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CMT-uno > Neuro /Bells Palsy/TN/Myasthenia Gravis > Flashcards

Neuro /Bells Palsy/TN/Myasthenia Gravis Flashcards

1
Q

Amygdala

A

fear and aggression, facial evaluation, social processing, (and odor processing)

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2
Q

Cerebellum

A

implicit/procedural/motor memory

Implicit memory is skills, action, and emotional conditioning

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3
Q

Prefrontal Cortex

A

memory encoding and retrieval

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4
Q

Limbic System

A

Involved in emotional responses:
-controls emotional experience and expression
-can modify the way a person acts
-produces such feelings of fear, anger, pleasure & sorrow
-recognizes life threatening disruptions in a person’s physical or psychological condition and counters them

Initiates fight-or-flight (SNS) system
-Guides a person into behavior that may increase chances for survival

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5
Q

choroid plexus

A

500 mL CSF formed each day (mainly) by choroid plexus in lateral ventricles.

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6
Q

Cerebellum

A

General Functions:
Muscle memory
Balance (proprioception)
Equilibrium (vestibular)
Muscle Tone
Coordination
Motor Learning

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7
Q

Bulbar Nerves

A

CN IX
CN X
CN XI
CN XII
-common “function” of chewing, swallowing, head/neck movement

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8
Q

Lower motor neuron

Alpha motor neurons

A

To extrafusal muscle fibers
Force generating contractions

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9
Q

lower motor neuron

gamma motor neuron

A

To intrafusal muscle fibers
Muscle tension and reflex contractions

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10
Q

Bell Phenomenon

A

Left eye rolls upward and inward

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11
Q
A

bells palsy

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12
Q
A

bells palsy

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13
Q

Bell palsy essentials of dx

A

-Sudden onset of lower motor neuron facial palsy.
Deficits evolve in 72 hours
-Hyperacusis or impaired taste may occur.
-No other neurologic abnormalities.

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14
Q

Bell palsy other potential findings (pain)

A

Post auricular pain
Concurrent or prodrome

Trigeminal neuralgia ~ 8%

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15
Q

Bells palsy

Sx onset and prognosis

A

Deficits evolve in 72 hours

Recovery of normal facial function occurs in majority

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16
Q

Bell Palsy: Epi

A
  • Most common etiology of unilateral facial nerve palsy
  • Usually adults, peak ages 20-40
  • Men and women equally affected
  • More often on right side of face
  • Rarely occurs in summer
  • DM, immunocompromise, preeclampsia
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17
Q

Bells palsy

etiology

A

HSV hypothesis: after causing primary infection on lips (cold sores), virus travels up sensory nerve axons and resides in geniculate ganglion. At times of stress, virus reactivates and causes local damage to myelin.

Autopsy studies have shown HSV in geniculate ganglion of patients with Bell palsy.

Other potential causes: Lyme disease, syphilis, EBV infection, CMV, HIV; inflammation alone; microvascular disease (DM andHTN). Has also been known to follow recent URI.

May be secondary to autoimmune reactions that cause facial nerve to demyelinate.

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18
Q

bells palsy

Patho

A
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19
Q

bell palsy

Dx

A

Unilateral facial palsy of acute onset
Evolved within 72 hours
Ipsilateral postauricular pain/mild to moderate otalgia/hyperacusis or phonophobia
Hypo or dysgeusia
Subjective tongue and facial hypoesthesia
Pfizer vaccine

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20
Q

Facial palsy of known etiology (e.g. Lyme Disease), or a palsy that is progressive, waxing and waning or affects facial zones in an uneven fashion—

A

is NOT Bells Palsy

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21
Q

Bells palsy

PE

A

Focused neuro exam, complete head and neck exam including detailed CN exam, otoscopy, and tuning fork exams - Except for ipsilateral facial palsy, the exam should be unremarkable

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22
Q

Bells palsy

Upper vs Lower motor neuron

A
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23
Q

possible bells palsy?

Uneven distribution?

Vesicles (auditory canal or auricle)?

A

Suggestive of neoplasm –> imaging

Zoster

24
Q

bell palsy

red flags

A
25
Q

Bells palsy

Dx testing

A

Imaging when indicated to rule out stroke or neoplasm

Lyme testing if known tick bite or travel to tick endemic area

26
Q

bell palsy

Tx

A
27
Q

bells palsy

eye protection

A

Artificial tears during the day, tape shut at night with lubricant

28
Q

bell palsy

Severe cases Tx

A

For severe cases:
Refer to a Neuro-ophthalmologist and Neurologist for further evaluations and treatments > surgery???

29
Q

bell palsy

prognosis and follow up

A
30
Q

Trigeminal Neuralgia

Essentials of Dx

A

Brief episodes of stabbing facial pain. [attacks following sensory distribution of CN V, usually right sided]
Pain is in the territory of the second and third division of the trigeminal nerve.
Pain exacerbated by touch.

31
Q

trigeminal neuralgia

International Headache Society criteria

A
32
Q

trigeminal neuralgia

Patients can localize their pain precisely

A
33
Q

Trigeminal neuralgia

triggers

A

Chewing, talking, smiling
Drinking cold or hot fluids
Touching, shaving, brushing teeth, blowing nose
Encountering cold air from open automobile window

Patients carefully avoid rubbing the face or shaving trigger area, in contrast to other facial pain syndromes, in which they massage the face or apply heat or ice
Many patients try to hold face still while talking, to avoid precipitating an attack

34
Q
A

trigeminal neuralgia

35
Q

trigeminal neualgia

more about TN pain

A
36
Q

Trigeminal neuralgia

Epi

A

More likely biologic females than biologic males
Usually begins after age 40, typically 60-70 years
HTN is risk factor

37
Q

TN

Dx

A

Characteristic pain distinguishes it from other causes
Labs and imaging not always needed
May use labs as baseline for monitoring treatment drug effects
Imaging if lesion is suspected

38
Q
A
39
Q

TN

Tx

A

AEDs: Carbamazepine and oxcarbazepine
Inhibit neuronal sodium channel activity, reducing excitability of neurons

Gabapentin, esp in patients with M
Modulation of excitatory transmitters involved in pain

Lamotrigine
Inhibits release of glutamate (excitatory amino acid) and inhibits neuronal sodium channel activity, which stabilizes neuronal membranes, reducing excitability

40
Q

TN

Surgical Tx (3)

A

Microvascular decompression

Gamma Knife treatment damages trigeminal nerve to stop transmission of pain signals

Radiofrequency damages trigeminal nerve to stop transmission of pain signals

41
Q

Tn

complications of surgery

A

Complications of surgery include permanent anesthesia over face or disabling, spontaneous postop pain (can be worse than original trigeminal neuralgia, and often untreatable)
Many patients require pain medication even after surgery

42
Q

TN

prognosis

A

Tends to be chronic
Treatments may fail

43
Q
Serum positive for antibodies to ACh receptors nerve stimulation studies show decreased motor neuron responsiveness
A

Myasthenia Gravis (MG)

44
Q

Myasthenia Gravis (MG)

general

A

Autoimmune disorder of postsynaptic membrane at neuromuscular junction

Characteristics
rare
presents at any age
males and females
fatigable muscle weakness:
eyelids (ptosis common) and EOM fatigue
face, neck, extremities & respiratory muscles

45
Q

Myasthenia Gravis

S/Sx

A

Partial paralysis of eye movements(ophthalmoparesis), double vision (diplopia), and droopy eyelids (ptosis) are usually among the first symptoms.

> 50% present with ocular symptoms of ptosis and/or diplopia.
Of those who present with ocular sx, half will develop generalized disease within two years.

Weakness and fatigue in neck and jaw also can occur early (Bulbarweakness — impairment of function of CNIX, X, XI, XII) — dysarthria, dysphagia, difficulty holding up the head. About 15% of patients.

46
Q

Myasthenia gravis

generalized Sx

A

weakness spreads from face/neck to upper limbs, hands, then lower limbs. (difficult to lift arms overhead, rise from sitting position, walk long distances, climb stairs, grip heavy objects).
Limb weakness alone in 5%

47
Q

MG

Patho

A

Immune system attacks Ach receptors on muscle, so muscle can no longer contract in response to Ach release from motor neurons

48
Q

Mg

Ice Pack test

A

part of neuro exam if ptosis; based on principle that neuromuscular transmission improves at lower muscle temperatures.

Assess ptosis, fill surgical glove with ice, place on closed lid for two minutes; remove ice and reassess ptosis; improvement is positive test result.

49
Q

MG

Edrophonium (“Tensilon”) test (historical)

A

Drug = acetylcholinesterase inhibitor with rapid onset (30 to 45 seconds) and short duration of action (5 to 10 minutes); prolongs presence of acetylcholine in neuromuscular junction and results in immediate increase in muscle strength.

50
Q

MG

blood Work up

A

Serum anti-AChR antibodies
positive in 80-90% with generalized MG

Anti-muscle-specific tyrosine kinase (MuSK) antibodies
positive in up to 70% of anti-AChR negative patients
facial, respiratory, proximal muscle weakness

Seronegative for both antibodies ~10%

Consider screening for concurrent thyroid disease

51
Q

MG

electrical work up

A

EMG testing: repetitive nerve stimulation shows decremental change in amplitude of muscle response

52
Q

MG

Imaging

A

CT or MRI: thymus gland abnormality (thymoma)

53
Q

MG

Tx
Meds and surgical

A
  • Symptomatic (acetylcholinesterase inhibition) to increase amount of acetylcholine (ACh) available at neuromuscular junction
  • Chronic immunosuppressive therapies (glucocorticoids) to target underlying immune dysregulation
  • Rapid but short-acting immunomodulating treatments (therapeutic plasma exchange and intravenousimmune globulin[IVIG])
  • Surgical treatment (thymectomy)
54
Q

MG

Mild disease management

A
  • no treatment
  • pyridostigmine (cholinesterase inhibitor)
  • add corticosteroids if unresponsive to inhibitor
55
Q

MG

Crisis (severe weakness, respiratory failure)
Tx

A
  • intubation and mechanical ventilation
  • plasma exchange/IV immunoglobulin
56
Q

MG

Moderate disease Tx

A

pyridostigmine + immunosuppressant (steroids, cyclosporine, tacrolimus)

57
Q

MG

Thymectomy

A

patients with thymoma (any age)
May not benefit MuSK antibody+ patients
patients with generalized MG and AChR
antibodies < 60 years of age

CMT-uno (54 decks)

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