Facial palsy/Trigeminal Neuralgia

For BDS stuents from Davidson

1. Facial Palsy/ Trigeminal Neuralgia Dr Avatar Verma KIST MCTH 2076/02/10

2. Trigeminal neuralgia Unilateral lancinating facial pain, most commonly involving the second and/or third divisions of the trigeminal nerve territory, usually in patients over the age of 50 years

3. Pathophysiology Irritative lesion involving the trigeminal root zone, in some cases an aberrant loop of artery Other compressive lesions, usually benign, are occasionally found Trigeminal neuralgia associated with multiple sclerosis may result from a plaque of demyelination in the brainstem

4. Clinical features Pain is repetitive, severe and very brief may be triggered by touch, a cold wind or eating Physical signs are usually absent, although the spasms may make the patient wince and sit silently (tic douloureux) Similar in multiple sclerosis or with other brainstem lesions, in which case there may be associated sensory changes in the trigeminal nerve territory or elsewhere There is a tendency for the condition to remit and relapse over many years

5. Management Carbamazepine: low dose and increase gradually Not tolerable to Carbamazepine: Gabapentin, Pregabalin Amitriptyline or steroids may be effective The possibility of surgical treatment should be entertained, especially where response is incomplete in younger patients Decompression of the vascular loop encroaching on the trigeminal root is said to have a 90% success rate Otherwise, localised injection of alcohol or phenol into a peripheral branch of the nerve may be effective

6. Facial weakness Bell’s palsy: One of the most common causes of facial weakness is Bell’s palsy, a lower motor neuron lesion of the 7 th (facial) nerve, affecting all ages and both sexes The lesion is within the facial canal Symptoms usually develop subacutely over a few hours, with pain around the ear preceding the unilateral facial weakness

7. Patients often describe the face as ‘numb’, but there is no objective sensory loss (except to taste if the chorda tympani is involved) Hyperacusis may occur if the nerve to stapedius is involved, and there may be diminished salivation and tear secretion Examination reveals an ipsilateral lower motor neuron facial nerve palsy Vesicles in the ear or on the palate may indicate primary herpes zoster infection

8. Steroids improve recovery rates if started within 72 hours of onset but antiviral drugs are not effective Taping the eye shut overnight helps prevent exposure keratitis and corneal abrasion About 80% of patients recover spontaneously within 12 weeks Plastic surgery may be considered for the minority left with facial disfigurement after 12 months

9. Recurrence is unusual and should prompt further investigation Aberrant re-innervation may occur during recovery, producing unwanted facial movements, such as eye closure when the mouth is moved (synkinesis), or ‘crocodile tears’ (tearing during salivation)

10. Unlike Bell’s palsy, lesions with an upper motor neuron origin partly spare the upper face Cortical lesions may cause a facial weakness either in isolation or with associated hemiparesis and speech difficulties

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