# Clinical Cases: Cranial Nerves ## Case 1: Bell's Palsy (Lower Motor Neuron Facial Nerve Palsy) ### Patient Presentation **Demographics:** 38-year-old female **Chief Complaint:** Right-sided facial drooping noticed upon awakening this morning **History of Present Illness:** The patient woke up this morning and noticed her face looked "crooked" in the mirror. She cannot close her right eye completely, and the right side of her mouth droops. She has difficulty drinking water as it dribbles out the right side. She noticed some mild pain behind her right ear starting yesterday evening. She denies any arm or leg weakness, speech difficulty (other than from the facial droop), hearing changes, or vision problems. She had a cold with runny nose about a week ago. She has no significant past medical history. **Physical Examination:** - Vital signs: BP 118/72, HR 68, T 36.8C - General: Anxious appearing female, right facial asymmetry - Neurological: - Mental status: Alert, oriented, speech clear but distorted by facial weakness - Cranial nerves: - II: Visual acuity and fields normal - III, IV, VI: Extraocular movements intact; right eye does not close completely when attempting to blink (lagophthalmos); Bell's phenomenon present (eye rolls up when attempting to close) - V: Facial sensation intact in all three divisions bilaterally - VII: Right-sided facial paralysis affecting BOTH upper and lower face: unable to raise right eyebrow, unable to close right eye fully, flattened right nasolabial fold, drooping right corner of mouth, cannot puff right cheek - VIII: Hearing grossly intact; no hyperacusis - IX, X: Palate elevates symmetrically; gag intact - XII: Tongue midline - Motor: 5/5 strength in all extremities - Sensory: Intact throughout - Reflexes: 2+ and symmetric **Workup:** - **Physical examination findings:** Complete right lower motor neuron facial weakness (forehead involved, distinguishing from stroke) - **No imaging required** in typical presentation without red flags - **Lyme serology:** Obtained given geographic area (endemic); pending - **Glucose:** 98 mg/dL (to evaluate for diabetes, a risk factor) **Diagnosis:** Bell's palsy (idiopathic peripheral facial nerve palsy) **Treatment:** - Prednisone 60 mg daily for 7 days - Artificial tears and lubricating ointment for eye protection - Tape right eye closed at night to prevent corneal exposure - Valacyclovir 1000 mg three times daily for 7 days (added given within 72 hours of onset) - Follow-up in 2 weeks **Clinical Course:** At 2-week follow-up, the patient showed early signs of recovery with ability to wrinkle her forehead slightly. By 6 weeks, she had recovered approximately 70% of facial movement. At 3-month follow-up, she had nearly complete recovery with only subtle asymmetry when smiling. **Clinical Pearl:** Bell's palsy causes lower motor neuron facial weakness affecting the entire hemiface including the forehead. This distinguishes it from upper motor neuron lesions (like stroke), which spare the forehead due to bilateral cortical innervation of the upper face. Most patients (70-80%) recover completely without treatment, but corticosteroids started within 72 hours improve outcomes. Eye protection is critical to prevent corneal ulceration from incomplete lid closure. --- ## Case 2: Third Nerve Palsy from Posterior Communicating Artery Aneurysm ### Patient Presentation **Demographics:** 52-year-old female **Chief Complaint:** Double vision and droopy right eyelid for 2 days, with new headache **History of Present Illness:** Two days ago, the patient noticed her right eyelid was drooping and she began seeing double. The double vision is horizontal and worsens when she tries to look to the left. She also developed a new headache, dull and constant, located behind her right eye. The headache is moderate in severity and not the worst headache of her life. She has a history of hypertension. Her mother had a "brain hemorrhage" at age 58. **Physical Examination:** - Vital signs: BP 162/94, HR 76, T 37.0C - General: Uncomfortable appearing, holding right eye closed to avoid diplopia - Neurological: - Mental status: Alert and oriented; appropriate - Cranial nerves: - II: Visual acuity normal; visual fields full - III (Right): Complete ptosis; when lid lifted manually: pupil 6 mm and unreactive to light (direct or consensual); eye is deviated "down and out" (lateral and inferior); cannot adduct, elevate, or depress the eye (medial rectus, superior rectus, inferior rectus, inferior oblique all weak) - III (Left): Normal - IV: Right superior oblique intact (eye intorts when attempting to look down and in) - VI: Right lateral rectus intact (can abduct) - V, VII, VIII, IX, X, XI, XII: Normal - Motor: 5/5 throughout - Neck: Supple **Workup:** - **CT head without contrast:** No hemorrhage - **CT angiography:** 7 mm saccular aneurysm arising from the junction of the right internal carotid artery and posterior communicating artery, projecting inferolaterally - **MRI brain:** Aneurysm confirmed; no recent infarction **Diagnosis:** Right third cranial nerve palsy secondary to unruptured right posterior communicating artery aneurysm **Treatment:** - Emergent neurosurgical and neurointerventional consultation - Blood pressure control (goal SBP <140) - Endovascular coiling of aneurysm performed on hospital day 1 - Aspirin 81 mg initiated post-procedure **Clinical Course:** The patient tolerated aneurysm coiling without complication. Her headache improved within 24 hours. The ptosis and pupillary dilation persisted at discharge. At 3-month follow-up, ptosis had partially improved, and the pupil had regained some reactivity (though still larger than left). At 6 months, she had near-complete recovery of eye movements with only mild residual ptosis. **Clinical Pearl:** An acute, painful third nerve palsy with pupil involvement is an aneurysm until proven otherwise. The posterior communicating artery aneurysm compresses the third nerve as it courses between the PCA and superior cerebellar artery. The pupil-involving pattern (mydriasis) occurs because parasympathetic fibers traveling on the outside of the nerve are compressed first. This "surgical" third nerve palsy contrasts with "medical" third nerve palsies from diabetes or vasculopathic disease, which typically spare the pupil (due to ischemia affecting the center of the nerve but sparing peripheral parasympathetic fibers). --- ## Case 3: Trigeminal Neuralgia ### Patient Presentation **Demographics:** 62-year-old male **Chief Complaint:** Severe shooting facial pain for 2 months **History of Present Illness:** The patient describes 2 months of recurrent, excruciating pain on the right side of his face. The pain is "like electric shocks" or "lightning bolts," occurring in the right cheek and jaw. Each episode lasts only a few seconds but is so severe he stops whatever he is doing. The pain is triggered by chewing, brushing his teeth, shaving, or even a light breeze on his face. He has had up to 20-30 episodes per day. He has lost 8 pounds because eating triggers the pain. Between attacks, he has no pain. The pain has never occurred on the left side or awakened him from sleep. **Physical Examination:** - Vital signs: BP 148/86, HR 72, T 36.9C - General: Appears apprehensive; has not shaved right side of face; protective of right cheek - Neurological: - Mental status: Normal - Cranial nerves: - Light touch to right V2 and V3 distributions triggers severe lancinating pain lasting 2-3 seconds (patient withdraws and grimaces) - Between triggers, sensation to light touch, pinprick, and temperature is NORMAL in all trigeminal divisions - Corneal reflex intact bilaterally - Motor function of V3 (masseter, temporalis) intact - All other cranial nerves normal - Motor/Sensory/Reflexes: Normal throughout **Workup:** - **MRI brain with thin cuts through posterior fossa:** No mass lesion; tortuous loop of right superior cerebellar artery in close contact with the right trigeminal nerve root entry zone, consistent with neurovascular compression - **No laboratory abnormalities:** TSH, basic metabolic panel, CBC normal **Diagnosis:** Classical trigeminal neuralgia (tic douloureux) with neurovascular compression **Treatment:** - Carbamazepine 100 mg twice daily, titrated to 200 mg three times daily - Baseline CBC and hepatic function panel (monitor for carbamazepine toxicity) - HLA-B*15:02 testing (patient of Asian descent - risk of severe cutaneous reactions) **Clinical Course:** Pain frequency decreased by 80% within 2 weeks of reaching therapeutic carbamazepine dose. At 3-month follow-up, he was experiencing only 1-2 mild attacks per day. He discussed surgical options (microvascular decompression) if medication becomes ineffective or intolerable but elected to continue medical management for now. **Clinical Pearl:** Trigeminal neuralgia is characterized by severe, brief, shock-like pain in the distribution of one or more trigeminal divisions, triggered by innocuous stimuli. V2 and V3 are most commonly affected. Between attacks, the neurological examination is normal - any sensory deficit should raise concern for a structural lesion or secondary cause. Most cases are caused by vascular compression of the trigeminal root entry zone. Carbamazepine is first-line treatment; microvascular decompression surgery is highly effective for refractory cases. --- ## Clinical Image ![Bell's palsy facial weakness](case_01_image.jpg) **Image Description:** Clinical photograph or illustration demonstrating characteristic features of lower motor neuron facial nerve palsy (Bell's palsy), including inability to close the eye, flattening of the forehead (distinguishing from UMN lesions), and drooping of the corner of the mouth. The entire hemiface is affected because all facial nerve motor fibers pass through the same peripheral pathway. **Attribution:** Image from Radiopaedia (https://radiopaedia.org/), Creative Commons Attribution-NonCommercial-ShareAlike 3.0 license.