed as third nerve nuclearlesion with bilateral ptosis, suspected with midline tuberculoma at midbrain.(Case 19, Figure 5) Kumar et al. reported a third nerve nuclear lesion due to midbrain tuberculoma that presented as isolated bilateral ptosis.[22] Midbrain tuberculoma with associated inflammatory edema can affect the fascicular course of the third nerve.[23,24] But they often have accompanied neurological features like contralateral hemiparesis, extrapyramidal signs and/or cerebellar ataxia, providing them a localizing value.[25] Cranial nerves can be involved in the subarachnoid space or the cavernous sinus.[26-30]
Conjugate eye movement abnormalities localize to a process at a supranuclear or internuclear level.[8] Our patient (Case 21) presented with no primary deviation but right adduction limitation with left abducting (ataxic) nystagmus and absent convergence of internuclear ophthalmoplegia. Neuroimaging revealed a rostral lesion in the midbrain involving the right medial longitudinal fasciculus (MLF). Convergence is usually spared if the lesion affects the MLF in the pons (Cogan’s posterior INO), but may be affected in rostral mesencephalic lesion, where the convergence input to the medial rectus subnucleus may be involved (Cogan’s anterior INO).[31,32] Certainly, INO is a very discrete localizing sign with significant clinical value.[33] TBM can present as INO secondary due to vasculitic ischemia of the MLF or a midline midbrain tuberculoma resulting into Wall-eyed Bilateral Internuclear Ophthalmoplegia (WEBINO).[34,35] One-and-half syndrome can be a seldom presentation with tuberculous granulomas in the brainstem.[36-38] Horizontal gaze palsy places the lesion at the paramedian pontine reticular formation (PPRF). It can present as an isolated finding with pontine tuberculoma. [39,40] Furthermore, association of ipsilateral lower motor neuron facial palsy alongwith a gaze palsy, gives a definite evidence of lesion at the facial colliculus involving the CN VI nucleus with PPRF and the loop of CN VII. (Case 22)
Our cohort presents the prevalence of OMD among patients of CNS TB who were referred by the treating neurologists – thereby reflecting an underlying referral bias. Given this bias, our findings cannot project the incidence of OMD among CNS TB patients in general. The study is limited by its sample size and inadequate follow up. A longer follow up is warranted to study the course of OMD and ophthalmic disability. The patients evaluated were on combination therapy, the induction of which was variable (less than 2 weeks from presentation) and this may have affected the ocular motility findings. Nonetheless, recognizing motility patterns in CNS tuberculosis and correlating with neuroimaging findings can enhance diagnostic accuracy. OMD in afflicted children can prove to be amblyogenic, if left untreated beyond the critical period of plasticity. We believe this study throws light over novel insights of this entity and opens avenue for further research.
Conclusion
Neuro-ophthalmic manifestations of CNS TB often go unnoticed in the melee of other sinister neurological manifestations. The disease has significant systemic morbidity that improves or prevents death with administration of appropriate therapy. Yet, the prediction of prognosis for a neuroclinician involves disability and death. A thorough ophthalmic and ocular motility assessment may help in diagnosing anddetermine the extent of CNS disease. A variety of OMD can be noted among patients with CNS-TB, the prognostic value of which remains to be assessed entirely. Many of the OMD respond well to treatment and ameliorate as the general condition of the patient improves. Ophthalmologists and neurologists should be sensitive to the detection and resolution of OMD during the course of treatment of patients with CNS-TB.
References:
- Dye C, Scheele S, Dolin P, Pathania V, Ravigliione MC. Consensus statement. Global burden of tuberculosis: estimated incidence, prevalence, and mortality by country. WHO surveillance and monitoring project. JAMA 1999; 282:677-686.
- Prasad K, Singh MB, Ryan H. Corticosteroids for managing tuberculous meningitis. Cochrane Database of Systematic Reviews 2016, Issue 4. Art. No.: CD002244. DOI: 10.1002/14651858.CD002244.pub4.
- Medical Research Council Report. Streptomycin treatment of tuberculous meningitis. Lancet 1948;1(6503):582–96.
- Sinha MK, Garg RK, Anuradha H, Agarwal A, Singh MK, Verma R, et al. Vision impairment in tuberculous meningitis:predictors and prognosis. J Neurol Sci. 2010;290:27–32.
- Sinha MK, Garg RK, Anuradha H, Agarwal A, Singh MK, Verma R, et al. Vision impairment in tuberculous meningitis:predictors and prognosis. J Neurol Sci. 2010;290:27–32.
| Table 1. Demographic frequencies of the cohort (n=22) | |
| Age-yr (Mean SD) (Range) | 22.2 ±12.3 (6-55) |
| Sex (%)
Male Female |
13 (59%) 09 (41%) |
| BMRC*
I II III |
05 (22.7%) 12 (54.5%) 05 (22.7%) |
| Follow up duration (months) (Mean SD) (Range) | 05 ±03 (1-12) |
| Ocular Motility Disorder
Pathologic Gazed Evoked Nystagmus Bruns Nystagmus Downbeat Nystagmus Ataxic Nystagmus CN VI Palsy (Bilateral/Unilateral) CN III Palsy CN VI+VII Palsy Gaze Palsy + CN VII palsy Internuclearophthalmoplegia |
08 (36.3%) 05 (22.7%) 02 (9%) 01 (4.5%) 10 (45.4%) 02 (9%) 01 (4.5%) 01 (4.5%) 01 (4.5%) |
| Neuroimaging abnormalities
Tuberculous Meningitis Tuberculoma Tuberculous Brain Abscess Hydrocephalus Tuberculous Meningitis &Tuberculoma Tuberculoma& Tuberculous Brain Abscess |
09 (40.9%) 06 (27.2%) 01 (4.5%) 06 (27.2%) 04 (18.1%) 02 (9%) |
| 3 months follow up on treatment
Persistent OMD Resolution Death Lost follow up |
06 (27.2%) 12 (54.5%) 04 (18.1%) 0 (0) |
| 6 months follow up
Persistent OMD Persistent Resolution New Resolution Lost follow up |
03 (13.6%) 04 (18.1%) 04 (18.1%) 11 (50%) |
| *British Medical Research Council criteria: Stage 1- Fully conscious and no focal neurological deficits; Stage 2- Altered consciousness, not comatose with moderate neurological deficit; Stage 3- Stuporous or comatose with severe neurological deficit. | |
| TABLE 2: Profile of Ocular motility disorders and correlational neuroimaging | ||||||
| Case No | Age (y), Sex(M/F) | BMRC | Ocular motility disorder | Neuroimaging diagnosis | ||
| Nystagmus | Cranial Nerve Palsy | Conjugate gaze deficit | ||||
| 1 | 8 M | 1 | PGEN | Tubercular Brain Abscess + Tuberculoma | ||
| 2 | 14 M | 2 | PGEN+ | Tuberculous Meningitis + Hydrocephalus | ||
| 3 | 18 M | 2 | PGEN+ | Tuberculous Meningitis + Hydrocephalus | ||
| 4 | 22 F | 3 | PGEN+ | Tuberculous Meningitis + Tuberculoma and Hydrocephalus | ||
| 5 | 45 M | 2 | PGEN | Tubercular Brain Abscess | ||
| 6 | 19 M | 2 | PGEN+ | VI (bl) | Tuberculous Meningitis | |
| 7 | 20 M | 2 | PGEN+ | VI (bl) | Tuberculous Meningitis | |
| 8 | 30 F | 2 | PGEN+ | VI (bl) | Tuberculous Meningitis | |
| 9 | 32 M | 3 | Bruns | Tuberculous Meningo-Encephalitis with Tuberculoma and Hydrocephalus | ||
| 10 | 9 M | 1 | Bruns | VI | Tuberculous Meningitis + Tuberculoma | |
| 11 | 16 F | 2 | Bruns+ | VI | Tubercular Brain Abscess + Tuberculoma | |
| 12 | 26 F | 1 | Bruns | VI | Tuberculoma | |
| 13 | 8 F | 1 | Bruns | VI, VII | Tuberculoma | |
| 14 | 20 F | 3 | Downbeat | Tuberculous Meningitis | ||
| 15 | 40 M | 2 | Downbeat | Tuberculoma | ||
| 16 | 10 M | 1 | VI | Tuberculous Meningitis | ||
| 17 | 20 F | 3 | VI | Tuberculous Meningitis | ||
| 18 | 32 F | 2 | VI (bl)+ | Tuberculous Meningitis + Hydrocephalus | ||
| 19 | 6 M | 2 | III | Tuberculous Meningitis + Tuberculoma | ||
| 20 | 15 M | 2 | III** | Tuberculoma | ||
| 21 | 24 M | 2 | Ataxic | INO | Tuberculoma | |
| 22 | 55 F | 3 | VII | GAZE PALSY+ | Tuberculoma + Hydrocephalus | |
| TOTAL | 16 (72.7%) | 13 (59%) | 2 (9%) | |||
| ** Patient presented with focal neurological deficit of contralateral hemiparesis. (Weber syndrome)
+ Fundus examination showed papilledema. bl, bilateral |
||||||
| Table 3. Follow up Summary | ||||
| CASE | OMD at presentation | Follow up Duration (m) | OMD at
3 months |
OMD at
6 months |
| 1 | PGEN | 6 | Resolution | Resolution |
| 2 | PGEN | 4 | No Resolution | Lost FU |
| 3 | PGEN | 12 | No Resolution | No Resolution |
| 4 | PGEN | 6 | No Resolution | No Resolution |
| 5 | PGEN | 3 | Resolution | Lost FU |
| 6 | PGEN, VI CNP | 4 | Resolution | Lost FU |
| 7 | PGEN, VI CNP | 7 | Resolution | Lost FU |
| 8 | PGEN, VI CNP | 9 | Resolution | Lost FU |
| 9 | BRUNS | 1 | Deceased | |
| 10 | BRUNS, VI CNP | 6 | Resolution | Lost FU |
| 11 | BRUNS, VI CNP | 6 | Resolution | Lost FU |
| 12 | BRUNS, VI CNP | 12 | Resolution | Resolution |
| 13 | BRUNS, VI, VII CNP | 3 | No Resolution | Lost FU |
| 14 | DOWNBEAT | 3 | Resolution | Lost FU |
| 15 | DOWNBEAT | 6 | No Resolution | No Resolution |
| 16 | VI CNP | 3 | Resolution | Resolution |
| 17 | VI CNP | 2 | Deceased | |
| 18 | VI CNP | 1 | Deceased | |
| 19 | III CNP | 3 | No Resolution | Resolution |
| 20 | III CNP | 6 | Resolution | Lost FU |
| 21 | INO | 5 | Resolution | Lost FU |
| 22 | GAZE PALSY, VII CNP | 2 | Deceased | |
| McNemar’s exact test | p<0.001 | |||
Legends
Table 1. Demographic frequencies of the cohort
Table 2.Profile of Ocular motility disorders and correlational neuroimaging
Table 3. Follow up summary
Figure 1. (1A) A young male with binocular diplopia, bilateral abduction limitation and papilledema (1B) (Case 6), was found to have bilateral pseudo-abducens palsy, falsely localizing due to raised intracranial tension in tuberculous meningitis, (1C) seen as spider leg appearance on contrast enhanced computed tomography (CT).
Figure 2. (2A) A young female with inward deviation of the left eye with headache and fever had left sixth nerve palsy. (Case 12) (2B,2C) MRI revealed multiple intracranial lesions along with lower pons lesions. T1W contrast showed hyperintense ring with hypointense centre that corresponded to hypointense lesion with surrounding vasogenic edema on T2W.
Figure 3. (3A) An adolescent boy with left hemiparesis with drooping right upper eyelid. (Case 20)Right third nerve palsy with pupil involvement localizing to the right cerebral peduncle in Weber syndrome and warranted neuroimaging. (3B) MRIT1W Post contrast, STIR, T2W images confirmed a fascicular lesion of tuberculomas at the right cerebral peduncle.
Figure 4. (4A) A young male complaining of binocular diplopia diagnosed with right internuclearophthalmolplegia. (Case 21) (4B) Convergence inability suggesting rostral lesion that was confirmed on MR imaging (4C) showing hyperintense lesion of tuberculous granuloma in the midline rostral brainstem (arrowhead).
Figure 5. Cranial nerve palsy resolving after ATT with adjunctive steroids on follow up. (5A) A young child(Case 19)presented as bilateral ptosis, predominant right exotropia and motility limitation, (5B) experienced improvement in ptosis and exotropia at 6 months. Absence of diplopia was attributed to suppression of the right eye. (5C) A young woman (Case 8) with headache, mental confusion and diplopia was found to have bilateral lateral rectus palsy at presentation. (5D) At 3 months after treatment, the motility deficit resolved completely.
Figure 6. Comparative prevalence of ocular motor cranial nerve palsies in central nervous system tuberculosis.
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