Bell's palsy

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

The first comprehensive description of Bell’s palsy was first discovered by Abū Bakr Muhammad ibn Zakariyyā al-Rāzī, a Persian polymath, physician, alchemist, philosopher, in 9th century, although Sir Charles Bell, a Scottish surgeon, was the first to provide the anatomic basis for the condition that bears his name in 1821. For the first time, Razi provided accurate descriptions of facial muscles disorders. Razi describes a clinical method for distinguishing spasm and paralysis for the first time. In 9th century, the therapy of Bell’s palsy was developed by Abū Bakr Muhammad ibn Zakariyyā al-Rāzī. In 1821, Sir Charles Bell described the lesions of the seventh cranial nerve produce facial paralysis. Bell described the Bell’s palsy is caused by problem of 7th cranial nerve(facial nerve).

Bell’s palsy may be classified into five categories according to laterality and recurrence and alternating of the palsy include: unilateral nonrecurrent, unilateral recurrent, simultaneous bilateral, alternating bilateral and recurrent bilateral type.

The exact pathophysiology of Bell’s palsy is not known. Bell’s palsy occurs due to failure to function in a normal manner of the facial nerve (VII cranial nerve). The malfunction of the facial nerve caused involuntary spasm in the facial muscles which called facial palsy. Bell’s palsy causes the lower motor neuron type paralysis. Although the exact etiology of Bell’s palsy is unknown, there is some evidences that implies there may be some relation between vasospasm, from any cause, along any facial nerve branch, with Bell’s palsy. There is no established association between genetic factors and Bell’s palsy. Hereditary components may play a role in familial recurrent Bell’s palsy. On microscopic histopathological analysis, thickened perineurium, infiltrates of inflammatory cells between nerve bundles and around blood vessels are characteristic findings of Bell’s palsy. It appears that the histology of the facial nerve in Bell’s palsy is similar to Herpes Zoster infection, suggestive of an infectious cause.

The exact cause of Bell’s palsy is unknown but there are some evidences which implies Bell’s palsy may be caused by: herpes simplex virus reactivation, herpes Zoster, cytomegalovirus, epstein Barr virus, rubella virus, mumps, influenza B, coxsackievirus, Rickettsial infection, borrelia burgdorferi, acute HIV infection, ischemic mononeuropathy, diabetes mellitus, thyroid disorders and compression of the facial nerve.

Bell’s palsy must be differentiated from other diseases that cause weakness or total paralysis on one side of the face, difficulty making facial expressions in one side, impaired facial nerve reflexes, salivation and unintended eye closure, such as Ramsay-Hunt Syndrome, Lyme Disease, stroke, Skull fracture, head or neck tumor, and Multiple sclerosis.

The incidence of Bell’s palsy is approximately 30 per 100,000 individuals. The lifetime prevalence of Bell’s palsy was 642.8 cases per 100,000 population age 15 years and above in one study. The incidence of Bell’s palsy increases with age. There is no racial predilection to Bell’s palsy. Bell’s palsy affects men and women equally. The ratio of male to female patients was 48:52 in one study. There is no geographic difference in incidence of Bell’s palsy.

The most potent risk factor in the development of Bell’s palsy is diabetes mellitus. Other risk factors include lyme disease, arterial hypertension, autoimmune inflammatory disorders, viral infections and lipid disturbances.

There is insufficient evidence to recommend routine screening for Bell’s palsy.

The onset of Bell’s palsy is sudden and symptoms typically peak fast, within a few days. The main symptom is acute peripheral facial weakness. The hallmark of Bell’s palsy is unilateral, acute paresis or paralysis of facial movement. A positive history of viral infections, Ischemic mononeuropathy,Diabetes mellitus and Thyroid disorders is suggestive of Bell’s palsy. Patients with Bell’s palsy may also have a positive history of: Herpes simplex virus reactivation, Herpes Zoster, cytomegalovirus, Epstein Barr virus, rubella virus, mumps, influenza B, coxsackie virus, rickettsial infection, borrelia burgdorferi, acute HIV infection, ischemic mononeuropathy, diabetes mellitus and thyroid disorders. Complications of Bell’s palsy include: incomplete eyelid closure with resultant dry eye, permanent facial weakness with muscle contractures, motor synkinesis , crocodile tears (tears when eating due to misdirection of regenerating gustatory fibres destined for the salivary glands, so that they become secretory fibres to the lacrimal gland and cause ipsilateral tearing while the patient is eating), contracture of facial muscles, reduction or loss of taste sensation and problems with dysarthria due to facial muscle weakness. Prognosis of Bell’s palsy is generally good. If left untreated approximately 71% of patients with Bell’s palsy recover normal function and around 13% are left with slight weakness and around 4% with severe weakness resulting in major facial dysfunction. The presence of complete palsy, advanced age and Herpes zoster infection is associated with a particularly poor prognosis among patients with Bell’s palsy. The Bell’s palsy recurs in 7% of patients. The House-Brackmann grading system was devised both as a clinical indicator of severity and also an objective record of progress.

There is no single diagnostic study of choice for the diagnosis of Bell’s palsy. Bell’s palsy is a diagnosis of exclusion of other causes of facial nerve palsy. The Magnetic resonance imaging (MRI) or computerized tomography (CT) may be performed to rule out other possible causes of facial nerve palsy. Laboratory studies are not routinely needed in the diagnosis of Bell’s palsy and are only recommended in patients with recurrence or absence improvement after more than 3 weeks of therapy. Blood studies for an underlying systemic disease or infection may also be considered in patients with Bell’s palsy. There is no test that provides prognostic information early enough to be used for guiding treatment or prognosis.

Common symptoms of Bell’s palsy include: rapid onset of mild weakness to total paralysis on one side of the face within hours to days, difficulty making facial expressions in one side, such as closing eye, smiling, whistling and frowning, salivation, facial droop, pain around the jaw or ear and numbness in the skin of affected side. Less common symptoms of Bell’s palsy include: Altered taste, changes in the amount of tears and saliva and ear problems (increased sensitivity to sound on the affected side, dizziness).

Patients with Bell’s palsy usually appear normal. Physical examination of patients with Bell’s palsy is usually remarkable for: unintended eye closure with an effort to smile, incomplete closure and the of the eye when patient attempts to close the eyes, inability to puff the cheek in affected side and impaired or absent taste in affected side, reduced hearing acuity, tenderness upon palpation of the ear, facial tenderness in distribution of facial nerve and asymmetric smile. Facial nerve reflexes may be impaired, including: impaired orbicularis oculi and impaired corneal reflex.

Laboratory studies are not routinely needed in the diagnosis of Bell’s palsy and are only recommended in patients with recurrence or absence improvement after more than 3 weeks of therapy. Blood studies for an underlying systemic disease or infection may also be considered in patients with Bell’s palsy. There is no test that provides prognostic information early enough to be used for guiding treatment or prognosis.

There are no ECG findings associated with Bell’s palsy.

There are no x-ray findings associated with Bell’s palsy. However, an x-ray may be helpful in the diagnosis of other causes of facial nerve palsy.

There are no echocardiography findings associated with Bell’s palsy. Ultrasound of the facial nerve may be used to predict functional outcomes in patients with Bell’s palsy. Ultrasound may show increase in facial nerve diameter and side-to-side difference in diameter in patients with facial nerve palsy compared to controls. The diameter of the affected side may be significantly larger than that of the healthy side in patients with Bell’s palsy. Ultrasound also may be helpful in the diagnosis of other causes of facial nerve palsy.

There are no CT scan findings associated with Bell’s palsy. However, an CT scan may be helpful in the diagnosis of other causes of facial nerve palsy.

MRI findings are not specific and necessary for diagnosis of Bell’s palsy. Findings on MRI suggestive of of Bell’s palsy include: swelling of facial nerve and Intraoperative swelling of geniculate ganglion of facial nerve. MRI also may be helpful in the diagnosis of other causes of facial nerve palsy.

There are no other imaging findings associated with Bell’s palsy.

There are no other diagnostic studies associated with Bell’s palsy.

Pharmacologic medical therapy is recommended among all patients with Bell’s palsy. Most patients with Bell’s palsy recover fully without treatment. Corticosteroids may reduce the risk of unsatisfactory recovery in patients with Bell palsy and are highly recommended for treatment of Bell’s palsy. Antiviral agents, when administered with corticosteroids, may be associated with additional benefit. Pharmacologic medical therapy in adults include: prednisolone 60 mg PO q24h for 5 days then reduced by 10 mg per day (for a total treatment time of 10 days) and 50 mg per day (in two divided doses) for 10 days and acyclovir 2000 mg PO q24h for 7-10 days. Pharmacologic medical therapy in children include: prednisolone 1 mg/kg PO per day q24h for 10 days . There is low quality evidence that tailored facial exercises can help to improve facial function in patients with bell’s palsy. There is low quality evidence that facial exercise reduces sequelae in acute cases of bell’s palsy.

Surgical intervention is not recommended for the management of all patients with Bell’s palsy as spontaneous recovery occurs in most cases. Surgery is usually reserved when degeneration of facial nerve reaches 90% to 94% within one to 21 days after onset of the symptoms of Bell’s palsy or when presence of a tumor is suspected or when there is high probability of nerve ischemia.

There are no established measures for the primary prevention of Bell’s palsy.

Effective measures for the secondary prevention of Bell’s palsy complications include early treatment of disease within 24h after onset of the symptoms.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

The first comprehensive description of Bell’s palsy was first discovered by Abū Bakr Muhammad ibn Zakariyyā al-Rāzī, a Persian polymath, physician, alchemist, philosopher, in 9th century, although Sir Charles Bell, a Scottish surgeon, was the first to provide the anatomic basis for the condition that bears his name in 1821. For the fiest time, Razi provided accurate descriptions of facial muscles disorders. Razi describes a clinical method for distinguishing spasm and paralysis for the first time. In 9th century, the therapy of Bell’s palsy was developed by Abū Bakr Muhammad ibn Zakariyyā al-Rāzī. In 1821, Sir Charles Bell described the lesions of the seventh cranial nerve produce facial paralysis. Bell described the Bell’s palsy is caused by problem of 7th cranial nerve(facial nerve).

• The first comprehensive description of Bell’s palsy was first discovered by Abū Bakr Muhammad ibn Zakariyyā al-Rāzī, a Persian polymath, physician, alchemist, philosopher, in 9th century, although Sir Charles Bell, a Scottish surgeon, was the first to provide the anatomic basis for the condition that bears his name in 1821.^[1]
  • For the first time, Razi provided accurate descriptions of facial muscles disorders.
  • Razi describes a clinical method for distinguishing spasm and paralysis for the first time.
  • Razi also gave the earliest description of bilateral facial palsy.

• In 9th century, the therapy of Bell’s palsy was developed by Abū Bakr Muhammad ibn Zakariyyā al-Rāzī.
• The treatment given by Razi was:
  • Massage until the “skin turns red,”
  • Warming oils and ointments
  • Warm compresses
  • Inhaled and intranasal medicines (emphasis on inducing sneezing)
  • Oral medications (emphasis on gargling)
  • Special diets
  • Phlebotomy
  • Application of a bandage to the distorted area to counteract the unbridled pull of the muscles
• In 1821, Sir Charles Bell described the lesions of the seventh cranial nerve produce facial paralysis.^[2]
  • Bell described the Bell’s palsy is caused by problem of 7th cranial nerve(facial nerve).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Bell’s palsy may be classified into five categories according to laterality and recurrence and alternating of the palsy include: unilateral nonrecurrent, unilateral recurrent, simultaneous bilateral, alternating bilateral and recurrent bilateral type.

• Bell’s palsy may be classified into five categories according to laterality and recurrence and alternating of the palsy:^[1][2]
  • Unilateral nonrecurrent
  • Unilateral recurrent
  • Simultaneous bilateral
  • Alternating bilateral
  • Recurrent bilateral type

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

The exact pathophysiology of Bell’ palsy is not known. Bell’s palsy occurs due to failure to function in a normal manner of the facial nerve (VII cranial nerve). The malfunction of the facial nerve caused involuntary spasm in the facial muscles which called facial palsy. Bell’s palsy causes the lower motor neuron type paralysis. Although the exact etiology of Bell’s palsy is unknown, there is some evidences that implies there may be some relation between vasospasm, from any cause, along any facial nerve branch, with Bell’s palsy. There is no established association between genetic factors and Bell’s palsy. Hereditary components may play a role in familial recurrent Bell’s palsy. On microscopic histopathological analysis, thickened perineurium, infiltrates of inflammatory cells between nerve bundles and around blood vessels are characteristic findings of Bell’s palsy. It appears that the histology of the facial nerve in Bell’s palsy is similar to Herpes Zoster infection, suggestive of an infectious cause.

• The exact pathophysiology of Bell’ palsy is not known.^[1]
  • Bell’s palsy occurs due to failure to function in a normal manner of the facial nerve (VII cranial nerve).^[2]
  • The malfunction of the facial nerve caused involuntary spasm in the facial muscles which called facial palsy.^[2]
  • Bell’s palsy causes the lower motor neuron type paralysis.^[3]
• Although the exact etiology of Bell’s palsy is unknown, there is some evidences that implies there may be some relation between vasospasm, from any cause, along any facial nerve branch, with Bell’s palsy.^[4]

• There is no established association between genetic factors and Bell’s palsy.
• Hereditary components may play a role in familial recurrent Bell’s palsy.^[5]

1. Blepharospasm^[6]

• Blepharospasm has been rarely seen in patients whit with Bell’s palsy.
• In most cases blepharospasm appeared within a month after the onset of Bell’s palsy.

2. Herpes zoster infection^[7]

• On microscopic histopathological analysis, thickened perineurium, infiltrates of inflammatory cells between nerve bundles and around blood vessels are characteristic findings of Bell’s palsy.^[8]

• It appears that the histology of the facial nerve in Bell’s palsy is similar to Herpes Zoster infection, suggestive of an infectious cause.^[7] ==References==

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

The exact cause of Bell’s palsy is unknown but there are some evidences which implies Bell’s palsy may be caused by: herpes simplex virus reactivation, herpes Zoster, cytomegalovirus, epstein Barr virus, rubella virus, mumps, influenza B, coxsackievirus, Rickettsial infection, borrelia burgdorferi, acute HIV infection, ischemic mononeuropathy, diabetes mellitus, thyroid disorders and compression of the facial nerve.

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of Bells palsy.

The exact cause of Bell’s palsy is unknown but there are some evidences which implies Bell’s palsy may be caused by:

• Viral infections:
  • Herpes simplex virus reactivation^[1]
  • Herpes Zoster^[2]
  • Cytomegalovirus^[3]
  • Epstein Barr virus^[4]
  • Rubella virus^[5]
  • Mumps^[6]
  • Influenza B^[7]
  • Coxsackievirus^[8]
  • Rickettsial infection ^[9]
  • Borrelia burgdorferi^[10]
  • Acute HIV infection^[11]
• Ischemic mononeuropathy^[12]
• Diabetes mellitus^[13]
• Thyroid disorders^[14]
• Compression of the facial nerve^[15]

Cardiovascular	Ischemic mononeuropathy
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	No underlying causes
Endocrine	Diabetes mellitus, Thyroid disorders
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Inactivated intranasal influenza vaccine
Infectious Disease	Acute HIV infection, Adenovirus, Coxsackievirus, Cytomegalovirus, Epstein-Barr virus, Herpes simplex virus, Herpes zoster, Inactivated intranasal influenza vaccine, Influenza B, Mumps, Rickettsial infection, Rubella, Varicella-zoster virus, Borrelia burgdorferi
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	Compression of the facial nerve, Facial nerve inflammation, Ischemic mononeuropathy, Tumors of the facial nerve
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Tumors of the facial nerve
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Inactivated intranasal influenza vaccine
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Compression of the facial nerve, Facial nerve inflammation, Idiopathic

• Herpes simplex virus reactivation is the most likely cause of Bell’s Palsy.
• Herpes Zoster may be the second most common viral infection.
• Cytomegalovirus
• Epstein Barr virus
• Adenovirus
• Rubella virus
• Mumps
• Influenza B
• Coxsackievirus
• Rickettsial infection
• Ehrlichiosis
• Borrelia burgdorferi
• Acute HIV infection

• Facial nerve inflammation
• Tumors and compression of the facial nerve
• Ischemic mononeuropathy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Bell’s palsy must be differentiated from other diseases that cause weakness or total paralysis on one side of the face, difficulty making facial expressions in one side, impaired facial nerve reflexes, salivation and unintended eye closure, such as Ramsay-Hunt Syndrome, Lyme Disease, stroke, Skull fracture, head or neck tumor, and Multiple sclerosis.

• Bell’s palsy must be differentiated from other diseases that cause weakness or total paralysis on one side of the face, difficulty making facial expressions in one side, impaired facial nerve reflexes, salivation and unintended eye closure, such as Ramsay-Hunt Syndrome, lyme Disease, stroke, Skull fracture, head or neck tumor, and Multiple sclerosis.

Diseases	Clinical manifestations						Gold standard of diagnosis	Additional findings
	Symptoms			Physical examination
									Weakness or total paralysis on one side of the face	Difficulty making facial expressions in one side, such as closing eye, smiling and whistling	Salivation	Impaired Facial nerve reflexes	Unintended eye closure with an effort to smile	Incomplete closure and the of the eye when patient attempts to close the eyes Inability to puff the cheek in affected side
Bell’s palsy	++	++	++	++	++	++	Exclusion of other causes of facial nerve palsy	Facial droop Pain around the jaw or ear Numbness in the skin of affected side
Ramsay-Hunt Syndrome	++	++	++	++	++	++	Diagnosis is clinical PCR test may be used to confirm the diagnosis	Ramsay Hunt syndrome is caused by the Varicella virus (Herpes zoster) that also causes chickenpox and shingles
Lyme Disease	-/+	-/+	-/+	-/+	-/+	-/+	Enzyme-linked immunosorbent assay (ELISA) Western blot	Erythema chronicum migrans Young patient Heart block Arthritis Vertigo Hearing loss
Stroke	-/+	-/+	-/+	-/+	-/+	-/+	MRI	Sudden unilateral motor and sensory deficit in a patient with a history of atherosclerotic risk factors (diabetes, hypertension, smoking) or atrial fibrillation.
Skull fracture	-/+	-/+	-/+	-/+	-/+	-/+	MRI	History of head injury
Head or neck tumor	-/+	-/+	-/+	-/+	-/+	-/+	MRI	slow onset of the symptoms Headaches Vision problems Difficulty with balance Speech difficulties Personality or behavior changes Seizures
Multiple sclerosis	Rare	-/+	Rare	-/+	-/+	Rare	MRI	Fatigue Mood problems Spasticity Bowel, bladder dysfunction Eye movement problems Sexual dysfunction Visual loss.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

The incidence of Bell’s palsy is approximately 30 per 100,000 individuals. The lifetime prevalence of Bell’s palsy was 642.8 cases per 100,000 population age 15 years and above in one study. The incidence of Bell’s palsy increases with age. There is no racial predilection to Bell’s palsy. Bell’s palsy affects men and women equally. The ratio of male to female patients was 48:52 in one study. There is no geographic difference in incidence of Bell’s palsy.

• The incidence of Bell’s palsy is approximately 30 per 100,000 individuals.^[1]

• The lifetime prevalence of Bell’s palsy was 642.8 cases per 100,000 population age 15 years and above in one study.^[2]

• The incidence of Bell’s palsy increases with age.^[2]

• There is no racial predilection to Bell’s palsy.

• Bell’s palsy affects men and women equally.
• The ratio of male to female patients was 48:52 in one study.^[1]

There is no geographic difference in incidence of Bell’s palsy.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

The onset of Bell’s palsy is sudden and symptoms typically peak fast, within a few days. The main symptom is acute peripheral facial weakness. The hallmark of Bell’s palsy is unilateral, acute paresis or paralysis of facial movement. A positive history of viral infections, Ischemic mononeuropathy,Diabetes mellitus and Thyroid disorders is suggestive of Bell’s palsy. Patients with Bell’s palsy may also have a positive history of: Herpes simplex virus reactivation, Herpes Zoster, Cytomegalovirus, Epstein Barr virus, rubella virus, Mumps, influenza B, coxsackie virus, rickettsial infection, Borrelia burgdorferi, acute HIV infection, ischemic mononeuropathy, Diabetes mellitus and Thyroid disorders. Complications of Bell’s palsy include: incomplete eyelid closure with resultant dry eye, permanent facial weakness with muscle contractures, motor synkinesis , crocodile tears (tears when eating due to misdirection of regenerating gustatory fibres destined for the salivary glands, so that they become secretory fibres to the lacrimal gland and cause ipsilateral tearing while the patient is eating), contracture of facial muscles, reduction or loss of taste sensation and problems with dysarthria due to facial muscle weakness. Prognosis of Bell’s palsy is generally good. If left untreated approximately 71% of patients with Bell’s palsy recover normal function and around 13% are left with slight weakness and around 4% with severe weakness resulting in major facial dysfunction. The presence of complete palsy, advanced age and Herpes zoster infection is associated with a particularly poor prognosis among patients with Bell’s palsy. The Bell’s palsy recurs in 7% of patients. The House-Brackmann grading system was devised both as a clinical indicator of severity and also an objective record of progress.

• The onset of Bell’s palsy is sudden and symptoms typically peak fast, within a few days.^[1][2]
• the main symptom is acute peripheral facial weakness.
• The hallmark of Bell’s palsy is unilateral, acute paresis or paralysis of facial movement. A positive history of viral infections, Ischemic mononeuropathy,Diabetes mellitus and Thyroid disorders is suggestive of Bell’s palsy.

Patients with Bell’s palsy may have a positive history of:

• Viral infections:
  • Herpes simplex virus reactivation^[3]
  • Herpes Zoster^[4]
  • Cytomegalovirus^[5]
  • Epstein Barr virus^[6]
  • Rubella virus^[7]
  • Mumps^[8]
  • Influenza B^[9]
  • Coxsackievirus^[10]
  • Rickettsial infection ^[11]
  • Borrelia burgdorferi^[12]
  • Acute HIV infection^[13]
• Ischemic mononeuropathy^[14]
• Diabetes mellitus^[15]
• Thyroid disorders^[16]

• Complications of Bell’s palsy include:^[17][18]
  • Incomplete eyelid closure with resultant dry eye
  • Permanent facial weakness with muscle contractures
  • Motor synkinesis (involuntary movement of muscles occurring at the same time as deliberate movement, e.g. involuntary mouth movement during voluntary eye closure)
  • Crocodile tears (tears when eating due to misdirection of regenerating gustatory fibres destined for the salivary glands, so that they become secretory fibres to the lacrimal gland and cause ipsilateral tearing while the patient is eating)
  • Incomplete recovery
  • Contracture of facial muscles
  • Reduction or loss of taste sensation
  • Problems with dysarthria due to facial muscle weakness

• Prognosis of Bell’s palsy is generally good.^[19]
• If left untreated approximately 71% of patients with Bell’s palsy recover normal function and around 13% are left with slight weakness and around 4% with severe weakness resulting in major facial dysfunction.^[18]
• The presence of complete palsy, advanced age and Herpes zoster infection is associated with a particularly poor prognosis among patients with Bell’s palsy.^[19]
• The Bell’s palsy recurs in 7% of patients.^[19]
• The House-Brackmann grading system was devised both as a clinical indicator of severity and also an objective record of progress.^[20]

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