Peripheral Nervous System Disorders II Flashcards
1
Q
What is Bells palsy/facial nerve paralysis
A
- Unilateral facial paralysis due to compression of CN VII caused by inflammation & swelling
2
Q
Incidence of Bells palsy/facial nerve paralysis
A
- Develops suddenly over hrs to days
- Causes one side of face to droop, become stiff over time
- Mostly temporary
- Affects 20-30 per 100,000 people/year
- Common age group 15-45 yrs
3
Q
Etiology and pathology of Bells palsy
A
- Suspected to be triggered by viral infections but lacks direct evidence, many cases lack signs of acute viral infection preceding onset
- More likely caused by re-activation of a latent virus rather than direct infection
- Most likely caused by herpes simplex/zoster, mumps, rubella
- Inflammation of the nerve causes compression that could lead to ischemia, demyelination, & axonal degeneration
4
Q
Risk factors of Bells palsy
A
- DM
- Pregnancy
- Hypothyroidism
5
Q
Describe the facial nerve course
A
- Passes through long bony canal causing increased risks for compression with inflammation & swelling
6
Q
Clinical manifestations of Bells palsy
A
- Unilateral facial paralysis, asymmetrical facial appearance
- Sx develop rapidly, often overnight
- Corner of mouth droops, nasolabial fold flattens, eyelids do not close
- CN VII also innervates stapedius muscle, receive taste sensation & provides autonomic innervation for salivation & lacrimation
- Compression proximal to chorda tympani branch can cause loss of taste
- If stapedius muscle innervation lost = sounds become louder
- Autonomic involvement causes dry/red eyes (lack. of tearing), thicker saliva
- Severe/chronic = pain, contractures, semi-facial spasms
- Bell’s reflex: rolling up of eyeball during attempts to close eye
7
Q
After severe injury axonal regrowth/rewiring could be misdirected & can cause
A
- Synkinesis: involuntary & undesirable facial movements associated with voluntary facial movements
- Voluntary activation of one muscle group can activate other muscles (blinking can activate mouth twitch & smelling can cause blink
- Autonomic misdirection can also happen: involuntary lacrimation while eating (crocodile tears)
8
Q
Describe how to diagnose Bells palsy
A
- Observation & physical exam
- Ask patient to wrinkle forehead, close eyes tightly, smile, whistle and observe for symmetry
- Electrodiagnostic tests: NVC/EMG can determine demyelination vs axonal degeneration
- NVC/EMG: Amplitude 90% drop = less than complete recovery; loss >98% = significant residual weakness & synkinesis
9
Q
Differential diagnosis between Bells palsy(facial nerve) and a stroke
A
- Observe forehead wrinkle, eye closing, & voluntary smiling
- Facial nerve/Bells palsy will effect one whole side of face while a stroke will only effect the lower half of face
10
Q
House Brackmann grading scale for Bells palsy severity categorization
A
- (1) Normal = normal facial function in all areas
- (2) Mild dysfunction = slight weakness noticeable only on close inspection; no synkinesis, contracture, or hemifacial spasm
- (3) Moderate dysfunction = pts who have obvious but no disfiguring synkinesis, contracture, and/or hemifacial spasm. are grade III. regardless of degree of motor activity
- (4) Moderately severe dysfunction = pts with synkinesis, mass action, and/or hemifacial spasm severe enough to interfere with function are grade IV regardless of motor activity
- (5) Severe dysfunction = only barely perceptible motion; synkinesis, contracture, and hemifacial spasm usually absent
- (6) Total paralysis = loss of tone, no motion
11
Q
Treatment for Bells palsy
A
- Early Tx with corticosteroids: anti-inflammatory effect can reduce the swelling of the facial nerve/compression in the facial canal
- General care includes proper eye care using artificial tears & ophthalmic ointment to prevent corneal abrasion & ulceration
12
Q
Prognosis for bells palsy
A
- Favorable that 85% show recovery within 3 wks
- 71% show. full recovery
- Degree of severity at onset is an important factor
- EMG results: A 90% drop in amplitude predicts less than complete recovery, and loss greater than 98% predicts significant residual weakness and synkinesis
- Absence of improvements at 3-4 mo should raise concerns regarding diagnosis & lead to search for alternative diagnoses
13
Q
Bells palsy implications for PT
A
- Neuromuscular re-ed using EMG biofeedback to regain motor control: helpful for synkinesis Tx
- Muscle stretches & exercises like wrinkling, puffing, closing eyes tightly, smiling, chin tuck, etc. can help maintain flexibility, decrease pain, & improve circulation in the affected muscles
- Facial E-stim lacks much evidence
14
Q
What is Charcot Marie Tooth disease
A
- Inherited motor & sensory neuropathy (HMSN)
- Slowly progressive disorder
- Characterized by distal limb weakness & wasting, skeletal deformities, distal sensory loss & reduced DTRs
- Fibular (peroneal) nerve is frequently affected 1st, aka perineal muscular atrophy (PMA)
- Progressive muscular atrophy foot.lower legs, progressing to hands/forearms
15
Q
Etiology and pathology of Charcot Marie Tooth disease
A
- Relatively common neuropathy
- Mostly autosomal dominant pattern of genetic mutation (autosomal recessive is rare)
- 2 genetic subtypes: CMT1 & 2
- Frequent de-/re- myelination causes hypertrophic ‘onion bulb’ formation around affected axon segments that contains Schwann cells & its processes (creates palpable areas along the peripheral nerves)