bells palsy.pptxNerve Injuries from Mandibular Third Molar Removal Roger A. Meyer, DDS, MS, MDa,*, Shahrokh C. Bagheri, DMD, MDb,c,d,

In surveys of oral and maxillofacial surgery practice, removal of teeth is the most frequently
performed operation. Removal of an impacted mandibular third molar tooth (M3) presents unique
surgical challenges. One such challenge is the risk of injury to the peripheral branches of the
trigeminal nerve, which provide sensation to the oral and facial regions. Indeed, in the practice of oral
and maxillofacial surgery, because of their unfavorable effects on orofacial sensation and related
functions (such as eating, drinking, washing, speaking, shaving, kissing), nerve injuries are currently
the most frequent cause of litigation against oral and maxillofacial surgeons (OMFSs) in the United
States. Since the seminal work of Merrill in the 1960s to 1970s on the injury, pathophysiology, and
repair of inferior alveolar and lingual nerve (LN) injuries, much research and clinical work has been
directed toward the prevention and treatment of peripheral trigeminal nerve injuries.
During the removal of an M3, the inferior alveolar nerve (IAN), lying adjacent to M3’s roots, and
the LN, often located just medial to M3’s crown at or near the mandibular lingual alveolar crestal
bone, are at risk of injury from the various surgical maneuvers composing the operation. Such injuries
may not resolve in a reasonable period but instead persist and result in significant permanent sensory
dysfunction in the distribution of the involved nerve. On the other hand, the long buccal nerve (LBN)
is frequently knowingly transected during the standard incision for exposure of the M3, but only
rarely does this maneuver cause bothersome sensory aberration (Fig. 1).
Nerve injury is a known and accepted risk of the removal of M3s and it may occur despite the best
of care. Proactive measures during evaluation and removal of M3s may reduce the incidence of nerve
injury and the disturbance of sensory alteration. When nerve injury caused by the removal of an M3
fails to resolve promptly and the resulting paresthesias and/or dysesthesias are unacceptable to the
patient, timely treatment gives the patient the best chance of a favorable outcome. In surveys of oral and maxillofacial surgery practice, removal of teeth is the most frequently
performed operation. Removal of an impacted mandibular third molar tooth (M3) presents unique
surgical challenges. One such challenge is the risk of injury to the peripheral branches of the
trigeminal nerve, which provide sensation to the oral and facial regions. Indeed, in the practice of oral
and maxillofacial surgery, because of their unfavorable effects on orofacial sensation and related
functions (such as eating, drinking, washing, speaking, shaving, kissing), nerve injuries are currently
the most frequent cause of litigation against oral and maxillofacial surgeons (OMFSs) in the United
States. Since the seminal work of Merrill in the 1960s to 1970s on the injury, pathophysiology, and
repair of inferior alveolar and lingu

1. BELL’S PALSY

2. The symptoms of Bell's palsy include sudden weakness in your facial muscles. In most cases, the weakness is temporary and significantly improves over weeks. The weakness makes half of your face appear to droop. Your smile is one-sided, and your eye on that side resists closing. Bell's palsy, also known as acute peripheral facial palsy of unknown cause, can occur at any age. The exact cause is unknown. For most people, Bell's palsy is temporary. Symptoms usually start to improve within a few weeks, with complete recovery in about six months. A small number of people continue to have some Bell's palsy symptoms for life. Rarely, Bell's palsy can recur. OVERVIEW

3. An idiopathic paresis or paralysis of the facial nerve of sudden onset (unilateral lower motor neuron paralysis of sudden onset, not related to any other disease elsewhere in the body). The name was ascribed to Sir Charles Bell, who in 1821, demonstrated the separation of the motor and sensory innervation of the face. DEFINITION Sir Charles Bell

4. Bell's palsy is an idiopathic condition with several proposed etiological theories. These include The rheumatic hypothesis (nerve compression due to swelling) The cold hypothesis (triggered by cold exposure), The ischemic hypothesis (disrupted blood flow causing nerve damage), The immunological hypothesis (an autoimmune response similar to guillain-barré syndrome. It is postulated that in vivo sensitization of lymphocytes to peripheral nerve myelin gives rise to a cell mediated autoimmune response in both conditions. ), and The viral hypothesis (linking bell’s palsy to herpes simplex virus, with ramsay hunt syndrome involving facial paralysis and herpetic eruptions). Multiple factors may contribute to its development ETIOLOGY

5. CLINICAL FEATURES Sudden onset, often noted upon waking in the morning. Unilateral facial paralysis involving the entire side of the face. Loss of muscle control: inability to smile, close the eye, wink, or raise the eyebrow on the affected side. Difficulty whistling and drooping of the mouth, causing drooling. Bell’s sign: upward rolling of the eyeball when attempting to close the eyelid. Inability to wrinkle the forehead or move the lips. Excessive tearing due to inability to close the eye. Widened palpebral fissure, loss of blinking reflex, and obliteration of the nasolabial fold. Mask-like facial appearance and slurred speech. Altered or lost sense of taste in some cases.

6. Are pregnant, especially during the third trimester, or who are in the first week after giving birth Have an upper respiratory infection, such as the flu or a cold Have diabetes RISK FACTORS

7. Following basic functions are examined: 1. Raising the eyebrows to test frontalis corrugator activity. 2. Tightly closing the eyes for orbicularis oculi sphincter function. 3. Asking the patient to grin or smile, to examine the retractor muscles acting on the angles of the mouth. 4. Taste may also be tested. 5. Patient is asked to blow out the air, hold air in mouth and whistle. DIAGNOSIS

8. Feature UMN Type LMN Type Affected Areas Lower face only; upper face unaffected Both upper and lower face affected Emotional Movements Unaffected in unilateral cases Lost Bell’s Phenomenon Absent Present Facial Muscle Atrophy None Atrophy and fasciculations present Taste Sensation Retained May be lost Corneal Reflex Not affected Absent Hemiplegia Associated with ipsilateral hemiplegia May be isolated or crossed Plantar Response Extensor on paralysed side Flexor on paralysed side, may be extensor on opposite side Examples Stroke, CNS neoplasm, multiple sclerosis Bell’s palsy, Lyme disease Difference between upper motor neuron (UMN) and lower motor neuron (LMN) type of cranial nerve (CN) VII palsy

9. (A)Upper motor neuron lesion (UMNL) sparing the upper half of the face. (B) Lower motor neuron lesion (LMNL) affecting the entire half of face on the affected side (Bell’s Palsy).

10. Any patient presenting with facial paralysis should undergo formal audiological testing, including pure tone, air and bone conduction, speech discrimination, reflexes and tympanometry. If asymmetry is found on the audiogram, an auditory brainstem response (ABR) and/or MRI should be obtained DIAGNOSTIC TESTS Test Nerve Tested Function Assessed Schirmer Test Greater superficial petrosal nerve (GSPN) Lacrimation rate Stapedial Reflex Test Stapedial branch Hyperacusis Taste Testing Chorda tympani nerve Taste loss Salivary Flow Test Chorda tympani Salivary flow rate and pH Topognostic Testing These tests localize the lesion based on loss of function in branches distal to the injury:

11. Electrophysiologic Tests Useful in complete paralysis to determine prognosis and guide decompression surgery. Imaging Studies Facial Bone CT or X-ray: Detects fractures or bony metastases. CT Brain: Evaluates for stroke, multiple sclerosis, or CNS infections (e.g., AIDS). MRI: Identifies neoplasms in the temporal bone, parotid gland, brain, or other structures. It also maps the course of the facial nerve.

12. Prognosis for Bell’s palsy is generally good; with 85%–90% of the patients fully recover within 1 month. Other 15% show no signs of recovery for 3–6 months due to complete degeneration. Complications are higher in those where the recovery is slow. The degree of paralysis determines the prognosis of the patient. Incomplete paralysis have good prognosis than the complete paralysis. PROGNOSIS

13. MANAGEMENT OF BELL'S PALSY Physiotherapy Prevents muscle atrophy and maintains muscle tone. Techniques include electrical stimulation (galvanism), gentle massage, and facial exercises. Medication Early treatment (within 2–3 weeks of onset): Prednisolone: 1 mg/kg/day for 10–14 days with gradual tapering (e.g., 60 kg patient: 10 mg tabs – 3 tabs twice daily for 4 days, taper as prescribed). Vitamins B1, B6, B12 may be added. Late presentation (after 3–4 weeks): Steroids are ineffective.

14. Eye Protection For incomplete eye closure: Use artificial tears, eye taping, or surgical options (spring, gold weight, or tarsorrhaphy). Baseline ophthalmologic evaluation is recommended. Chronic Sequelae Hyperkinesias : Muscle denervation or botulinum toxin injections (temporary muscle paralysis for 4–6 months). Hypokinesia: May require nerve or muscle transfers, or static slings.

15. Advanced Interventions Facial nerve decompression (if >90% nerve action potential loss in 2 weeks): Internal decompression: Relieves pressure within the fallopian canal, removes adhesions. External decompression: Releases the epineural sheath from scar tissue or bone. Nerve anastomosis and grafting: Reanimation with hypoglossal or spinal accessory nerves. Grafting for neuromas or nerve segment loss.

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