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1 week Prior to SAH, _____ can occur Sentinel Bleed, which presents as brief, but terrible HA
Next Step with SAH Angiography and Neurosurgery consult
Highest Risk of rebleeding is 24 hrs
TX SAH Nimodipine to prevent cerebral vasospasm
If presents as SAH, but CT is normal, whats the next step? LP
High dose steroids immediately, even if vision loss has already
TX Temporal Arteritis
occurred, so as to prevent contralateral vision loss.
Unilateral neck and face pain after mild trauma. Difficuly talking
Carotid Dissection leading to Horners syndreome and ischemic
and finding words.
stroke
Has ptosis and constricted pupil on same side
DX Carotid Dissection MR or CT Angio
TX Carotid Dissection Anticoagulation v Antiplatelet to prevent thrombus formation
Transforming intermittent HA into a chronic daily HA, associated
Analgesic rebound HA
with freq use of abortant or analgesic pain meds
What imaging for a tymor MRI w/ contrast
When is Dexamethasone used with increased ICP Symptomatic mass effect
If focal signs are present, as abcess may be causing increased
When do you get a CT before an LP
ICP.
Headache with papilledema, increased BP, confusion, and no Hypertensive encephalopathy
signs of ICH, stroke, or meningitis. Dx of exclusion
TX Hypertensive Encephalopathy Labetolol and Nicardipine
Posterior Reversible Encephalopathy Syndrome, which presents
What is PRES with posterior signal on MRI in the setting of acute increase in BP
May also present with cortical visual disturbance and seizure.
transient visual loss, pulsatil tinnitus or gradual visual field loss if
Psuedotumor Sxs
sever
CT to r/o mass
DX Pseudtumor
Followed by LP
Acetazolamide
Lasix can also be used
Weight loss
TX Pseudotumor
If visual field loss, optic n. sheath fenestratiosn can relieve pres-
sure.
TX Refractory cases with VP shunt
Intracrainal Hypoension, due to loss of fluid and continued dural
Sxs of Post-LP HA
leak causing HA when sitting or standing, and relief when flat
Fluid and Bed Rest
TX Post LP HA
Caffeine may help
Clinically, but MRI can show meningeal enhancement and sag-
Dx Post LP HA
ging of cerebellar tonsils
1) Lasts 4-72 hours
2) Is either unilateral, pulsating, moderate, or aggravated by phys-
Migraine Criteria
ical activity
3) either nausea, photophobia, or phonophobia after migraine
When to use migraine prophylaxis If severly disabling or occur greater than 4 times/month
What are prophylactic agents Propranolol, TCAs, depakote, or topomax
NSAIDs or daily TCA
TX Tensions HA
Avoid Triggers and relaxation techniques
Same time each day for weeks or months, accompanied by au-
How does cluster HA present tonomic symptoms on the ipsilateral face (tearing, runny nose,
flushing, Horners)

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Oxygen
TX Cluster HA Prophylaxis Can be prednisone short term or verapimil for chronic
PPx
TX Refractory Trigeminal Neuralgia Interventional nerve block
Dx CO poisoning Measure percentage of carboxyhemoglobin in blood
TX CO poisoning 100% O2
Compressive CN 3 nerve lesion from herniation pressure building
Dilated Pupil and Down and out indicates what?
from expanding hematoma
Trauma with raccon eyes. Clear fluid dripping from the nose or ear,
Presentation of Basilar Skull fracture
ecchymosis behind the ears suggests basilar skull fracture.
Neurosurg consult
TX Basilar skull fracture Prophylactic abx if direct communication between environment
and intracranial caivty
HA, irritability, mild cognitive difficulties, dizziness, depression,
Concussion Presentation
and anxiety
TX Concussion Brain rest, not doing any activities
Often after trauma, throbbing pain that is very sensitive and not
Presentation of Complex Regional Pain Syndrome responsive NSAIDs or opiates
If extremitiy, may apear diaphoretic, erythematous, and swollen
Sympathetic block may be considered or anticonvulsant/steroid
TX Complex Regional Pain Syndrome
for sxs control
Pathophys of TIA Stenosis/Plaque of carotid a
Dx TIA CTA, MRA, Carotid Duplex or angiogram
Carotid endarterectoy
TX TIA
Antiplatelet agents may also be done
How do verterbral TIAs present Repeated epsode of spinning room, blurry vision, slurred speech
Antiplatel therapy
TX Vertebral TIAs
If refractory, stent
Transient episode of weakness followed by severe HA with nausea
Presentation of Hemiplegic Migraine
and photophobia
Avoid Triptans due to increased risk of stroke, otherwise TX like
TX Hemiplegic migraines
normal migraine
If stroke pt is over 6 hrs, what are the options Clot retrival if between 6-8 hrs,
If cardioembolic origin, DVT w/ PFO, hypercoaguable disorder,
When indicated to use coumadin for secondary prevention of
Aortic arch athlerosclorosis, sinus venous thrombosis
stroke
NOT EMBOLIC ENDOCARDITIS
Progressive defects after initial onset, decreasing consciousness,
Clues that its hemorrhage
and signs of increased ICP
BP management (Btw 140-160)
Measure INR
TX Intraparenchymal Hemorrhage Manage incr. ICP with elevation, hyperventilation and Mannitol as
needed
Consult Neurosurgy
Most likely cause of hemorrhage in young pt vascular malformation
Most likely cause of hemorrhage in older patients HTN esp if posterior fossa, thalamic, or basal ganglia
Most likely cause of older patient with multiple cortical he-
Cerebral amyloid angiopathy
morhages
Severe, persistent HA in hypercoaguable pt
Presentation of Venous SInus Thrombosis
Bilateral thalamic or corpus callosum infarct on DWI
DX Venous Sinus Thrombosis MR venogram
TX Venous SInus Thombosis IV Heparin
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3 Hz spike and wave pattern Absence Seizure
TX Ethosuximide resitant Absence Seizure Lamictal or Depakote
Olfactory aura demonstrates what lobe of the brain Temporal
Shaking starts in the hand and gradually expands to involve the
Jacksonian March
arm and whole body.
T/F Do you start AEDs after one seizure episode If EEG is normal, then no
Where do visual seizure symptoms occur Occipita lobe
Where motor seizure symptoms occur Frontal
What studies are ordered on any patient with new onset seizure EEG and MRI (to look for structural cause)
Absence seizures do not have post ictal confusion fact
Patient with alteration of conciousness, automatisms (finger rub-
Complex partial seizure
bing, lip smacking, chewing) and post ictal confusion
Although syncope may have few myoclonic jerks, syncope does
Differentiating syncope from seizure not have post ictal confusion, urinary incontinence, or tongue
biting to suggest seizure.
Orthostatic BP-a drop in 20 systolic or 10 diastolic confirms,
Dx Syncope
can also do a tilt table
Dysautonomia-fluid rehydration, compression hose, leg strenthing
TX Refractory Orthostatic Hypoptension
exercise and fludrocortisone or midodrine can be used
Fear, emotional response, blood, posttussive or straining cause
Triggers for vasovagal syncope over active parasympathetic which can lead to cardiac inhibitor or
vasodilation
SSRI
If no triggers what is the TX of vasovagal syncope
Otherwise avoid triggers
Benzos acutely and scheduled for taper of withdrawl.
TX Alchol withdrawly
NO AEDS ARE INDICATED
3-7 days after stopped drinking
Presentation of Delirium Tremes Marked by autonomic instability, impaired mental function such as
agitation, febrile and can have hallucinations, diaphoretic
Presentation of alchol withdrawl hallucinations Often start 12-24 hrs after stop, and resolve in 24-48 hrs
Sweaty, tremulous, anxious, confused with some palpitations,
Presentation of hypoglycemic seizure
followed by seizure
Stressors at home, seizures last longer than 30 mins without sig-
nificant sequalae or post ictal confusion, alternating movements,
How to differentiate psychogenic seizures from organic seizures shaking head side to side with closed eyes, intact concuiusness
while shaking bilaterally.
STILL NEED TO R/O WITH EEG
IV Ativan
Then IV Ativan again and Fosphenytoin
How do you treat SE
Then other IV ativan again, consider intubation with Propofol or
Phenobarb
What is potential problem with the TREATMENT of SE and how Respiratory depression from benzos
is it managed Intubate
Lasts more than 15 mins, focal defecits, or more than one in 24
When is a more through work up of a febrile seizure indicated
hrs
Hepatotoxicity
Pancreatitis
SFx Valproic Acid Weight gain
Hair thinning
Tremor
SFx Carbamezapine and Oxacarbazine Hyponatremia
SFx Phenytoin Gingival hypertrophy, ataixia, hypertrichosis
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SFx Keppra Agitation, Neuropsychiatric disturbance
SFx Topiramate Mild cognitive difficulties and word finding difficulties
Symptoms of toxic or overdosed AED Nystagmus, N/V and ataxia
Difficulty with anterograde memory formation, word finding dif-
ficulties, and visuospatial skills (lost while driving) resulting in
Early Alzheimers
functional impairment
Note normal aging has no functional impairment
R/O other causes by working up depression, TSH, B12, RPR, and
DX Dementia
MRI (r/o multi infarct, hydrocephalus, or inflammatory lesions)
Donepezil first line
TX Alzheimers NMDA Antagonist (Memantine added for moderate to severe cas-
es)
Significant impairment in cognitive domal more so than normal
aging, but without significant affect on ADLS.
What is Mild cognitive impairment i.e. Pt may have memory diffiulties but can still maintain ADLs
Often miss a couple points on MMSE, and have an increased risk
of dementia going forward
Hallucinations, delusions, sleep disorders, aggression or para-
noia. Incotincence, apraxia (inability to use utensils), and eventu-
Late Alzheimers ally can be bed bound due to poor motor control, along with poor
swallowing and minimal speech
Often die due to infection
Get UA, Electrolytes to search for common causes
What is the first step in managing delirium Delirum more common in patient with underlying neuro disease,
can also be caused by anticholinergic meds
Dx Vascular Dementia MRI shows multiple infarcts
TX Vascular Dementia Cholinesterase Inhibitors
Changes with personality, which may include hyperorality or lan-
guage defecits. Memory and visuospatial skills are typically re-
Presentation of Frontotemporal Dementia
tained early
Late stage may have global dementia
Dx FTD MRI shows frontotemporal atrophy
TX FTD Supportive psych meds as needed
Present initially with dementia characterized by fluctuating levels
of alertness, visual hallucinations, falls and often REM sleep
disorders
Later shows features of Parkinsons
Presentation of Lewy Body Dementia Anticholinergics may trigger delirium like state
L-Dopa worsens hallucinations, when used to try and treat Parkin-
sons features
Typical Antipsychotics cause sedation, Parkonsonism, and Neu-
roleptic Malignant Syndrome
Dx Lewy Body Dementia Clinical
ACHei-Donepezil is first line
TX Lewy Body Dementia
Can also carefully add L Dopa
Parkinsons dementia has the cognitive impairment develop 1 year
How to differentiate Lewy Body Dementia from Parkinsons De-
or more after the motor symptoms
mentia
Note it can also have visual hallucinations in later stages
Often young, with subacute dementia, startle myoclonus, and gait
CJD Presentation
incoordination
EEG shows periodic generalized discharges
Dx CJD
CSF can show 14-3-3 protein
Triad of Normal Pressure Hydrocephalus

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Apraxic Gait
Dementia
Urinary Incontinence
MRI/CT shows enlarged ventricles not caused cortical atrophy
Dx NPH High Volume LP with pre and post gait assessment, can be diag-
nositc if improved
Ventricular shunting
TX NPH Better prognosis if gait disorder appear first and are more promi-
nent than cognitive dysfxn
Ataxia, Confusion, and oculomotor involvement (nystagmus, gaze
Signs of Wernickes Encephalopathy
palsy) in an alcholic
First Step in Mangement of Wernickes Encephalopathy IV thiamine, BEFORE Flucose
Patient with memory difficulties, with cognitive testing that is gen-
Pseudementia
erally better objectively than subjective complaints
Unresponsiveness (coma)
Brainstem death-evidenced by absent BST reflexes (no oculo-
Definition of Brain Death
cephalic response) and absent spontaneous breathing (failing the
apnea test)
Presence of Respiratory Drive and response of Cranial nerve
How to differentiate coma from brain death reflexes
Still wont respond to voice or sternal rub
Have sleep-wake cycles
No observable response to external stimuli
How to differentiate Persistent Vegitative state from coma?
No response for 3 months to be considered persistent in non
traumtic cases and 1 yr in traumatic cases
Vanc + Ceftriaxone
Empiric TX Meningitis
Ampicillin if over 50 yo
If patient has FND along with meningitic signs, what should be
CT to r/o abcess that may lead to increased ICP
done?
DX Aseptic Meningitis LP WITH PCR for HSV and Enterovirus
Signs of encephalitis Confusion, seizures, severe mental status changes
Subacute fever, HA, and FND
Signs of Brain abcess
Increased ICP
Bactermeia, preceding infection near the brain (sinusitis, otitis), or
Risk Factors of Brain abcess
immunocompromised state
Dx Brain Abcess TX based on Hx, Aspiration or blood CX to target TX
Presentation of HIV Associated Dementia Toxic immune repsonse from HIV virus in CNS, typically insidious
MRI to r/o focal pathology and oppurtunistic infxn, presents as
DX HIV associated dementia
mild diffuse atrophy with prominent sulci and ventricles
Presentation of Toxo CNS Focal signs and increased ICP
Positive serology and MRI
DX Toxo CNS Can also do therapuetic trial and see if they respond even if still
testing for CNS lymphoma
Insidious onset of focal signs/sxs and multiple areas of demyelina-
Presentation of PML tion on MRI, often confluent subcortical matter, that dont enhance
or produce mass effect
Dx PML CSF JC PCR
EBV in the CSF
DX CNS Lymphoma May present similar to toxo otherwise as can be either single or
multiple lesions, with or without enhancement
TX CNS Lymphoma HAART therapy, steroids, radiation, and potentially chemo

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Subacutely in immunocompromised pts
HA or Cranial Neuropathies
Presentation of Fungal meningitis
MRI with basilar enhancement
Mononuclear pleocytosis in CSF
Meningitis, radiculopathy, neuropathy, encephalopathy, or Bells
Neuro manifestations of Lymes Disease
Palsy
TX Lymes Meningitis IV Ceftriaxone
TX Lymes Bells Palsy Oral doxycycline
Lymes Disease
Causes of Bilateral Bells Palsy
Sarcoid
Hydrophobia due to painful contraction of larynx, pharynx and
diaphragmatic muscle in response to swallowing liquids
Presentation of Rabies
Paresthesias, pain or pruritis at inoculation site that develop prior
to encephalitis
If unvaccinated person bit by dog, and it gets away what is the
Give post exposure prophylaxis with Rabies Ig
next step?
If vaccinated person bit by dog, and it gets away, what is the next
Give booster shots
step
Facial swelling, painful swelling around eye, diplpia and numbness
What is Cavernous Sinus Syndrome over upper aspects of the face due to Mucor infection of arteries
resulting in infarction
Next Step in Cavernous Sinus Syndrome Immediate surgical debridement + Amphoterecin
Dx Tabes Dorsalis CSF VDRL
Partial seizure with secondary generalization suggesting focal
Presentation of neurocysticercosis pathology, and headache, enchancing cystic lesions due to cys-
ticerci lodging in brain parenchyma
MRI-cysts or clacification, and serum Ab
Dx Neurocysterocosis
Can also Bx
Intense pain with redness, pupil is mid dilated and fixed. May be
Presentation of acute angle glaucoma
precipitate by anticholinergics or sympathetics
DX Acute angle glaucoma Ocular tonometry
Acetazolamide and Beta Blocker
TX Acute angle glaucoma 1 hr later, Pilocarpine
Consult opthamology urgently
Emergency!
Next step when signs of Compressive 3rd nerve palsy
Angio to r/o Posterior communicating a. aneurysm, and clip
What else can cause compressive 3rd nerve palsy, that is an
Uncal herniation
emergency?
What can cause uncal herniation Edema from large CVA 3-5 days after the insult
Like any increased ICP
Mannitol, Intubation, and ventilation
TX Uncal Herniation
NOTE STEROIDS ARE NOT EFFECTIVE FOR ISCHEMIC EDE-
MA
Cover one eye, if it relieves the double vision than neuro cause,
First step with diplopia such as myastenia gravis, CN III, IV or VI palsies
If it doesnt, than its an inherent ocular dz or conversion disorder
Await recovery as most likely microvascular palsy.
Next Step for Trochlear Palsy
Trauma may also cause it
Ptosis, anhidrosis, and miosis
Horners Syndrome Presentation and Cause
Pancoast Tumor, next step is Chest CT
Oculomotor palsy due to either microvascular cause (normal
Causes of Ptosis
pupil), or compression (blown pupil), Horners Syndrome

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Presents in young women with tonic pupils (dont constrict to light
Adies Syndrome
bright light, but do to near stimulus), and weak/absent reflexes.
TX Adies Syndrome None
MLF carries signal from the abducens nucleus to the contralateral
How does INO occur
occulomotor nucleus in adducting eye
Next Step when INO presents MRI to r/o MS
Paralysis of upward gaze, with tonic deviation of eyes downward.
What is Parinauds Syndrome
Light near dissocaition present
What causes Parinauds Syndrome Pineal Tumor AND Hydrocephalus
Next Step In Parinauds Syndrome MRI and Surgical Evaluation
What does fundus show in pt with Amaurosis Fugax Cholesterol depositis in the retinal a.
Image Carotid a., b/c most likey due to emboli from carotid a. going
Next step after Amaurosis Fugax
into the retinal a.
TX Carotid a. Carotid endarterectomy if patient has sxs, followed by antiplatelet.
Pain in eye, worse with movement
Presentation of optic neuritis
Blurriness in eye, and relative afferent pupillary defect
What signs can Prolactinoma produce Bitemporal hemianopsia, galactorrhea, hypogonadism
Homonymous hemianospia can be due to defecits in either Optic tract lesions or from occipital stroke
Slit Lamp Exam! Consult optho and mae sure patient gets a
Next Step in Herpes Zoster Opthalmicus corneal exam with fluorescein staining to look for herpetic lesions
on the cornea
TX Herpes Zoster Ophtalmicus Oral Antivirals.
Decreased visual acuity, visual field testing performed showing
Presentation of Open Angle Glaucoma
peripheral vision loss in both eyes
Beta blockers, Carbonic anhydrase inhibitors, alpha 2 agonists,
TX Open Angle Glaucoma
and prostaglandin analogs.
Typical progressive action tremor and head noding, alleviated by
Essential Tremor Presentation
alchol, often in people with FHx
Propranolol or primidone
TX Essential Tremor
If medication refractory, DBS
Loss of dopaminergic neurons in subsantia nigra and deposition
Pathology of Parkinosons of Lewy bodies in the brain
Lewy bodies are comprised of alpha synuclein.
Dopamine blocking agents such as metoclopramide or neurolep-
What agents cause Drug induced Parkinosnism
tics (haldol)
What are historical clues for drug induced Parkinosonism as
Abrupt onset, bilateral onset (PD usually starts on one side)
opposed to Parkinsonons
TX Drug induced Parkinsonism, if cant take them off the drug Give anticholinergics
Parkinsons + autonomic failure or cerebellar dysfunction, espe-
What is the presentation of Mutliple System Atrophy
cially if these other features are acute
Parkinsons + downward gaze palsy (!!!!) , early falls, dysarthria,
Progressive Supranuclear Palsy presentation
frontal-lobe cognitive problems and rapid progression
Parkinsons + Alien limb (limb performs involuntary purposeful
Presentation of Corticobasal degeneration
movements, and person can not command any movements).
What physical exam trick can be done for spasmodic torticollis
Lightly touching head, relieves some of the sxs
(cervical dystonia)
Hyperextnded with arms extended, eyes rolled back, and mouth
Acute dystonia secondary to neuroleptic use presentation
open with tongue protruded
TX Acute dystonia secondary to neuroleptic use Anticholinergic meds (Benztropine or tihexyphenidyl)

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Need to move, develops subacutely after haloperidol or typical
What can cause akathisia
antipsychotic exposure
TX Tardive Dyskinesia Wean Haldol and consider atypical antipsychotic
Presentation of Huntingtons Chorea , and mood changes (depression, acting impulsively)
MRI-Caudate Atrophy
Next step in diagnosing Huntingtons
Gene sequencing shows CAG expansion on c4
Involves one muscle group vs. coordinated involvement of multiple
Complex v. Simple motor tic
muscle groups
Next Step with Motor Tic If not affecting the patients life, ressurance. Often outgrow these
-Multiple motor tics
Criteria for Tourettes -Vocal tic
-Present for at least one year
What are comorbidites of Tourettes ADHD, OCD, Anxiety, Depression
If interefering with life, TX alpha agonist (clonidine or guanfacine),
Next Step in Tourettes
or even an atypical antipsychotic
Ipsilateral, lesion on rt causes gait instability, nystagmus when
Cerebellar sxs are ipsilateral or contralateral?
looking right, dysmetria in rt, dysdiadochokinesia in rt hand.
Next Step when Cerebellar signs MRI to look pathology
Tumor, infarction, chronic alchol (which primarily affects the ver-
Possible causes of cerebellar signs
mis causing ataxia, MRI reveals atrophy)
Copper deposits in basal ganglia causing Parkinosonian signs,
Pathophys of Wilsons Dz
ataxia, dysarthria, dysphagia, and dystonia
Liver bx with quantitative assay (other blood work can be sugges-
DX Wilsons Dz
tive but not diagnostic)
TX Wilsons Dz Penicillamine
Next Step Hemiballismus MRI to show lesion in contralateral subthalamic nucleus
When you have patient smile looks like they are snarling Myasthenia Gravis
Pathophys Myasthenia Gravis AutoAb to AChR on postsynaptic nerve terminal
Auto Ab
Dx Myasthenia Gravis
If Neg and still supsect, MUSK
Next stepp after dx myasthenia gravis Chest CT to r/o Thymoma
TX Myasthenia Gravis AChEi and immunosuppresants
Fever, with ptosis, difficulty speaking, decreased facial move-
Myashtenic Crisis Presentation ments, which are weaker than baseline, unable to lift extremities
May be triggered by infection
Evaluate respiratory parameter in order to see if need intubation
Then Start plasmapheresis or IVIG
Next Step when Myasthenic Crisis presents
Do not give high doses of AChEi as this can cause cholinergic
crisis
Autonomic sxs (dry mouth and impotence)
Lambert Eaton abn sxs
Hyporeflexia
Pathophys Lambert Eaton AutoAb against Ca channels
Sympotmatic 3,4 Diaminopyridine, as well as immunosuppresive
TX Lambert Eaton
TX
Bulbar sxs followed by generalized weakness with diminished
Presentation of Botulism reflex. Also may be autonomic sxs such as dry mouth, pupillary
dilation.
Dx Botulism With serum toxin assay
TX Botulism Equine antitoxin, with respiratory monitory and early intubation
TX boutlism in child Immediate intubation, ventilatory support, and botulism Ig

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After tick attachment, that presents with ascending paralysis, that
can involve bulbar/facial/ respiratory muscles
Presentation of Tick Paralysis
May be hyporeflexive
No change in sensory
DX Tick Paralysis Finding the tick
TX Tick Paralysis Remove the tick, and just supportive care
Areflexive, acending paralysis involving distal and proximal mus-
cles
GBS
Sensory and autonomic sxs may occur, such as decreased sen-
sation or painful tingling
Clinical
But if LP done, will show high protein, with normal WBC.
GBS Dx
Nerve conduction studies show acute demyelination w/ or w/o
axonal damage.
TX GBS IVIG or Plasmapharesis
1) Presents subacutely
Difference between CIDP (Chronic Inflammatory Demyelinating 2) Can be either chronic progressive or relappsing-remitting
Polyneuropathy) Otherwise similar ascending paralysis with possible sensory and
autonomic sxs
LP should show increased protein, and NCS will show demyeli-
DX CIDP
nation
TX CIDP IVIG or PLEX, same as GBS
Gradual sensory loss in stocking glove distribution, may be asso-
Presentation of Diabetic Neuropathy ciated with pins and needles sensation, motor sxs may occur later
and autonomic sxs can occur
Test for Glucose tolerance test, r/o nutrition (B1, B6, B1), immune
DX Diabetic Neuropathy disorder such as MM, MGUS, or waldenstroms), tociv (EtOH,
chemo) or thyroid
Yes, such as orthostatic hypoTN, impotence, urinary inconti-
Can Diabetic Neuropathy eventually lead to autonomic sxs
nence, abn sweating, gastroparesis, constipation, dry mouth
What nutrition deficiencies most likely cause sensory changes B1 and B6
such as paresthesias and decreased sensation Most often in alcholics
What are drugs that can cause Neuropathy, and how do they Taxol, vincristine, thalidomide, Cisplatin, Antiretrovirals
present? Cause distal loss to pain, temp, light touch, and proprioception
Distal senoriomotor loss, wasting occurs as weakness progresses
Presentation of Charcot Marite Tooth
and hammer toes/high arches present at early age
Dx Charcot Marie Tooth Genetic Testing
CMT1-Demyelinating neuropathies
Difference between CMT1 and CMT2
CMT 2-Axonal neuropathy
Dx Carpal tunnel syndrome Nerve conduction studies to determine severity
Numbness and tingling in thumb, and after repetitive hand move-
Sxs of Carpal Tunnel
ment. Some thenar weakness/wasting
Dx Ulnar nerve entrapment Nerve Conduction Studies
Tx Ulnar nerve entrapment Elbow pads or behavior modification
Radiculopathy associated with neck pain, and multiple muscle
Difference between radiculopathy and peripheral nerve
groups.
Dx Radiculopathy MRI/EMG
Conservative TX, analgesics with rest and cervical collar.
Tx Radiculopathy
Surgery if significant motor defecits or Intractable pain
If shoulder dislocated posterior what is at risk? Axillary n.
How do you test damage to axillary n. Test shoulder abduction and sensation of lateral shoulder

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What is susceptible injury if fracture humerus Radial n.
Entrapment of lateral cutaneous n. cause numbness over antero-
Presentation and Cause of Meralgia Paresthetica lateral thigh
Seen in patients with rapid weight gain or obese patients
Reassurance
TX Meralgia Paresthetica Can also TX with NSAIDs, drugs for neuropathic pain, or local
corticosteroid injection
Multifocal mononeuropathies often due to inflammatory cause
What is Mononeuritis Multiplex
(SLE, Churg Strauss, PAN, RA)
Aggressive immunosuppresion with high dose steroids and po-
TX Mononeuritis Multiplex
tentially cyclophosphamide
Change in taste and hyperacusis due to no innervation in
Other sxs of Bells Palsy
stapedius muscle
TX Bells Palsy Predisone + Symptomatic treatment i.e. eye protection
Possible causes for Central Bells Palsy Contralateral cerebral lesion
Next Step when find Central bells Palsy Imaging
Carbamazepine
TX Trigemnial Neuralgia Refractory cases recieve interventional block of trigeminal gan-
glion
First, EMG which shows increased spontaneous activity with pos-
itive sharp waves and short duration, low amplitude polyphasic
units on voluntary activity
Dx Polymiositis and findings
Then, Muscle Biopsy, CD8 T cells within muscle fasciles bound to
MHC molecules on the sarcolemma
(Should also screen for underlying malignancy)
TX Polymyositis Corticosteroids and other immunosuppresants
EMG first, shows signs of myopathy
DX Dermatomyositis and Findings
Then, Biopsy, which shows inflmmatoin and perifascicular atrophy
More common in elderly. present with similar proximal weaknness
Presentation of Inclusion Body Myositis
as others, but also FINGER FLEXOR weakness (decreased grip)
Dx Inclusion Body Myositis Biopsy shows rimmed vacuoles and amyloid staining
Proximal muscle weakness without irritability on EMG (no spont
How to differentiate steroid induced myopathy from other my-
discharges) and normal CK
opathies
Also often have other signs of steroid use
What is a common complication for Duchennes Cardiomyopathy
Dystrophin deficiency on muscle bx or mutation analysis of pe-
Dx Duchennes
ripheral leukocytes.
TX Duchennes Glucocorticoids have been shown to slow progression
Beckers patient can walk past 15 yo, and most survive into 4th or
Defintion differences in Duchennes and Beckers
5th decade
What should be monitored in Duchennes and Beckers outside of
Cardiomyopathy
musculoskeletal problems?
Weakness mainly in neck, hands and feet
Frontal balding, temporal wasting, cataracts
Presentation of Myotonic Dystrophy Often have lag time in relaxing if tighten eye or hit thumb
May also have dorsiflexor weakness
Often have cardiomyopathy as well
EMG shows Myotonia, Muscle biopsy may show atrophy of type I
Dx Myotonic Dystrophy
fibers
Muscle weakness in proximal muscles, and pain
Reflex testing has prolonged relaxation phase
Presentation of hypothyroid Myopathy
CK is often eleveated slightly
Other sxs, weight gain, feeling cold, and constipation
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Clincally see both UMN and LMN, and EMG confirms 3 or 4 levels
DX ALS
of neuraxis with motor neuron degeneration
TX ALS Riluzole
Next step when presented with optic neuritis MRI, so can see enhancement, and r/o other MS lesions
MS Types Chronic Progressive or Relapsing-Remitting
MRI lesions presenting as periventricular ovoid white matter le-
sions perpendicular to ventricles or white matter lesions affecting
Dx MS
corpus callosum.
LP with CSF analysis for oligoclonal bands
More often in older pt (40) and can be male or female. Gradually
Primary progressive MS presentation progressive sxs
This type responds poorly to TX
NMO presentation Bilateral optic neuritis and myelitis w/o brain involvement
Dx NMO Aquaporin-4 Ab
IV Steroids acutely, and immunosuppressants or rituximab may
TX NMO
be used chronically
Typically presents after vaccination or illness. Inital recovery, then
Presentation of Acute Disseminated Encephalomyeltis patient has HA, neck stiffness, and encephalopathy (sleepy con-
fused, seizures) , UMN signs.
MRI: Extensive white matter lesions of brain and spinal cord,
DX ADEM which enhance with contrast.
LP shows lymphocytic pleocytosis
Steroids for 5-7 days iwth oral steroid taper for 2 weeks, if not
TX ADEM
improving PLEX/IVIG
DX of Central Pontine Myelinolysis Brain MRI shows symmetric high signal in basis pontis
TX Central Pontine Myelinolysis Stop Na
Constant pain, that worsens with movement and awakens at night
Presentation of Myelopathy and possible causes Nerve signs with UMN
Could be cancer, could be abcess if associated with fever
Next Step with Myelopathy MRI contrast to look for compressive lesion
If due to cancer, Decompressive surgery if neuro defecits
IV Steroids acutely
TX Myelopathy
If due to Abcess, urgent decompressive laminectomy with de-
bridement, IV Abx
OA of cervical spine leading to radicular arm symptoms (pain) and
What is Spondylitic Myopathy and how does it present compressing the cervical cortiospinal tract (so that there is lower
extremity sxs).
Painful dermatome with development of signs below the lesion
Presentation of a myeltis (i.e. weakness or numbness), additionally may be incontinent
MRI shows lesion
Post infectious, acute infectious, related to systemic disorder or
Causes of Transverse myeltis
demyelinating disorder
TX Transverse Myelitis IV Methylpred
Weakness and numbness to LT, pain and temp, usually below T9,
Presentation of anterior Spinal A. syndrome but vibration and proprioception are intact
This often due to surgery/embolism/stenosis
Decrease pain and temp sensation often over shoulders, with
Presentation of Central Cord Syndrome
decreased strength in hands, while LE is normal
MRI of cervical spine, as it shows cavitation/CSF signal of central
Next Step in Central Cord syndrome
cord.
T4
Nipples are what dermatome? Umbilicus?
T10
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Lower back pain that radiates the legs, leg weakness, numbness
Sxs of Cauda Equina in a saddle like distribution, urinary incontinence, hyporeflexia
Potentially caused by spinal stenosis
Dx Cauda Equina Syndrome MRI to evaluate
TX Cauda Equina Syndrome Neuro surgical intervention and Steroids if due to tumor
Dorsal Column and Corticospinal/ spinocerebellar tract dysfxn
Presentation of B12 deficiency
,ay also have stocking Glove Neuropahy
Serum B12, Elevated MMA, Elevated Homocysteine
Next Step with B12 deficiency
MRI shows hyperintense lesions in dorsal column
Leg pain, paresthesias radiating down leg when walking
Presentation of Neurogenic Claudication
Relieved with rest and flexing at waist
Dx Neurogenic Claudication MRI Lumbar Spine
TX Neurogenic Claudication Neurosurgical consultation for decompression
Often in spinal cord injury above T10, when patients feel noxious
stimuli (distended bladder, stool impaction) below this sensory
Autonomic Dysreflexia Presentation and how does it occur
level, increased BP and activation Sympathetic tone, when nor-
mally low BP
Next step with Autonomic Dysreflexia Search for noxious stimuli and can give clonidine to lower Bp
Next Step in Restless Leg syndrome Check for iron deficiency anemia
TX Restless Leg Syndrome Roprinirole, Pramipexole, or levodopa
Polycythemia, Nocturia (ANP released due to Rt atrial enlarge-
What are some weird characteristics of OSA
ment pumping against pulm HTN, and brain fog
Mean Sleep latency which shows early onset REM + cataplexy
DX Narcolepsy (paralysis with emotion)
Can also be associated with hypocretin/orexin in CSF
Modafinil
TX Narcolepsy Antidepressants can be used for cataplexy, hallucinations, sleep
paralysis
Acute onset of vertigo with hearing loss. Will intially be constant,
Presentation of Acute viral Labrinthytitis
and then become periodic, exacerbated by sudden moveents
Clinical
DX Acute Viral Labrinthytis If did audiogram, would show sensonurial hearing loss
OR Electronystagmogram would show caloric hypofunctioning
Supportive antiemetics, hydration
TX Acute Viral Labrinthytis
Benzos or Meclizine may help
Idiopathic neuropathy of CN VIII,
Vestibular Neuritis Presentation Similar presentation to viral labrinthitis, but no associated hearing
loss because the cochlea is not inflamed
Benzos, Anticholinergics, antihistamines, antiemetics, short
TX Vestibular Neuritis
course of steroids
Recurrent unilateral vestibular dysfunction with associated low
Presentation of Menieres Disease
tone hearing loss, tinnitus, and aural fullness
Symptomatic TX acute vertigo
TX Menieres Disease Low salt diet for prevention
Refractory spells, ablative procedure
Recurrent unilateral vestibular disfunction without hearing loss,
Vestibular migraines Presentation
and history of migraine HA
TX Vestibular Migraines Migraine Prevention
Bilateral hearing loss, oscillopsia (bouncy and blurry vision), dif-
Presentation of Aminoglycoside toxicity
ficulty walking
Presentation of BPPV

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Short attacks of vertigo, less than 1 minute that occur when
turning the head. No hearing loss associated
DX and TX BPPV Dix-Hallpike and Epley (canalith repositioning)
Acoustic neuroma
Progressive unilateral hearing loss, should raise concern for Tinnitus and HA may also occur. Subtle balance problems may
also occur
TX Acoustic neuroma Surgical removal v. Stereotactic radiotherapy v. observation
Constant mild sensation generally with out hearing loss
Presentation of central vertigo Other CN defecits more likely central process
Vertical Nystagmus is specific for Central vertigo
DX Central Vertigo STAT CT, for possible bleed
If stroke-tpa,
TX Central Vertigo H1 receptor antagonist and benzos can improve vertigo as they
act centrally
Dx Prescubysis Audiometry-loss of high tone
TX Prescubysis Hearing Aid
Bx Brain tumor-Spindle shaped cells and Rosenthal fibers Pilocytic Astrocytoma
TX Pilocytic Astrocytoma Surgical Resection
Bx Brain Tumor-Hyperchromatic nuclei in pseudorosette pattern Medulloblastoma
What is MC presenting sxs of medulloblastoma? Hydrocephallus due to compression of 4th ventricle
Dx Medulloblastoma Bx
TX Medulloblastoma Surgery, Radiation, Chemo
1) Confined to ventricles
Clues that point to ependymoma rather than medulloblastoma 2) Calcifications on CT
3) Blepharoplasts on biopsy/pathology
Bx Brain Tumor-Focal necrosis with pseudopalisading of malig-
GBM
nant nuclei and endothelial proliferation resembling a glomerus
Bx Sheet of regular cells with spherical nuclei surrounded by halo
Oligodendroglioma
of clear cyto, resembling a fried egg
MRI-Calfications
Dx Oligodedromglioma
Bx
TX Oligodendroglioma Surgery with Systemic Chemo
Pt has B cell lymphoma somewehere else that metastasized to
Secondary CNS Lymphoma means
the CNS
Visual field defects, hypopituitarism, HA
Epidimiology and Presentation of Craniopharyngioma
Often in 5-10 yo or 60-70 yo
DX Craniopharyngioma Cystic Suprasellar mass
TX Craniopharyngioma Transcranial or transphenoidal surgical resection
Most likely cancers to metstasize to the brain Breast, lung, melanoma, and Renal Cell carcinoma
Proptosis, vision loss, and possibly strabismus
Presentation of optic nerve glioma May have optic atrophy as well
Often in NF
Dx Optic Nerve Glioma Fusiform enlargement of optic n.
Uniform dural-based mass along the sagittal sinus compressing
MRI of meningioma temporal lobe
Often in NF II
TX Menigioma Resection is curative
Cutaneous lesions (ash leaf spots, adeoma sebaceum, shagreen
Presentation of TS
patches), seizures, and MR

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Dx TS MRI shows Cortical Tubers and/or subependymal nodules
Echo-Cardiac rhabdomyoma
Renal US-Renal Angiomyolipoma
Next Step when Dx TS
Periodic MRI to look for subependymal giant cell astrocytomas
(which cause hydrocephalus)
TX Infantile spasms ACTH as most due to TS, Prendisolone also used
CNS Hemangioblastomas (including retinal, cerebellar, spinal),
VHL Characterisitics
renal/liver cysts, RCC and Pheochromocytoma
Next Step when Dx VHL Renal Imaging-RCC and Pheo
TX Cerebellar Hemangioma Surgical Resection
Dialted Artery leading from the optic disc to peripheral tumor with
Presentation of hemangioma fundoscope and MRI findings an engorged vein.
MRI shows well defined hypervascular enhancing mass
Type of Tumor Sturge Weber is associated with Leptomeningeal angiomas
CT Calficications
Dx Sturge Weber
MRI Pial ANgiomas
Intractable seizures, developmental delay, stroke like episodes,
Concern in Sturge Weber
development of glaucoma
MRI Ataxia Telangiectasia Cerebellar atrophy and dilated 4th ventricle
Most common tumor in Ataxia Telangiectasia Hodgkin Lymphoma
Pathophys of Ataxia Telangiectasia Defect in DNA damage repair
Dx Rb US or CT
Pituitary Adenoma, Parathyroid hyperplasia, and Pancreatic Neu-
MEN I
roendocrine Tumor
Chronic HA and neck pain, worse with couging
Chiari I presentation
DIminished pain and temp sensation in BUE
Inferior portion of cerebellar tonsils lie below foramen magnum
MRI Chiari
(can obstruct CSF, causing hydrocephalus and syringomyelia)
TX Chiari Decompressive surgery
DX Hydrocephalus in NEWBORN CT or MRI
Onset early adolense
Presentation of Juvenile Myoclonic Epilepsy Intial seizures are myoclonic jerks that develop into generalized
seizures in few years
TX Juvenile Myoclonic Epilepsy Depakote
Hemifacial or secondarily generalized seizures which are preced-
Benign Rolandic epilepsy presentation ed by somatosensory aura in that area, and occur more frequently
during sleep
EEG Benign Rolandic Epilepsy Centrotemporal Spikes
Mutliple Seizure types
Preentation of Lennox Gastaut Syndrom Cognitive dysfxn
EEF with <3 Hz spike and wave discharges
Triad of spasms
Infantile Spasms (West Syndrome) EEG with Hypsarrthymia
MR
Periventricular Leukomalacia is a hint for CP
Genetic Abn in Fragile X Increased CGG repeat on X chromosome
Angelman Syndrome presentation Speech delay, motor delay, ataxic gait, hand flapping and happy
Prominent speech delay with minimal use of words
Prader Willi Presentation Hypotonia as child, and now uncoordinated
Later always eating, gaining weight

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Regression of developmental mile stones when less than 1 yo,
Rett Syndrome
also have hand wringing and self mutilation
MR
Neuro complications with Down Syndrome Atlantoaxial instability
Early onset Alzheimers
Has impaired social development, but normal language and cog-
Difference between Aspergers and Autism Spectrum Disorder
nitive abilities
Lab abn in Malignant hyperthermia Potassium, CPK, and urine myoglobin increased
Cooling and IV hydration, alkalization to prevent renal failure
TX Neuroleptic Malignant Syndrome
Also use bromocriptine and dantrole
Serotoonin Syndrome presentation Rigid, tremulous extremities with clonus, HTN, tachycardia, fever
TX Serotonin Syndrome Cyproheptadine
Li Toxicity Bilateral coarse tremor and ataxic gait

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