Neurology Flashcards
What is CT scan? When is it used?
produces XR similar to conventional XR but produces cross sectional images without superimposing tissues on each other - used in trauma situations due to speed and superiority over plain film
used in initial CVA/neuro studies but NOT preferred over MRI
fat is black on a CT scan (vs white on MRI)
What is SPECT? When is it used?
Single position emission CT; function CT scan of the brain
used in dx of dementia
What is unique about a PET scan?
reveals the cellular level metabolic changes occuring in an organ/tissue (important bc this is where disease proceses often begin; earlier detection)
imaging of choice for nervous system
MRI
what is the procedure of choice in CNS diagnosis?
Imaging (MRI) except in cases of meningitis > lumbar puncture
Low Ach =
decreased memory, delirium, delusions
high ach =
aggression, depression
low dopamine =
dementia, movement disorders, depression
high dopamine =
psychoses, anxiety, confusion, aggression
low norepi =
depression, dementia
low GABA =
anxiety
high GABA =
affective decrease, lethargy
low glycine =
anxiety
high glycine =
affective decrease, lethargy
low NO =
vasospasm, potential hyperactivity
high NO =
sedation, vasodilation, visual hallucinations
low histamine =
depression
high histamine =
mania
“Downers” (neurotransmitters)
GABA
glycine
NO
histamine (special instances)
neurosteroids
“uppers” (neurotransmitters)
serotonin
ach
dopamine
NE
histamine
glycine (special instances)
neuroleptic MOA and classes
dopamine blocking
phenothiazine
benzisoxazole (respiradone)
butyrophenon (haloperidol)
dibenzodazepine (clozapine, quetiapine)
thienebenzodiazepine
adverse effects of neuroleptics/antipsychotics
tremors/parkinsonian effects
spasms/movements you cant control
tardive dyskinease
POTS
blurred vision, dry mouth, constipation, urinary retention
sexual dysfunction
drowsiness
what is neuroleptic malignant syndrome? how does it present, and what is the tx?
too much neuroleptic drug; catatonia, fluctuating BP, dysarthria, and fever
fatal unless antipsychotic immediately discontinued and tx with dopamine agonist such as bromocriptine
If you are looking at doing AA therapy with somebody, what is an important consideration?
make sure their B vitamin/mineral cofactor levels are at proper level
supplement for concentration/cognitive support
phosphatidylcholine - donates choline for ach syntehesis
supplement for sleep-wake regulation
phosphatidylserine - donates choline, supports dopamine production
supplement for serotonin affected syndromes
phosphatidylinositol - sensitizes serotonin receptors
NT therapy for the tx of depression
catecholamine therapy (need uppers)
serotonin therapy (need leveling)
combination?
NT therapy for the tx of anxiety/sleep/seizure/mania
GABA
glycine
NMDA antagonist
NO
histamine
supplements for depression
SAMe
phenylalanine
tyrosine
(inc dopamine and norepi)
what nutrients are precursors for catacholeamines and should be avoided if someone is on a dopamine reuptake inhibitor?
tyrosine
phenylalanine
reuptake of dopamine is blocked by:
cocaine
buproprion
benzatropine
amphetamine
norepi reuptake is blocked by
tricyclics
amphetamine
serotonin comes from the breakdown of ____
tryptophan >
> serotonin > melatonin
> niacinamide (low niacin might steal tryptophan for its pathway)
serotonin is degraded by
MOA
aldehyde dehydrogenase
what is key for SSRI lowering/removing?
tryptophan and cofactors (B3, iron, B5, B6, B12, folate)
taper drug almost all the way/fully first before adding nutrients
signs/sx of serotonin syndrome
fever
hyperreflexia
BP changes
coma
death
tricyclic drugs MOA
“combinations” catecholamines AND serotonin
tricylcic discontinuation considerations
watch for rebound insomnia, replace NE and 5HT with SLOW tapering
drugs for depression and central pain
citalopram (SSRI)
escitalopram (SSRI)
duloxetine (SSNRI)
drugs for fibromyalgia
mostly antidepressants raising serotonin, NE, DOPA, or all three
one is an atypical anti-seizure med
histamine effects in the brain
H1 (stimulating)
H2 (stimulating)
H3 (inhibiting)
H4 (inhibiting)
so h1/h2 blockers can produce somnelesence > used for insomnia
3 Bs of GABA reception
booze
barbiturates
benzodiazepines
GABA overdose
GABA comes from ____
glutamine
glutamine > GABA (relaxing)
glutamine > glutamate (stimulating)
inhibitory activity of the CNS is caused by
chloride channel opening (by GABA or glycine)
why is progesterone considered a neurosteroid?
binds to GABA receptor
what is the class effect of barbituates/benzos?
amnesia (faster hits ur brain = more amnesia)
what is an anxiety drug with no GABA effect/addictive qualities?
buspirone
there is a need for extreme caution in patients with what dx in glycine supplementation?
bipolar; potential NMDA (glutamate) receptor triggering > mania
excitatory action NMDA receptors
- glycine (in some cases)
- glutamate
- zinc
how to dx epilepsy
can NOT dx with secondary seizure cause (tumors, organic dz, etc)
MRI image of choice, LP may be done in some cases
simple partial seizure
limited to single part of body/one aspect of bx
consciousness preserved
focal motor (convulsive jerks) or somatosensory (paresthesia or tingling)
jacksonian seizure
spread to “march” to diff parts of limb to body
sensory sx (light flashes, smells, buzzing, songs)
autonomic sx (flushing, sweating, epigastric sensations)
complex partial seizure
s/s may change during attach (hallucinations > complex motor acts)
change in or loss of consciousness
deja vu, fear, pleasure, anger
can lead to tonic-clonic/complete seizure
generalized seizures
may evolve from partial seizures
paroxysmal neuronal d/c generalized to both sides of the brain
usually has alteration or LOC
two major kinds - absence (petit mal) and tonic clonic (grand mal)
absence (petit mal) seizures
begin 2-12
+ fhx
two types: simple absence (1-2 sec, blank stare, spacing out), complex absence (15-30 sec, head drops, arms jerk, every 10-100 days, hyperventilating can trigger > can lead to grand mal as adults)
tonic clonic (grand mal)
most extreme, can begin at any age
triggered by fatigue, fever, low Ca, glucose, magnesium
may be preceded by prodrome of mood change, apprehension, loss of appetite
tonic (10-20 sec) body stiff/arch, cyanotic
clonic (series of jerks, loss of sphincter control, bite tongue)
post ichtal - flaccid relaxation, heavy breathing/salivating
> wake up, sleep for several hours, start new convulsion (status epilepticus)
what is an important dietary consideration for a pt on lithium?
NEVER low sodium diets! lithium interferes with sodium ions in the brain (and rest of body)
common long term kidney adverse effects
kidney dz
hypothyroidism
what nutrient used with ritalin improves ADHD sx control in children?
zinc
bacterial meningitis etiology, presentation
e coli, h flu, meningococcus
HA with photophobia
purpuric rash on trunk, fever
nuchal rigidity (not always in peds/neonates)
obtundation (dec alertness)
toxic appearance
most common organisms and tx for meningitis in ages: 0-4 weeks
group B strep, e coli, listeria
ampicillin + cefotaxime
most common organisms and tx for meningitis in ages: 4-12 weeks
strep pneumo, group B strep, e coli, listeria
ampicillin, third generation cephalosporin
most common organisms and tx for meningitis in ages: 3 mo-18 years
s pneumo, n meningitidis, h flu
third gen cephalosporins
most common organisms and tx for meningitis in ages: 15 years-50 years
s pneumo, n meningitis
third generation cephalosporin
most common organisms and tx for meningitis in ages: >50 years
s pneumo, n meningitis, listeria, aerobic gram - bacilli
third generation cephalosporin + ampicillin
encephalitis presentation and etiology
severe: HA with systemic sx, focal neuro deficit
sub acute: similar to severe viral illness, HA persists as systemic sx wax and wane
viral: CMV, HIV, polio, rabies
bacterial: listeria, TB, syph, rickettsia, toxoplasma gondii
EEE (togaviridae) from bird as reservoir (ppl and horses get the disease)
MMR/chicken pox > AI encephalitis
HSV 1+2
what sign/sx can differentiate between meningitis and encephalitis?
focal neuro deficit present in encephalitis
presentation rabies
dog or wild carnivore bite
negri bodies in hippocampus and cerebellum
paresthesias around wound, spasms, hydrophobia
respiratory failure
presentation poliomyelitis
non specific gastroenteritis - flaccid paralysis, hyporeflexia, secondary invasion of LMN
post polio syndrome - progressive weakness 25-35 years later, muscle wasting, pain, virus not found
what ddx can commonly be mistaken for vertebral back pain?
herpes zoster recurrence
bells palsy etiology, presentation, tx
unilateral facial paralysis of sudden onset
usu viral infxn with swelling CN7 (facial)
pain behind ear may precede paralysis
no sensory loss, except taste
tx: difficult; steroids, PT, eye patching to prevent keratitis, B12, hypericum, acyclovir if viral
guillian barre synrome presentation
follows flu/recent viral infxn
symmetric weakness with paresthesias, beginning in legs and moving upward (most reach max paralysis in 2-3 weeks), half have facial involvement
DTRs lost, sphincter control maintained
inc CSF protein
generally self limited; supportive care
ddx: botulism
botulism presentation
**descending flaccid paralysis **
dry mouth, diplopia, ptosis, loss of accomodation and pupillary light reflex
GI sx precede > N/V, cramps, diarrhea
NO FEVER
how may infant botulism present differently?
most often seen at 2-3 months
caused by colonization of gut (honey, soil, spore contaminated foods)
constipation may preceded other sx
may progress to “flobby baby”
stool analysis confirms dx
where do brain/CNS tumors tend to occur?
in adults - ABOVE tentorium cerebelli
in children - BELOW
astrocytoma presentation and grading
usu involves frontal lobe in adults, cerebellum in children
recent/worsening HA, N/V, altered mental status, visual disturbances, lack of coordination/sensation
grade 1-2: benign
grade 3: malignant
grade 4: glioblastoma multiforme - AGGRESSIVE, MALIGNANT
what is the most common primary brain tumor in adults?
glioblastoma multiforme (grade 4 astrocytoma)
peripheral nerve tumors
schwannomas: benign
acoustic neuroma: CN 8 (severe vertigo)
neurofibromas: benign if solitary
neurofibromastosis = von recklinghausens, AD & mutations
wernicke korsakoff syndrom
thiamine (b1) def due to alcoholism
confabulations, no short term memory
typically reverses with IV B1
pellegra
niacin/b3 def
dementia, dermatitis, diarrhea (death)
b12 def
macrocytic anemia
degeneration of spinal cord (spasticity, weakness, dementia, loss of proprioception)
NOT cured by folate supplementation, tho the anemia will clear
key points of ischemic cerebrovascular dz/stroke
new recurrent, nondescript HA often occur before event: new HA in pts > 50 should be investigated
signs of increased ICP
papilledema (swelling of disk) and brain herniation
cerebral edema
brain has no lymphatics, BBB controls fluid transport
edema secondary to inc vascular permeability, altered regulation of fluid or transudation
common after injury, radiation, long term HTN
hydrocephalus
enlarged ventricles
inc CSF produced in choroid plexus
lateral third and fourth ventricles swell
what type of necrosis occurs in cerebral infarction/stroke?
liquifaction necrosis
most common arteries to be affected in stroke
middle cerebral arteries
intracranial hemorrhage
HTN, rupture of aneurysms (charcot bouchard)
confusion, drowsiness, HA, nausea
vascular malformations in the brain
AVM = congenital, anywhere, chronic HA, hemorrhage, seizures, neuro deficit
cerebral:
- berry = most common; congenital, ant middle and post communicating arteries; sudden excruciating HA with rupture “worst ha of my life”
- fusiform (atherosclerotic)
- mycotic: sec to staph/strep
hypertensive encephalopathy
DP > 120
grade 4 retinal changes
confusion, drowsiness, HA, nausea
may lead to rupture and hemorrhage
CNS vascular compromise
various neuro deficits
often from vascular compression (tumors, acute disk compression)
occlusion from remote causes (aortic surgery, dissecting aneruysm)
time frame that TIA and RIND affect pt
TIA: sx/signs of stroke <24 hours
RIND: sx/signs of stroke >24 hr BUT RESOLVE COMPLETELY
most common presentation of TIA
acute onset, last 2-30 min
no permanent sequelae
90% affect carotid > ipsilateral blindness, CL hemiparesis
neuro exam normal
type of stroke with: speech not impaired
right cortical stroke
type of stroke with: impaired attention
corticol stroke
type of stroke with: impaired cognition
large cortical or bilateral stroke
type of stroke with: total hemiplegia
sub cortical stroke
type of stroke with: lower CN involved
sub cortical stroke
type of stroke with: cerebellar signs
sub cortical stroke
what could be a non-typical presenting sx of stroke?
seizures
personality change
what is unique bx to a cluster headache?
restless behavior (evil lil gnome hitting u with hammer..taking break…hitting again - bc they know pain is coming but dont know when so they are extremely agitated)
ddx of headache as a sign
infectious (encephalitis, meningitis)
brain tumors
eye
sinus
vascular (AVM, aneurism, HTN, giant cell arteritis)
cluster, tension, migraine
trigeminal neuralgia
migraine tx
goal is vasoconstriction
triptans are specific 5HT effectors
ergot drugs are alpha effectors
consideration for triptans
highest action in basilar artery
CI in basilar artery migraine (comes from base of skull, radiates upwards) > can cause rupture (inoperable death sentence)
important finding in trigeminal neuralgia to differentiate it from more serious causes
no sensory loss or motor weakness
giant cell/temporal arteritis presentation and tx
malaise, proximal muscle pain, jaw claudication, tender scalp arteries, unilateral HA
untreated > blindness in 50% of those who present with HA (from opthlamic branch)
ESR 100+ biopsy of artery
tx: immediate steroids
first ddx of someone waking up in the morning with a headache
carbon monoxide poisoning
DEA control of pain meds
- central muscle relaxants - nonDEA
- central pain control - DEA and non DEA scheduled
- peripheral pain control (NSAIDS, steroids) - non DEA scheduled
MOA muscle relaxants
work on proprioception; drive to have muscle contraction (why overdose can lead to respiratory depression)
all opiates share what SE?
PSLYTIC activity
constipation, N/V, rebound insomnia
itching
overdose = death from respiratory distress
MOA opiates
central (kappa / mu)
disassociation from pain
naloxone vs naltrexone
naloxone (IV) = EMS opiod overdose tx
naltrexone = same but also used orally low dose in CA and AI
adult dose threshold acetominophen
4 g / 24 hours
#1 overdose/toxicity in the world
toxicity = hepatotoxic necrosis (etoh inc hepatotoxicity at 3 drinks/day)
no dialysis/way to get out of system. NAC assists in excretion.
acetominophen MOA
hypothalmic pain threshold
peripheral pain control
shut down cytokines
NSAIDS, steroids, gout meds
main SE aspirin
salycism (severe vertigo); tinnitus, hearing loss
whats a risk in IV NSAIDS that is more of a long term risk in oral?
kidney damage
dose calculations b/w prednisone and cortisone
prednisone:cortisone = 4:1
(5 mg prenisone = 20 mg prednisone)
physiologic cortisone dose
25-40 mg orally
MS etiology, presentation, workup
chronic remitting dz with demyelination of patches in the brain and spinal cord > multiple neuro sx
glove and stocking paresthesias
onset between 20 and 40
weakness, numbness, tingling, unsteadiness, spasticity, diplopia, sphincter disturbance, chronic recurrent optic neuritis
MRI to show plaques (paraventricular white matter lesions)
dx in muscular dystrophy
muscle biopsy
cerebral palsy
motor manifestations of nonprogressive brain damage sustained during prenatal/postnatal life (low birth weight, anoxia at birth)
spastic; quadraplegic, hemiplegic, diplegic
ALS
progressive degeneration of corticospinal tracts and/or anterior horn cells and/or bulbar motor nuclei; mut on chromo 21
both upper AND lower neuron dysfunction
mid and later life; progressive; most die in 3-6 years (respiratory failure)
myasthenia gravis
AI disorder caused by ab to ACh receptor of skeletal muscle
women in 20s, men in 40s-50s
weakness (starts in face, head, neck)
weakness on exertion that is progressive!
no sensory loss
what is the most common movement disorder?
benign essential tumor
fhx
inc with skilled movements (esp with hands) and with tension/stress
absent at rest
tremor of head and voice
parkinsons
dec dopamine; slowly progressive degenerative dz of CNS
- slow movement (bradykinesia)
- muscular rigidity (affects the face; mask like features), diff initiating movements
- resting tremor/pill rolling tremor (dis with sleep, worse w excitement/fatigue)
- postural instability (shuffling gait, no arm swing)
huntingtons
AD; dec GABA; manifests in 3rd/4th decade
starts as fidgeting or restlessness > writhing, purposeless movements/ hyperactive DTRs > dementia > death in 15-20 years
alzheimers
diffuse cotical atrophy, neurofibrillary tangles
senile plaques in cortex (abnormal tau protein in nerve processes, microglia, and astrocytes)
progressive impairment of higher intellectual function
MUST rule out other causes of dementia; blood sugar, sleep deprivation, etc…
dx criteria alzheimers
clinical exam and MMSE (deficits in 2+ areas)
SPECT scanning
progressive worsening
no disturbance of consciousness
absence of systemic or other brain dz to acct for sx
use of MMSE
dx / follow mental deficit disorders (such as alzheimers)
graded by education level
what NT is central for memory
Ach
for more Ach/chole sparing agents
-inhibit ach esterase (keep it from breaking down, stay in neural synapse)
supplement for memory
phosphatidylcholine
first step in workup for syncope
EKG; esp to rule out silent heart block
very common cause of syncope
too much HTN meds/meds with alcohol
NT MOA cannabis
dopamine is released: more neuro activity
anti-inhibition of GABA neurons: more relaxed
cocaine MOA
blocks reuptake of
dopamine (euphoria)
serotonin (confidence)
norepi (energy)
ecstasy MOA
potentiates norepi and dopamine
STRONG affinity for serotonin transporters (more serotonin = more break from reality)
acoustic neuroma presentation/workup
benign primary intracranial tumor of myelin forming cells
U/L hearing loss, tinnitus, disequilibrium
workup: MRI
meningioma presentation
raised intracranial pressure > papilledema, CN dysfunction
workup and tx for herpes zoster
Tzanck test to see multinucleated giant cells
acyclovir/valacyclovir before rash
gabapentin for post herpetic neuralgia
tx rabies
passive immun with human rabies IG into wound site
active imm with killed rabies virus vaccine
bacteria causing tetanus
clostridium tetani
tx cluster HA
oxygen, sumatriptan
tx migraine
triptans
NSAIDs
aspirin
triptans are CI in what pathology
basilar artery migraines
tx tension HAs
heat, massage, analgesics, TCAs
workup and tx TMJ disorder
MRI to look for articular disk placement
NSAIDs, benzodiazepines, moist heat, massage
tx trigeminal neuralgia
carbamazepine
seizure tx
EMS
high conc O2
roll on side
check glucose
give glucose
IV with ringers/NS
diazepam IV > phenytoin IV
tx huntingtons
diazepam + risperidone for chorea
bupropion and TCAs
MS tx
INF-B
methotrexate
benzos
TCA
carbamazepine
gabapentin
amantadine
modafinil
parkinson tx
amantidine
rivastigmine
levodopa
carbidopa
bromocriptine
pramipexole
scopolamine
schizophrenia criteria A that distinguishes it from delusions
2+ of the following over one month
- delusions
- hallucinations
- disorganized speech
- grossly disorganized catatonic bx
- negative sx (lack of affect, alogia, avolition)
rule out other mood, medical disorders
tx schizophrenia
risperdal
antipsychotics
anxiolytics
bipolar disorder tx
lamotrigine
lithium
quetiapine
GAD tx
short term benzos
SSRIs
TCAS
BB
OCD tx
SSRIs (fluoxetine, higher doses and longer duration)
atypical and typical antipsychotics
what meds to avoid with phobias
TCAs like amitripyline
tx PTSD
SSRIs (fluoxetine)
benzos
atypical antipsych (risperidone)
sedatives
hypnotics
