Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
136 Cards in this Set
- Front
- Back
|
What are 5 UMN signs? |
- spasticity - hyperreflexia - clonus - pyramidal pattern - upgoing toes |
|
|
What are 4 LMN signs? |
- flaccidity - hyporeflexia - downgoing toes - muscle atrophy |
|
|
Compare the onset of vascular insults vs. inflammatory events in the nervous system |
vascular - abrupt onset inflammatory - gradual onset |
|
|
What are 6 symptoms of a neuromuscular junction disorder? |
- pure motor - ptosis - diplopia - bulbar symptoms - limb weakness - fluctuating symptoms |
|
|
What are 4 symptoms of acquired myasthenia gravis? |
- ptosis, ophthalmoparesis - weakness @ facial muscles, bulbar, neck flexors & extensors, limbs - dyspnea - fluctuating & fatiguable weakness |
|
|
What is the pathophysiology of acquired myasthenia gravis? |
autoimmune antibodies against the ACh receptor |
|
|
What are 3 diagnostic tests for acquired myasthenia gravis? |
- bedside test (Tensilon test) - electrodiagnostic tests (eg. RNS) - serology |
|
|
How do you manage acquired myasthenia gravis? |
symptomatic: Mestinon, IVIg, plasma exchange disease-modifying: steroids, azathioprine, cyclosporine, mycophenolate mofetil (?thymectomy) |
|
|
What are 2 symptoms of a myopathy? |
- pure motor syndrome - proximal upper & motor limb weakness |
|
|
What are 4 investigations (other than bloodwork) that you would do for myopathy? |
- EMG, nerve conduction - MRI - muscle biopsy - genetics |
|
|
What are 3 symptoms of a diffuse motor neuron disorder? |
- progressive pure motor disorder - mixed UMN & LMN signs - involves bulbar & limb muscles |
|
|
What is ALS? |
amyotrophic lateral sclerosis progressive disorder of the UMNs & LMNs |
|
|
What is the treatment for ALS? |
supportive only (no cure) |
|
|
What are 2 types of ALS? |
spinal onset: upper limb onset > lower limb, unilateral, distal focal limb weakness & atrophy bulbar onset: dysphagia, dysarthria, aggressive disease |
|
|
What is the normal speed of nerve conduction? |
40-60 m/s |
|
|
What are 4 mechanisms of nerve injury? |
- disrupted axonal transport - nerve infarction - nerve inflammation - compressive / direct trauma |
|
|
What is a glove-stocking pattern? What disorder / syndrome is it associated with? |
- length-dependent pattern of nerve damage - related to deficiency in axonal transport associated w/ polyneuropathy |
|
|
What are clinical features of polyneuropathy? (3 categories) |
sensory: itching, burning, freezing, tingling, numbness motor: cramps, weakness ANS: syncope, arrhythmia, perspiration changes, GI, bladder dysfunction, visual changes, sexual dysfunction |
|
|
What are 8 common specific etiologies of distal symmetric polyneuropathies? |
- diabetes (most common in developed world) - B12 deficiency - thyroid disease - paraproteinemia - medications - alcohol - renal disease - infections (HIV, syphilis, leprosy) |
|
|
What are 4 features of hereditary neuropathy? |
- insidious - symmetric - often no pain or positive sensory/motor symptoms - bony / cutaneous abnormalities |
|
|
What is an example of hereditary neuropathy? |
Charcot-Marie-Tooth disease |
|
|
Compare nerve conduction studies vs. electromyography |
NCS: delivers current to skin, to evaluate certain motor & sensory neurons in distal arm and leg EMG: uses micro-electrode inserted into the muscle; can evaluate nerve & muscle lesions @ any accessible muscle |
|
|
What do NCS & EMG studies provide info on? (4) |
- location of damage - extent of damage - type of damage - duration of dysfunction |
|
|
T/F: NCS & EMG studies can tell you about the etiology of injury, and can provide information about CNS disorders too |
False! NCS & EMG does NOT tell you about etiology, or central / non-neuro disorders |
|
|
What are 6 patterns of peripheral nerve dysfunction? |
- mononeuropathy - mononeuropathy multiplex - plexopathy - radiculopathy - polyneuropathy - demyelinating |
|
|
What are 6 red flags in peripheral nerve dysfunctions? |
- early / simultaneous upper limb symptoms - cranial nerve involvemt - rapid progression - focality - pure motor involvement - bowel / bladder symptoms |
|
|
T/F: Other than treating the underlying disease (eg. B12 deficiency, toxin, infection, etc), symptomatic treatment is the main method of management in peripheral nerve dysfunction |
True |
|
|
Which cranial nerve & nucleus are affected in headaches? |
CN V (trigeminal) trigeminal nucleus caudalis |
|
|
What is your ddx for a headache? (4) |
primary headache: migraine, trigeminal autonomic cephalgias, tension type secondary headache |
|
|
What 3 features are used to classify headaches? |
- frequency - associated features (migrainous, SNS, PNS) - duration |
|
|
What are 3 types of headaches with duration >4 hrs? |
- migraine - tension type - hemicrania continua |
|
|
What are trigeminal autonomic cephalgias? What are 3 types? |
- CN V1 pain, ipsilateral ANS features, very severe headaches for <4 hours duration - cluster headache - paroxysmal hemicrania - SUNCT / SUNA |
|
|
What are 7 features of migraine without aura? |
- ≥5 attacks, 4-72 hrs each - unilateral - pulsating - moderate-severe intensity - aggravated by / avoids activity - nausea / vomiting - photophobia, phonophobia |
|
|
T/F: After puberty, migraine without aura is equally common between men and women |
False! More common in women after puberty |
|
|
What are 3 childhood migraine equivalents? |
- cyclical vomiting - motion sickness - abdominal migraine |
|
|
What are 3 principles of treatment of young migrainers? |
- lifestyle & behaviour modification (eg. protein, hydration, sleep, exercise) - acute treatment (NSAIDs, triptans) - preventative treatment (if ≥1/week) |
|
|
What are 3 features of auras (before migraines)? |
- fully reversible visual symptoms - fully reversible sensory symptoms - fully reversible dysphasic speech symptoms (no motor weakness) |
|
|
What are features of migraine with aura? |
- ≥2 attacks with aura - each symptom lasts between 5-60 minutes - headache follows aura within 60 minutes |
|
|
What are 4 clinical features of migraine with aura? (eg. triggers) |
- unilateral (60%) - more on holidays & weekends - worse @ menses, ovulation, stress, sleep disruption, weather changes - less frequent in 1st trimester pregnancy |
|
|
T/F: migraine has an inverse relationship with estrogen levels |
True |
|
|
What is the pathophysiology of aura? |
- cortical spreading depression - vascular correlate: wave of hyperemia, followed by oligemia |
|
|
T/F: migraine without aura increases stroke risk |
False!! Migraine w/o aura does not increase stroke risk |
|
|
T/F: migraine with aura increases stroke risk |
True; even higher risk with hormone replacement therapy & smoking |
|
|
How do you acutely treat mild-moderate migraines? |
NSAIDs - naproxen (short acting) - nabutone (long acting) |
|
|
How do you acutely treat moderate-severe migraines? |
triptans |
|
|
T/F: The maximum number of times a patient should take triptans each month is approximately 20. |
False; max 8/month |
|
|
What are 5 absolute & 3 relative contraindications for triptans? |
absolute: - ischemic heart disease - uncontrolled hypertension - PVD - stroke - basilar / hemiplegic / ophthalmoplegic migraine relative: SSRIs, SNRIs, MAOi |
|
|
What is your ddx for chronic headache? (4) |
- chronic migraine - chronic tension type headache - new persistent daily headache - hemicrania continua |
|
|
What is a chronic migraine? |
≥15d headache per month |
|
|
What is chronification of migraine? Why should we prevent it? |
- when headache symptoms don't return to baseline in between episodes because of persistent central sensitization - increases risk of comorbidities (eg. depression, anxiety, sleep disorders) |
|
|
What are risk factors for chronic migraine? (7) |
- attack frequency - treatment patterns - chronic back pain - low SES, stressful life events, caffeine, snoring, obesity - head injury - psychiatric illness - allodynia |
|
|
What is a medication overuse headache? |
an interaction between a therapeutic agent and a susceptible patient with analgesic use for ≥2-3 days / week |
|
|
What are 4 characteristics of medication overuse headaches? |
- increasing dose w/ less effectiveness - withdrawal symptoms - incomplete relief - anxiety about next attack |
|
|
T/F: Adverse childhood events are associated with inflammatory markers, and are a risk factor for migraine |
True |
|
|
What is the most important non-modifiable risk factor for stroke? Are strokes more likely in men or women? |
- age - men |
|
|
Trace the vascular anatomy to the right side of the brain (eg. from the aortic arch) |
aortic arch --> brachiocephalic trunk brachiocephalic trunk --> subclavian --> vertebral brachiocephalic trunk --> common carotid --> internal carotid |
|
|
Trace the vascular anatomy to the left side of the brain (eg. from the aortic arch) |
aortic arch --> subclavian --> vertebral aortic arch --> common carotid --> internal carotid |
|
|
What 2 vessels supply the brainstem? |
basilar & vertebral arteries (penetrating branches) |
|
|
What 3 vessels supply the cerebellum? |
PICA AICA SCA |
|
|
What vessel supplies the basal ganglia? |
MCA perforating arteries |
|
|
What 2 vessels supply the thalamus? |
basilar & proximal PCA (perforating arteries) |
|
|
What are 3 features of ACA syndrome (i.e. ACA ischemia)? |
- contralateral hemianesthesia - contralateral hemiparesis - leg affected more than arm / face |
|
|
What are 7 features of MCA syndrome (i.e. MCA ischemia)? |
- contralateral hemianesthesia - contralateral hemiparesis - leg affected the same / less than arm & face - contralateral homonymous hemianopsia - contralateral hemineglect - ipsilateral gaze deviation - language impairment |
|
|
Compare expressive & receptive aphasia |
expressive aphasia: lesions @ left posterior-inferior frontal lobe (Broca's) receptive aphasia: lesions @ left posterior-superior temporal lobe (Wernicke's) |
|
|
What is the main feature of PCA syndrome (ie. PCA ischemia)? |
contralateral homonymous hemianopsia |
|
|
What are 5 features of brainstem ischemia? |
- crossed face-body deficits - abnormal eye movement - diplopia - nausea / vomiting - dysphagia |
|
|
What are 2 features of a cerebellar lesion at the vermis? |
gait ataxia truncal instability |
|
|
What are 4 features of a cerebellar lesion at one hemisphere? |
ipsilateral limb ataxia nystagmus vertigo nausea / vomiting |
|
|
T/F: lacunar syndromes only present as pure motor deficits |
False; can have pure hemi-motor stroke, hemi-sensory stroke, hemi-sensorimotor stroke, ataxic hemiparesis, dysarthria |
|
|
What is the most common feature of thalamic lesions? |
contralateral sensory loss |
|
|
What are 4 main etiologies of stroke? |
- thrombus - embolus - intracranial hemorrhage - systemic hypoperfusion |
|
|
How does a thrombus arise, leading to a stroke? |
- triggered by local pathology @ endothelium eg. - atherosclerotic plaques - plaque rupture / ulceration - turbulent flow due to plaques |
|
|
What is the most common cause of intracerebral hemorrhage? |
hypertension |
|
|
What are 4 modifiable risk factors for stroke affecting the arteries? |
- hypertension - diabetes - dyslipidemia - lifestyle |
|
|
T/F: decreasing blood pressure lowers stroke risk only if the patient is hypertensive |
False! Lowering BP = reduced stroke risk for normotensive & hypertensive patients |
|
|
Why is diabetes a risk factor for stroke? |
poorly controlled glycemia = microvascular & macrovascular complications |
|
|
What is the target for glycemic control (related to diabetes as a risk factor for stroke)? |
HbA1c <7% |
|
|
Why is dyslipidemia a risk factor for stroke? |
strong relationship w/ atherosclerosis |
|
|
T/F: both fibrates & statins provide sufficient reduction of stroke risk |
False! Fibrates reduce cardiovascular risk only. Statins are best at reducing stroke risk |
|
|
What is a modifiable risk factor for stroke affecting the heart? How can you address this factor? |
atrial fibrillation anti-coagulation |
|
|
T/F: aspirin is equally good as warfarin for preventing strokes in a fib |
False! warfarin > ASA in preventing strokes in a fib |
|
|
What are 2 disadvantages of using warfarin? |
- requires regular blood tests - many drug interactions |
|
|
What are 3 alternatives to warfarin? How are they different from warfarin? (3) |
dabigatran, apixaban, rivaroxaban - equal / superior to warfarin - lower risk of bleeding complications - easier to use |
|
|
What is a TIA? |
transient ischemic attack self-limited episode of neurologic dysfunction from focal temporary cerebral ischemia without infarction |
|
|
Why should you treat a TIA? |
b/c they have increased stroke risk in the next 90 days |
|
|
What is the approach to stroke prevention & treatment of TIAs? |
manage risk factors (eg. hypertension, statin, diabetes, lifestyle, anticoagulants) treat established problems (eg. ASA) |
|
|
Why is ASA used so often if there is small absolute benefit? |
- widely available - low cost - minimal adverse effects |
|
|
What is a 1st line antiplatelet? What are 2 2nd line antiplatelets? |
1st line: ASA 2nd line: aggrenox, plavix |
|
|
What are 2 ways to manage carotid disease? |
- carotid endarterectomy (esp. if >70 years old) - carotid stent |
|
|
What is the time window for tPA? What is its main risk? |
4.5 hours intracranial hemorrhage |
|
|
How are major strokes managed? (2) |
- tPA (within 4.5 h) - endovascular therapy (embolectomy) |
|
|
Compare intra-axial, extra-axial, and intraventricular brain tumours |
intra-axial: in brain parenchyma extra-axial: outside brain parenchyma intraventricular: in ventricles |
|
|
Where do pediatric tumours usually occur? |
posterior fossa |
|
|
How do posterior fossa tumours present? (2) |
hydrocephalus cerebellar signs |
|
|
T/F: WHO Grade I tumours are infiltrative & surgically curable |
False! Grade I tumours are non-infiltrative and surgically curable |
|
|
How does an IDH-1/2 mutation affect prognosis in lower-grade gliomas? |
IDH mutation = better prognosis |
|
|
Which WHO Grade of gliomas are incurable? |
WHO Grade II - IV (b/c they're infiltrative) |
|
|
How do low grade tumours present (ie. symptoms)? |
with seizure (not neurological deficit) |
|
|
How do low grade tumours present on imaging (CT, MRI) |
hypodense on CT hypodense on T1 hyperdense on T2 |
|
|
T/F: low grade tumours usually contrast-enhance and have calcification on CT |
False; low grade tumours usually don't enhance & have calcification |
|
|
What is an infiltrating cancer (in context of brain tumours)? |
cancer that has spread beyond the layer of tissue in which it developed & is growing into surrounding healthy |
|
|
T/F: Malignant tumours contrast-enhance |
True |
|
|
T/F: Rapid progression of symptoms is associated with benign tumours |
False! They're associated with malignant tumours |
|
|
Where do adult brain tumours usually arise? |
supratentorial |
|
|
Compare epileptic seizure vs. epilepsy |
epileptic seizure: transient occurrence of symptoms; abnormal excessive synchronous activity epilepsy: disorder with enduring predisposition to epileptic seizures; ≥1 unprovoked seizure |
|
|
What is the age range for onset of childhood absence epilepsy? |
2-12 years old |
|
|
What is the age range for juvenile myoclonic epilepsy? What are 3 types of seizures seen in it? |
8-25 years old - myoclonic seizures (mandatory) - generalized convulsive seizures - absence seizures |
|
|
What is the age range for epilepsy with generalized tonic-clonic seizures? What can their seizures be provoked by? |
11-20 years old lack of sleep, fatigue, alcohol |
|
|
What are 5 predisposing factors for remote symptomatic seizures? |
- birth insult - febrile seizures - meningitis / encephalitis - traumatic brain injury - family hx |
|
|
What are 4 acute precipitants of seizures? |
- drugs / withdrawal - altered metabolism - meningitis, abscesses - ICH, stroke |
|
|
What are two purposes of doing EEG for seizures? |
diagnosis (confirm / classify) prognosis |
|
|
T/F: a negative EEG rules out epilepsy |
False! |
|
|
What are 5 predictors of recurrent seizures? |
- abnormal EEG - known etiology - post-ictal Todd's paresis - nocturnal occurrence - prior seizure |
|
|
T/F: having multiple seizures in the 1st 24h is a good predictor of recurrence |
False! Multiple seizures in the 1st 24h are NOT predictors of recurrence |
|
|
T/F: Most anti-epileptic drugs can be used to treat generalized tonic-clonic & myoclonic epilepsy |
False-ish; generalized tonic-clonic & partial seizures can be treated by most drugs |
|
|
What 3 types of epilepsy should you treat with broad-spectrum anti-epileptics? |
- myoclonic - atonic / clonic - absence |
|
|
What are 5 examples of broad-spectrum anti-epileptics? |
- valproic acid - benzodiazepines - phenytoin - lamotrigine - levetiracetam |
|
|
What are 6 side effects of carbamazepine? |
- dizziness - headache - sedation - diplopia - ataxia - incoordination |
|
|
What are 3 side effects of valproic acid? |
- tremor - hair loss - weight gain |
|
|
What are 2 side effects of lamotrigine? |
- rash - Steven Johnson syndrome |
|
|
What are 2 side effects of levetiracetam? |
- irritability - behaviour change |
|
|
What is a side effect of topiramate? |
nephrolithiasis |
|
|
What are 6 anti-epileptic medications at high risk for decreasing the efficacy of oral contraceptives? |
- phenobarbitol - phenytoin - primidone - carbamazepine - oxcarbazepine - topiramate |
|
|
What is status epilepticus? |
≥5 min continuous seizure, OR ≥2 discrete seizures w/o complete recovery of consciousness |
|
|
What is the management of status epilepticus? (4) |
1) ABCs 2) check serum glucose 3) meds (eg. benzos) 4) treat underlying cause |
|
|
What should do you if the 1st appropriate anti-epileptic medication doesn't work? (3) |
- right dx? - compliance? - titrate up as tolerated |
|
|
What is refractory epilepsy? |
not well controlled after 2 appropriate 1st-line drugs |
|
|
T/F: patients should only be referred to epilepsy surgery after 2 years of trying medications |
False; should refer after 9 months |
|
|
T/F: dementia is a diagnosis |
False! dementia is NOT a diagnosis; need to find a cause! |
|
|
What are 5 signs of cognitive impairment? |
- inability to acquire new info - lack of reasoning - poor visuospatial abilities - poor language function - change in personality |
|
|
What are 2 types of Alzheimer Disease? |
- amnestic presentation - non-amnestic presentation |
|
|
What are 2 causes of dementia that involve alpha synuclein? |
Lewy Body dementia Parkinson's disease dementia |
|
|
What are features of Lewy body dementia? |
dementia, +2 of... - fluctuation - visual hallucination - parkinsonism |
|
|
What are 5 neurodegenerative diseases causing dementia? |
- Alzheimer's disease - Lewy body dementia - Parkinson's disease dementia - vascular dementia - frontotemporal lobar dementia |
|
|
What are 4 features of mild cognitive impairment? |
- concern about cognitive changes - impairment in ≥1 cognitive domain - preservation of independence - no dementia |
|
|
What are 8 risk factors for dementia? |
- smoking - diabetes, hypertension, obesity - education level - depression - lack of physical activity - lack of cognitive stimulation |
