neuro test 2 Flashcards
how do you test CN I?
olfactory
sensory recognition of common odors (soap, coffee, tobacco, etc)
how do you test CN II?
optic
visual acuity (with corrective lenses)
far vision- SNELLEN CHART
near vision- ROSENBAUM POCKET SCREENER OR READING NEWSPRINT
visual fields (assessment of peripheral vision)
funduscopic exam
-optic disc color (creamy yellow)
-optic disc clarity (flat and sharp)
-increased intraocular pressure (glaucoma) cause optic
disk to depress-‘cupping’
-increased intracranial pressure causes optic disc to
elevate (“papilledema”)
-spontaneous venous pulsations are a normal finding
how do you test CN III?
oculomotor
Motor: EOMs (also CN IV and VI)
parasympathetic branch (PSNS constricts pupil, SNS dilates pupil)
how do you test CN IV?
trochlear
motor- EOMs (also CN III , VI)
how do you test CN V?
trigeminal
motor : muscles of mastication (temporalis, masseter) bulk
sensory:
-sensation in 3 divisions (ophthalmic, maxillary and manibular divisions) of Trigeminal nerve
-corneal touch reflex
how do you test CN VI?
abducens
motor: EOMs (also CN III, IV)
* *Eye can not move laterally
How do you test CN VII?
facial
Motor:
- facial symmetry and movements (smile, puff cheeks, raise eyebrows)
- close eyelids tightly against resistance
- labial speech sounds (b,p,m)
sensory: sweet and salty taste on anterior 2/3 of tongue
how do you test CN VIII?
vestibulocochlear
SENSORY:
vestibular division (semicircular canal/vestibular nerve tests)
-stand on one leg and keep balance
-nylen-barany test (head movements to induce
nystagmus)
-cold calorics (cold water introduced into ear to induce
nystagmus)
cochlear division (hearing division)
- assess auditory acuity (whisper or watch tick)
- Rinne test (using 512 Hz tuning fork)
- Weber test (using 512 Hz tuning fork)
- Schwaback test (using 512 Hz tuning fork)
how do you test CN IX?
sensory and motor
glossopharyngeal
sensory:
- gag response (also CN X)
- sour/bitter taste on posterior 2/3 of tongue
motor:
- movement of soft palate upon phonation (say “ahh”)
- swallowing function (swallow cup of water - also CN X)
how do you test CN X?
vagus
sensory:
- gag response (also CN IX)
motor:
- movement of soft palate upon phonation (say ‘‘ahh’’)
- swallowing function (swallow cup of water - also CN IX)
how do you test CN XI?
accessory nerve
motor: trapezius and SCM muscle strength, against resistance
how do you test CN XII?
hypoglossal
motor:
- tongue midline position, movement and strength
- atrophy or fasciculations of tongue
- lingual speech sounds (l,t,d,n)
normal DTRs are?
bilaterally summetrical
DTRs
- simple spinal reflex arcs
- normally prevented from being hyperactive by inhibitory upper motor neurons - if they’re damaged (ie stroke), DTRs will be hyperactive on one side of the body)
Bicep DTR?
C5
brachioradialis DTR?
C6
triceps DTR?
C7
patellar DTR?
L2,L3,L4
Achilles DTR?
S1
what is a normal grade for a DTR?
2+
multiple contractions and relaxations of a muscle group occurring in rapid succession after forcefully moving the joint
clonus - just a couple beats of clonus is normal ( you must test for clonus in both upper and lower extremities)
normal DTRs are what?
bilaterally symmetrical. An absent of asymmetrically diminished DTR suggests a problem at that level of the spinal cord.
what does a hyperreflexive DTR suggest damage to?
the inhibitory upper motor neuron (often from a stroke)
superficial reflexes are decreased or absent if there is damage to what?
upper motor neurons
what refers to how loose or rigid (spastic) an extremity is when moved?
tone
what is normal strength?
5 (movement against gravity and full resistance)
4/5 - movement against gravity and some resistance
3/5 movement against gravity only
2/5 movement if gravity is eliminated
1/5 slight contractility (flicker) but no movements
0/5 no movement at all
what is the palmar (pronator) drift test and what do it test?
tests muscle power
patient is asked to extend his arms with the palms up and hold them there
this test is very sensitive for subtle motor motor strength weakness
abnormal test: the weak arm droops downward and pronates
what are “stress” gait evaluation?
walk on heels
walk on toes
“tandem” gait (heel-toe walking)
headaches due to another medical or neurological condition are what?
secondary headaches
this headache develops within the first few days after trauma and usually has a rapid resolution (days)
post-traumatic headache
10% of patients with persistent HA or other symptoms - average duration 3 months
when is ICP typically increased?
when laying down, not necessarily better when upright
what suggests chronicity of increased ICP?
papilledema on exam
when is intracranial hypotension worse?
when upright, better/resolves when laying down
may have worsening with cough/valsalva (paradoxical)
what is a classic example of intracranial hypotension?
post-lumbar puncture headage
treatment for intracranial hypotension
blood patching
caffeine
bed rest
is a headache a common symptom of ischemic stroke?
no, rare - must more strongly suggestive of hemorrhage (any type)
what headache should be considered for older patients (over 50 or 60) with new headache and repeated episodes of monocular vision loss? and what is the treatment?
temporal arteritis
treatment: steroids should be given before TA biopsy
red flags for secondary headache
new headache or change in headache quality (“worst headache of my life”)
age > 50 without prior history of headaches
trauma or known systemic disease associated with secondary headaches
focal neurologic deficits, impaired consciousness
systemic symptoms (fever, weight loss)
abrupt onset (“thunderclap”)
biggest cause of disability among headache disorders
migraine
phases of migraine
prodrome- several hours or more before “the migraine” starts. sleepiness, irritability, mood changes, food cravings
aura
attack (usually few hours)
postdromal phase -can last hours to days. tiredness, confusion, sluggishness, mild persistent headache
what is migraine aura?
present for about 20% of migraineurs, though not necessarily with every attack
precedes the attack by seconds to 60 minutes
usually has onset gradually and frequently stops with/before headache onset
most common are visual
what is necessary for a migraine diagnosis?
one of the following:
nausea and/or vomiting
both photophobia and phonophobia
also need at least 5 attacks over lifetime to make definitive diagnosis
acute treatment for migraines
rest/sleep
OTC analgesics
combination analgesics
triptans - serotonin receptor 1B agonists
migraine prevention drugs
propranolol, other beta blockers non-dihydropyridine calcium channel blockers antidepressants anticonvulsants riboflavin CoQ10
lifestyle modifications (avoid trigger foods, alcohol, caffeine)
regular sleep and meals, staying hydrated, exercise
stress reduction
migraine with aura doubles the risk of what?
ischemic stroke (compared to migraine without aura) - more common with women
smoking and OCP use independently increase that risk further
true or false: migraine not considered a risk factor after age 50
true (much greater impact from HTN, DN, etc)
what is the most common headache disorder?
tension-type headache (70% in men, 85-95% in women)
what are the symptoms of a tension headache?
“band-like” tightness around the head
bilateral, occipital vs. frontal/temporal
should have no other associated neurological sx
can have photophobia or photophonia but not both
what is acute therapy for tension headaches?
NSAIDs, acetaminophen probably best
combination analgesics
narcotics can provide temporary relief but not a good long term option
heat and/or ice packs
muscle relaxers
what is chronic management of tension headaches?
tricyclic antidepressants
stretching, massage, heat/ice - PT
other migraine prophylaxis options all tried and can be effective (exception - propranol probably has no role)
family of primary headache disorders with a few common features:
unilateral severe headache, usually forehead/eye
associated ispilateral autonomic symptoms (lacrimation, congestions, conjunctival injection, rhinorrhea, sweating, miosis)
trigeminal autonomic cephalalgias
diagnosis hinges on timing, frequency, and duration of headaches
treatment is very different among the subtypes, so identifying the right syndrome is most important
characteristics of cluster headaches
attacks last 15m-3 hr
frequency btw every other day and 8x/day
clusters of headaches lasting weeks-months, with periods of remission lasting months-years
only primary headache syndrome more common in men
classic description- “restless”, pacing around —contrast migraines (want to rest, avoid physical activity)
cluster headache treatment
first line: oxygen
headaches usually too short to respond to pills
prevention: verapamil (board answer), lithium
corticosteroids during a cluster
headache attacks that last 3-20 minutes. frequency at least 5x/day, though can have periods of less frequent attacks. have to have at least 20 lifetime attacks. response to indomethacin is necessary for diagnosis
paroxysmal hemicrania
headaches that last 5 seconds-5 minutes. frequency anywhere from 3-200 per day. clinically can resemble trigeminal neuralgia (autonomic features not present in TN, and TN more likely V2/V3 rather than around the eye). always forehead and periorbital
SUNCT/SUNA
treatment for a spinal cord injury
ABCs
spinal immobilization
state imaging : MRI preferred
IV steroids
36 y/o male with no PMH presents with one week of tingling in legs, eventually spreading to arms. unable to walk; beginning to feel SOB
Neuromuscular respiratory failure
GUILLAIN-BARRE SYNDROME - preceded by infection (C jejuni, EVB, CMV)
diff dx: myasthenia gravis tetanus botulism organophosphate toxicity
what causes Guillian-barre syndrome?
preceded by infection - URI most common preceding, but C jejuni enterits is most commonly isolated organism
what is in the CSF for guillian-barre syndrome?
CSF with albuminocytologic dissociation (high protein, no WBCs- with the exception of HIV patients)
how do you know when someone is in respiratory distress?
increased RR and use of accessory muscles
inability to count to 20 on one breath
hypoxia is a late finding, usually hypercarbic and decreased mental status first- do not rely on pulse oximetry to monitor patients
what is the acute management of neuromuscular respiratory failure?
intubation (VC
what is the definition of status epilepticus?
continuous electrical or clinical seizure activity
or
repetitive seizures without regaining consciousness
> 5 min
can be generalized, focal (partial), nonconvulsive
causes of status epilepticus
**AED noncompliance
**EtOH related (withdrawal)
drug toxicity
CNS infection
CNS tumor
treatment for status epilepticus
ABCs
thiamine, glucose, IVF
AED levels (make sure complient), labs
BENZODIAZAPENES
lorazepam
(or diazepam or midazolam)
ANTICONVULSANTS
fosphenytoin, valproate, phenobartibal
signs of increase ICP
altered consciousness (can’t count backwards)
cushing reflex (bradycardia, hypertension, irregular respirations)
dilated, fixed pupils (CN 3 palsy)
CN 6 palsy
papilledema (late finding)
projectile vomiting
treatment of increased ICP?
immediately: designed to facilitate venous outflow
- head of bed up, head midline
- hyperventilation (bridge therapy) **manually
- mannitol or hypertonic (>.9%) saline
osmotherapy or steroids
remove mass, consider decompression craniectomy
acute bacterial meningitis symptoms and physical findings
headache, photophobia
vomiting
lethargy
seizures
fever
impaired consciousness
kernig or brudzinski sign
nuchal rigidity
bacterias responsible for community acquired bacterial meningitis
S pneumoniae (47%) N. meningitides (25%) - communal living, dorms, prisons
bacterias responsible for acquired bacterial meningitis in patients older than 50
S. pneumoniae
bacterias responsible for acquired bacterial meningitis in immunocompromised
listeria monocytogenes
treatment for acute bacterial meningitis
ABCs
treat empirically: cefotaxime or ceftriaxone vancomycin consider ampicillin (for listeria) steroids
image (CT) - cancer, seizures, alcoholics, comatose, elderly
LP
“no situation where you would pick one over the other” - do all at once
how do you treat viral meningitis
supportive +/- acyclovir (herpes family only)
who is at risk for wernicke’s encephalopathy?
chronic alcoholism or patients with other nutritional deficiency states (post gastric bypass, NPO)
symptoms of wernicke’s encephalopathy
3 As
Ataxia
Ocular Abnormalities
Altered mental status/confusion
42 year old man, history of alcohol abuse. found by his family at home, confused and unsteady.
exam shows: disoriented, inappropriate, abnormal eye movements, nearly falls when trying to walk
wernicke’s encephalopathy
78 year old woman. 2 weeks of vertex headaches, painful to comb hair. brief left eye visual loss “like a shade being pulled down”. 2 month history of malaise, diffuse muscle aches. pain on chewing, soreness in hips. * nodular, ropey temporal artery. frail appearing, leg movement causes pain in hips/thighs, scalp tender to palpatiation. swollen optic disk and 20/200 in L eye.
giant cell arteritis
what should you do for giant cell arteritis?
**stat ESR and CRP
steroids (oral)- IV if visual symptoms/loss
superficial temporal artery biopsy
chest CT and yearly CXR - aortic/thoracic aneurysms
25 y/o man who took an unknown medication, presenting with confusion, temperature of 101.4, confusion, arms difficult to move, with myoclonus.
neuroleptic malignant syndrome
symptoms of neuroleptic malignant syndroms
rigidity, myoclonus
dysautonomia
altered mental status
fever
treatment for neuroleptic malignant syndroms
discontinue offending agent
dysautonomia, altered mental status, myoclonus, hyperreflexia, seizures
serotonin syndroms
what is the cause of malignant hyperthermia?
halogenated inhaled anesthetics
symptoms of malignant hyperthermia?
rigidity fever dysautonomia acidosis rhabdomyolysis
treatment of malignant hyperthermia?
dantrolene
state of being neither awake or aware
coma
damage to ascending reticular activating system (brainstem, bilateral thalami, bilateral cortex)
coma
treatment for coma
ABCs physical exam correct hypothermia thiamine, glucose, consider naloxone labs (ABG, glu, CMP, everything) CT/consider therapy for elevated ICP consider LP consider EEG
most common type of brain tumor
metastatic tumors (1/2)
where are most metastatic brain tumors from?
lung cancer
brain tumor causing abulia, dementia, personality changes, apraxia, hemiparesis, dysphasia is likely where?
frontal lobe
inability to perform particular purposive actions, as a result of brain damage.
apraxia
brain tumor causing auditory or olfactory hallucinations, deja vu, memory impairment, visual field changes is likely where?
temporal lobe
brain tumor causing contralateral motor or sensory impairment, homonymous hemianopsia, agnosia, apraxia is likely where?
parietal lobe
brain tumor causing contralateral visual field deficits and alexia (impaired reading)
occipital lobe
brain tumor causing cranial nerve deficits, ataxia
posterior fossa
tumor is slow growing, extra axial, usually benign, arises from the arachnoid mater
meningioma
tumor presenting with hormonal effects (cushing disease, acromegaly), bitemporal hemianopsia
pituitary adenoma
most malignant brain tumor
astrocytoma WHO grade IV (median survival less than a year)
standard steroid used in brain tumors and other meds
decadron
anti-epileptic medications , Keppra
DVT/PE - second leading cause of death in cancer patients- treat with LMWH (more efective than coumadin)
any condition that affects the structure and/or function of the peripheral motor or sensory nerves
neuromuscular disorder
neurological disorders related to the spinal cord.
may be structural (compressive) from spondylosis, neoplasms, MS, syringomyelia, abscesses etc. Or can be noncompressive from radiation, vascular disease, infections, metabolic.
myelopathy
cervical myelopathy signs
neck pain without radiation
chronic DJD (degenerative joint disease)
posterior column symptoms (sensory changes, balance problems)
increase reflexes
progressive motor loss of upper and lower motor neurons
Amyotrophic Lateral Sclerosis (ALS)
average age of onset of ALS
60 (males 2-3x more likely than females)
life expectancy from date of diagnosis of ALS
3 -5 years - shorter for bulbar predominant patients
classic symptoms of ALS
painless weakness & atrophy, muscle fasciculations and cramping
laryngospasm
respiratory muscle weakness
head drop
2/3 of patients with ALS present with what?
limb onset/LMN-D or PMA presentation
one of the most common neurological problems. Pain along the course of one dermatone. elicited by specific maneuvers: straight leg raise, reverse straight leg. sensory or motor symptoms in one segment (cervical, thoracic, lumbosacral). diminished DTR
radiculopathies
most common radiculopathies
L5 and S1
impingement of lumbar nerve (L5-S1 space). commonly a lifting injury with acute onset. Unilateral. symptoms increase with sitting. decreased motor and sensation
lumbar radiculopathy
clinical features: multiple levels of degenerative disease with compression of several nerve roots.
morning stiffness, increase pain with activity and prolonged standing
joint space narrowing and osteophyte (bone spurs) formation
BILATERAL pain, numbness and tingling
lumbar stenosis
this neuromuscular disorder typically presents as pain restricted to a single limb - multiple nerve distributions can be affected if they share partial innervations. symptoms are usually pain, numbness, weakness, or absent reflexes
plexopathies
brachial plexus plexopathies
upper trunk palsy
lower trunk palsy
“erb palsy” typically during childbirth. “waiter’s tip” position .weak upper arm, strong hand
upper trunk palsy
“klumpke” pulling arm up in child, cervical rib or lung tumor (pancoast tumor with Horner’s syndrome) Ulnar nerve. weak hand but strong upper arm
lower trunk pasy
NM condition recognized by the combination of motor and sensory deficits localized to one nerve distribution. signs and symptoms should be distal to the site of injury
mononeuropathy
which nerve fiber would present with decreased vibration and proprioception and + tingling
large fiber
which nerve fiber would present with decreased pain and temperature and + burning
small fiber
diagnostic tests recommended by the AAN to evaluate for distal symmetric polyneuropathy
fasting glucose, B12, SIFE
this tests for motor and sensory problems through repetitive stimulations. a delayed response (F waves and H reflexes) - assess more proximal nerve segments
Nerve conduction studies (NCS)
this is a needle examination that assesses spontaneous activity, motor unit action potentials (MUAPs), and recruitment rate. this is a single fiber analysis
electromyography (EMG)
this NM condition has symmetric involvement and mainly affects distal nerves first. Sensory or motor nerves involved- often one predominate. patients experiences a burning/numbness in distal extremities ie “stocking glove distribution”
polyneuropathies
neuropathy related to duration and severity of hyperglycemia. due to vascular insufficiency or nerve infarction. pure sensory and may lead to foot ulcers
diabetic neuropathy
an acute inflammatory demyelinating polyneuropathy. clinical features are rapidly evolving areflexic motor paralysis with or without sensory involvement. “rubbery legs” 70% occur after infection.
CSF: elevated protein, normal cell counts
guillian barre syndrome
treatment for GBS
IVIG or plasmapharesis
what occurs in median mononeuropathy/carpal tunnel syndrom
thenar atrophy
sensory loss in digits 1,2,3
DTRs intact
worse at night
autoimmune disorder caused by antibodies directed at acetylcholine receptors of skeletal muscle.
bimodal age of onset in second and seventh decades of life.
clinical presentation: fatigable, painless, asymmetric, muscle weakness
myasthenia gravis
up to 85% of MG patients will have initial symptoms involving what?
ocular muscles (ptosis, diplopia or blurred vision)
triad of muscle weakness, autonomic dysfunction, and hyporeflexia
lambert eaton syndrom
muscles diseases are also known as what?
myopathies - typically involve shoulder, and hip girdle muscles ie large proximal muscles
most frequent myopathy in adults; autosomal dominant. presents with myotonia (inability to relax after contraction -eyes)
myotonic dystrophy
increased risk factors for MS
geographical location females (2-2.5X) race timing genetics (not hereditary but there is a genetic link)
neurological white matter
optic nerve brainstem basal ganglia spinal cord lateral ventricles
how does MS happen?
inflammation
scarring
degeneration
of myelin in white matter
what is the classic first presentation of MS?
optic neuritis (unilateral pain, vision loss)
other clinical signs of MS
sensory symptoms (decreased pain, position, light touch) Lhermitte's phenomenon pain (back pain, visceral pain, spasms) vertigo nystagmus weakness, coordination
how does MS progress?
relapse/flare- weeks on then unknown remission, more frequent early in course, can happen with fever, activity
usually demyelinating events are in similar locations
pregnancy’s effect on MS
decreases flares, especially in the third trimester, but flares increase in the post partum period
term for MS involving a single attack consisting of 1 or more neurological symptoms secondary to a demyelinating inflammatory event.
clinically isolated syndrome
term for MS - acute flares during which symptoms increase, plateau and resolve. +/- progression of disease during remission.
relapsing/remitting
criteria used for MS
McDonald
what diagnostic test is used for MS?
MRI, no single lab test
95 % of patients will have abnormal brain lesions
test where peripheral stimulation evokes CNS electrical events that are measurable. VER/VEP used for MS if diagnosis is unclear
evoked potential testing
how do you treat MS?
high dose steroids - methyprednisone
oral or IV both equally effective
life expectancy of MS
30 years from onset
most common type of seizure disorder?
partial seizure
can’t see, can’t pee, can’t climb a tree
anykylosing spondylitis - an inflammatory disease that can cause some of the vertebrae in your spine to fuse together.
Ptosis, miosis and anydrosis
horner’s syndrome
Paralysis of one side, vertigo, difficulty speaking and contralateral leg weakness. Likely type of stroke?
basilar stroke
