Cranial Nerve Palsies in Streptococcus
pneumoniae Meningitis Mary Lynn Y. Chu, MD*, Nathan Litman, MD+, David M. Kaufman, MD*, and Shiomo Shinnar, MD, PhD *t
Cranial nerve palsies are uncommon in nontuberculous bacterial meningitis. We report a patient with Streptococcus pneumoniae meningitis, multiple cranial nerve involvement, and cerebellar signs suggestive of basilar meningitis. Nontuberculous bacterial meningitis should be considerefl in the differential diagnosis of basilar meningitis. C h u M L Y , L i t m a n N, K a u f m a n D M , S h i n n a r S. C r a n i a l n e r v e palsies in Streptococcus pneumoniae m e n i n g i t i s . Pediatr Neurol 1990;6:209-10.
Introduction C r a n i a l n e r v e p a l s i e s are c o m m o n l y f o u n d in p a t i e n t s with chronic basilar meningitis. For example, tuberculous m e n i n g i t i s f r e q u e n t l y c a u s e s a b d u c e n s n e r v e palsy or facial diplegia. C o n v e r s e l y , n o n t u b e r c u l o u s b a c t e r i a l m e n i n gitis usually affects the c o n v e x i t i e s o f t h e b r a i n so that such p h e n o m e n a are u n c o m m o n . W e r e p o r t a p a t i e n t w i t h Streptococcus pneumoniae ( p n e u m o c o c c a l ) m e n i n g i t i s , multiple cranial nerve involvement, and cerebellar findings.
Case Report This 13-year-old black male had an upper respiratory tract infection 2 weeks before admission. He did well until 4 days prior to admission when he developed fever and a generalized throbbing headache. He was treated with cephalexin (750 mg/day in 3 divided doses), continued to be symptomatic, and on the day of consultation, he complained of neck stiffness and diplopia. On arrival at the emergency room, he had a temperature of 38.9°C. Physical examination was unremarkable except for marked nuchal rigidity.
From the Departments of *Neurology and tPediatrics; Montefiore Medical Center; Albert Einstein College of Medicine; Bronx, New York.
Neurologic examination revealed a lethargic but oriented boy who was coherent but slow in responding to questions. Fundoscopic examination demonstrated spontaneous venous pulsations and no evidence of papilledema. Pupils were equal and reactive. He had bilateral lateral rectus muscle palsies and a mild facial diparesis with inability to whistle or fully puff his cheeks. His hearing was normal. He had mild appendicular dysmetria and truncal ataxia. Motor examination demonstrated grade 5/5 strength without asymmetry or weakness. Deep tendon and plantar reflexes were normal. Sensation was intact. Cranial computed tomography (CT), including cuts of the posterior fossa and sinuses, was performed with and without contrast enhancement. No intracranial abnormalities were found. Air-fluid levels were observed in the frontal, maxillary, and sphenoid sinuses. A lumbar puncture yielded cloudy cerebrospinal fluid (CSF) under an opening pressure of less than 10 cm H20. CSF contained 1,170 leukocytes/mm3 (95% neutrophils, 5% lymphocytes), 560 erythrocytes/mm3, protein 363 mg/dl, and glucose 5 mg/dl. Gram stain revealed many Gram-positive diplococci in pairs. Stain for mycobacteria was negative. The administration of ampicillin and chloramphenicol was based on the presumptive diagnosis of Streptococcuspneumoniaemeningitis. Blood and CSF cultures subsequently grew Streptococcuspneumoniaesensitive to penicillin; the patient received a 14-day course of intravenous penicillin. The patient's dysmetria improved after 3 days. Five days after admission, extraocular muscle movement was full and he was able to whistle. Fever resolved in 1 week. Repeat sinus films revealed slight mucoendosteal thickening with loss of the previous air-fluid level in the left maxillary sinus antrum. After a 14-day course of antibiotics, he was completely asymptomatic and was discharged. Subsequently, he has been asymptomatic with no neurologic residua. Follow-up examination revealed no hearing loss.
Discussion O n l y a few reports o f n o n t u b c r c u l o u s bacterial m e n i n gitis with cranial n e r v e a b n o r m a l i t i e s h a v e b e e n p u b l i s h e d . C o o k et al. r e p o r t e d a 2 4 - y e a r - o l d p a t i e n t with Corynebacterium hemolyticum w h o p r e s e n t e d w i t h a n a b d u c e n s n e r v e palsy w h i c h they a t t r i b u t e d to an i s o l a t e d s p h e n o i d sinus i n f l a m m a t i o n [ 1 ]. F o c a l n e u r o l o g i c deficits o c c u r in as m a n y as 15% of c h i l d r e n w i t h m e n i n g i t i s [2-4] a n d are a s s o c i a t e d w i t h a d v e r s e o u t c o m e s [5]. T h e u n d e r l y i n g p a t h o l o g y is bel i e v e d to b e cortical v e n o u s or arterial t h r o m b o s i s s e c o n d a r y to e d e m a a n d i n f l a m m a t i o n [3,4]. I s o l a t e d c r a n i a l n e r v e palsies are not the usual p r e s e n t a t i o n . O u r p a t i e n t p r e s e n t e d w i t h diplopia. H e h a d b i l a t e r a l a b d u c e n s palsy, facial diparesis, a n d m i l d ataxia, all of w h i c h g r a d u a l l y i m p r o v e d with t r e a t m e n t o f Streptococcus pneumoniae m e n i n g i t i s . I n c r e a s e d i n t r a c r a n i a l p r e s s u r e m a y c a u s e bilateral a b d u c e n s palsy in a p a t i e n t with m e n ingitis [6], b u t o u r p a t i e n t h a d n o e v i d e n c e o f i n c r e a s e d i n t r a c r a n i a l pressure. T h e p r e s e n c e o f lateral rectus palsy, facial d i p a r e s i s , a n d m i l d ataxia s u g g e s t b r a i n s t e m inv o l v e m e n t p r o b a b l y d u e to b a s a l i n f i l t r a t i o n o f the m e n i n ges. A l t h o u g h it w a s fairly rapid, the clinical r e s o l u t i o n o f
Communications should be addressed to: Dr. Shinnar; Division of Pediatric Neurology; VCP-207; Montefiore Medical Center; 111 East 210th Street; Bronx, NY 1(/467. Received December 5, 1989; accepted February 14, 1990.
Chu et al: Cranial Nerve Palsies 209
symptoms was sufficiently prolonged to make edema an unlikely etiology. Other infectious causes of acute cranial nerve palsies include tuberculous meningitis which is notorious for presenting with multiple cranial nerve palsies. In 40 patients studied by L a m b a et al., 72.9% had ocular manifestations [7]. Common abnormalities included fundus lesions (62.5%), pupillary changes (48%), and cranial nerve palsies (28%). Direct infiltration at the base of the brain is more likely to involve the oculomotor nerve than any other. Abducens nerve palsy, though less common, has a higher mortality (50%) because it usually reflects increased intracranial pressure. Wyllie et al. reported 37 patients with isolated inflammatory sphenoid sinus disease at the Mayo Clinic between 1935 and 1972 [8]. The patients were divided into those with chronic sinusitis and those with mucoceles or pyoceles. Fifty-four percent of the latter group had visual disturbances, but only 1 patient bad bilateral abducens palsy. The neurologic findings in this patient cannot be explained on the basis of sinusitis, though it may well have been the source of infection. Ataxia, which has been reported as a temporary or permanent c o m p l i c a t i o n of bacterial meningitis [4,9], is believed to be due to vestibular damage, probably secondary to drug therapy. It usually is associated with deafness due to cochlear nerve involvement. When ataxia is not associated with deafness, Schwartz suggested cerebellar dysfunction as the etiology [9]. Our patient had ataxia on presentation, prior to therapy; therefore, drugs could not have been the cause. It was also clinically different from that observed in eighth nerve involvement because there was no rotatory nystagmus. The ataxia was similar to that observed with involvement of the cerebellum or the intraaxial brainstem and cerebellar connections.
210 PEDIATRIC NEUROLOGY Vol. 6 No. 3
Cranial nerve palsies are rarely observed in nonlubcr culous bacterial meningitis. Our case reporl suggests Ihal nontuberculous bacterial meningilis can present with cranial nerve palsies and ataxia, clinical signs usually ob served in chronic meningitis.
Dr. Shinnar is supported in part by a Teacher Investigator Development Award 1 K07 NS00930 from the National Institute of Neurological Disorders and Stroke.
References
[1] Cook IE Cabral DA, Reed WD, Bond RJ, Henderson A. lntracranial complications of sphenoid sinus inflammation. Med J Aust 1981;1:366. [2] Klein JO, Feigin RD, McCracken GH Jr. Report of the task force on diagnosis and management of meningitis. Pediatrics 1986,78 (Suppl):959-82. [3] Swartz MN, Dodge PR. Bacterial meningitis--A review of selected aspects. N Engl J Med 1965;272:725-30. [4] Feigin RD. Bacterial meningitis beyond the newborn period, tn: Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. Philadelphia: WB Saunders, 1981;293-304. [5] Kaplan SL, Feigin RD. Clinical presentations, prognostic factors and diagnosis of bacterial meningitis. In: Sande M, Smith AL, Root RK, eds. Bacterial meningitis. New York: Churchill Livingstone, 1985;83-4. [6] Donelly WJ. Meningitis and cranial nerve V1 palsy. Postgrad Med 1968;43:214-9. [7] Lamba PA, Bhalla JS, Mullick DN. Ocular manifestations of TB meningitis, a clinico-biochemical study. J Pediatr Ophthalmol Strabismus 1986;23:123-5. [8] Wyllie JW, Kern EB, Djalilian M. Isolated sphenoid sinus lesion. Laryngoscope 1973;83:1252-65. [9] Schwartz JF. Ataxia in bacterial meningitis. Neurology 1972; 22:1071-4.
pneumoniae Meningitis Mary Lynn Y. Chu, MD*, Nathan Litman, MD+, David M. Kaufman, MD*, and Shiomo Shinnar, MD, PhD *t
Cranial nerve palsies are uncommon in nontuberculous bacterial meningitis. We report a patient with Streptococcus pneumoniae meningitis, multiple cranial nerve involvement, and cerebellar signs suggestive of basilar meningitis. Nontuberculous bacterial meningitis should be considerefl in the differential diagnosis of basilar meningitis. C h u M L Y , L i t m a n N, K a u f m a n D M , S h i n n a r S. C r a n i a l n e r v e palsies in Streptococcus pneumoniae m e n i n g i t i s . Pediatr Neurol 1990;6:209-10.
Introduction C r a n i a l n e r v e p a l s i e s are c o m m o n l y f o u n d in p a t i e n t s with chronic basilar meningitis. For example, tuberculous m e n i n g i t i s f r e q u e n t l y c a u s e s a b d u c e n s n e r v e palsy or facial diplegia. C o n v e r s e l y , n o n t u b e r c u l o u s b a c t e r i a l m e n i n gitis usually affects the c o n v e x i t i e s o f t h e b r a i n so that such p h e n o m e n a are u n c o m m o n . W e r e p o r t a p a t i e n t w i t h Streptococcus pneumoniae ( p n e u m o c o c c a l ) m e n i n g i t i s , multiple cranial nerve involvement, and cerebellar findings.
Case Report This 13-year-old black male had an upper respiratory tract infection 2 weeks before admission. He did well until 4 days prior to admission when he developed fever and a generalized throbbing headache. He was treated with cephalexin (750 mg/day in 3 divided doses), continued to be symptomatic, and on the day of consultation, he complained of neck stiffness and diplopia. On arrival at the emergency room, he had a temperature of 38.9°C. Physical examination was unremarkable except for marked nuchal rigidity.
From the Departments of *Neurology and tPediatrics; Montefiore Medical Center; Albert Einstein College of Medicine; Bronx, New York.
Neurologic examination revealed a lethargic but oriented boy who was coherent but slow in responding to questions. Fundoscopic examination demonstrated spontaneous venous pulsations and no evidence of papilledema. Pupils were equal and reactive. He had bilateral lateral rectus muscle palsies and a mild facial diparesis with inability to whistle or fully puff his cheeks. His hearing was normal. He had mild appendicular dysmetria and truncal ataxia. Motor examination demonstrated grade 5/5 strength without asymmetry or weakness. Deep tendon and plantar reflexes were normal. Sensation was intact. Cranial computed tomography (CT), including cuts of the posterior fossa and sinuses, was performed with and without contrast enhancement. No intracranial abnormalities were found. Air-fluid levels were observed in the frontal, maxillary, and sphenoid sinuses. A lumbar puncture yielded cloudy cerebrospinal fluid (CSF) under an opening pressure of less than 10 cm H20. CSF contained 1,170 leukocytes/mm3 (95% neutrophils, 5% lymphocytes), 560 erythrocytes/mm3, protein 363 mg/dl, and glucose 5 mg/dl. Gram stain revealed many Gram-positive diplococci in pairs. Stain for mycobacteria was negative. The administration of ampicillin and chloramphenicol was based on the presumptive diagnosis of Streptococcuspneumoniaemeningitis. Blood and CSF cultures subsequently grew Streptococcuspneumoniaesensitive to penicillin; the patient received a 14-day course of intravenous penicillin. The patient's dysmetria improved after 3 days. Five days after admission, extraocular muscle movement was full and he was able to whistle. Fever resolved in 1 week. Repeat sinus films revealed slight mucoendosteal thickening with loss of the previous air-fluid level in the left maxillary sinus antrum. After a 14-day course of antibiotics, he was completely asymptomatic and was discharged. Subsequently, he has been asymptomatic with no neurologic residua. Follow-up examination revealed no hearing loss.
Discussion O n l y a few reports o f n o n t u b c r c u l o u s bacterial m e n i n gitis with cranial n e r v e a b n o r m a l i t i e s h a v e b e e n p u b l i s h e d . C o o k et al. r e p o r t e d a 2 4 - y e a r - o l d p a t i e n t with Corynebacterium hemolyticum w h o p r e s e n t e d w i t h a n a b d u c e n s n e r v e palsy w h i c h they a t t r i b u t e d to an i s o l a t e d s p h e n o i d sinus i n f l a m m a t i o n [ 1 ]. F o c a l n e u r o l o g i c deficits o c c u r in as m a n y as 15% of c h i l d r e n w i t h m e n i n g i t i s [2-4] a n d are a s s o c i a t e d w i t h a d v e r s e o u t c o m e s [5]. T h e u n d e r l y i n g p a t h o l o g y is bel i e v e d to b e cortical v e n o u s or arterial t h r o m b o s i s s e c o n d a r y to e d e m a a n d i n f l a m m a t i o n [3,4]. I s o l a t e d c r a n i a l n e r v e palsies are not the usual p r e s e n t a t i o n . O u r p a t i e n t p r e s e n t e d w i t h diplopia. H e h a d b i l a t e r a l a b d u c e n s palsy, facial diparesis, a n d m i l d ataxia, all of w h i c h g r a d u a l l y i m p r o v e d with t r e a t m e n t o f Streptococcus pneumoniae m e n i n g i t i s . I n c r e a s e d i n t r a c r a n i a l p r e s s u r e m a y c a u s e bilateral a b d u c e n s palsy in a p a t i e n t with m e n ingitis [6], b u t o u r p a t i e n t h a d n o e v i d e n c e o f i n c r e a s e d i n t r a c r a n i a l pressure. T h e p r e s e n c e o f lateral rectus palsy, facial d i p a r e s i s , a n d m i l d ataxia s u g g e s t b r a i n s t e m inv o l v e m e n t p r o b a b l y d u e to b a s a l i n f i l t r a t i o n o f the m e n i n ges. A l t h o u g h it w a s fairly rapid, the clinical r e s o l u t i o n o f
Communications should be addressed to: Dr. Shinnar; Division of Pediatric Neurology; VCP-207; Montefiore Medical Center; 111 East 210th Street; Bronx, NY 1(/467. Received December 5, 1989; accepted February 14, 1990.
Chu et al: Cranial Nerve Palsies 209
symptoms was sufficiently prolonged to make edema an unlikely etiology. Other infectious causes of acute cranial nerve palsies include tuberculous meningitis which is notorious for presenting with multiple cranial nerve palsies. In 40 patients studied by L a m b a et al., 72.9% had ocular manifestations [7]. Common abnormalities included fundus lesions (62.5%), pupillary changes (48%), and cranial nerve palsies (28%). Direct infiltration at the base of the brain is more likely to involve the oculomotor nerve than any other. Abducens nerve palsy, though less common, has a higher mortality (50%) because it usually reflects increased intracranial pressure. Wyllie et al. reported 37 patients with isolated inflammatory sphenoid sinus disease at the Mayo Clinic between 1935 and 1972 [8]. The patients were divided into those with chronic sinusitis and those with mucoceles or pyoceles. Fifty-four percent of the latter group had visual disturbances, but only 1 patient bad bilateral abducens palsy. The neurologic findings in this patient cannot be explained on the basis of sinusitis, though it may well have been the source of infection. Ataxia, which has been reported as a temporary or permanent c o m p l i c a t i o n of bacterial meningitis [4,9], is believed to be due to vestibular damage, probably secondary to drug therapy. It usually is associated with deafness due to cochlear nerve involvement. When ataxia is not associated with deafness, Schwartz suggested cerebellar dysfunction as the etiology [9]. Our patient had ataxia on presentation, prior to therapy; therefore, drugs could not have been the cause. It was also clinically different from that observed in eighth nerve involvement because there was no rotatory nystagmus. The ataxia was similar to that observed with involvement of the cerebellum or the intraaxial brainstem and cerebellar connections.
210 PEDIATRIC NEUROLOGY Vol. 6 No. 3
Cranial nerve palsies are rarely observed in nonlubcr culous bacterial meningitis. Our case reporl suggests Ihal nontuberculous bacterial meningilis can present with cranial nerve palsies and ataxia, clinical signs usually ob served in chronic meningitis.
Dr. Shinnar is supported in part by a Teacher Investigator Development Award 1 K07 NS00930 from the National Institute of Neurological Disorders and Stroke.
References
[1] Cook IE Cabral DA, Reed WD, Bond RJ, Henderson A. lntracranial complications of sphenoid sinus inflammation. Med J Aust 1981;1:366. [2] Klein JO, Feigin RD, McCracken GH Jr. Report of the task force on diagnosis and management of meningitis. Pediatrics 1986,78 (Suppl):959-82. [3] Swartz MN, Dodge PR. Bacterial meningitis--A review of selected aspects. N Engl J Med 1965;272:725-30. [4] Feigin RD. Bacterial meningitis beyond the newborn period, tn: Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. Philadelphia: WB Saunders, 1981;293-304. [5] Kaplan SL, Feigin RD. Clinical presentations, prognostic factors and diagnosis of bacterial meningitis. In: Sande M, Smith AL, Root RK, eds. Bacterial meningitis. New York: Churchill Livingstone, 1985;83-4. [6] Donelly WJ. Meningitis and cranial nerve V1 palsy. Postgrad Med 1968;43:214-9. [7] Lamba PA, Bhalla JS, Mullick DN. Ocular manifestations of TB meningitis, a clinico-biochemical study. J Pediatr Ophthalmol Strabismus 1986;23:123-5. [8] Wyllie JW, Kern EB, Djalilian M. Isolated sphenoid sinus lesion. Laryngoscope 1973;83:1252-65. [9] Schwartz JF. Ataxia in bacterial meningitis. Neurology 1972; 22:1071-4.
