Bell's palsy Flashcards
What is Bell’s palsy?
Bell’s Palsy is an acute, unilateral lower motor neuron (LMN) facial nerve (cranial nerve VII) paralysis of unknown cause, leading to weakness or paralysis of facial muscles on the affected side. It is thought to be due to inflammation and viral reactivation (e.g., herpes simplex virus).
What are the branches of the facial nerve?
Temporal branches
Zygomatic Branches
Buccal Branches
Marginal Mandibular branch
Cervical branche
What is the cause of Bell’s palsy?
The exact cause of Bell’s palsy is uncertain, but it is believed to be linked to viral infections that trigger inflammation of the facial nerve (cranial nerve VII). The most commonly implicated virus is the herpes simplex virus (HSV-1), which is responsible for cold sores. The virus may become reactivated in the body, leading to inflammation and swelling of the facial nerve, resulting in the symptoms of Bell’s palsy.
What type of motor neurone defecit is Bell’s Palsy?
Lower motor neurone deficit. Upper and lower face paralysed.
It involves both upper and lower muscles of facial expression.
What is the pathophysiology of Bell’s palsy?
Atietology is generally unclear
Diagnosis of exclusion once other causes for facial nerve palsy have been considered
If no other cause is found, idiopathic Bell’s Palsy is diagnosed
What are the risk factors of Bell’s Palsy?
Pregnancy
What are the symptoms and clinical features of Bell’s palsy?
Facial Weakness (LMN Pattern) – Unilateral, affects entire face (including forehead).
Eye & Mouth Issues – Can’t close eye, drooping mouth, difficulty smiling.
Sensory & Autonomic Symptoms – Loss of taste (anterior ⅔ tongue), hyperacusis, dry eyes, reduced saliva.
Sudden Onset – Develops over hours to days, peaks within 72 hours.
No Stroke Features – No limb weakness, speech issues, or sensory loss.
What is the difference between an upper motor neurone lesion and lower Motor lesion?
An upper motor neuron (UMN) lesion occurs due to damage in the corticospinal or corticobulbar tracts within the brain or spinal cord, while a lower motor neuron (LMN) lesion affects the cranial nerves, spinal nerves, or anterior horn cells in the spinal cord. These two types of lesions result in distinct clinical features.
In UMN lesions, muscle weakness presents with spasticity (increased muscle tone) due to the loss of inhibitory control from the brain. Reflexes are exaggerated (hyperreflexia), and the Babinski sign is positive (toes extend upwards when the sole is stroked). However, muscle atrophy is minimal, as the muscles still receive some input, although disuse atrophy may occur over time. Common causes of UMN lesions include stroke, multiple sclerosis, and spinal cord injury.
In contrast, LMN lesions cause flaccid paralysis (decreased muscle tone) due to direct damage to motor neurons. Reflexes are diminished or absent (hyporeflexia), and muscle atrophy is severe, as the muscle loses direct neural input. Fasciculations (muscle twitches) may be seen due to spontaneous firing of degenerating motor neurons. The Babinski sign is negative, with toes flexing downward or no response. LMN lesions are seen in conditions such as Bell’s palsy, Guillain-Barré syndrome, and polio.
How does Bell’s palsy differentiate from a stroke?
Bell’s is a LMN lesion whereas Stroke is an UMN lesion thus they will have different signs and symptoms:
Bell’s: Forehead not wrinkled and asymmetric
Palpebral fissure widened
Nasolabial fold is flat
Mouth drooping
Stroke: Forehead wrinkling intact and asymmetrical
Palpebral fissure not widened
Nasolabial fold is flat
Mouth drooping
How is Bell’s Palsy diagnosed?
Clinical diagnosis based on characteristic symptoms (sudden unilateral facial weakness or paralysis).
Exclusion of other conditions (e.g., stroke, tumors) through clinical examination.
No need for imaging (e.g., CT/MRI) if the diagnosis is clear and no red flags are present.
What are the investigations of Bell’s palsy?
Clinical - based on history and physical examination
Patients do not require any imaging unless symptoms are atypical, recurrent or persist for >2 months
When imaging is considered, MRI is the method of choice
What are the differential diagnoses?
Lyme disease
Ascending inflammatory demyelinating polyneuropathy (AIDP or Guillain-Barré syndrome)
Sarcoidosis
Autoimmune disease
Malignant or benign facial nerve tumour
Herpes zoster oticus (Ramsay Hunt syndrome)
Otitis media
Stroke/TIA
HIV
MS
What is the management of Bell’s palsy?
Oral corticosteroids
Start within 72 hours of symptom onset
Do not use antivirals ( evidence doesn’t show its effective)
Eye protection
Transparent eye shield
Artificial tears for lubrication
Tape eye shut at night
Surgical decompression
Some patients may benefit from referral to aneuro-otoloigst
What is the long term management of Bell’s palsy?
Review patient within 1 to 2 weeks of the initial visit, to monitor response to pharmacologic treatment and to assess the condition of the eye.
Subsequently, follow-up may occur monthly or at 3-month intervals to monitor recovery.
Absence of recovery of function at 3-4 months should prompt further imaging to investigate for an alternative diagnosis
What are the complications of Bell’s Palsy?
Cosmetic:
Long-term sequelae like facial weakness or synkinesis may occur but usually improve over time.
Psychological
Social implications
What are the treatment interventions of Bell’s according to NICE?
Treatment:
Prednisolone (steroid therapy) is recommended for all adults with acute Bell’s palsy to improve recovery outcomes:
Prednisolone 40 mg daily for 10 days (starting within 72 hours of symptom onset).
Use is most effective if started early, ideally within 48–72 hours.
Antiviral treatment (e.g., aciclovir) is not routinely recommended unless there are concerns about herpes zoster or severe cases with evidence of viral involvement.
Symptom Management:
Eye care is crucial to prevent dry eye and potential damage from the inability to close the eyelid:
Lubricating eye drops or ointment.
Eye patching at night if unable to fully close the eye.
Facial exercises: Some evidence suggests that facial exercises may help in restoring function but should be done under supervision.
