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Clin Med III Unit 3 > Head and Facial Disorders > Flashcards

Head and Facial Disorders Flashcards

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1
Q

What are the most common etiologies of general facial palsies?

A 
Infectious
Traumatic
Tumor
Cerebrovascular disease
Toxin exposure
Idiopathic***
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2
Q

Acute facial nerve palsy of unknown cause that makes up 50% of facial nerve palsies

A

Bell’s Palsy

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3
Q

What two conditions dramatically increase your odds of getting Bell’s Palsy?

A

PREGNANCY (3x increase)

Diabetes (5-10% of BP patients)

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4
Q

When is the risk of Bell’s palsy highest for pregnant women?

A

During the 3rd trimester and immediately postpartum

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5
Q

There is some link between _____ and Bell’s Palsy but often unable to confirm and therefore the condition is labeled idiopathic

A

HSV

It can still be helpful to give HSV tx

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6
Q

Clinical presentation of Bell’s Palsy

A

Sudden onset of unilateral facial paralysis (within hours)
• Inability to close eye
• Facial drooping with flattening of nasolabial fold
• Decreased tearing
• Hyperacusis
• +/- Loss of taste to anterior 2/3 of tongue

*May also present with additional cranial nerve neuropathy

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7
Q

What other conditions should be on your DDx for Bell’s Palsy?

A 
Herpes zoster
Otitis media
Lyme
Guillain-Barre
Tumor
Stroke
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8
Q

Cephalic herpes zoster with facial nerve involvement or herpes zoster oticus

A

Ramsay Hunt Syndrome

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9
Q

How do you differentiate Ramsay Hunt from Bell’s Palsy?

A

Evaluate for vesicles near external meatus and ask about preherpetic neuralgia

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10
Q

How do you differentiate Lyme disease from Bell’s Palsy?

A

BILATERAL (though can also be unilateral) lasting less than 2 months

May be associated with Lyme meningitis

Evaluate in young patient and other associated symptoms including erythema/swelling prior to palsy

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11
Q

How do you differentiate Guillain-Barre from Bell’s Palsy?

A

Progressive, SYMMETRIC and BILATERAL

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12
Q

How do you differentiate a tumor from Bell’s Palsy?

A

GRADUAL onset over 2+ weeks

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13
Q

How do you differentiate a stroke from Bell’s Palsy?

A

SPARES FOREHEAD!!!

Rarely, upper motor neuron strokes affect ipsilateral facial nerve nucleus or tract, but in general, they’ll be able to wrinkle their forehead and they can’t in Bell’s Palsy

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14
Q

UMN lesion affecting the contralateral portion of the lower face with forehead spared

A

Central Facial Palsy

Think about STROKE, TUMOR, MS, or trauma to motor cortex/corticobulbar tracts

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15
Q

LMN lesion affecting the ipsilateral side of the face and involving the forehead

A

Peripheral Facial Palsy

Think of BELL’S PALSY, Guillain-Barre, otitis media, Lyme, Ramsay Hunt

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16
Q

How is Bell’s Palsy diagnosed?

A

Typically a clinical diagnosis

  1. Diffuse facial nerve involvement
  2. Acute onset in 1-2 days —> progressive with max severity within 3 weeks —> improvement/recovery in 6 months
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17
Q

What is the progression of symptoms in Bell’s Palsy

A

Acute onset (1-2 days)

Max severity in 3 weeks

Resolution in 6 months

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18
Q

When do you need to order diagnostic studies for Bell’s Palsy?

A

Atypical symptoms
No significant improvement in 4 months
Progression beyond 3 weeks

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19
Q

If you DO decide you want diagnostic studies for Bell’s Palsy, what you ordering?

A

Electromyography (EMG)/Nerve Conduction Study (NCS)

CT/MRI

Labs:
• Serology for Lyme/HSV
• Fasting blood sugars in patients with risk factors for DM

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20
Q

How do you treat Bell’s Palsy?

A

Mild cases may resolve spontaneously within 2 weeks

PREDNISONE 60 mg qd x 5 days then taper by 10mg daily x 5 days OR 60-80 mg qd x 7 days

+/- Valacyclovir 1g TID x 7 days

Best results if treatment initiated within 3 days of Sx onset

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21
Q

What do you need to do about your patient’s eyes if they have Bell’s Palsy?

A

Because they can’t close one of their eyes, increased risk of drying, corneal abrasion, or corneal ulceration

Artificial tears (liquid or gel) applied hourly during the day

Eye ointments (mineral oil and petrolatum) at night, +/- patch

Sunglasses

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22
Q

85% of Bell’s Palsy patients improve within _______

A

3 weeks

Normal function returns in 3-6 months

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23
Q

What is the prognosis for Bell’s Palsy?

A

Generally good

New axon growth may be disorganized/synkinesis
• Blinking causes twitch in corner of mouth
• Smiling causes eye to wink

Recurrence rate 7-15% (pregnancy and genetics increase risk)

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24
Q

What is the other fancy name for Trigeminal Neuralgia?

A

Tic doulaureux

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25
Recurrent brief episodes of severe, unilateral pain along CN V
Trigeminal Neuralgia One or more branches of the trigeminal nerve may be triggered Pain is an electrical (shock-like) sensation
26
Who gets Trigeminal Neuralgia more, men or women?
Women
27
Incidence of trigeminal neuralgia increases with _____
Age Onset typically >50 yo Familial association is rare
28
_____ may be a risk factor for Trigeminal Neuralgia
Hypertension
29
What is the pathophysiology of Trigeminal Neuralgia?
Compression of CN V causes nerve demyelination Classic TN: • Idiopathic or vascular compression of the trigeminal nerve root Painful Trigeminal Neuropathy (Secondary Trigeminal Neuropathy): • Other causes: herpes zoster, vestibular Schwan MOA, meningioma, cyst, MS (may be bilateral)
30
Clinical presentation of trigeminal neuralgia
Paroxysms of shooting pain lasting a few seconds and may occur repetitively Frequency of episodes varies (daily or several times/month) Episodes of remission last for 6+ months Recurrence is often more frequent and disabling Typically UNILATERAL presentation Affects V2 and/or V3 most often (V1 may be associated with autonomic sx)
31
Unilateral or bilateral: Trigeminal neuralgia
Unilateral
32
Which branches of the trigeminal nerve are most often affected in TN?
V2 and/or V3
33
What can trigger an attack in trigeminal neuralgia?
Light touch can trigger - patient guarding is common Other triggers include chewing, talking, shaving, brushing teeth, cold air etc Physical exam may be completely normal
34
What is pretrigeminal neuralgia?
Continuous, dull ache in the jaw prior to classic TN symptoms present Rule out dental causes
35
What is the International Classification of Headache Disorders’ Diagnostic criteria for Trigeminal Neuralgia?
At least 3 paroxysmal episodes of unilateral facial attacks: severe intensity, shock-like/shooting quality Affects trigeminal nerve distribution only No neurological deficits
36
How do you diagnose trigeminal neuralgia?
Clinical suspicion should be followed by evaluation for secondary cause MRI with and without contrast preferred ? MRA for vascular compression in classic presentation
37
What is the pharmacologic therapy for trigeminal neuralgia?
Carbamazepine 100mg-200mg BID Increase gradually w/ typical maintenance dose of 600mg-800mg total daily Side effects: drowsiness, dizziness, n/v, leukopenia, and rarely aplastic anemia
38
When prescribing Carbamazepine for your patient’s trigeminal neuralgia, what precautions do you need to take?
Follow CBC routinely (b/c risk of agranulocytosis) Screen for HLA-B 1502 allele in Asian population (increased risk of Steven-Johnson syndrome if positive)
39
What are some alternatives if your TN patient can’t have carbamazepine?
Other anticonvulsants: Oxcarbazepine, gabapentin, phenytoin, lamotrigine Baclofen 40-80mg daily may be used alone or in combo with carbamazepine Topical lidocaine may be beneficial Maybe opioids (but need high dose so maybe not) Botox, glycerol injections Radiofrequency thermal lesioning Surgery if refractory to meds
40
What surgical options are available for TN if patient is refractory to pharmacologic therapy?
Microvascular decompression Ablation: Rhizotomy, Gamma knife radiosurgery
41
Chronic vasculitis of medium and large vessels —> diffuse inflammatory cells leading to wall thickening and decreased lumen
Giant Cell Arteritis
42
What are the two main things we worry about with Giant Cell Arteritis?
Ophthalmic artery occlusion —> blindness Basilar artery occlusion —> brain stem infarct
43
Incidence of giant cell arteritis increases with ______
Age Typically presents >50 yo and average age is 77
44
What population has the highest incidence of giant cell Arteritis?
Scandinavian descent
45
40-50% of GCA patients also have _________
Polymyalgia rheumatica
46
Possible presenting symptoms of GCA
NEW HEADACHE w/ extracranial vessel involvment • Unilateral, severe, +/- throbbing sensation • Aggravated by pressure or cold exposure Visual disturbances (diplopia/transient blindness - amaurosis fugax)***** Symptoms associated with polymyalgia rheumatica JAW CLAUDICATION Unexplained fever or other constitutional symptoms
47
Pathognomonic clinical sign of giant cell arteritis
Jaw claudication (present in 70% of cases)
48
Physical exam findings for GCA
HEENT: vision eval Tender, palpable temporal artery • Pulse is decreased or absent • Auscultate for bruits Muscle tenderness in neck and shoulders Check for carotid bruits
49
What labs you wanna get for your potential GCA case?
Anemia may be present, so CBC ESR = most useful screening tool CRP (elevated TEMPORAL ARTERY BIOPSY
50
And ESR of _____ is 95% specific for GCA, while ______ is about 60% specific
>50 mm/hr >100 mm/hr
51
What are you looking for on temporal artery biopsy to definitively diagnose giant cell arteritis?
Minimum of 1-2 cm section of artery (“skip lesions”) Presence of multi-nucleated cells is diagnostic
52
What are the American College of Rheumatology diagnostic criteria for Giant Cell Arteritis?
(3/5 sufficient for diagnosis) 1. Age of onset >50 2. New, localized headache 3. Temporal artery tenderness, decreased temporal pulse 4. ESR >50 mm/hr 5. Positive temporal artery biopsy
53
What is the goal in treating giant cell arteritis?
Prevent blindness or stroke**** Promptly initiate glucocorticoid treatment If suspicion is high then start prior to confirming diagnosis
54
What pharmacologic agents do you use to treat giant cell arteritis?
Prednisone 40-60mg PO daily; taper slowly starting at 2-4 weeks or with symptom control Continue with 10-20mg daily for 9-12 months Recurrence may require lifelong steroids Follow ESR/CRP
55
TMJ Dysfunction is characterized by...
Pain associated with TMJ misalignment —> muscular hypertrophy with malocclusion and arthritis
56
Who gets TMJ Dysfunction?
W>M Onset typically 20-40 years
57
Which condition puts a patient at a higher risk of TMJ dysfunction?
Rheumatoid Arthritis ``` May also be associated with: Bruxism Gum chewing Pencil biting Pipe smoking Musical instruments Trauma Mood and psych disorders ```
58
Clinical presentation of TMJ dysfunction
Periauricular pain and tenderness of TMJ and muscles of mastication HA or ear discomfort may also be associated Pain may radiate to ear, temporal, or periorbital areas CREPITUS WITH JAW MOVEMENT (clicking/popping, audible or palpable on exam)
59
What PE findings are suggestive of TMJ dysfunction
Subluxation/dislocation of jaw (catching vs locking) Decreased ROM - may demonstrate asymmetric opening and closing (Malocclusion) Abnormal dental wear
60
How is TMJ dysfunction diagnosed?
CLINICAL DIAGNOSIS Further eval if associated with other systemic sx: • CBC, ESR, RF, ANA • Plain films (panoramic) to eval erosions, osteophytes, arthritis • CT/MRI considered in extreme pain, abnormal radiographs, changes in cranial nerves, previous surgery to TMJ
61
How do you manage TMJ dysfunction?
Dental referral Heat Soft diet, avoid chewing gum Jaw exercises Oral appliances (occlusal splint) - $$$$
62
What pharmacologic agents can be used to treat chronic pain associated with TMJ dysfunction
Tylenol NSAIDs Muscle relaxants Trigger injections or surgery for refractory TMJ dysfunction

Clin Med III Unit 3 (5 decks)

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