Neurology Flashcards
1
Q
syncope
A
- loss of consciousness/postural tone 2ary to acute dec in cerebral blood flow; 20% pts have 1ary dx of anxiety, mood, or substance abuse
- Ddx:
- seizure
- cardiat et: arrhythmias (sick sinus, v-tach, AV block, rapid SVT), obstruction of blood flow (aortic sten, HCM, mitral valve prolapse), massive MI
- vasovagal: ↑parasymp, ↓symp stim, MCC, emotional stress, fear, etc.; premonitory sxs = pallor, sweat, light-headed, N, dec vision, roaring in ears; Tilt table study to reproduce sxs; tx = supine, elevate legs, BB
- orthostatic HoTN: caused by ganglionic blocking agents, DM, old, defect in vasomotor reflexes; posture is main cause, + tilt table, tx with inc sodium and fluids, fludrocortisone
- TIA, hypoglyc, hypervent, hypersensitivity, mech reduction of venous return (valsalva, postmicturition), meds
- EKG FOR ALL PTS
2
Q
Seizure
A
- synchronoous dc of electrical activity or chonic disorder or recurrent, idiopathic seizures not reporduced by 2ary cause
- causes: 4Ms and 4Is
- Metabolic (hyponatremia, H2O tox, hypoglycemia, hyperglyc, hypocalc, uremia, thyroid storm, hypertherm
- Mass lesions (brain met, 1ary brain tumor, hemorrhage)
- Missing drugs (noncompliance w/ anticonvusants, withdrawal from ETOH, benzos, barbituates)
- Miscellaneous: pseudosiezures (psych), eclampsia, HTN enceph, febrile
- Intox (cocaine, lithium)
- Infxn (septic shock, bact, viral meningitis, brain abscess)
- Ischemia (embolic stroke, TIA, syncope)
- Increased ICP (dt trauma)
3
Q
epilepsy
A
- chronic, reccurent seizures not produced by 2ary cause
- Triggers: sleep dep, emotional stress, meds, infxn, alc
- Causes: childhood and age
- sxs: dz requires 2+ separate seizures (unprovoked)
- dx: if known epileptic → check anticonculsant levels, if 1st seizure → CBC, CMP, gluc, renal fn, urinalysis
- EEG(abnormal pattern is NOT dx on its own), CT, MRI, LP, preg, PRL (serum levels rise abruptly in postictal state only in true epilepsy)
- tx: ABCs, check for noncompliance, check drug levels, increase dose of first anticonvulsant if persistent, add second drug if szs still uncontrolled. if controlled on 2 drugs, continue for 2y and then taper
- first seizure: EEG with neuro consult, if normal then recurrence is low.
- dont tx most pts with only one seizure
- start antiepileptics only if EEG abnl, MRI abnl or status epilepticus
4
Q
simple partial seizure (focal), or aura
A
- sxs: consciousness INTACT (not impaired)
- seizure is localized but may evolve - can be described as a sensation (N, epigastric sensation), abnl thought (fear, deja vu), or involuntary mvmt
- pt can interact normally w/ enviro except for limitations imposed by seizure itself on local brain fns
- may involve transient unilateral clonic-tonic mvmt
- 60% of pts with partial epilepsy
- dx: EEG
- tx: phenytoin and carbamazepine (alternatives = phenobarb, depakote, primidone)
5
Q
Complex partial seizure
A
- consciousness IMPAIRED (spans from minimal to complete unresponsiveness), preceding aura, ictal manifestations (1-3 mins), eyes usually open during ictus, automatisms (purposeless, involuntary, repetitive mvmts), epigastric sensation or vague cephalic sensation, olfactory or gustatory hallucinations, deja vu, micropsia, macropsia, fear, pleasure, anger, voices, music, speech arrest, absence-like sxs
- contralateral: eye dev, arm extens, fencing posture, clonic mvmts of face, fingers, hand, foot
- postictal confusion (fatigue, ipsilateral HA, mins to hours)
- dx: EEG
- tx: trileptal, lamictal, phenytoin and carbamazepine
6
Q
Generalized tonic clonic (grand mal) seizure
A
- eyes open and “roll to back of head”, begins with sudden LOC, apnea, urinary incontinence, vomiting
- Tonic phase: extensor posturing for 20-60s (rigid trunk, limb extension, bilaterally symmetrical)
- clonic phase: progressively longer periods of inhibition → lasting up to 60s
- postictal phase: transient deep stupor → 15-30min of lethargy, confusion → hours to days of HA, muscle soreness, mental dulling, mood changes
- signs: cyanosis, foaming at mouth, tongue biting, hypoxemia
- dx: lactic acidosis, elevated catecholamines, increased CK, PRL, corticotropin, cort
- EEG: generalized high amp rapid spiking
- tx: roll pt onto side, levetiracetam, topiramate, zonisamide, phenytoin and carbamazepine, phenobarb, depakote, primidone
7
Q
absence (petitmal) seizures
A
- school aged children, resolves with age
- sxs: disengage from current activity, “stare into space”, minor clonic activity (eye blinks, head nodding), brief (lasts a few seconds), but quite frequent (up to 100x/d), impairment of consciousness, no loss of postural tone and no postictal confusion
- dx: EEG shows 3/s spike and slow wave activity
- tx: ethosuximide, depakote, zonisamide
8
Q
myoclonic seizures
A
- rapid recurrent, brief muscle jerks of face or hands → massive bilat spasms simultaneously affecting head, limbs, trunk
- occurs bilaterally, synchronously or asynchronously, may occur shortly after waking up, but can occur at any time
- dx: EEG
- tx: keppra (levatiracetam), depakote (valproic acid)
9
Q
Status epilepticus
A
- causes: noncompliance, ETOH widrawal, intracranial infxn, neoplasm, metabolic dz, drug overdose
- sxs: prolonged, sustained unconsciousness w/ persistent convulsive activity lasting longer than 30 min OR 2 or more sequential seizures without full recovery of consciousness between them
- dx: EEG, MRI
- tx: ABCs, IV, O2, monitor, CMP, Ca, Mg, Phos, CBC, UTox, troponin, AED levels, gluc
- if hypoglyc, give 100mg IV thiamine and 50ml 50% dextrose, 0.1 mg/kg IV lorazepam, repeat if persistent
- IV fosphenytoin or IV phenytoin 20mg/kgIV, monitor HR and BP
- Intubation, IV phenobar
10
Q
Parkinson’s dz
A
- loss of dop containing neurons located in substantia . nigra and locus ceruleus, usually >50yo, meds that cause park = chlorpromazine, metoclopramide, reserpine
- sxs: pill rolling tremor at rest, bradykinesia, cogwheel rigidity . (rachet like jerking, test tone in one limb while pt clenches opposite fist), poor postural reflexes, difficulty initating walking, shuffling steps, masked facies, micrographia, dementia, personality changes early (withdrawn, apathetic, dependent, depression)
- significant disability within 5-10y
- dx: clinical dx
- tx: no cure, carbidopa levodopa (Sinemet) (can . cause dyskinesias after 5-7yrs of tx, N/V/anorex, “on-off” phenomena dt dose response relationship), dopamine receptor agonists (bromocriptine, pramipexole) - INITIATE FIRST! delay need for levodopa, Selegiline (MAOI inhib - adjunct tx, enhances effect of levodopa), amantadine, anticholinerg, amitryp, surg
11
Q
essential tremor
A
- familial (autosomal dom)
- sxs: worse with certain postures, head tremor, vocal tremulousness, improved with alc
- tx: propranolol (1st line), primidone, alprazolam, small amnts alc, gabapentin, topiramate or nimodipine, deep brain stim
12
Q
Bell’s palsy
A
- hemifacial weakness/paralysis of mm innervated by CN VII dt swelling of cranial nerve
- uncertain cause, possibly viral
- sxs: URI preceding event, acute onset unilateral facial weakness/paralysis, both upper and lower parts of face - mastoid pain, decreased tearing, cannot raise eyebrow on affected side, weak orbicularis oculis (unable to close eye), impairment or loss of taste
- signs: check ext ear canal for rash or vesicles to r/o Ramsay Hunt, hyperacusis (tuning fork)
- dx: clinical, consider Lyme dz (dont use steroids), EMG testing if paresis fails to resolve in 10d
- tx: no tx required, short course of prednisone and acyclovir, wear eye patch to prevent abrasion, surg decompress of CN VII, prognosis good (80-90% full recovery in 6wk-3mo)
13
Q
Delirium
A
- “waxing and waning”, rapid onset, “sundowning” = worse at night
- sxs: rapid deterioration in mental status (h-d), fluctuating level of awareness, disorientation, abnl vitals, may have visual hallucinations, dont have to be agitated but may have slow blunted responsiveness
- dx: MMSE, labs (CMP, B12/folate), LP in febrile delirious pt (cerebral edema)
- tx: almost always reversible - tx underlying cause, haloperidol for agitation/psychosis, supportive care
14
Q
causes of delirium
A
- Causes: SMASHED and P. DIMM WIT
- SMASHED =
- Structural brain abnlity (stroke, hematoma, tumor, etc.)
- Meningitis/mental illness
- Alc/acidosis
- Seizures (postictal)/substrate deficiency (thiamine)
- Hypercapnia/hyperglycemia
- Endocrine (addisonian crisi, thyrotox, hypothyroid)/encephalitis/encephalopathy,
- Drugs
- P. DIMM WIT =
- Postop state
- Dehydration
- Infxn
- Meds (TCAs, roids, antichol, hallucinogens, coke)
- Metals (heavy)
- Withdrawal (ETOH, benzos)
- Inflammation (fever)
- Trauma (burns)
15
Q
Dementia
A
- RF: old age
- sxs: insidious, progressive, preserved consciousness, rarely hallucinations, no tremor unless dt parkinson
- tx: typically irreversible unless cause = hypothyroid, neurosyph, vitB12/folate/thiamine def, meds, hydroceph, depression, subdural hemotoma
- pharm tx: vitE, tacrine, donepezil
16
Q
vascular dementia
A
- multi-infarct, stepwise decline dt series of infarcts
- M>W
- sxs: forgetfulness in absence of depression and inattentiveness
- cortical - speech difficulty, trouble performing routine tasks, sensory interpretation difficulty, confusion, amnesia, executive dysfn
- subcortical - gait problems, urinary difficulties, motor deficits, personality changes
- tx: control HTN and metabolic disorders, tx same as Alzheimer dz
17
Q
frontotemporal dementia
A
- frontal lobe sxs: behavioral sx (euphoria, apathy, disinhibition) and compulsive disorders
- primitive reflexes (frontal release signs): palmomental, palmar grasp, rooting reflexes
- dx: MRI (frontal or ant temp lobe atrophy), PET (frontal and/or ant temp hypometabolism)
- tx: supportive care, SSRIs for depression
18
Q
Lewy body dementia
A
- Features of alzheimer and Parkinson dz but progression more rapid than in Alzheimer dz
- sxs: visual hallucinations predominate, extrapyramidal features and fluctuating mental status, sensitive to adverse effects of neuroleptics (make worse)
- tx: neuroleptics for hallucinations . and psychosis, cholinesterase inhibitors: donepezil, rivastigmine, galantamine, selegiline (slows progression)
19
Q
ischemic stroke
A
- 85%
- etiology in young pts: OCP, hypercoagulable states (preg, malig, vWF, antiphospholipid Ab syndrome), vasoconstrictive druge use (cocaine, amphet, polycythemia vera, sickle cell)
- RF: age and HTN, smoking, DM, HLD, afib, Fhx of stroke, previous stroke/TIA, carotid bruit, drugs
- dx: CT noncon differentiates hem vs ischem, MRI, EKG, carotid duplex scan, MRA (definitive test for stenosis of vessels of ehad/neck and for aneurysms)
- tx: acute (IV O2 monitor), GRADUAL BP control (IV labetalol, DONT GIVE ANTIHTN MEDS UNLESS SBP >200, DBP >120, or MAP >130)
- prevention: control HTN, DM, smoking, HLD, obesity, ASA, carotid endarterectomy
- Stable stroke: t-PA tx (unless >3 hrs after event, uncontrolled HTN, bleeding dz, hx of surg or trauma), ASA, anticoagulants
- if w/in 3h give thrombolytics
- if after 3h give aspirin
- anticoags, assess pts ability to protect airway, keep NPO, elevate HOB