# Clinical Cases: Face and Scalp ## Case 1: Bell's Palsy ### Patient Demographics - **Age:** 38 years old - **Sex:** Female - **Occupation:** Marketing executive ### Chief Complaint Sudden onset of right-sided facial droop and inability to close the right eye, noticed upon waking this morning. ### History of Present Illness The patient went to bed feeling well and awoke this morning to find the right side of her face drooping. She noticed that she could not fully close her right eye, her smile was asymmetric, and she was drooling from the right corner of her mouth. She reports that food and drink spill from the right side of her mouth. She also notes that sounds seem louder in her right ear (hyperacusis) and that she has diminished taste sensation on the right side of her tongue. She denies hearing loss, vertigo, limb weakness, numbness, speech difficulty, or vision changes. She had a mild upper respiratory infection approximately 1 week ago. She has no history of diabetes, recent travel, or tick exposure. ### Physical Examination - **Vitals:** Within normal limits - **Neurological examination:** - Facial nerve (CN VII): Right-sided facial weakness involving BOTH the upper and lower face; unable to wrinkle forehead on right, unable to close right eye against resistance (Bell's phenomenon present - eye rolls upward on attempted closure), asymmetric smile with right-sided droop, unable to puff out right cheek - Taste: Diminished on anterior two-thirds of tongue on right - Other cranial nerves: Normal, including hearing - Motor/Sensory: Normal strength and sensation in all limbs - **Ear examination:** External auditory canal and tympanic membrane normal; no vesicles (rules out Ramsay Hunt syndrome) - **Eye examination:** Incomplete right eyelid closure; conjunctiva mildly injected due to exposure ### Clinical Image ![Bell's Palsy](case_01_image.jpg) *Photograph demonstrating typical facial appearance in Bell's palsy with inability to close the eye and asymmetric facial droop.* **Image Source:** Wikimedia Commons - Bellspalsy.jpg, CC BY-SA 3.0 ### Diagnosis **Bell's Palsy** (idiopathic facial nerve paralysis) ### Anatomical Correlation The facial nerve (CN VII) has a complex course with multiple segments. After exiting the brainstem at the cerebellopontine angle, it enters the internal acoustic meatus and traverses the facial canal within the petrous temporal bone. Within the canal, it gives off the greater petrosal nerve (carrying parasympathetic fibers to the lacrimal gland), the nerve to stapedius (which dampens loud sounds), and the chorda tympani (carrying taste fibers from the anterior two-thirds of the tongue). The nerve exits through the stylomastoid foramen and enters the parotid gland, where it divides into five terminal branches (temporal, zygomatic, buccal, marginal mandibular, cervical) that innervate the muscles of facial expression. Bell's palsy is thought to result from viral inflammation and edema of the facial nerve within the narrow confines of the facial canal, causing compression and ischemia. The characteristic finding is a lower motor neuron (peripheral) pattern of facial weakness affecting ALL muscles on the ipsilateral side, including the forehead (frontalis). This distinguishes it from an upper motor neuron lesion (such as stroke), where the forehead is spared because the frontalis muscle receives bilateral cortical input. The involvement of taste (chorda tympani) and hyperacusis (stapedius nerve) indicates that the lesion is within the facial canal, proximal to where these branches arise. ### Treatment 1. **Corticosteroids:** Prednisone 60-80 mg daily for 7 days, then taper (improves outcomes if started within 72 hours) 2. **Antivirals:** Consider adding valacyclovir if severe; evidence is less robust than for steroids 3. **Eye protection:** Critical to prevent exposure keratopathy - Artificial tears during the day - Lubricating ointment at night - Tape eyelid closed during sleep - Consider moisture chamber or eye patch 4. **Physical therapy:** Facial exercises may help recovery 5. **Prognosis:** 70-85% recover completely within 3-6 months; incomplete recovery more likely in older patients, those with complete paralysis, or delayed treatment --- ## Case 2: Cavernous Sinus Thrombosis ### Patient Demographics - **Age:** 25 years old - **Sex:** Male - **Occupation:** College student ### Chief Complaint Severe headache, eye swelling, and double vision for 3 days following a facial infection. ### History of Present Illness The patient developed a "pimple" on the right side of his nose approximately 1 week ago. He attempted to squeeze and pop the lesion multiple times. Over the following 3 days, he developed progressive right periorbital swelling, headache, and fever. He presented to an urgent care clinic and was prescribed oral antibiotics for facial cellulitis. Despite 2 days of antibiotics, his symptoms worsened significantly. He now has bilateral eye swelling (initially only right, now spreading to left), severe headache, double vision, and high fevers (up to 39.5C). He also reports right facial numbness over the cheek and forehead. ### Physical Examination - **Vitals:** HR 115 bpm, BP 100/65 mmHg, Temp 39.8C, appearing toxic - **Head examination:** - Bilateral periorbital edema with erythema (right worse than left) - Proptosis (forward displacement of the eye) bilaterally - Chemosis (conjunctival swelling) bilaterally - Crusted lesion on right nasal ala with surrounding cellulitis - **Neurological examination:** - CN III: Right pupil dilated, sluggish response; limited upward, downward, and medial gaze on right - CN IV: Limited downward gaze when adducted (right) - CN VI: Limited lateral gaze (right) - CN V1/V2: Decreased sensation over right forehead and cheek - Fundoscopy: Papilledema bilaterally, dilated retinal veins ### Imaging Workup 1. **CT head with contrast:** Filling defects in both cavernous sinuses, more prominent on right; proptosis bilaterally; inflammatory changes in the right orbit and face 2. **MRI/MRV brain:** Confirms bilateral cavernous sinus thrombosis with surrounding inflammatory changes ### Laboratory Studies 1. **Blood cultures:** Positive for Staphylococcus aureus 2. **CBC:** WBC 22,000 with left shift 3. **Inflammatory markers:** CRP 285 mg/L, Procalcitonin elevated ### Diagnosis **Septic Cavernous Sinus Thrombosis** secondary to nasal furuncle (facial infection in the "danger triangle") ### Anatomical Correlation The "danger area of the face" is the triangular region bounded by the corners of the mouth and the bridge of the nose. This area drains via the facial vein and angular vein, which communicate with the cavernous sinus through two routes: (1) the superior ophthalmic vein, which drains directly into the cavernous sinus, and (2) the deep facial vein, which connects to the pterygoid plexus, which in turn communicates with the cavernous sinus. Critically, these veins are valveless, allowing blood (and infection) to flow in either direction. The cavernous sinuses are paired dural venous sinuses located on either side of the sella turcica. They have a complex trabeculated structure containing several important structures: the internal carotid artery and abducens nerve (CN VI) pass through the center, while the oculomotor nerve (CN III), trochlear nerve (CN IV), and ophthalmic (V1) and maxillary (V2) divisions of the trigeminal nerve course within the lateral wall. When infection spreads to the cavernous sinus, thrombosis and inflammation affect these structures, producing the classic findings: ophthalmoplegia (CN III, IV, VI), facial sensory loss (CN V1, V2), proptosis and chemosis (venous congestion), and papilledema. Bilateral involvement occurs because the cavernous sinuses communicate via intercavernous sinuses. ### Treatment 1. **Broad-spectrum IV antibiotics:** Vancomycin plus ceftriaxone or meropenem; adjust based on cultures 2. **Prolonged antibiotic course:** Typically 3-4 weeks IV followed by oral antibiotics 3. **Anticoagulation:** Controversial but generally recommended to prevent thrombus propagation 4. **Surgical drainage:** Of primary infection source if abscess present 5. **ICU monitoring:** High mortality condition requiring close observation 6. **Prognosis:** Mortality 20-30% even with treatment; high rate of neurological sequelae