cranial nerves:

1 olfactory-smell
2.Optic- vision
3.Oculomotor- eye movements and pupillary reflexes
4. Trochlear- ocular rotation
5. Trigeminal- muscles of mastication and sensory to the face
6. Abducens- ocular abduction
7. facial- motor to the facial muscles
8. Acoustic- hearing and vestibular function
9. Glossopharyngeal- sensory to pharynx
10. vagus- motor to pharynx and visceral sensation
11. accessory- shoulder shrug
12. hypoglossal- tongue

EXAM SIDE NOTES: finger tapping test is a sensitive method for detecting hemiparesis. When you check sensation dont forget the face. Abnormal monofilament examination can predict future foot ulceration. UMN is babinski and Hoffman (flick middle finger and the index finger will flex as indicates an UMN problem). Pronator drift indicates central dysfunction.
if there is language difficulties after a stroke than the L hemisphere is affected.
Radiculopathy: weakness and numbness in distribution of nerve root.
Myelopathy: weakness below level of lesion and can see UMN signs
Myopathy: proximal upper and lower ext weakness which is symmetric and w/o numbness
Peripheral neuropathy: symmetric sensory loss, initially affecting feet then arms
LP notes: perform in decubitis to get opening pressure and to avoid person going vasovagal, in this position face bevel to ceiling to avoid large whole in meninges, ALWAYS replace stylet before removing needle or you may suck out a nerve; bed rest 30min after
LP diagnostic numbers:
Bacterial - cloudy, inc pressure, cells, low glucose, inc protein
TB- clear fluid, inc pressure, inc cells, n/low glucose, inc protein
fungal- clear fluid, inc pressure, inc cells, low glucose, inc protein
viral- clear fluid, normal/inc pressure, inc cells (lymph), nl glucose, inc protein
acute syphilis- clear fluid, inc pressure, inc cells, n/low glucose, inc protein
Carcinomatous- clear fluid, inc pressure, inc lymphs, dec glucose, inc protein
SAH- bloody fluid, inc pressure, inc RBC, n/low glucose, inc protein
MS- clear fluid, nl pressure, 0-20 lymphs, nl glucose, inc protein
PML- clear fluid, only inc cells seen
GBS- clear fluid with only inc protein
Pseudo tumor: clear fluid with only increased pressure
warning signs of secondary headaches: weakness, numbness, anisocoria >1mm, worse in the AM, worse with valsalva, Papilledema, need imaging of head if focal neuro deficits
MIgrane tx is usually triptans unless there is CV contraindication or hx of stroke (MOA is vasoconstriction). Migraine with aura have increased risk of stroke and it is further increased by smoking and OCP use. if over 65 need a cardio workup before using triptans. NSAIDs and caffeine compunds are second line agents because they can make migraines chronic if used too much. Oppiods are discouraged due to risk of habituaiton and rebound HA. If have 1-2 HA a week need preventative meds- elavil, topamax (SE weight loss, renal stones, acute angle glaucoma, not used in young women and need folate supplement). Depakote (SE is facial hair but also a teratogen), BB, Neurontin and lyrica, botox (SE droop eyelids and if spreads could cause dysphagia-would need a PEG for 3mos).
cluster HA treatments: O2, triptans, lithium, steroids, valproate, and verapamil
Common causes of symptomatic HA: HTN, Tumor (slowly prog and worsens with change in position and valsalva, dull ache), Hydrocehalus (consider with h/o of menegitis), Pseudotumor cerebri (overproduce CSF--need MR venogram to r/o sinus thromobosis), IC hypotension (Post LP, treated with bed rest and hydration)
SAH- need CT and if negative LP...if positive then CTA and neurosurg consult. Risk factors- PCKD, HTN, smoking. Can see stroke due to vasospasm in 48-72hrs so start nimodipine (60 Q4).
bacterial meningitis treated with ceftriaxone +/- steroids
viral meninigitis treated with Acyclovir till PCR says no HSV
trigeminal neuralgia- MRI brain to evaluate causes of increased pressure on nerve and tx with tegretol or trileptal
Ataxia causes:
acquired- stroke-cerebellar or brainstem, tremors, ETOH, Dilantin, 5FU, cytosine, arabinoside, vit E def, Paraneoplastic
inheritied- fragile X, Fredrich's ataxia, Spinocerebellar ataxia
Parkinson's disease tx: Carbidopa/levodopa (if hallucinates use)-Amantadine, requip, Mirapex, Stalevo, Comtan, (SE- dyskinesias, vivid dreams, ortho hypotension, pathologic gambiling), DBS, Sinemet (try to save till end and SR used for sleep disturbances)
Multi system atrophy: parkinsons, ataxia and autonomic dysfunction (ED, constipation, Diarrhea, Urinary incontinence, ortho hypotension)--symptomatic tx to increase BP but few respond to sinemet
Progressive supranuclear palsy: gait impairment with falls, slurred speech, dysphagia, parkinsonism, impaired vertical eye movements, dysarthria, decreased facial expression and blink, lack a tremor; no diff in treatment
Corticobulbar degeneration: gait impaired, dystonia, myoclonus, tremor, slurred speech, ASSYMETRIC rigidity, bradykinesia, and dystonia
Essential tremor: tx propranolol and primidone, DBS, botox; will see head and voice changes; meds that cause it Depakote, steroids and lithium
dystonia (sustained contraction)- can be caused by dopamine blockers (tx benadryl, benztropine, or biperidine), cervical dystonia (tx botox), Spasmodic dystonia (effects voice and tx with botox)
Causes of Chorea: lithium, cocaine, antihitamines, TCA, tumor, stroke, HD, sydenham's post infection, idiopathic
RLS: can be idiopathic; secondary to ESRD, Fe def, and preg; associated with PD and periodic limb movements in sleep
MS: presentations include optic neuritis, lehermitte's sign (flex neck and electrical shock runs down), fatigue, heat sensitivity, INO. Dx with MRI, CSF, RA screen. Tx delay immunizations for 4-6wks after attacks, halt DMARDs, consider pseudoexacerbation like UTI, IV methylprednisone 1gm QD x 3-5d, interferons- Avonex, Betaseron, Rebif, Copaxone (glatirimer), Natalizumab; Mitoxantrone; PT
NPH has a magnetic gait---feet stuck to the floor
MCI precursor to AD
Cortical dementia- aphasia, apraxia, agnosia
AD: prog memory loss, anomia, apraxia, anosgnosia (unaware of decline); no clear Dx tests; tx: Donepizil and memantine (ACH esterase inhibitors), NMDA agonists, Atypical Antipsychotics (quetiapine), AntiAch can worsen symps
lewy body dementia: PD + AD, greater EPS on antipsychotics
ABCDD score can tell if in the next 7 days what the risk of a person with TIA will have a stroke (score of 60, BP>140/90, presentation: speech w/o weakness or unilateral weakness, Duration under an hour or over an hour, diabetes.
sequelae of IVH is obstructive uropathy
BP goal with stroke, hold meds if BP
review TPA scoring form and exclusion and NIH score sheet
if see stroke and new onset Afib: start on ASA and Comadin, no heparin bridge
tx stroke: TED or SQ heparin, no steroids, surgery for swelling, DM tx, HTN, Lipids control, smoking cessation, CEA (2 weeks of small stroke and 6 weeks from larger stroke)--70-99% stenosis with more than 5 years life expectancy
tx of noncardiogenic stroke is ASA, plavix or aggrenox
tx of arterial dissection causing stroke is 3-6mos of Coumadin
Concussion image those with persistent HA of greater than 72 hrs alteration of mentation or focal neuro signs
Grade 1 concussion is momentary concussion, Grade 2 MS abn more than 15mins and if over an hour need observation, grade 3 LOC. Grade 1 or 2 1 week to return, grade 3 brief LOC 1 week to return, grade 3 prolonged LOC (minutes) 2 weeks to return, Multiple grade 3- 1month or more to return. In general practice we dont let patient return as long as symps present and till they improve.
CNS lymphoma most due to B cells, 20% have occular symps, Dx with MRI and CSF, withold steroids to increased yield of LP and Bx; tx is intrathecal chemo and whole brain RT; 5 year survival 25-40%
Cancers that met to brain: lung, breast, Melenoma
SCLC can cause LEMS syndrome
second seizure in life now called epilepsy and requires AED medications
Myoclonic seziures happen in anoxia
Simple partial seziures have no LOC but complex partial do.
Be aware that dilantin and Phenobabatal can cause Osteopersis so need a DEXA
if seziures are refractory to 2 or more meds consider surgery
status tx: Ativan 2mg x 2, load Cerebyx 1gm IV instead of dilantin, if no resp then depakote 1 gm IV, if no response than phenobarb load and intubation, alt propofol and add VEEG
Spinal cord compression EMERGENT MRI to see if Met v Epidural abcess (one gets steroids and other doesnt)
other causes of spinal cord dys: B12, tabes from syphilis, AVM, Syrinx (enlarged central canal), Spinal stenosis
tx carpal tunnel with splint then steroids then surgery if needed.
DM is most common cause of perph neuropathy in USA and leprosy is most common cause world wide; bx not always needed but can help in certain conditions and if cause still uncertain
Diabetic neuropathy pain mgmt: TCA, Gabapentin, Carbamazepine, NSAIDs, Tramadol, Mexilitine, Capsaicin cream, Lidoderm
neck flexors affected in MG, ALS, and GBS.
GBS: weakness, resp failure, pain, loss of DTRs, Dysautonomia, SIADH; tx plasma exchange and IGG, NO STEROIDS and supportive care and pain control; 75% nadir in a week then recovery
CIDP is a slow progressive type of GBS that is hard to diagnose on one visit and here steroids actually work, support, plasma exchange, IVIG, cyclophosphamide, mycophenolate, cyclosporin, Azathioprine, INF; can be associated with DM and look like nepropathy but it is now!!!
UMN and LMN signs with 2-5 year survival, see weakness and fasiclation and atrophy; SENSORY and Autonomic dys NOT SEEN; will need PEG and trach soon; only med Rilutek but only increase life span by 2-3mos
MG: antibodies to postsynaptic ACH receptors, NEVER give Penacillamine, if doesnt generalize from eye in 2 years most likely wont. Tensilon test showed improved function (cholinesterase inhibitors)--SE abd cramps, fasiculations, brady and syncope--keep atropine at bedside. False positives are possible like in ALS so need a strong clinical suspicion to start. Old tests were the ice pack test and sleep test.
Drugs that worse MG: Aminoglycosides, cipro, erythromycin, ampicillin, BB, Li, Mag, Procanimide, Verapimil, Quinidine, Chloroquine, Prednisone (at high doses so in tx start low and go slow), Timolol, AntiAchs
MG tx: Pyridostigime (mestinon), prednisone, azathioprine, cyclosporine, Mycophenolate, plasma exchange, IVIg, thymectomy
exacerbate LEMS: neuromuscular block agents used in intubation can keep a patient on vent for days, Aminoglycosides, Fluoroquinolines, Mag, CCB, IV contrast; it never begins with ocular weakness and usually has weakness in legs>arms. LEMS have reduced release of Ca presynaptically so when there is repeated stimulation the muscle function improves unlike in MG; tx +/- pyridotigmine, immunosuppression, and tx neoplasam.
weakness w/o sensory loss= myopathy; inclusion body myopathy see in finger flexors and quads, Mitochondrial myopathies you see ocular weakness, Usually myopathies are painless unless metabolic cause, Limb girdle muscular dystrophy seen more in french-canadian descent, if has rash than DM. Metabolic causes check thyroid d/o, HPTH, vit D def. Can check EMG but prefer to do after Bx unless r/o ALS for example. If steroid myopathy you see NO EMG changes

	Created by Jaimie Shah over 10 years ago

Board Review Cards Note on Neurology, created by Jaimie Shah on 18/09/2013.

Neurology