Clinical Nrurology und ~Yeurosur~ery,94 (1992) I-5 0 1992 Elsevier Science Publishers

CLINEU

B.V. All rights reserved

0303-8467192/s

05.00

00160

AbdulKader

Daif, Tahir Obeid, Basim Yaqub and Mohammed AbdulJabbar qfNeurolog_v

Division

(381, King Khulid Uniwrsit~ (Received (Revised.

17 October,

Tuberculous Arabia;

We present initially

meningitis;

Geographic

AIDS;

CSF examination,

consciousness.

The third

patient

Tuberculoma;

1991)

1991)

Internuclear

ophthalmoplegia;

meningitis

with atypical

one developed presented

internuclear

with paranoid

bacterial meningitis and he developed right hemianopia pletely with anti-tuberculous treatment.

clinical

features

is still endemic cx llUlll”Il n,lmhe=r u

cases of TB in association

in developing

psychosis,

with AIDS

and the fourth

in the

of the nervous

Cu.se 1 A 2%year-old

count.

zures,

hemiparesis,

thalmoplegia

papilloedema

[5,7]. The clinical

reported,

such as sei-

it is important

or internuclear

oph-

and cerebrospinal

fluid

days later.

Corre.~ponclmm Neurology,

can result in severe disability

that unusual

Division

manifestations

to: Dr. Abdulkader of Neurology

tal, P.O. Box 7805. Riyadh

Daif,

11472, Saudi Arabia.

or death.

of the disease

Assistant

(38). King Khalid

mimicking

All recovered

we present

acute com-

a few such

Professor

University

of

Hospi-

was admitted

with a 7-day

vomiting and fever. He was oriented was 38.5”C and BP 125170. Blood

urea and electrolytes

brain

(CSF) abnormalities vary, and acid-fast bacilli smears yield few positive results [4]. CSF examination may be initially normal or simulate pyogenic meningitis [6]. As delay in diagnosis

In this report

male patient

berculous

been

by MRI.

of

Patients

history of headache, and his temperature

have

had a picture

detected

system frequently presents with baffling features [l-3]. A number of observations of unusual presentation of tumeningitis

had

rennrtd ‘vy”‘cb’u

infection

yet. Tuberculosis

Two patients

countries,

nf have “A C~IIA;PC UCUUlVU 11u.u

USA and Haiti [8,16]. In Saudi Arabia, where tuberculosis is endemic, AIDS is still a rare disease and no association has been reported

Saudi

while the other had deterioration

are widely known. instances.

Tuberculosis

psychosis;

and CSF findings.

ophthalmoplegia,

due to a tuberculoma

Introduction

althnr,rrh rc=.r~ntlx/ UfiC”“Ub” ‘“VV”“,

Paranoid

medicine

4 cases of tuberculous

normal

26 March,

Rixudh 11472, Saudi Arrrhitr

1990)

received 25 March.

(Accepted

Key words:

Hospital.

were normal.

CT and CSF examinations the patient

became

Chest X-ray,

were normal. drowsy

A few

with mild neck

rigidity and bilateral lower motor neuron facial nerve palsy. He had bilateral internuclear ophthalmoplegia with slow and incomplete both eyes with nystagmus

adduction and abduction of in the abducting eye and fail-

ure of convergence. Deep tendon reflexes were exaggerated and both plantar responses were extensor. A repeat CSF showed high white blood cell (WBC) count w,ith predominant neutrophils and Koch bacillus were found (Table 1). Anti-tuberculous (Anti- TB) medication was started: isoniazid 300 mg. rifampicin 600 mg. pyrazinamide 1.5 g and ethambutol 700 mg orally with predni-

TABLE

I

CEREBROSPINAL

FLUID

BEFORE

AND FOLLOWING

ANTI-TB

CHEMOTHERAP‘I c’..-....

-_-.-‘il

Jugat

IIII‘IULII

A

r.11

A,-n

(I? = 2,s 4)

_____ 18-01-08

.-.--..-

24-02-08

5 77

03-02-08 23-03-08

128 40

22-03-10

4 162

28-03-10

0.48 60% Neutro.

96% Lymph.

0.68 0.81 0.84

3.4 0.8

cultLire

+

~!

_

+

-

-.

0.9 0.8

0.40 1.72

3.1

2.86 I.6

2.9

3.08

3.7 1.9 1.3 I.5

18-06-10 06-07-10 28-Q7- ! 0

16 0

07-05-10

8 0

90% Lymph.

3.1

225

55% Lymph.

0.77 I .63

18-05-10 23-05-10

98% Lymph.

st11eat

__-

..- ~~.--.

7

1.2

3.9

___~----.AFB: acid fast bacilli. ZN: Ziehl-Neelsen

60 mg daily. This produced a progressive provement leading to full recovery 5 months later. solone

im-

Case 2

clinic with a 2-week history of headache, vomiting and drowsiness. He was drowsy, afebrile, without focal neurological signs. Brain CT was normal. CSF examination showed normal cells, protein and glucose. One week later his general condition deteriorated and he became confused and agitated, but remained afebrile. Another brain CT revealed mild hydrocephalus with meningeal enhancement. CSF revealed 162 WBC, 97% lymphocytes. 0.9 g/l protein and 1.5 mmol glucose. Anti-TB treatment (isoniazid, rifampicin, pyrazinamide and ethambutol combined with dexamethasone) was started orally. His general condition improved progressively. On follow-up 6 months later, he had fully recovered. Cuse 3 A 5 1-year-old male patient was admitted to the psychiatric ward with a history of acute delirium and was diagnosed as paranoid psychosis. On examination he was confused without focal neurological signs. Chest X-ray showed bilateral multiple disseminated ill-defined opaci-

ties of variable size with some calcification. Biochemical investigation revealed hypernatremia of 162 mmol/l. This was well controlled with subcutaneous and subsequently oral DDAVP Contrast-enhanced brain CT ,h,..,,rl On 0-h on,.;nn moon ;n tha ~n..r.~nsJl.ar .-~n;nn Jll”WclUall LI111‘LUlMll~ ‘,lQJJ 111U,&,JUy‘uJU‘rr* ‘k+‘V,‘ IE‘;m ,I lej. 1). LP done after 5 days showed 16 cells 98% lymphocytes (Table 1). Anti-psychotic drugs were stopped and anti-TB medication was instituted (isoniazid, rifampicin, pyrazinamide and ethambutol combined with dexamethasone). His clinical condition improved within 10 days. After 6 months of treatment the patient was perfectly well. Case 4 A 33-year-old male patient was seen in a private clinic complaining of headache, generalized fatigue, and loss of appetite. On examination he was febrile, without meningeal or focal neurological signs. He was diagnosed as a case of typhoid fever and treated with chloramphenicol. On referral to us, he was drowsy, with meningeal signs. and a temperature of 38°C. Laboratory investigations showed normal blood count, urea, electrolytes, and liver function tests. Chest X-ray was normal. Brain CT showed a mild hydrocephalus with meningeal enhancement. LP showed 8 WBC, 3.1 g/l protein and 1.9 mmol

Fig. 1. Post-contrast

CT shows an enhancing mass on suprasellar region.

glucose. A partially pected and hence

treated pyogenic meningitis was suspenicillin and dexamethasone were

given to which the patient

responded

quite well. Four-

Fig. 2. Magnetic resonance imaging (MRI) with gadoliniumDTPA enhancement shows an isodense mass located in the left hypothalamic area extending into the suprasellar cistern and the medial and anterior aspect of the left frontal lobe.

high protein

and low or normal

glucose content

and fa-

teen days later another LP revealed no cells and 0.77 g/l protein. Therefore. drug therapy was discontinued. Two

vourable response to anti-tuberculous treatment are regarded as evidence indicative of tuberculous meningitis

days later the patient

[2]. Definitive

deteriorated

again with drowsiness,

confusion, fever and meningeal signs. Another LP was done which showed 225 WBC (55% lymphocytes) and a protein

content

of

1.62 g/l.

Anti-TB

(isoniazid,

ri-

fampicin, pyrazinamide and ethambutol orally) combined with dexamethasone were started. He improved progressively and dexamethasone was stopped 4 weeks later. While on regular therapy, the patient started to complain of his vision after 2 months. On examination he proved to have a right-sided homonymous CT and MRI of brain showed an isodense in the left hypothalamic area extending lar cistern and the medial and anterior

hemianopia. mass located

into the supraselaspects of the left

frontal lobe (Fig. 2). After 4 months of anti-TB medication neurological and ophthalmological examinations showed

progressive

MRI had shrunk

improvement.

The lesion shown

on

(Fig. 3).

Discussion

of tuberculous

infection

in our pa-

tients was provided by positive culture of Mycohacterium tuberculosis in 3 cases, and all 4 patients had a good response to anti-TB treatment with follow- up for at least 9 months. An early diagnosis

of tuberculous

meningitis

is highly

relevant to the treatment and prognosis of the disease. A common difficulty in developing countries is to distinguish TB meningitis from partially treated bacterial meningitis,

fungal

meningitis.

or neurobrucellosis.

especially

if the clinical presentations are unusual [2,9]. Kennedy and Fallon [3] reported 52 cases with TB meningitis in whom meningeal signs were absent in IO%. cranial nerve palsy was present in 19% and focal features in 25%. Internuclear

ophthalmoplegia

and paranoid

psychosis

are

highly unusual clinical presentations in TB meningitis [7]. Teoh et al. [7] reported 2 cases of internuclear ophthalmoplagia in TB meningitis in whom CT of the brain was normal. In one case, autopsy meningitis with diffuse brainstem to widespread

The diagnosis of tuberculous meningitis rests on the clinical picture. CSF findings and subsequent clinical response to adequate anti-tuberculous therapy. In the absence of a positive smear for mycobacterial tuberculosis, a compatible clinical picture plus lymphocytic CSF of

proof

panarteritis.

showed severe basal infarction secondary

In tuberculous

basal menin-

gitis. the vessels around the base of the brain arc most prone to develop inflammatory occlusion [I 1. I?]. Hence. the very vessels supplying the brain stem and the limhic system were involved and cause internuclear ophthalmoplegia, cranial nerve palsies. diabetes insipidus and para-

cal picture but also the absence of the classical CSF findings. The CSF changes in untreated TB meningitis are lymphocytic pleocytosis with high protein and low glucose [15]. The CSF may not initially show any abnormalities in patients with severe TB infection of the brain or spinal cord. This was seen in 2 of our patients (cases I and 2). Taylor et al. [6] and Kocen et al. [lo] reported fen cases of TB meningitis where the CSF was normal. Our patient no. 4 had a clinical course and CSF findings compatible with a partially treated pyogenic meningitis. We recommend a repeat CSF examination as soon as possible in patients with clinical features of meningitis when the initial CSF was normal or atypical, as delay in establishing the diagnosis of TB meningitis will eventually lead to increased morbidity and mortality. In endemic areas such as Saudi Arabia. the clinical manifestations and CSF findings may mimick the features of neurobrucellosis as reported by Bahemuka et al. [16]. The absence of the classical clinical picture and C‘S): findings should not misguide the treating physician, and the patient has to be started on anti-TB drugs, if there is a high index of clinical suspicion. Acknowledgements

Fig. 3. Magnetic resonance imaging (MRI) with gadoliniumDTPA enhancement, after four months of anti-TB treatment shows decrease in the size of the mass previously seen in Fig. 2.

noid psychosis

as illustrated

in 2 of our patients

(cases I

References

and 3).

In TB meningitis

The authors wish to express appreciation to Ibrahim AlOrainey, Professor of Infectious Disease, for helpful advice and reading of this manuscript, and Lydia Gallardo for secretarial assistance.

the appearance

symptoms and signs may indicate cerebral tuberculomas which may

of new neurological the development of occur in the first 2

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