Bell’s palsy mimicker in Infant: Tuberculoma presenting as peripheral facial nerve palsy

INTRODUCTION

Bell’s palsy is defined as, an acute, idiopathic, unilateral, lower motor neuron paralysis of the facial nerve (cranial nerve VII), resulting in sudden weakness or paralysis of the muscles on one side of the face.^[1] Although in a few cases, it may be bilateral. Many neurological disorders can present as an acute-onset peripheral facial nerve palsy. Facial nerve palsy can be upper motor neuron (UMN)/central as well. Differentiating between UMN and lower motor neuron (LMN) facial palsy, looking for neighborhood signs and localization of lesion along the nerve are important aspects for etiological differential diagnosis of facial nerve palsy. We are presenting a case of disseminated tuberculosis (TB) mimicking Bell’s palsy to emphasize the importance of early diagnosis and prompt initiation of etiology-specific intervention to improve the outcome in such cases.

CASE REPORT

A 3½-month-old male baby from a lower socioeconomic family developed an acute onset of deviation of the mouth towards the left side and inability to close the right eye. A diagnosis of Bell’s palsy was considered at an outside health facility. At 5 months of age, the child was brought to our tertiary care center with persistence of facial deviation and cough from 7 days. There was no history of fever, seizures, abnormal movements, limb weakness, and jerky eye movements. The baby was looking well with normal sensorium but tachypneic (respiratory rate: 54/min). Neurological examination showed right LMN facial palsy (Grade 4 on House–Brackmann scale) with normal lacrimation and subtle right sixth nerve palsy. Other CNS examination was non-contributory. General examination revealed hepatomegaly and mild pallor. The ear examination was normal.

Laboratory reported high C-reactive protein (25.21mg/L), total leukocyte count 17410, and raised erythrocyte sedimentation rate (42 mm/h). The baby was anemic (hemoglobin 9.1 g/dL, mean corpuscular volume 57.4 fL, and mean corpuscular hemoglobin 16.9 pg). Mantoux test was positive (15 mm). Cerebrospinal fluid (CSF) routine and microscopy showed lymphocytic pleocytosis (cells 25, lymphocytic predominant, high protein (110 mg/dL), and normal glucose (60 mg/dL against blood glucose of 76 mg/dL). CSF and gastric aspirate CBNAAT for TB were negative. Magnetic resonance imaging (MRI) of the brain, T1 contrast sequence revealed multiple rings enhancing lesions in brainstem, cerebellum, and supratentorial region, and one large lesion was seen in the dorsal pons. These lesions were hypointense on T2 sequence. Chest X-ray was suggestive of miliary TB [Figure 1a-d]. Diagnosis of probable CNS TB without microbial confirmation was considered, strongly supported by positive Mantoux test, miliary pattern on chest X-ray, classical MRI brain findings, and CSF findings.

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Figure 1:

(a) Loss of forehead wrinkling (star), wide palpebral fissure (thin arrow), and loss of nasolabial fold (thick arrow) suggesting right lower motor neuron facial weakness, (b) chest X ray showing miliary tuberculosis (thin arrow), (c) Magnetic resonance imaging brain T2 sequence showing hypointense lesion in the right dorsal pons (thick arrow), and multiple similar lesions in cerebellum (thin arrows), (d) T1 contrast image showing ring enhancement of lesions (thick arrow).

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The patient was treated with ATT (HRZE) and dexamethasone along with pyridoxine and supportive care. On follow-up, after 2 months, child’s facial weakness improved. Dexamethasone was given for 4 weeks, followed by tapering over the next 4 weeks.

DISCUSSION

Facial nerve palsy is the most commonly encountered cranial neuropathy, yet it encompasses a wide spectrum of possible etiologies. Bell’s palsy, or idiopathic acute peripheral facial nerve palsy, is the most common cause in both children and adults (accounting for 65–80% of pediatric cases).^[2] Bell’s palsy is characterized by an acute onset, usually unilateral LMN facial weakness without other neurological signs, and it remains a diagnosis of exclusion.

The pathophysiology of Bell’s palsy is presumed to be active or reactivated herpes simplex virus (HSV) type 1 or varicella–zoster virus (VZV), leading to inflammatory edema of the nerve within the narrow facial canal.^[1,2] However, a range of secondary causes, such as infectious, inflammatory, vascular, neoplastic, and traumatic, must be excluded by careful clinical history and examination.

Infectious causes of facial palsy are viral (HSV, VZV, Cytomegalovirus, Epstein–Barr Virus, etc.), and bacterial infections (acute otitis media, mastoiditis, Lyme disease, TB, etc.). Tuberculous lymphadenitis in neonates and infants has been described as a rare but important cause of LMN palsy, especially in endemic areas.^[3] Multiple sclerosis, Guillain– Barré syndrome (GBS) and sarcoidosis, can involve the facial fascicle or nucleus in the pons, sometimes with abducens palsy, usually in older children.^[4] Neoplastic etiologies such as cerebellopontine angle (CPA) tumors and brainstem gliomas may present as isolated facial weakness at disease onset. Other causes are trauma (temporal bone fracture, birth injury or during surgery), brainstem stroke (Millard– Gubler syndrome-ipsilateral 6^th and 7^th Nerve palsy with contralateral hemiparesis), Melkersson–Rosenthal syndrome (recurrent facial nerve palsy, orofacial swelling, and a fissured tongue), and Moebius syndrome (congenital hypoplasia of facial and abducens nerve nuclei).^[2,5]

We used a four-step approach for localization in cases of facial nerve palsy. Step one is to classify facial palsy as LMN versus UMN. Equal involvement of all three segments, for example, frontalis, orbicularis oculi, and lower face muscles (nasolabial fold), indicates LMN palsy (nuclear or infranuclear lesion) while a gradient in weakness with sparing of the forehead indicates UMN palsy (supra nuclear lesion). In our case, all three segments were equally involved.

Step two is to look for neighborhood signs. Pontine lesions will lead to abducens nerve palsy, hemiparesis, or both. Ipsilateral LMN facial and abducens palsy with contralateral hemiparesis suggests Millard–Gubler syndrome indicate ventral pontine stroke. Congenital bilateral LMN facial with abducens palsy indicates Mobius syndrome, while isolated facial palsy with or without 6^th nerve palsy indicates dorsal pontine involvement. Ipsilateral LMN facial palsy and VIII nerve involvement (hearing loss, imbalance) suggest a CPA tumor. Our patient had associated abducens nerve involvement without pyramidal weakness.

Step three is the localization of the lesion along the nerve. Normal lacrimation, salivation and taste with hyperacusis (lowered tolerance or increased sensitivity to everyday environmental sounds) indicate a nuclear lesion, while loss of lacrimation with hyperacusis indicates a lesion distal to the nucleus but proximal to the nerve to stapedius. Preserved lacrimation without hyperacusis indicates a lesion distal to the nerve to stapedius. Ear examination is compulsory in all LMN facial nerve palsy. Our case had normal lacrimation. Right LMN facial palsy with ipsilateral 6^th nerve palsy with normal power and lacrimation, suggestive of dorsal pontine lesions.

Step four is identifying the etiology for LMN facial palsy. Congenital facial palsy should be ruled out by a proper history of neonatal onset. Bilateral LMN facial palsy is seen in Lyme disease, GBS, and sarcoidosis. Clinical clues for specific etiology are the presence of ear discharge (otitis media), vesicular lesions of the auricle or oral epithelium (Ramsey–Hunt syndrome), erythema chronicum migrans (Lyme disease), evidence of trauma to the face, temporal area, or skull, or other cranial nerve involvement (malignancy, sarcoidosis, GBS).^[6]

Neuroimaging is required for progressive facial weakness, persistent facial weakness (no improvement over 2 months), recurrent facial palsy, UMN facial palsy, and in atypical cases. MRI brain with contrast with facial nerve cuts, including the brain stem, CPA, and facial canal, are indispensable to rule out inflammation, demyelination, tumors or granulomatous lesions of the brainstem and facial nerve.^[6-8] CSF studies may be helpful for basal meningitis or GBS. Serological tests for HSV, VZV, EBV, Lyme disease, and HIV are guided by clinical context. Histopathology or fine-needle aspiration cytology may be diagnostic in cases with associated cervical lymphadenopathy, as in tuberculous lymphadenitis.^[3]

CONCLUSION

Symptomatic facial palsy should be excluded in infants presenting as LMN facial palsy by thorough history, clinical examination, and investigations. The four-step approach can help in localization and differential diagnosis. MRI brain with contrast with facial nerve cuts should be considered to rule out demyelination, tuberculoma, glioma, or other focal pathologies in atypical, persistent, progressive, and recurrent facial palsy. Early diagnosis and prompt initiation of etiology-specific intervention improve the outcome. Written informed consent was obtained from the parents/legal guardians for publication of the case details and the clinical photograph.