{
 "topic": "Facial Nerve Palsy",
 "slug": "facial-nerve-palsy",
 "category_id": 15863,
 "passage_count": 14,
 "source_chars": 12472,
 "enough_material": true,
 "references": [
  {
   "title": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024",
   "author": null,
   "pages": [
    3591,
    3946
   ]
  },
  {
   "title": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "author": null,
   "pages": []
  },
  {
   "title": "Cover",
   "author": "Vitalsource Download",
   "pages": [
    8586,
    8587
   ]
  },
  {
   "title": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition",
   "author": "Hay, William W., Levin, Myron J., Deterding, Robin R., Abzug, Mark J.",
   "pages": [
    62,
    853
   ]
  },
  {
   "title": "MedStudy Pediatrics Core 11th Edition 2024-2025",
   "author": null,
   "pages": [
    453
   ]
  },
  {
   "title": "Gomella's Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs, Eighth Edition",
   "author": "Tricia Lacy Gomella, Fabien G. Eyal and Fayez Bany-Mohammed",
   "pages": [
    106
   ]
  },
  {
   "title": "Zitelli and Davis' Atlas of Pediatric Physical Diagnosis: Expert Consult - Online",
   "author": null,
   "pages": [
    80
   ]
  },
  {
   "title": "Ghai Essential Pediatrics, 9e (Vinod K Paul, Arvind Bagga)",
   "author": "CamScanner",
   "pages": [
    571
   ]
  }
 ],
 "passages": [
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 3591",
   "text": "movements (e.g., smiling, raising the eyebrows, inflating the cheeks). A facial nerve palsy may be congenital; idiopathic **(Bell palsy)** ; or secondary to trauma, demyelination (Guillain- Barr\u00e9 syndrome), infection (Lyme disease, herpes simplex virus, HIV), granulomatous disease, neoplasm, or meningeal inflammation or infiltration. Facial nerve lesions that are proximal to the junction with the chorda tympani will result in an inability to taste substances with the anterior two thirds of the tongue. If necessary, taste can be tested by placing a solution of saline or glucose on one side of the extended tongue. Normal children can identify the test substance in <10 seconds. Other findings that may be associated with facial nerve palsy include hyperacusis, resulting from stapedius muscle involvement, and impaired tearing."
  },
  {
   "source": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "text": "Weakness in the distribution of cranial nerve VII (facial) may be produced by either central (upper motor neuron) or peripheral (lower motor neuron) dysfunction. Peripheral disease is most common in children, particularly when the facial weakness is an isolated finding. Bell palsy refers to peripheral facial nerve weakness with no identifiable underlying cause. It is believed to be caused by edema of the facial nerve as it passes through the facial canal within the temporal bone. There is often a history or preceding upper respiratory tract infection, and in at least a subset of patients, there is evidence of reactivation of infection with Epstein\u2013Barr virus or HSV. Seventh nerve palsy may occur in association with otitis media, in which case it may indicate the presence of mastoid involvement. Facial palsy may also be a manifestation of early-disseminated Lyme disease. In general most cases of facial nerve palsy in children are of the idiopathic (or viral reactivation) type; however, in endemic areas, Lyme"
  },
  {
   "source": "Cover, p. 8586",
   "text": "## **FACIAL NEUROPATHIES** _Facial palsies_ are among the most common mononeuropathies seen in children and may be classified into congenital or acquired categories. _Congenital facial palsies_ range from 1.8 to 7.5 per 1000 births and can be due to prenatal or obstetric compression of the facial nerve, a congenital neuromuscular disorder such as congenital muscular dystrophy, or a congenital myopathy or a malformation syndrome such as Mobius syndrome or CHARGE syndrome. _Acquired facial neuropathies_ are much more common (90% of facial palsies in children) and include idiopathic Bell palsy, which is a diagnosis of exclusion, Ramsay Hunt syndrome, Lyme disease, otogenic facial palsy, and traumatic or"
  },
  {
   "source": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition, p. 62",
   "text": "Facial nerve palsy is sometimes associated with forceps use but more often results from in utero pressure of the baby\u2019s head against the mother\u2019s sacrum. The infant has asymmetrical mouth movements and eye closure with poor facial movement on the affected side. Most cases resolve spontaneously in a few days to weeks. Subgaleal hemorrhage into the large potential space under the scalp (Figure 2\u20134) is associated with difficult vaginal deliveries and repeated attempts at vacuum extraction. It can lead to hypovolemic shock and death from blood loss and coagulopathy triggered by consumption of clotting factors. This is an emergency requiring rapid replacement of blood and clotting factors. ## **INFANTS OF MOTHERS WHO ABUSE DRUGS**"
  },
  {
   "source": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "text": "Facial Nerve Palsy Neonatal facial nerve palsy arises either from a traumatic birth injury or from hereditary agenesis of the facial nerve nucleus (Moebius syndrome). Traumatic peripheral nerve injury takes place when the facial nerve is compressed as it exits the stylomastoid foramen or branches within the ramus of the mandible. Compression of the facial nerve may occur during pregnancy or during delivery and may occur as a result of oblique midforceps application, or pressure on the face by extreme prolonged pressure by the sacrum, other fetal parts or uterine fibroid tumors. Peripheral injury is unilateral and may be associated with brachial nerve palsy. Traumatic central nerve injury results from destruction of contralateral brain tissue within the posterior fossa or the temporal bone. Traumatic central injury is rare and can affect other cranial nerves."
  },
  {
   "source": "Cover, p. 8587",
   "text": "_Bell idiopathic facial palsy_ accounts for up to 50% of acquired facial neuropathies in children. An antecedent upper airway infection occurs in approximately one-third of children. It is followed by ear or periauricular pain followed by a fairly rapid progression of facial weakness over hours or days. The weakness involves the muscles that are innervated by the facial nerve, which include the frontalis, orbicularis oculi, nasalis, and orbicularis oris. Bell palsy can occur in children of any age but is most frequently seen after age 8 years. Treatment with steroids and acyclovir has not been shown to improve recovery in children, and care is largely symptomatic. It is important to protect the exposed cornea with lubrication and an eye patch. Complete spontaneous recovery is seen in as many as 90% of children, with a younger patient having a more favorable prognosis. Between 7% and 15% of patients with Bell palsy may have recurrent symptoms, which should prompt a workup to rule out an intracranial or"
  },
  {
   "source": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition, p. 853",
   "text": "Acquired peripheral facial weakness (Bell palsy) is common in children. Some cases are postinfectious, although an increasing body of evidence suggests that Bell palsy is a viralinduced cranial neuritis. It may be a presenting sign of Lyme disease, infectious mononucleosis, herpes simplex, or GBS and is usually diagnosable by the history, physical examination, and appropriate laboratory tests. Chronic cranial nerve VII palsy may be a sign of brainstem tumor. Bilateral facial weakness in early life may be due to agenesis of the facial nerve nuclei or muscles (part of M\u00f6bius syndrome) or may even be familial. Myasthenia gravis, Miller-Fisher syndrome, fascioscapulohumeral muscular dystrophy, and myotonic dystrophy must be considered."
  },
  {
   "source": "MedStudy Pediatrics Core 11th Edition 2024-2025, p. 453",
   "text": "exiting from the pons, accounts for approximately half of the cases of facial nerve palsy. The pathogenesis of Bell's palsy is believed to be viral but may also be postinfectious immune-mediated demyelination. HSV is the likely cause in most cases, followed by herpes zoster. Other causes include Lyme disease, trauma, and neoplasms. Congenital facial nerve palsy can be due to trauma to the peripheral (extracranial) facial nerve or due to cranial nerve nucleus abnormalities, often referred to as M\u00e9bius syndrome. It is caused by hypoplasia or agenesis of the facial nucleus and/or nerve and is accompanied by CN 6 (abducens) abnormalities causing ocular abduction impairment. Other cranial nerves can also be involved. 12-19 ##"
  },
  {
   "source": "Gomella's Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs, Eighth Edition, p. 106",
   "text": "**1. Trauma.** The most common cause is birth trauma. Risk factors include an injury from forceps, a large baby, and primiparity. On physical examination, there is facial asymmetry with crying, the corner of the mouth droops, there is drooling on the side of the paresis, the nasolabial fold is absent in the paralyzed side, and there is partial closing of the eye (ptosis). Most symptoms disappear within the first week of life, but sometimes it may take several months. If the palsy persists, absence of the nerve should be ruled out. **2. Agenesis of the facial nerve nucleus** (Moebius syndrome) is a rare congenital neurologic disorder that is due to the underdevelopment of cranial nerves VI (lateral eye movement) and VII (facial expression). Infants have facial paralysis, are unable to move their eyes from side to side, and have difficulty swallowing."
  },
  {
   "source": "CURRENT Diagnosis and Treatment Pediatrics, Twenty-Fourth Edition, p. 853",
   "text": "In the few children with permanent and cosmetically disfiguring facial weakness, plastic surgical intervention at age 6 years or older may be of benefit. New procedures, such as attachment of facial muscles to the temporal muscle and transplantation of cranial nerve XI, are being developed. Gronseth GS, Paduga R; American Academy of Neurology: Evidence-based guideline update: steroids and antivirals for Bell palsy: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology 2012;79(22):2209\u20132213 [PMID: 23136264]. Kennedy PG: Herpes simplex virus type 1 and Bell\u2019s palsy-a current assessment of the controversy. J Neuroviol 2010;16(1):1\u20135 [PMID: 20113184]. Pavlou E et al: Facial nerve palsy in childhood. Brain Dev 2011;33(8):644\u2013650 [PMID: 21144684]. Rioja-Mazza et al: Asymmetric crying facies. J Matern Fetal Neonatal Med 2005;18(4):275\u2013277 [PMID: 16318980]. ## **CHRONIC POLYNEUROPATHY** ## ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES"
  },
  {
   "source": "Zitelli and Davis' Atlas of Pediatric Physical Diagnosis: Expert Consult - Online, p. 80",
   "text": "![](/tmp/pdf-images/pdf-0080-06.png) **Figure 2-39** Facial nerve palsy. This infant incurred injury to the right facial nerve, resulting in loss of the nasolabial fold on the affected side and asymmetrical movement of the mouth. The side of the mouth that appears to droop is the normal side. normal side. The differential diagnosis includes M\u00f6bius syndrome (usually bilateral) and absence of the depressor anguli oris muscle, which may be associated with cardiac anomalies. The latter condition is distinguishable from facial nerve palsy by the absence of involvement of the forehead, eyelid, or nasolabial area. The prognosis for facial nerve palsies is excellent, and recovery usually occurs within the first month. In the meantime, prevention of corneal drying is essential. Surgery is reserved for cases in which clear-cut severing of the facial nerve has occurred. Referral should be made if there is no improvement after 2 to 3 months."
  },
  {
   "source": "Ghai Essential Pediatrics, 9e (Vinod K Paul, Arvind Bagga), p. 571",
   "text": "Birth trauma; intracranial hemorrhage Hyperbilirubinemia; hypoglycemia Central nervous system (CNS) infection Postnatal CNS infection Hypoxia Trauma; toxins affecting 2-3 infants per 1000 live births. While perinatal asphyxia was considered the most common cause, it accounts for less than 10% of cases. Various causes are listed in Table 19.6. Clinical Features The most common presentation is with developmental delay. Physical findings are persistence of neonatal reflexes, increased tone, fisting with cortical thumb, scissoring of legs, toe-walking, abnormal posture and gait, abnormal movements and/or hyperreflexia. Common comorbidities include intellectual disabili ty, microcephaly, seizures, behavioral problems, difficulty in speech, language, swallowing or feeding, blindness, deafness, squint, malnutrition, sleep disturbances and excessive drooling. Contractures may develop that are inibally dynamic and later fixed. Classification Cerebral palsy is classified topographically as"
  },
  {
   "source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 3946",
   "text": "Bell palsy is an _acute- onset_ peripheral facial nerve palsy that is not associated with any other cranial nerve neuropathies or brainstem dysfunction. It is a common disorder at all ages from infancy through adolescence, usually developing suddenly about 2 weeks after a presumed viral infection. Numerous viruses have been linked with Bell palsy (Table 657.1). Active or reactivation of herpes simplex or varicella- zoster virus are the most common causes of Bell palsy (Fig. 657.1). In **Ramsay Hunt syndrome** (herpes zoster oticus), an acute facial nerve palsy is associated with painful vesicles in the external auditory canal or auricle. Hereditary forms of Bell palsy are rare. Bell palsy rarely occurs in the context of systemic hypertension or type 1 diabetes mellitus. _Unilateral or bilateral facial nerve palsy is often a sign of Lyme disease._ In addition, Lyme- associated facial palsy is often preceded by fever, malaise, headache, myalgias or arthralgias, all symptoms uncommon in idiopathic Bell palsy."
  },
  {
   "source": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub",
   "text": "In children with facial nerve palsy caused by Lyme disease, there may be bilateral involvement in contrast to Bell palsy, in which weakness is always unilateral. Additionally, facial nerve palsy can be the sole presenting symptom of Lyme disease. Thus, even in the absence of other findings, serologic evidence for systemic Lyme infection should be sought in all children with isolated cranial nerve VII paresis in endemic areas. The sensitivity of serologic testing increases with time after infection, so repeat titers are indicated in circumstances where suspicion is high but initial titers are negative. An LP should be performed if there is evidence of meningoencephalitis such as severe headache or nuchal rigidity; however, the need for LP in a child at risk for Lyme disease with isolated facial nerve palsy is controversial. For patients with facial nerve palsy due to Lyme disease, oral antibiotic treatment for 14 to 21 days is indicated as for other manifestations of early-disseminated Lyme disease (see"
  }
 ]
}