Neuro-peripheral Flashcards by Lux Smith

controls the 1. Muscles of facial expression

VII- facial
You’re lucky if you get a facial

if you’re lucky you are smiling

all come out of the parotid

Temporal
Zygomatic
Buccal
Mandibular
Cervical

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what CN involves the muscles of mastication

V- Trigeminal

snesory

if you TRI to kiss me i will feel it

V1-tip of the nose
V2
V3

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the first brachial arch is innervated by the

trigeminal -5

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the second brachial arch ins innervation by the

facial -7

remember nerves are in place before development and then carried with development

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MCC of facial pain

Trigeminal nerve issue

dental, triggers include hot, cold, sweet foods

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what is the term used to describe pain in the trigeminal nerve

Lancinating pain like zaps

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dx associated with CNV pain

trigeminal neuralgia

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tic douloureux”

trigeminal neuralgia

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what divisions are most commonly hit by trigeminal neuralgia

V2 and V3

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if you have neuralgic looking pain that is bilateral or in a young person what ddx do you want to consider

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nueralgic pain is usually described as iv. Pain at ____ points,_____ sensory deficit

iv. Pain at trigger points, without sensory deficit

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tx for neuralgic pain

Neuropathic pain - AVOID narcotics
Antiepileptic agents have proven effective

a. Carbamazepine, phenytoin (Dilantin), gabapentin

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what do you want to be careful of with antieplileptic prescribed for nerualgia?

need to titrate in order to avoid a seizure

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what is the surgical intervention for neuralgic facial pain

a. Usually attempts to relieve decompression by tortuous vasculature in the posterior fossa or along path of CN V

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why do we see hyperacusis with damage to the to the facial nerve

chorda typmani is a branch of the facial nerve If paralyzed, the TM moves more and it sounds louder

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shingles like eruption in pharynx, ear canal distinguish what should we suspect

i. Ramsay Hunt

can cause facial paralysis and hearing loss in the affected ear.

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geniculate ganglion vs CN VII

geniculate ganglion an L-shaped collection of fibers and sensory neurons of the facial nerve located in the facial canal of the head.

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Bell’s palsy affects what CN

VII

this is why we see v. Hyperacusis

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recover with bell’s palsy

60% recover c/o treatment
Only 10% with permanent disfigurement or disability
Assess severity in early disease

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indicators of poor prognosis with bell’s palsy

Poor prognosis associated with age, hyperacusis (b/c its more into the CNS), severe early pain

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two major classifications of neuropathies

mono =compression/trauma thing

poly= metabolic, toxic or hereditary cause

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why do we typically see stocking-glove distribution with neuropathies

longest nerves are affected first

iv. Begin distally, usually (stocking-glove distribution) and move proximally

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MC mono neuropathies

MC:
ulnar (elbow or lateral part of hand),
median (carpal tunnel), peroneal/common fibular (in the leg near tib/fib)

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what predisposes you to mononeuropathies

pregnancy
DM
arthritis
tumors

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positive and negative sxs associated with poly neuropathies

Positive (paresthesias = pins and needles) negative (numbness) symptoms

preserved muscle bulk is a sign of uMN or LMN

UMN LMN seen wiht atrophy

what type of muscle tone would we expect to see in UMN dz

spasctic knife opening

spontaneous movement seen with UMN or LMN dz

LMN fasciculations

reflexes are increased in UMN or LMN

UMN kickin can of preserved muscle bulk that you have to open wiht a knife and fan our like a bb

bibinski's sign is present UMN or LMN

UMN

what is an example of UMN dz

CVA or MS

ii. Position in space and vibration tell us about

posterior columns)

Pain and temperature

spinothalamic tract

Discriminative sensations

involve cortical input

Most prevalent inherited ataxia

a. Friedreich's Ataxia

first disturbance in friedreich's ataxia

iv. Gait is first disturbance

onset of friedreich's ataxia

ii. Presents in childhood (5-15), early adulthood

babinski positive of negative in friedreich's ataxia

Babinski --> UMN

what is most commonly the cause behind trigeminal neuralgia

90% of the time caused by compression of CN by the superior cerebral artery especially in older pt with less compliant artery

ddx of bells palsy

CVA/TIA, Lyme, herpes Zoster

classification of peripheral neuropathies

a. Axonal b. Paranodal/segmental demyelination c. Mononeuropathies by compression

the diminished ability to perceive pain, temperature, touch, or vibration.

hypoesthesia

decreased sensitivity to painful stimuli.

hypalgesia

ability of the patient to identify numbers or letters drawn in the palm of the hand.

●Graphesthesia

ability to recognize common objects such as keys, coins or paper clips by touching or handling them with one's eyes closed. ●

Stereognosis

evaluated by simultaneously touching two separate points on either side of the body.

Extinction

why do we see a positive romberg test

when the patient has lost proprioception from feet

Mononeuropathies

pathology affecting an individual peripheral nerve

Radiculopathies refers to

Radiculopathies refer to pathology affecting the nerve root,

anterolateral spinothalamic tract AP are perceived as

pain

AP carried over the dorsal column medial lemniscal system are perceived as

touch or pressure

describe the neural transmition of touch of pressure

occurs through the medial lemniscal pathway posterior columns receive signal on first order neuron that is translated to the medulla which then synapses with a second motor neuron and crosses over where it is transmitted to the thalamus synapses to a 3rd order neuron and then reach the sensory cortex of the brain (parietla lobe) you can also have the transmission of pain going directly from the posterior horn to the anterior horn --> reflexes

describe the neural pathway of pain

synapse is made in the posterior horn

vascular ischemic theory of diabetic neuropathy

1. Hyperglycemic damage of capillaries that feed nerve cells so they can't deliver proper blood flow (not enough blood to feed the axon)

iii. Laminin theory behind Diabetic neuropathy

lack of normal laminin in basement memebrane, effects growth of nerve fiber and capillaries

iv. Autoimmune theory behind diabetic neuropathy

1. Immunogenic disruption of endotheliumí nerve damage

v. Altered neurotrophic effect

1. Altered production/transport of NGF (nerve growth factor) that results in damage to the nerve

ii. Follows infection (Campylobacter), vaccine, surgery seen commonly with Gi symptoms and involves respiratory complaints 40% of the time

Guillain barre LMN

lab diagnostics for guillain abrre

protein in the CSF (you also see this with MS)

carpal tunnel is most bothersome at what part of the day

night

tx for carpal tunnel

Modify 2. Splint 3. Drugssss iii. NSAIDs - pain relief in 20-30 mins; anti-inflammatory effects in 7-10 days -- Keep the inflammation down w/ ices

etiologies of UMN lesions

stroke multiple sclerosis cerberal palsy brain or spinal cord damage

etiologies of LMN lesions

``` guillan barre syndrome botulism poliomuelitis cauda equina syndrome bells palsy ```

spastic paralysis is more associated with umn or lmn lesions

UMN

fasciculation are associated with UMN or LMN

End stage LMN

iv. Discriminative sensations involve what type of input from the brain

cortical

if you can't stimulate the ventral horn with sensory input you get

hyporeflexia ventral horn is another name for the anterior horn

What can lack of Position and vibration sensation indicate?

posterior columns lesions, Fingers and toes first

What can lack of light touch sensation indicate?

posterior and spinothalamic

What can lack of discrimination sensation indicate?

involve cortical input

Describe the presentation of Diabetic Neuropathy

1] Sensory before motor, 2] Dulled perception of vibration, pain and temperature 3] Denervation of small muscles results in toe clawing, 4] Decreased pain, high pressures leads to ulcers 5] Also effects autonomic nerves

Antibodies to Cj cross react with nerve fibers

Describe pathophysiology of Guillain Barre Syndrome due to Campyloabacter

Neuro-peripheral Flashcards

(72 cards)