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A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease
Brain & Development xxx (2017) xxx–xxx www.elsevier.com/locate/braindev
Case Report
A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease Chizuko Nakamura a,b, Yuji Inaba b,c,d,⇑, Keiko Tsukahara a, Mie Mochizuki a, Emi Sawanobori a, Yozo Nakazawa b, Kouki Aoyama a a Kofu Municipal Hospital, Kofu, Japan Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Japan c Center for Perinatal, Pediatrics and Environmental Epidemiology, Shinshu University School of Medicine, Matsumoto, Japan d Division of Neurology, Nagano Children’s Hospital, Azumino, Japan b
Received 31 March 2017; received in revised form 31 August 2017; accepted 1 September 2017
Abstract Background: Cat scratch disease is a common infectious disorder caused by Bartonella henselae that is transmitted primarily by kittens. It typically exhibits a benign and self-limiting course of subacute regional lymphadenopathy and fever lasting two to eight weeks. The most severe complication of cat scratch disease is involvement of the nervous system, such as encephalitis, meningitis, and polyneuritis. Peripheral facial nerve palsy associated with Bartonella infection is rare; few reported pediatric and adult cases exist and the precise pathogenesis is unknown. Case report: A previously healthy 7-year-old boy presented with fever, cervical lymphadenopathy, and peripheral facial nerve palsy associated with serologically confirmed cat scratch disease. The stapedius muscle reflex was absent on the left side and brain magnetic resonance imaging revealed a mass lesion at the left internal auditory meatus. The patient’s symptoms and imaging findings were gradually resolved after the antibiotics and corticosteroids treatment. Conclusions: The suspected granulomatous lesion was considered to have resulted from the host’s immune reaction to Bartonella infection and impaired the facial nerve. This is the first case report providing direct evidence of peripheral facial nerve palsy caused by a suspected granulomatous lesion associated with cat scratch disease and its treatment course. Ó 2017 Published by Elsevier B.V. on behalf of The Japanese Society of Child Neurology.
Keywords: Bartonella henselae; Cat scratch disease; Facial nerve palsy; Magnetic resonance imaging; Minocycline
1. Introduction Cat scratch disease (CSD) is a human infection caused by Bartonella henselae (B. henselae), a gramnegative bacillus commonly found in feline erythrocytes and fleas. B. henselae can contaminate feline saliva and
⇑ Corresponding author at: Division of Neurology, Nagano Children’s Hospital, 3100 Toyoshina, Azumino 399-8288, Japan. E-mail address: [email protected] (Y. Inaba).
infect humans through biting or scratching [1]. As Bartonella species are difficult to culture, the serological study of specific immunoglobulin (Ig)G is generally recommended for CSD diagnosis. A positive IgM test suggests acute infection, although the production of IgM is brief in CSD [2]. CSD generally afflicts children and young adults as a benign and self-limiting course lasting two to eight weeks [1,3,4]. Regional lymphadenopathy manifests one to two weeks after infection mainly in ipsilateral
http://dx.doi.org/10.1016/j.braindev.2017.09.001 0387-7604/Ó 2017 Published by Elsevier B.V. on behalf of The Japanese Society of Child Neurology.
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
2
C. Nakamura et al. / Brain & Development xxx (2017) xxx–xxx
upper extremities, the neck, and the jaw [1,5]. While the prognosis of CSD is generally good, it may become complicated with such neurological conditions as encephalitis, meningitis, and polyneuritis [5,6]. Peripheral facial nerve palsy associated with Bartonella infection is very rare; only a few published pediatric and adult cases of CSD exist, and its precise pathogenesis is unknown [3,4,7,8]. We herein describe the clinical course of a 7-year-old boy who had fever, cervical lymphadenopathy, and peripheral facial nerve palsy associated with serologically confirmed CSD. 2. Case report An otherwise healthy 7-year-old boy presented with a remittent fever reaching 40 degrees Celsius, left cervical lymphadenopathy of 1–2 cm in size, and left facial nerve palsy. He had experienced a transient fever with subsequent erosive lesions on the left cheek one month prior that recurred with left facial nerve palsy at crying a day before admission (Fig. 1). Initial laboratory findings included white blood cell (WBC) count 8200/lL and C-reactive protein (CRP) 0.2 mg/dl. Ultrasonography (US) revealed left cervical and parotid gland lymph node swelling. He was diagnosed as having peripheral facial nerve palsy and began treatment with intravenous acyclovir and prednisolone for 5 days followed by oral prednisolone for 11 days. His fever improved transiently but soon recurred with deteriorated laboratory findings of WBC count 24,200/lL and CRP 3.8 mg/dl. Despite switching to from acyclovir to flomoxef and azithromycin, the patient’s high fever, cervical lymphadenitis, and facial palsy persisted. He was transferred to our hospital at 23 days after the onset of facial nerve palsy. On admission, history taking on the erosive abrasion on his left cheek revealed that his family had started keeping a kitten three months prior to symptom onset. Left-side palsy prevented the boy from closing his eye
PSL ACV AZM FMOX
Fever
CTRX
AMPC
MINO
Fever
Erosion Left facial nerve palsy Cervical lymphadenopathy -30
-20
-10
0
-10
20
30
40
50
Days after the onset of facial nerve palsy
Fig. 1. Clinical course. Fever and cervical lymphadenopathy improved after the administration of CTRX and MINO, followed later by facial nerve palsy resolution by PSL. ACV, acyclovir; AMPC, amoxicillin; AZM, azithromycin; CTRX, ceftriaxone sodium; FMOX, flomoxef sodium; MINO, minocycline hydrochloride; PSL, prednisolone.
and lifting the corner of the mouth and eyebrow. According to the Yanagihara grading system [9] for facial palsy, his palsy was scored 8 (ranging from the score 0, complete palsy, to 40, no palsy) Other cranial nerve functions and neurological signs were normal, and no meningeal signs were observed. Laboratory findings disclosed WBC count 9400/lL, CRP 1.8 mg/dl, and no pleocytosis in the cerebrospinal fluid. US revealed multiple swollen lymph nodes at the left neck and parotid gland. Magnetic resonance imaging (MRI) identified a mass lesion at the left internal auditory meatus (Fig. 2a; arrow). The stapedius muscle reflex as tested by an otolaryngologist was absent on the left side, which was consistent with mass lesion causing facial nerve compression at the level of the facial nerve canal. Based on his history and findings, the boy was prescribed minocycline after obtaining informed consent from his parents about a possible teething issue. He was also administered ceftriaxone since Lyme disease could not be completely ruled out. His fever, lymphadenopathy, and laboratory findings all improved within a week. Oral prednisolone and amoxicillin were continued for two weeks since his facial nerve palsy persisted and the mass lesion remained enhanced in serial MRI on day 33 (Fig. 2b–d; arrows). Afterwards, the symptoms of facial nerve palsy slowly but gradually improved and became resolved at six months after onset. Follow-up MRI on day 70 showed the disappearance of the mass lesion at the left internal auditory meatus (Fig. 2e). Immunofluorescence assays revealed that B. henselaespecific IgM had been negative but IgG was greater than 1:1024 in previously obtained serum. 3. Discussion The most common neurological manifestation of CSD is acute encephalopathy, which occurs in 2–3% of patients and is more prevalent in adults. Seizures, cerebellar ataxia, hemiparesis, myelitis, hearing loss, abductor nerve palsy, and aphasia have all been associated with encephalopathy as well [10]. Other neurological manifestations in the absence of encephalopathy are uncommon but may include neuroretinitis and peripheral neuritis [10]. Peripheral facial nerve palsy associated with Bartonella infection is very rare, with only a few reported pediatric [3,7] and adult cases [4,8]. One report described a 9-year-old boy with parotitis complicated with partial facial nerve palsy of the mandibular marginal branch coursing through the parotid gland. The cause of the palsy was suspected to be direct compression by the parotid gland [7]. Another case exhibited peripheral facial nerve palsy associated with a granulomatous lesion in the parotid gland that was detected by MRI [4]. The remaining reports suggested a pathophysiology of disseminated B. henselae or bacterial spreading [3], but the above considerations on patho-
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
C. Nakamura et al. / Brain & Development xxx (2017) xxx–xxx
a)
3
d)
b)
c)
e)
Fig. 2. MRI findings. (a) T2-weighted image on day 23 revealed a mass lesion (arrow) adjoining the left facial nerve (arrowhead). (b) The mass lesion was apparent in a constructive interference in steady state (CISS) image, which was a T2-weighted image providing a high signal for cerebrospinal fluid that was well suited for examining the details of cranial nerves, on day 33. (c) and (d) The mass lesion was clearly enhanced by gadolinium on day 33. (e) Follow-up MRI on day 70 showed complete resolution of the mass lesion at the left facial nerve. Arrows, mass lesion; arrowheads, left facial nerve; double arrowheads, left vestibulocochlear nerve.
genesis were not based on direct evidence and were largely speculative. There have been several proposed pathologies for optic neuropathies associated with CSD, including neuroretinitis, edema, and compression by granuloma [11,12]. In the present case, an enhanced mass lesion, and not the facial nerve, was clearly implicated at the left internal auditory meatus by MRI. Differential diagnoses of the mass lesion included other infections, sarcoidosis, and such tumors as schwannoma or lymphoma. However, his clinical history of keeping a kitten, fever, skin lesion, and cervical lymphadenopathy all supported the mass lesion to be granulomatous and caused by Bartonella infection. Although a similar lesion was also observed in the left parotid gland, the absent stapedius muscle reflex indicated facial nerve palsy from the level of the facial nerve canal, presumably by compression of the facial nerve. This is the first known report of Bartonella infection inducing peripheral facial nerve palsy likely caused by a granulomatous lesion as evidenced by MRI. Lastly, the therapeutic course of this case supports the suspected pathogenesis of a granulomatous lesion. Minocycline was considered to effective in reducing the patient’s fever and improving his cervical lymphadenopathy, but the facial nerve palsy and mass esion in MRI remained. The fact that the palsy and lesion resolved after corticosteroid therapy indicated that it was immunologically reactive. An earlier case report described the pathological biopsy findings of a swollen lymph node in the left parotid gland displaying a reactive component and granuloma-like areas of eosinophilic histiocytes with incipient necrosis at the center and associated acute inflammatory infiltrates [4]. Taken together, corticosteroids in addition to antibiotics may
be considered for CSD treatment if a suspected granulomatous lesion is associated with other relevant symptoms. 4. Conclusion This report described a pediatric patient with rare peripheral facial nerve palsy associated with CSD. The palsy was likely caused by a granulomatous lesion at the left internal auditory meatus as directly evidenced by neuroradiological and electrophysiological studies. The patient was successfully treated by corticosteroids and antibiotics for Bartonella infection. References [1] Klotz SA, Ivans V, Elliott SP. Cat-scratch disease. Am Fam Phys 2011;83:152–5. [2] Sander A, Posselt M, Oberle K, Bredt W. Seroprevalence of antibodies to Bartonella Henselae in patients with cat scratch disease and in healty controls: evaluation and comparison of two commercial serological tests. Clin Diagn Lab Immunol 1998;5:486–90. [3] Walter RS, Eppes SC. Cat scratch disease presenting with peripheral facial nerve paralysis. Pediatrics 1998;101:e13. [4] Ganesan K, Mizen K. Cat scratch disease: an unusual cause of facial palsy and partial ptosis: case report. J Oral Maxillofac Surg 2005;63:869–72. [5] Carithers HA. Cat-scratch disease. An overview based on a study of 1200 patients. Am J Dis Child 1985;139:1124–33. [6] Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: II cat-scratch disease. Pediatr Infect Dis J 1997;16:163–7. [7] Premachandra DJ, Milton CM. Cat scratch disease in the parotid gland presenting with facial paralysis. Br J Oral Maxillofac Surg 1990;28:413–5.
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
4
C. Nakamura et al. / Brain & Development xxx (2017) xxx–xxx
[8] Thompson PK, Vaphiades MS, Saccente M. Cat-scratch disease presenting as neuroretinitis and peripheral facial palsy. J Neuroophthalmol 1999;19:240–1. [9] Yanagihara N. Grading of facial palsy. In: Facial Nerve Sergery. Birmingham, AL: Aesculapius Publishing Co; 1977. p. 533–5. [10] Carithers HA, Margileth AM. Cat-scratch disease. Acute encephalopathy and other neurologic manifestations. Am J Dis Child 1991;145:98–101.
[11] Schmalfuss IM, Dean CW, Sistrom C, Bhatti MT. Optic neuropathy secondary to cat scratch disease: distinguishing mr imaging features from other types of optic neuropathies. Am J Neuroradiol 2005;26:1310–6. [12] Aziz HA, Plesec TP, Sabella C, Udayasankar UK, Singh AD. Cat scratch disease: expanded spectrum. Ocul Oncol Pathol 2016;2:246–50.
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
Case Report
A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease Chizuko Nakamura a,b, Yuji Inaba b,c,d,⇑, Keiko Tsukahara a, Mie Mochizuki a, Emi Sawanobori a, Yozo Nakazawa b, Kouki Aoyama a a Kofu Municipal Hospital, Kofu, Japan Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Japan c Center for Perinatal, Pediatrics and Environmental Epidemiology, Shinshu University School of Medicine, Matsumoto, Japan d Division of Neurology, Nagano Children’s Hospital, Azumino, Japan b
Received 31 March 2017; received in revised form 31 August 2017; accepted 1 September 2017
Abstract Background: Cat scratch disease is a common infectious disorder caused by Bartonella henselae that is transmitted primarily by kittens. It typically exhibits a benign and self-limiting course of subacute regional lymphadenopathy and fever lasting two to eight weeks. The most severe complication of cat scratch disease is involvement of the nervous system, such as encephalitis, meningitis, and polyneuritis. Peripheral facial nerve palsy associated with Bartonella infection is rare; few reported pediatric and adult cases exist and the precise pathogenesis is unknown. Case report: A previously healthy 7-year-old boy presented with fever, cervical lymphadenopathy, and peripheral facial nerve palsy associated with serologically confirmed cat scratch disease. The stapedius muscle reflex was absent on the left side and brain magnetic resonance imaging revealed a mass lesion at the left internal auditory meatus. The patient’s symptoms and imaging findings were gradually resolved after the antibiotics and corticosteroids treatment. Conclusions: The suspected granulomatous lesion was considered to have resulted from the host’s immune reaction to Bartonella infection and impaired the facial nerve. This is the first case report providing direct evidence of peripheral facial nerve palsy caused by a suspected granulomatous lesion associated with cat scratch disease and its treatment course. Ó 2017 Published by Elsevier B.V. on behalf of The Japanese Society of Child Neurology.
Keywords: Bartonella henselae; Cat scratch disease; Facial nerve palsy; Magnetic resonance imaging; Minocycline
1. Introduction Cat scratch disease (CSD) is a human infection caused by Bartonella henselae (B. henselae), a gramnegative bacillus commonly found in feline erythrocytes and fleas. B. henselae can contaminate feline saliva and
⇑ Corresponding author at: Division of Neurology, Nagano Children’s Hospital, 3100 Toyoshina, Azumino 399-8288, Japan. E-mail address: [email protected] (Y. Inaba).
infect humans through biting or scratching [1]. As Bartonella species are difficult to culture, the serological study of specific immunoglobulin (Ig)G is generally recommended for CSD diagnosis. A positive IgM test suggests acute infection, although the production of IgM is brief in CSD [2]. CSD generally afflicts children and young adults as a benign and self-limiting course lasting two to eight weeks [1,3,4]. Regional lymphadenopathy manifests one to two weeks after infection mainly in ipsilateral
http://dx.doi.org/10.1016/j.braindev.2017.09.001 0387-7604/Ó 2017 Published by Elsevier B.V. on behalf of The Japanese Society of Child Neurology.
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
2
C. Nakamura et al. / Brain & Development xxx (2017) xxx–xxx
upper extremities, the neck, and the jaw [1,5]. While the prognosis of CSD is generally good, it may become complicated with such neurological conditions as encephalitis, meningitis, and polyneuritis [5,6]. Peripheral facial nerve palsy associated with Bartonella infection is very rare; only a few published pediatric and adult cases of CSD exist, and its precise pathogenesis is unknown [3,4,7,8]. We herein describe the clinical course of a 7-year-old boy who had fever, cervical lymphadenopathy, and peripheral facial nerve palsy associated with serologically confirmed CSD. 2. Case report An otherwise healthy 7-year-old boy presented with a remittent fever reaching 40 degrees Celsius, left cervical lymphadenopathy of 1–2 cm in size, and left facial nerve palsy. He had experienced a transient fever with subsequent erosive lesions on the left cheek one month prior that recurred with left facial nerve palsy at crying a day before admission (Fig. 1). Initial laboratory findings included white blood cell (WBC) count 8200/lL and C-reactive protein (CRP) 0.2 mg/dl. Ultrasonography (US) revealed left cervical and parotid gland lymph node swelling. He was diagnosed as having peripheral facial nerve palsy and began treatment with intravenous acyclovir and prednisolone for 5 days followed by oral prednisolone for 11 days. His fever improved transiently but soon recurred with deteriorated laboratory findings of WBC count 24,200/lL and CRP 3.8 mg/dl. Despite switching to from acyclovir to flomoxef and azithromycin, the patient’s high fever, cervical lymphadenitis, and facial palsy persisted. He was transferred to our hospital at 23 days after the onset of facial nerve palsy. On admission, history taking on the erosive abrasion on his left cheek revealed that his family had started keeping a kitten three months prior to symptom onset. Left-side palsy prevented the boy from closing his eye
PSL ACV AZM FMOX
Fever
CTRX
AMPC
MINO
Fever
Erosion Left facial nerve palsy Cervical lymphadenopathy -30
-20
-10
0
-10
20
30
40
50
Days after the onset of facial nerve palsy
Fig. 1. Clinical course. Fever and cervical lymphadenopathy improved after the administration of CTRX and MINO, followed later by facial nerve palsy resolution by PSL. ACV, acyclovir; AMPC, amoxicillin; AZM, azithromycin; CTRX, ceftriaxone sodium; FMOX, flomoxef sodium; MINO, minocycline hydrochloride; PSL, prednisolone.
and lifting the corner of the mouth and eyebrow. According to the Yanagihara grading system [9] for facial palsy, his palsy was scored 8 (ranging from the score 0, complete palsy, to 40, no palsy) Other cranial nerve functions and neurological signs were normal, and no meningeal signs were observed. Laboratory findings disclosed WBC count 9400/lL, CRP 1.8 mg/dl, and no pleocytosis in the cerebrospinal fluid. US revealed multiple swollen lymph nodes at the left neck and parotid gland. Magnetic resonance imaging (MRI) identified a mass lesion at the left internal auditory meatus (Fig. 2a; arrow). The stapedius muscle reflex as tested by an otolaryngologist was absent on the left side, which was consistent with mass lesion causing facial nerve compression at the level of the facial nerve canal. Based on his history and findings, the boy was prescribed minocycline after obtaining informed consent from his parents about a possible teething issue. He was also administered ceftriaxone since Lyme disease could not be completely ruled out. His fever, lymphadenopathy, and laboratory findings all improved within a week. Oral prednisolone and amoxicillin were continued for two weeks since his facial nerve palsy persisted and the mass lesion remained enhanced in serial MRI on day 33 (Fig. 2b–d; arrows). Afterwards, the symptoms of facial nerve palsy slowly but gradually improved and became resolved at six months after onset. Follow-up MRI on day 70 showed the disappearance of the mass lesion at the left internal auditory meatus (Fig. 2e). Immunofluorescence assays revealed that B. henselaespecific IgM had been negative but IgG was greater than 1:1024 in previously obtained serum. 3. Discussion The most common neurological manifestation of CSD is acute encephalopathy, which occurs in 2–3% of patients and is more prevalent in adults. Seizures, cerebellar ataxia, hemiparesis, myelitis, hearing loss, abductor nerve palsy, and aphasia have all been associated with encephalopathy as well [10]. Other neurological manifestations in the absence of encephalopathy are uncommon but may include neuroretinitis and peripheral neuritis [10]. Peripheral facial nerve palsy associated with Bartonella infection is very rare, with only a few reported pediatric [3,7] and adult cases [4,8]. One report described a 9-year-old boy with parotitis complicated with partial facial nerve palsy of the mandibular marginal branch coursing through the parotid gland. The cause of the palsy was suspected to be direct compression by the parotid gland [7]. Another case exhibited peripheral facial nerve palsy associated with a granulomatous lesion in the parotid gland that was detected by MRI [4]. The remaining reports suggested a pathophysiology of disseminated B. henselae or bacterial spreading [3], but the above considerations on patho-
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
C. Nakamura et al. / Brain & Development xxx (2017) xxx–xxx
a)
3
d)
b)
c)
e)
Fig. 2. MRI findings. (a) T2-weighted image on day 23 revealed a mass lesion (arrow) adjoining the left facial nerve (arrowhead). (b) The mass lesion was apparent in a constructive interference in steady state (CISS) image, which was a T2-weighted image providing a high signal for cerebrospinal fluid that was well suited for examining the details of cranial nerves, on day 33. (c) and (d) The mass lesion was clearly enhanced by gadolinium on day 33. (e) Follow-up MRI on day 70 showed complete resolution of the mass lesion at the left facial nerve. Arrows, mass lesion; arrowheads, left facial nerve; double arrowheads, left vestibulocochlear nerve.
genesis were not based on direct evidence and were largely speculative. There have been several proposed pathologies for optic neuropathies associated with CSD, including neuroretinitis, edema, and compression by granuloma [11,12]. In the present case, an enhanced mass lesion, and not the facial nerve, was clearly implicated at the left internal auditory meatus by MRI. Differential diagnoses of the mass lesion included other infections, sarcoidosis, and such tumors as schwannoma or lymphoma. However, his clinical history of keeping a kitten, fever, skin lesion, and cervical lymphadenopathy all supported the mass lesion to be granulomatous and caused by Bartonella infection. Although a similar lesion was also observed in the left parotid gland, the absent stapedius muscle reflex indicated facial nerve palsy from the level of the facial nerve canal, presumably by compression of the facial nerve. This is the first known report of Bartonella infection inducing peripheral facial nerve palsy likely caused by a granulomatous lesion as evidenced by MRI. Lastly, the therapeutic course of this case supports the suspected pathogenesis of a granulomatous lesion. Minocycline was considered to effective in reducing the patient’s fever and improving his cervical lymphadenopathy, but the facial nerve palsy and mass esion in MRI remained. The fact that the palsy and lesion resolved after corticosteroid therapy indicated that it was immunologically reactive. An earlier case report described the pathological biopsy findings of a swollen lymph node in the left parotid gland displaying a reactive component and granuloma-like areas of eosinophilic histiocytes with incipient necrosis at the center and associated acute inflammatory infiltrates [4]. Taken together, corticosteroids in addition to antibiotics may
be considered for CSD treatment if a suspected granulomatous lesion is associated with other relevant symptoms. 4. Conclusion This report described a pediatric patient with rare peripheral facial nerve palsy associated with CSD. The palsy was likely caused by a granulomatous lesion at the left internal auditory meatus as directly evidenced by neuroradiological and electrophysiological studies. The patient was successfully treated by corticosteroids and antibiotics for Bartonella infection. References [1] Klotz SA, Ivans V, Elliott SP. Cat-scratch disease. Am Fam Phys 2011;83:152–5. [2] Sander A, Posselt M, Oberle K, Bredt W. Seroprevalence of antibodies to Bartonella Henselae in patients with cat scratch disease and in healty controls: evaluation and comparison of two commercial serological tests. Clin Diagn Lab Immunol 1998;5:486–90. [3] Walter RS, Eppes SC. Cat scratch disease presenting with peripheral facial nerve paralysis. Pediatrics 1998;101:e13. [4] Ganesan K, Mizen K. Cat scratch disease: an unusual cause of facial palsy and partial ptosis: case report. J Oral Maxillofac Surg 2005;63:869–72. [5] Carithers HA. Cat-scratch disease. An overview based on a study of 1200 patients. Am J Dis Child 1985;139:1124–33. [6] Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: II cat-scratch disease. Pediatr Infect Dis J 1997;16:163–7. [7] Premachandra DJ, Milton CM. Cat scratch disease in the parotid gland presenting with facial paralysis. Br J Oral Maxillofac Surg 1990;28:413–5.
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001
4
C. Nakamura et al. / Brain & Development xxx (2017) xxx–xxx
[8] Thompson PK, Vaphiades MS, Saccente M. Cat-scratch disease presenting as neuroretinitis and peripheral facial palsy. J Neuroophthalmol 1999;19:240–1. [9] Yanagihara N. Grading of facial palsy. In: Facial Nerve Sergery. Birmingham, AL: Aesculapius Publishing Co; 1977. p. 533–5. [10] Carithers HA, Margileth AM. Cat-scratch disease. Acute encephalopathy and other neurologic manifestations. Am J Dis Child 1991;145:98–101.
[11] Schmalfuss IM, Dean CW, Sistrom C, Bhatti MT. Optic neuropathy secondary to cat scratch disease: distinguishing mr imaging features from other types of optic neuropathies. Am J Neuroradiol 2005;26:1310–6. [12] Aziz HA, Plesec TP, Sabella C, Udayasankar UK, Singh AD. Cat scratch disease: expanded spectrum. Ocul Oncol Pathol 2016;2:246–50.
Please cite this article in press as: Nakamura C et al. A pediatric case with peripheral facial nerve palsy caused by a granulomatous lesion associated with cat scratch disease. Brain Dev (2017), http://dx.doi.org/10.1016/j.braindev.2017.09.001