Neurology disorder Flashcards
Bell’s palsy
Idiopathic facial nerve
palsy.
Acute, spontaneous, unilateral facial paralysis
cranial nerve VII palsy
Bell’s palsy presentation
Disappearance of the nasolabial fold
decrease tearing on the affected side
inability to wrinkle the forehead
loss of taste sensation
inability to pucker lips
treatment of Bell’s palsy
prednisone
concussion
mild traumatic brain injury
GCS =13 or > Glasgow coma scale
concussion treatment
physical rest 24-48h with a gradual return to activity
cognitive rest minimizes cognitive activities that exacerbate symptoms
recurrent concussion
may indicate overexertion during recovery
if a migraine history, a concussion may trigger migraine HA
promote sleep it help recovery
cognitive recovery may be longer than physical recovery
refer for symptoms lasting >21 days or escalating symptoms after injury or multiple concussions
After a concussion when back to school or work?
when able to focus for 30-45 mins at a time
back to sports?
return-to-school success
symptoms free, no meds
normal neuro exam
Back to sports ?
light aerobic exercise (increase HR)
sport-specific exercises (add movement
noncontact participation
full contact practice (assess status)
normal game/physical activity
Headaches?
primary headaches: migraine, tension, cluster
Secondary headaches: underlying pathology “ red flag” headache
NB
New onset headache in a middle/older adult (>50) is usually secondary
papilledema
swelling of the optic disc due to increase ICP
Almost always bilateral
CT vs MRI
CT : radiation,look at cavities, intracranial hemorrage, tumor, hard thing, bones
quick 5min
MRI: no radiation. look at soft tissue, brain , spinal cord, ligament, tendon, injuries
nonemergent
Dx of migraine without aura
-headaches last 4-72 hours
has 2 of these characteristics unilateral, pulsating quality, mod to severe intensity, aggravated by routine activity
-during headache: N and /or V , photophobia or phonophobia (at least 1)
-5 or more attacks have occurred with these characteristics
-no other reason for the headaches occurrence
Dx migraine with aura
25% of pt have aura
-2 attacks of migraine with aura
-visual. sensory, motor, and brainstem. retinal. or speech change fully reversible
-develops over 5-60mins , headache develop within 60minutes
treatment
first line -Acetaminophen
NSAIDs
triptans
calcitonin gene-related peptide CGRP
prophylactic agents : beta blockers propranolol, timolol
antidepressant amitriptyline, venlafaxine
anticonvulsants: valproate, topiramate
Vertigo
either peripheral or central etiology
peripheral etiology involves the vestibular system (BPV)
central involves the brainstem or cerebellum (stroke)
is vertigo peripheral or central
peripheral (vestibular)
-visual fixation stops nystagmus
-walking preserved
-hearing may be impaired
-normal neuro check
Central
-visual fixation does not stop nystagmus
-often falls with walking
-hearing usually intact
-abnormal neuro exam
clue to etiology of vertigo
-Less than 1 minute, single episode - BPV
-Few minutes to hours, single, episode-migraine, TLA of labyrinth or brain stem
-Several mins or hours, recurrent- Meniere;s , vestibulopathy
-Days, prolonged and severe - vestibular neuritis, MS, brain stem infarct
The Dix-Hallpike
The Dix-Hallpike maneuver is the gold standard for diagnosing benign positional paroxysmal vertigo caused by a posterior canal otolith. The patient is positioned recumbent with the head back and toward the affected ear, causing the otolith to progress superiorly along the natural course of the canal.
The Dix-Hallpike test diagnoses the condition and the Epley maneuver treats it by encouraging the tiny calcium carbonate crystals to move back where they belong.
Treatment
-Meclizine-Antivert
-Dimenhydrinate-Dramamine
-Diphenhydramine-Benadryl
Diabetic Neuropathy
-Distal symmetric polyneuropathy
DSPN= diabetic neuropathy
-15-20% of DM neuropathy patients have pain
-symptomatic neuropathy is not usually reversible
Differential diagnosis of
=Metabolic-diabetes, B12, deficiency, hypothyroidism
=Toxic- Alcohol
= Diffuse motor without sensory- Guillain-barre syndrome, myasthenia gravis
=inflammatory infectious - sarcoidosis, lupus, Lyme disease
Preventive care
-glycemic control
-modify risk factors (BMI, Bp, A1c, minimal EtOH consumption , avoidance of smoking ect)
-foot care
Pharm treatment
SNRI: duloxetine (Cymbalta, Venlafaxine (Effexor)
TCA: amitriptyline, desipramine, nortriptyline
Gabapentinoid: pregabalin (Lyrica) , gabapentin (Neurontin)
patient evaluation
-Screening in asymptomatic patients is NOT recommended
- history of cognitive/behavioral changes (from family or significant other)
-Med history asks about analgesics anticholinergics, psychotropics, sedative-hypnotics
patient evaluation
-MMSE
-Montreal cognitive assessment (MoCA)
-if there is a discrepancy between cognitive testing and physical exam, further testing is need
Depression
Depression can worsen cognitive impairment
Always screen for depression (consider PHQ2)
Treatment of AD
Cholinesterase inhibitors: Donepezil, rivastigmine, galantamine.
NMDA receptor antagonist, memantine.
Advanced AD:
use in combo with cholinesterase inhibitors (donepezil/memantine)
pharm for severe , persistent symptoms
Olanzapine (consider first)
Quetiapine (consider as an alternative)
May increase mortality. side effects
cranial nerves
Oh Oh Oh To Touch And Feel Very Good Velvet AH
O-Olfactory
O-Optic
O-Oculomotor
T-Trochlear
T-Trigeminal
A-Abducens
F-Facial
V-Vestibulocochlear
G-Glossopharyngeal
V-Vagus
A-Accessory
H-Hypoglossal
