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KChan Saves the World > KC Neuro > Flashcards

KC Neuro Flashcards

1
Q

Describe the results of the ULTRA trial (TXA in SAH)

A

Population: Adults with signs and symptoms <24 hours indicating SAH confirmed on non contrast CT. Excluded traumatic SAH, ongoing treatment for VTE.
Intervention: 1G TXA bolus, repeated q8H
Control: Standard of care.
Outcome: Primary outcome 6 month clinical outcome using modified Rankin; ‘good’ mRS 0-3 and ‘poor’ 4-6. No difference in primary or secondary outcomes (excellent clinical outcome, mortality at 1 mo or 60 mo).

Double blind open label RCT with ~1000 pt

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2
Q

Describe the results of the POINT trial

A

Does the combination of asa + clopidogrel compared to ASA alone reduce the risk of stroke

Population: adult paints with minor stroke NIHSS <4 or TIA with ABCD2 >3. Head CT or MRI. Excluded patients with isolated numbness or dizziness, those who received thrombolytics or EVT
Intervention: 600mg clopidogrel + 75 daily + ASA
Control: placebo + ASA
Outcome: composite major ischemic events (stroke, MI, or death) with primary safety outcome of major hemorrhage. Lower rate of major ischemic events in DAPT and a increased risk of major hemorrhage (but due to non intracranial events). Trial stopped early due to higher risk of hemorrhage in DAPT.

5000+ randomized double blinded trial

DAPT reduces the risk of stroke in 3 months.

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3
Q

Describe the results of the DEFUSE trial

A

Bottom line: EVT at 6-16 hours improved functional neurological outcomes at 90 days compared with medical therapy alone

Population: 182 patients randomized, 38 hospitals in the US. Included if age 18-90, NIHSS 6+, baseline mRS 0-1, presenting 6-16 hours, + imaging: ICA or MCA with large mismatch
Intervention: thrombectomy + medical therapy
Control: medical therapy (ASA)
Outcome: modified Rankin scale. Median mRs at 90 days: 3 (IQR 1-4) vs. 4 (IQR 3-6).Functional independence (Modified Rankin 0-2) at 90 days – significantly increased with endovascular therapy.45% vs 17%, OR 2.67 (95% C.I. 1.6-4.48), p<0.001.Serious adverse events – no significant difference.

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4
Q

Describe the results of the DAWN trial

A

In patients 6-24 post stroke with a mismatch between clinical sx and infarct does thrombectomy improve care?

Population: >18 with ischemic stroke, failed IV tPA or contraindication for tPA, last seen normal 6-24 hours ago, baseline mRS 0-1, Ct occlusion ICA or M1, mismatch between severity of symptoms and infarct volume. Exclusion criteria included recent severe head trauma or bleeding, prior thrombectomy, seizure at stroke onset, sustained HTN SBP>185, infarct volume >1/3 MCA territory
Intervention: mechanical thrombectomy with the Trevo device plus standard medical therapy
Control: standard medical therapy alone
Outcome: modified Rankin scale and functional independence at 90d. Secondary outcomes include early therapeutic response, vessel recanalization at 24 hours, change in baseline infarct volume, safety outcomes.
Multicentre RCT 26 centres, unblinded open label

NNT 3 for functional independence for thrombectomy
Overall: Benefit of thrombectomy. Strict inclusion/exclusion criteria with small sample size.

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5
Q

*6 causes of spontaneous cerebral bleed

A

Hypertensive vasculopathy
Cerebral amyloid angiopathy
Vascular malformations
Drug intox
Malignant hypertension
Saccular aneurysms
Blood dyscrasias
Venous sinus thrombosis
Hemorrhagic transformation
Moya moya
Tumours

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6
Q

*Biggest risk factor for spontaneous bleed

A

Hypertension

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7
Q

*5 steps in management

A

IV access and cardiac monitoring
Admission to ICU or specialized unit
Rapid neuroimaging
Airway management
BP target
Reversal ACO
Lower ICP
Consult neuroSx
Treat hyperthermia and hypoglycemia

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8
Q

*Three clinical findings of ACA stroke

A

Contralateral weakness (legs>arms) and sensory loss
Impaired judgement/insight
Bowel/bladder incontinence
Apraxia/gait clumsiness

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9
Q

*Three clinical findings of PCA stroke

A

-Contralateral homonymous hemi-anopia
-Alexia without agraphia (cant read but you can write)
-Acalculia (cant process numbers or preform calculations)
-Memory deficit
-Contralateral sensory loss without motor
-Visual agnosia

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10
Q

*Three clinical findings of PICA stroke

A

-Ipsilateral cerebellar signs (ataxia, dysmetria)
-Ipsilateral Horner syndrome
-Ipsilateral paralysis of palate/laryngeal/pharyngeal muscles
-Loss of pain/T to contralateral body + ipsilateral face

N/V/nystagmus

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11
Q

*Three clinical findings of MCA stroke

A

Contralateral motor (arms>leg)
Contralateral sensory defects
Expressive aphasia (L), dysarthria/neglect (R)
Agnosia
Ipsilateral hemianopsia

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12
Q

*Old man found next to his bed in nursing or retirement home. Seen normal two hours ago at dinner. R sided hemiparesis. Unable to speak. What are absolute and relative contraindications to tPA despite the patient being the in the window.

A

Absolute
Active ICH
Active other bleed
Pt refusal or not in GOC

Relative m
CVA in last 3 months
Spine surgery in last 3 months
Spine or head trauma last 3 months

Active AD
Active IE

Platelets <100
DOAC

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13
Q

*What are 5 signs of stroke on a non contrast CT?

A

Hyperdense artery sign (thrombus in vessel)
Sulcal effacement
Loss of the insular ribbon
Loss of grey-white interface
Mass effect
Acute hypodensity

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14
Q

*What are 5 causes for this patient’s presentation other than stroke?

A

Hypoglycemia
Seizure
Migraine
Hyponatremia
Encephalitis
Wernicke’s
Intoxication

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15
Q

*Hypertension and normal non-contrast CT head — R sided hemiparesis 230/125
1. Six things on the differential of this presentation with a normal CT head?

A
  1. Acute ischemic stroke (can still have a normal plain CT brain in this case)
  2. Migraine
  3. Todd’s paralysis
  4. Internal carotid artery dissection
  5. GCA
  6. Aortic dissection
  7. CVT
  8. Hypoglycemia

Think of it in two categories - things you need different CT for (carotid dissection, aortic dissection, CVT) and then mimics (hypoglycemia, Todd’s paralysis, complex migraine, GCA)

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16
Q

*6 reasons to decrease BP in this patient?

A
  1. If you’re going to thrombolyse them (ie, ischemic stroke inside the window)
  2. If they’re having an aortic dissection
  3. Reduce risk of intracranial hemorrhage
  4. Signs of raised ICP
  5. Acute myocardial infarction
  6. Hypertensive encephalopathy (10-15% reduction)
  7. Severe left ventricular heart failure
  8. Should slowly reduce BP over 24h even in ischemic stroke not getting tPA (15-25%)
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17
Q

*ACEP vs CAEP guidelines for tPA windows. ACEP says 4.5 hours, CAEP doesn’t recommend 3-4.5 hour tPA. 3 reasons why CAEP does not recommend 3-4.5 hours?

A

Question is now irrelevant - seems everyone is on board with 4.5h. (following Canada’s stroke best practice guidelines)

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18
Q

*tPA airway complication? One thing

A

Angioedema

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19
Q

*Most common location of hypertensive hemorrhagic stroke

A

Putamen (44%)
Thalamus (13%)
Cerebellum (9%)
Pons (9%)
Other cortical areas (25%)

PT for CP

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20
Q

*Patients ICP is 40. BP is now 120/60. Calculate CPP

A

CPP = MAP – ICP
MAP = 1/3 (SBP – DBP) + DBP.
CPP = 80 - 40 = 40 mmHg

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21
Q

*What is the range over which CPP is auto-regulated.

A

50-160

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22
Q

*5 signs of increased ICP on CT

A
  • Compressed basal cisterns
  • Diffuse sulcal effacement
  • Diffuse loss of differentiation between gray and white matter
  • Midline shift
  • Compressed ventricle
  • Brain herniation
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23
Q

*4 treatment in the ED (non-operative) for increased ICP

A
  • Elevate head of bed
  • Maintain neutral head and neck position to avoid jugular venous compression
  • Mannitol
  • Hypertonic saline
  • Hyperventilate to PCO2 30-35 mmHg
  • Sedation
  • Analgesia
  • Anti-emetics
  • Treat fever
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24
Q

*Visual stim of pontine hemorrhage: three characteristic clinical findings of the lesion

A

decreased level of consciousness (most common)
long tract signs including tetraparesis
cranial nerve palsies
pinpoint pupils
seizures
Cheyne-Stokes respiration

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25
Q

*Elderly patient with ataxia, rotary nystagmus, nausea, and 2+ reflexes with normal power. Started a few hours ago and is worsening.
a. List 4 possible causes for this presentation

A
  1. Cerebellar or brainstem ischemia
  2. Cerebellar or brainstem hemorrhage
  3. Vertebral artery dissection
  4. brainstem met
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26
Q

*4 therapies you would initiate in the emergency department for acute ischemic stroke?

A
  • Thrombolysis (tPA) in consultation with stroke neurologist, if no contraindications
  • Initiate ASA therapy if patient not a candidate for thrombolysis
  • Avoid extreme hypertension (SBP < 185 mmHg, DBP < 110 mmHg if to receive tPA)
  • Optimize perfusion (target MAP 65 to 100 mmHg)
  • Optimize oxygenation (normoxia to mild hyperoxia, PaO2 80-120 mmHg)
  • Avoid fever, with acetaminophen and surface cooling (for T 38 Celsius and higher)
  • Avoid hyperglycemia (target 10 mmol/L or less)
  • Treat seizures
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27
Q

*What is Broca’s aphasia?

A

Inability to communicate verbally in an effective way, even though understanding may be intact (i.e. expressive aphasia)

Memory aide:
B is broke, B uses broken words, B is frustrated, expressive aphasia
W is like, “what?”, W doesn’t understand, W uses word salad; fluent receptive aphasia

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28
Q

*22-year-old presents with facial droop and hemiplegia. What is on the differential for other than stroke in this patient?

A
  • Seizure/Todd’s paralysis
  • Tumour
  • Complicated migraine
  • Alcohol intoxication
  • Psychiatric (e.g. conversion disorder)
  • Drug toxicity
  • Bell’s palsy
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29
Q

*What are CT features of an MCA stroke?

A
  • Hyperdense MCA sign
  • Parenchymal hypoattenuation
  • swelling of the grey-white matter junction
  • Mass effect
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30
Q

*What causes strokes in young people?

A
  • Hypercoagulable state (e.g. antiphospholipid Ab Sx, protein C/S deficiency)
  • Carotid/Vertebral artery dissection
  • Endocarditis/Septic embolism
  • Sickle cell anemia
  • Polycythemia
  • Fibromuscular dysplasia/Collagen vascular disease
  • Recreational drugs (e.g. cocaine)
  • Subarachnoid hemorrhage
    If female: Pregnancy, use of oral contraceptive
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31
Q

*5 stroke mimics

A
  1. Hypoglycemia
  2. Migraine with focal neurologic findings
  3. Seizure with Todd’s paralysis
  4. Encephalitis
  5. Bell’s palsy
  6. Epidural hematoma
  7. Subdural hematoma
  8. Tumors
  9. Abscesses
  10. Hypertensive encephalopathy
  11. Meningitis
  12. MS
  13. CVST
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32
Q

*4 features of a high risk TIA

A

(ABCD2 score) i. Age > 60 (1 point)
ii. Hypertension at triage >140/90 (1 point)
iii. Clinical features of TIA; unilateral weakness (2 points), speech disturbance without weakness (1 point)
iv. Duration >60 mins (2 points) 10-59 mins (1 point)
v. Hx DM (1 point)
0-3 low risk, 4-5 moderate risk, >6 high risk

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33
Q

*Define TIA

A

A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.

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34
Q

What are BP targets for hemorrhagic strokes?

A

140-160 in the first 24-48 hours as per Canadian Stroke Guidelines

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35
Q

List 5 factors associated with hemorrhagic strokes

A

Vascular malformations, aneurysms, hypertension, alcohol use, cocaine use, cerebral amyloid angiopathy

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36
Q

List 3 clinical tools that can be used to assess stroke

A

NIHSS, FAST (facial droop, arm weakness, slurred speech, time <24 hours), VAN (vision, aphasia, neglect)

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37
Q

List 5 components of the NIHSS

A

LOC, gaze, visual fields, facial droop, motor arms, motor legs, ataxia, sensory, language, dysarthria

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38
Q

List 5 findings on non contrast CT that suggest stroke

A

Dense MCA, loss grey-white differentiation, loss deep nuclei, sulcal or gyral effacement, insular ribbons, hemorrhage, mass effect

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39
Q

List 5 findings from stroke that can be seen on CTA

A

Posterior circulation better visualized, intravascular thrombi, intraluminal narrowing, dissection, AVM

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40
Q

What is a high risk TIA

A

aphasia, unilateral weakness, amaurosis fugax

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41
Q

What imaging is required for a stroke in the 0-4.5 hour window. What interventions are possible

A

CT head (CAEP). Most get CTA
TPA +/- thrombectomy

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42
Q

What imaging is required for a stroke in the 4.5-6 hour window. What interventions are possible

A

CT head + CTA
CT perfusion if +ve VAN or NIHSS >6
Thrombectomy

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43
Q

What imaging is required for a stroke in the >6 window. What interventions are possible

A

CT. CTA + CT perfusion if +ve VAN or NIHSS >10
Thrombectomy

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44
Q

What are blood pressure targets in acute stroke

A

<185/110 if planning to give tPA. Otherwise permissive hypertension up to 220/120, lowering 15% in the first 24 hours

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45
Q

List 5 features of a primary stroke centre

A

Continuous monitoring capability
Emergency physician
24 hour access to CT + CTA
Telehealth equipment for stroke consultation
TPA capability

Think of this one as Joe Brant

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46
Q

List 5 additional features of a comprehensive stroke centre

A

Primary stroke centre features +
Stroke neurology on site
Neurosurgical expertise on site
Neurointerventional on site
Central hub for telehealth consultations
EVT capabilities
Dedicated stroke unit for rehab

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47
Q

What is the dose of TPA

A

0.9mg/kg IV alteplase max dose 90mg, 10% of dose as a bolus over 1 minute

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48
Q

Patient with a high risk TIA is being discharged. What medications should be prescribed

A

If ABCD >4
ASA 160mg PO load then 81mg daily
Plavix 300mg PO load then 75 mg PO OD

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49
Q

*Two accepted definitions of status epilepticus

A

Seizure lasting longer than greater than 5 minutes duration, or
recurrent seizure activity without intervening return to baseline mental status

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50
Q

*Two NON IV treatments of status epilepticus

A

Midaz (IM, IN, buccal, IO)
Diazepam (IO, PR)

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51
Q

*Ideal first line treatment for status epilepticus, if have IV?

A

Lorazepam 2mg IV

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52
Q

*Specific seizing situations. Already gave benzos still seizing. Treatments?
a. MDMA
b. Patient who recently tested positive on TB skin test and is seizing
c. Eclampsia
d. Patient with history of schizophrenia and psychogenic polydipsia

A

a. Hypertonic saline 100mL
b. Pyridoxine max dose 5g (for presumed INH induced seizures)
c. Mag sulf 4g
d. Hypertonic saline 100mL

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53
Q

Describe the two main classification of seizures

A

Partial: no loss of consciousness. Can be simple (consciousness normal) or complex (change in consciousness)
Generalized: loss of consciousness. Includes absence, tonic/clonic, myoclonic, atonic, infantile spasms

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54
Q

List 10 potential etiologies of seizure

A

Withdrawals: anti-convulsants, alcohols, benzos, barbiturates, baclofen
Toxins that lower seizure thresholds: anticholinergics, ASA, salicylates, lithium, lidocaine, isoniazid, bupropion, flumazenil
Acute neuro injury: brain tumors, SAH, stroke, trauma, hypoxia, hydrocephalus
Infection:encephalitis, meningitis, abscess, malaria, neurocysticercosis, febrile seizure
Metabolic: sugars, hyponatremia, hypocalcemia, uremia, hepatic encephalopathy
Chronic epilepsy
Eclampsia (may occur up to 8 weeks postpartum)
Noncompliance with medications

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55
Q

List 3 options for first line agents to use in seizure

A

Lorazepam 0.1mg/kg IV, max 4mg
Midazolam 0.2mg/kg IV, max 10mg IM
Diazepam 0.5mg/kg PR

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56
Q

List 3 options for second line agents to use in seizure

A

Fosphenytoin or phenytoin 20mg/kg IV
Phenobarbital 20mg/kg IV
Valproic acid 40mg/kg IV
Levetiracetam 60mg/kg IV (usually 1g)
Others: ketamine, propofol

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57
Q

*Patients who is a young female (22). You suspect idiopathic intracranial hypertension.
What are 4 medication causes of IIH?

A

Vit A
Retinoids
Tetracycline
HGH

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58
Q

*What are three neurologic findings of IIH on exam?

A

Papilledema
Visual field defect/visual loss
Sixth nerve palsy

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59
Q

*What is one medication you can give for this? What are two alternatives?

A

Acetazolamide is the most potent medication for lowering ICP, and the usual starting dosage is 500 mg twice a day.
Other medications that have been used include furosemide, topiramate, and steroids.

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60
Q

*What are two non-medical treatment options for IIH if medical treatment fails?

A

CSF shunting
Optic nerve sheath decompression

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61
Q

*Most likely diagnosis for:
1. Headache after syncope:
2. Multiple family members with headache:
3. Headache with history of polycystic kidney disease:
4. Headache after entering dark room:
5. Headache with ataxia:
6. Headache after chiropractic manipulation:

A
  1. Subarachnoid hemorrhage/Intracranial hemorrhage
  2. Carbon monoxide toxicity
  3. Subarachnoid/Ruptured cerebral aneurysm
  4. Acute glaucoma
  5. Vertebral artery dissection/Posterior fossa mass or hemorrhage
  6. Vertebral A dissection
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62
Q

*5 causes of unilateral facial weakness besides Bell’s palsy

A
  • Stroke
  • Ramsay Hunt syndrome
  • Lyme disease
  • Bacterial infection (e.g. complicated otitis media/externa)
  • Trauma
  • Tumor
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63
Q

*6 indications for urgent CT in workup for atraumatic headache

A
  1. Fever
  2. AMS
  3. Lateralizing signs
  4. Thunderclap
  5. Recent neurosurgery
  6. Signs of uncal herniation
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64
Q

*6 parenteral therapies for migraine

A

Ketorolac, stemetil, metoclopramide, ondansetron, IV fluids, morphine, dexamethasone, dihydroergotamine

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65
Q

*1 treatment specific to cluster headache

A

High flow O2

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66
Q

*What diagnosis must be ruled out in patients with mydriasis and CN 3 palsy?

A

Pcomm aneurysm

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67
Q

*What are the 6 criteria as part of the SAH rule by Perry?

A

Age>40
Neck pain / stiffness
Thunderclap headache
Loss of consciousness
Exertional onset
Flexion of neck limited on exam

ANT LEaF

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68
Q

*What is the diagnostic gold standard used in the paper (SAH rule by Perry) (3 things)?

A

SAH on CT
Xanthochromia on CSF
Presence of RBC with >1x106 on CSF with aneurysm or AVM on CTA

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69
Q

*What is the sensitivity and specificity of the SAH rule by Perry?

A

Sensitivity 100%, specificity 13.6%

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70
Q

*Take home message from Perry’s SAH

A

Modern 3rd generation CT is extremely sensitive in identifying SAH when it is carried out within 6 hrs of headache onset and interpreted by a qualified radiologist

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71
Q

*The sensitivity and specificity of CT overall for SAH

A

sensitivity 93%, specificity 100%

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72
Q

*Sensitivity and specificity of the patients scanned within 6 hrs of headache onset

A

Sensitivity 100%, specificity 100%

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73
Q

*4 Inclusion criteria Perry’s SAH

A

i. age > 15 years
ii. GCS 15
iii. underwent ED head CT as part of their diagnostic investigation
iv. presents with non-traumatic (no falls or direct trauma to the head in the previous seven days) acute headache (maximum intensity in less than 1 hr after onset) or with syncope associated with headache

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74
Q

*% post LP headache

A

10-30% as per UTD

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75
Q

*How to improve LP success

A
  • Optimize positioning (e.g. flexion to open interspinous spaces, hips and shoulder in line with another)
  • Ultrasound (e.g. to check depth of insertion, confirm anatomic landmarks)
  • Trial lateral decubitus position
  • Assistant to
  • Pain management
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76
Q

*5 contraindications to LP vs CT first?

A

Overlying skin infetion
Platelets <50
INR > 1.4
Spinal Epidural Abscess
Think going to herniate

Papiledema
US increase in size on POCUS
Mass lesion on CT
Other signs of increased ICP

Weird exam contraindications
Immunocomppromised
Seizure
Hernation
Focal neuro
Altered

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77
Q

*What are methods to decrease incidence of post-LP headache

A
  • Orient needle bevel parallel to longitudinal axis of spine
  • Use of non-cutting spinal needle
  • Use of smaller-diameter needle (typically 20- to 22-gauge)
  • Replace stylet prior to spinal needle withdrawal
  • Limit number of lumbar puncture attempts
  • Early ambulation
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78
Q

*5 indications to CT before LP

A
  • clinical concern for a CNS abscess, bleed or mass lesion:
  • History of trauma
  • Known tumor or history of cancer
  • History of immune compromise
  • Focal neurological deficit
  • Focal seizures
  • aLOC
  • Clinical features of raised ICP (papilledema, severe headache, irritability, decreased HR)
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79
Q

*6 indications for urgent CT in workup for atraumatic headache

A

Sudden onset
“Worst ever headache” or “have never had a headache like this one”
Refractory symptoms despite treatment
Headache onset during exertion
Hx of HIV or immunocompromised
Altered mental status + headache
Meningismus
Unexplained fever
Focal neurological findings

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80
Q

*Acute, atraumatic headache, list EIGHT historical features that suggest a potentially serious etiology.

A

Sudden onset
“Worst ever headache” or “have never had a headache like this one”
Refractory symptoms despite treatment
Headache onset during exertion
Hx of HIV or immunocompromised
Altered mental status + headache
Meningismus
Unexplained fever
Focal neurological findings

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81
Q

*LP interpretation in SAH

A

In short, increased WBC, protein and decreased glucose = infection

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82
Q

What is the diagnostic criteria of migraine without aura

A

5+ attacks, 4-72 hours, 2 of: unilateral, pulsating, moderate, aggravation with activities; 1 of nausea/vomiting or photo and sonophobia

5,4,3,2,1
5 episodes
4 hours to 3 days
2 of MUPA (moderate, unilateral, pulsating, worse activity)
1 of N/A, photophobia, sonophpbia

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83
Q

What is the diagnostic criteria of migraine with aura

A

3 of (HA during or after aura, reversible aura, >4 mins, <60 mins), 2+ attacks

2,3,4, - two attacks of 3/4 criteria - in criteria 4 minutes to1 hour

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84
Q

What is the presentation of a tension headache

A

Gradual onset, band-like, bilateral often with associated neck and scalp muscle pain

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85
Q

What is the presentation of a cluster headache

A

Sudden unilateral retro orbital pain that occurs in clusters. May have ipsilateral autonomic symptoms ex. Ptosis, miosis

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86
Q

List 10 causes of secondary headaches

A

Life threatening: tumor, meningitis/encephalitis, bleed/SAH, PRES, central venous thrombosis
Optho: cute angle close glaucoma, GCA
Neuro: pseudotumor cerebri, sinusitis, intracranial hypertension, reversible cerebral vascular syndrome, cavernous venous thrombosis
MSK: occipital neuralgia
Vascular conditions: hemorrhage, stroke, venous sinus thrombosis, AVM, carotid or vertebral dissection
Metabolic: hypoxia, hypoglycaemia, hypercapnia, drug withdrawal, CO poisoning
HTN: preeclampsia, HTN emergency
Pregnancy: preeclampsia

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87
Q

List 5 risk factors for the development of CVST

A

OCP use, antiphospholipid syndrome lupus, protein C and S deficiency, factor V Leiden mutation, thrombophilia, sickle cell anesthesia, pregnancy

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88
Q

What is the diagnostic criteria of idiopathic intracranial hypertension

A

Headache that remits with normalization of CSF pressure
Papilledema
Nonfecal neurologic examination
CN 6 palsy
CSF opening pressure >250 in adults and >280 in children
Normal CSF diagnostic studies
Normal neuroimaging studies
No other cause of increased ICP identified

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89
Q

What are risk factors for SAH

A

Age, hypertension, smoking, alcohol consumption, sympathomimetic drugs, family hx of aneurysms, family hx of polycystic kidney disease, Marfan or connective tissue disorder

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90
Q

What is the components of the Ottawa SAH rule

A

ANT LEaF: Age>40, Neck pain, Thunderclap onset, LOC, Exertional onset, Flexion decreased
100% sensitive if no factors are present

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91
Q

What is the Hunt and Hess clinical grading scale for SAH

A

0 unruptured aneurysm
1 asymptomatic or minimal headache and slight nuchal rigidity
2 moderate or severe headache, nuchal rigidity, no neurologic deficit other than CN palsy
3 drowsiness, confusion, or mild focal deficit
4 stupor, moderate to severe hemiparesis
5 deep coma, decerebrate posturing, moribund appearance

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92
Q

What is the blood pressure target in SAH

A

<140-160

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93
Q

What specific therapy is indicated in SAH to reduce vasospasm

A

Nimodipine

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94
Q

What is the clinical presentation of carotid artery dissection

A

Unilateral headache or neck pain, ipsilateral partial Horner’s syndrome (ptosis, miosis, anhidrosis), blindness or contralateral motor deficits caused by cerebral ischemia

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95
Q

What is the clinical presentation of vertebral artery dissection

A

posterior headache with rapidly progressive neurologic cerebellar deficits ex. vertigo, severe vomiting, ataxia, diplopia, hemiparesis, tinnitus

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96
Q

What is the diagnostic criteria for delirium

A
  1. Acute onset with fluctuating course
  2. Disturbs attention and awareness (inattention)
  3. Disturbed Perception
  4. NOT better explained by another neurocognitive disorder

FAPE’N

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97
Q

What are the 4 components of the CAM screen

A
  1. Acute onset and fluctuating course
  2. Inattention
  3. Disorganized thinking OR
  4. Altered Level of consciousness

A TIA

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98
Q

List 10 causes of dementia

A

See photo - causes of dementia

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99
Q

List 3 bedside tests that can be used in the assessment of delirium

A

CAM, MMSE, clock drawing test, short portable mental status questionnaire, cognitive capacity screening examination

100
Q

What is the definition of dementia

A

Significant, gradual cognitive decline (in memory + one of aphasia, apraxia (motor), agnosia (recognizing objects), executive functioning) that represents a significant decline in function and do not occur in the context of delirium or another medical event

CIDE + LEAM

101
Q

Contrast delirium and dementia

A

Delirium: acute, fluctuating, reversible, decreased awareness/attention, disorganized thoughts
Dementia: chronic, gradual, progressive, permanent, normal consciousness, disinhibited thoughts

102
Q

What is the clinical presentation of Parkinson’s

A

TRAP Presentation: tremor, rigidity (cog-wheeling), akinesia (slow and small movements), postural instability. Also shuffling gait, masked facies.

103
Q

List the ADLs and IADLs

A

Basic ADLS (DEATH) - dressing, eating, ambulatory, toileting, hygiene
Instrumental ADLs (SHAFT) - shopping, housekeeping, accounting, food prep/meds, transportation. These are higher level societal functions

104
Q

*What are 5 causes of facial nerve injury (not idiopathic)?

A

Trauma
Tumor
Otitis media
Lyme disease
EBV
HSV

105
Q

*What is treatment for a mild case of Bell’s palsy (Name, Dose, Route, Frequency, Duration) [5 marks]

A

Prednisolone 50-60mg PO daily x10 days

106
Q

*What are 3 physical exam signs of SEVERE facial nerve paralysis (3 points)?

A

Inability to close eyes
Asymmetry at rest
No perceptible movement

107
Q

*Patients can get corneal scarring because they can’t close their eyes; what are 3 interventions to prevent this over short- or long-term?

A

Patching
Goggles
Ointment/artificial tears
Referral to ophtho

108
Q

*Visual stim: eye down and out. What is the diagnosis?
Most emergent diagnosis (cause)
5 other diagnoses that could cause this

A

CN 3 palsy
P comm aneurysm (or uncal herniation?)
o Microvascular ischemia/diabetes
o Tumor
o Hemorrhage
o Demyelination/multiple sclerosis
o Cavernous sinus thrombosis
o Trauma
o Migraine
o Myasthenia gravis
o Meningitis/infection

109
Q

*Vesicular rash anterior to ear, CN involved and eponymous syndrome

A

CN VII - Ramsay Hunt

110
Q

*Bitemporal vision loss (mechanism and common cause)

A

Lesion at optic chiasm eg. pituitary adenoma

111
Q

What nerve is affected in trigeminal neuralgia

112
Q

What medication can be used in the treatment of trigeminal neuralgia

A

Carbamazepine 100mg PO BID

113
Q

List all the cranial nerves and specific findings associated with CN palsies

114
Q

List 6 ddx for CN 7 palsy

A

Bell’s palsy, Ramsay hunt, lyme disease, OM
Guillain Barre, HIV infection
Tumor compression, stroke

115
Q

How can a central vs. peripheral cause of facial droop be differentiated?

A

Peripheral CN7 palsy INVOLVES the forehead (ex. Bell’s palsy)
Central cause SPARES the forehead (ex. Stroke)

116
Q

What are the clinical features of optic neuritis

A

acute or subacute vision, unilateral eye pain, +RAPD

117
Q

*Non traumatic ddx of cauda equina

A

Malignancy / path fracture
Epidural abscess
Epidural Hematoma
Spinal SAH
Potts disease

118
Q

*What are the 3 most common malignancies that can metastasize to spine?

A

Breast
Lung
Lymphoma

119
Q

*ED management of cauda equina

A

Dexamethasone 10mg IV edema decompression
Neurosurgery

120
Q

*MRI shows lytic lesion and spinal compression with elevated Cr, calcium with anemia. What is your presumed Dx and next lab test?

121
Q

*5 diagnoses requiring urgent spinal MRI in the ED

A

Transverse osteomyelitis
Cauda equina or conus medullaris syndromes
Epidural abscess
Epidural compression
Epidural hematoma

122
Q

*What are 3 physical exam findings suggestive of cauda equina in the ED

A
  1. Saddle Anesthesia
  2. Lower Extremity Weakness (use in L4/L5 distribution)
  3. Urinary Retention (in general, if complete, get retention*)
  4. Fecal Incontinence
  5. Decreased rectal tone
123
Q

*Describe 2 differences between neurogenic and vascular claudication.

A
  1. takes longer time to improve after rest (>15mins)
  2. better when bending forward (ie walking upstairs), worse walking down

(vs vasogenic immediately better with rest and worse walking down stairs)

124
Q

*65 F, with 12 weeks of back pain, bilateral leg, progressively worse with walking, urinary incontinence, negative straight leg raises x 2, still symptomatic after PT, opioids, NSAIDS, everything. 2 reasons to refer this patient to a spinal surgeon

A
  • Neurologic deficit/suspected cauda equina syndrome
  • Disabling pain despite 12 weeks conservative therapy
125
Q

*Table with L3-S1 dermatomes, muscular function and reflexes

A

o L3-4: Quadriceps power, patellar reflex
o L4-5: Heel walking, ankle dorsiflexion power
o L5: Great toe extension power
o S1: Great toe flexion power, ankle reflex

126
Q

*Most sensitive finding of Cauda Equina

A

Urinary retention

127
Q

*Most common organism for spinal epidural abscess

A

Staph aureus

128
Q

*Most urgent treatment for SEA

A

Abx (ceftri vanco) and surgical decompression - unsure which they are asking for here

129
Q

*List diagnosis, mechanism/most common cause
1. Vibration/position sens maintained; Motor & temp/pain impaired
2. Unilateral facial & body sensory deficit

A
  1. Anterior cord syndrome - forced flexion or injury to anterior spinal artery
  2. Hemibody syndrome - functional
130
Q

Describe the tracts of the spinal cord

A

Ascending lateral spinothalamic, pain and temperature, crosses at spinal cord
Ascending dorsal, proprioception and vibration, crosses at medulla
Descending corticospinal, motor, crosses at medulla
See photo

131
Q

Describe the clinical findings of a complete spinal cord lesion

A

Total loss of motor and sensation distal to the injury. Absolutely no signs of sparing (ex. No rectal tone)

132
Q

Describe the mechanism and clinical findings of a central cord lesion

133
Q

Describe the mechanism and clinical findings of a Brown Sequard lesion

134
Q

Describe the mechanism and clinical findings of an anterior cord lesion

135
Q

Describe the grading of neuromuscular weakness

136
Q

List 10 non traumatic causes of spinal cord dysfunction

A

Compressive lesions: hematoma, abscess, diskitis, cancer
Non compressive: MS, transverse myelitis, spinal subarachnoid hemorrhage, syringomyelia, HIV myelopathy, other myelopathies, spinal cord infarction

137
Q

Describe the dermatomes associated with: C5, C7, L1, L4, S1, S2

A

See photo - dermatomes

138
Q

Describe the myotomes associated with: C5, C7, L1, L4, S1, S2

A

See photo - myotomes

139
Q

What is transverse myelitis

A

Inflammation of the full width of the spinal cord, involving very lengths of cord. Can occur at any level, but often thoracic. Etiologies may be post infectious (ex. EBV, CMV, campylobacter) or autoimmune (SLE, APS) or idiopathic. Dx with MRI. Supportive care.

140
Q

What is Syringomyelia? What makes it worse? How does it present similarly to?

A

Fluid filled lesion within the spinal cord. Chronic progressive with headache, neck pain, gait abnormalities, numbness. Sx worsen with sneeze, cough, or Valsalva. Lower limb hyperreflexia. May present similar to a central cord.

141
Q

What is diskitis

A

Infection of the nucleus pulposus, secondary to infection of the cartilage. Often staph. May be secondary to surgery or spontaneous in patients who are immunocompromised or with systemic infection

142
Q

*List diagnosis, mechanism/most common cause: Weak dorsiflexion; sens 1st web space decreased

A

Deep peroneal nerve compression - habitual leg crossing

143
Q

How many peripheral spinal nerves are there?

A

12 cranial nerves and 31 spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal)

144
Q

List 10 causes of emergent weakness

A

Autoimmune: GBS, myasthenia gravis
Toxic: botulism, tick paralysis, metals, paralytic shellfish toxin
Metabolic: dyskalemia, hypophosphatemia, hypermagnesemia, porphyria
Infectious: poliomyelitis, diphtheria

145
Q

Which peripheral nerve disorder presents with purely motor symptoms

146
Q

Which peripheral nerve disorder presents with purely sensory symptoms

A

Gangliopathy

147
Q

Which peripheral nerve disorders present with symmetrical symptoms

A

Demyelinating (ex. GBS), distal polyneuropathy (ex. Diabetes)

148
Q

List 7 categories of peripheral nerve disorders and an example of each

A

Symmetrical:
Demyelinating: proximal + distal ex. GBS, CIDP
Distal Polyneuropathy ex. Diabetes
Asymmetric:
Radiculopathy and Plexopathy ex. Brachial plexus injury
Isolated mononeuropathy ex. Radial nerve palsy
Mononeuritis multiplex ex. Lyme disease
Motor neuron disease ex. ALS
Sensory neuron disease ex. ganglionopathies

149
Q

List 5 causes of demyelinating polyneuropathy

A

GBS, Miller-Fischer variant, CIDP, HIV, Diphtheria, buckthorn, malignancy

150
Q

List 5 causes of distal polyneuropathy

A

Diabetes, alcohol (most common)
Neoplastic, HIV, porphyria
Toxins: heavy metals, drug reactions (amiodarone, antiretrovirals, dapsone, isoniazid, phenytoin, statin)
Nutritional: thiamine, vitamin B deficiency
Hereditary: Charcot-Marie Tooth

151
Q

List 3 plexopathies

A

Brachial plexus, lumbar plexus, conus medullaris

152
Q

List 5 isolated mononeuropathies

A

Radial, median, ulnar, sciatic, femoral, peroneal, facial

153
Q

List 3 causes of mononeuropathies multiplex

A

Diabetes, lyme, vasculitis, HIV, neoplastic

154
Q

List 5 causes of ganglionopathies

A

Pyridoxine, HSV, VZV, heavy metals, paraneoplastic

155
Q

What is the clinical presentation of Miller Fischer syndrome

A

ophthalmoplegia, ataxia, and areflexia

156
Q

List 3 triggers of GBS

A

Post infectious campylobacter (30%), mycoplasma, CMV, EBV
Vaccinations

157
Q

Describe the clinical symptoms of GBS

A

Motor: peripheral, symmetrical ascending weakness or paralysis (including loss of reflexes) of more than one limb over days-week, hyporeflexia. Sparing of the anal sphincter; should be no bladder or bowel dysfunction
Sensory: mixed parasthesias in a distal and proximal pattern (usually positive rather than negative symptoms); generally very mild. Should not follow a sensory level
Bulbar: loss of cough (increased secretions), gag, swallow, poor neck strength, change in voice
Autonomic: HR changes (both tachycardia and bradycardia), hypo/hypertension, diaphoresis

158
Q

What measurements can be used to predict the need for intubation in a GBS patient

A

Vital capacity should be >20 cc/kg; MIP >30 ccH20; MEP >40 ccH2O

159
Q

What are the CSF findings of GBS

A

high protein and a low/normal cell count; albuminocytologic dissociation

160
Q

What two therapies can be used in the management of GBS

A

IVIG, plasmapheresis

161
Q

Which ulnar neuropathies will have sensory symptoms

A

The ulnar cutaneous nerve to the hand branches proximal before entering Guyon’s canal; a lesion at the wrist should not produce sensory abnormalities but one at the elbow would be expected to do so

162
Q

List 4 diseases associated with carpal tunnel

A

acromegaly, amyloid, diabetes, hypothyroid, obesity, pregnancy, renal failure, rheumatoid arthritis

163
Q

List signs of UMN vs LMN disease

A

UMN: Increased reflexes, increased muscle tone, +ve Babinski. No muscle wasting
LMN: Decreased reflexes, decreased muscle tone, -ve Babinski. Muscle wasting and fasciculations

164
Q

List 5 drugs that can precipitate a myasthenia crisis

165
Q

List 2 causes of ascending paralysis and 2 causes of descending paralysis

A

Ascending paralysis: Polio, GBS, Tick paralysis, Periodic (hypoK)
Descending paralysis: Miller Fischer (variant of GBS - starts with ophthalmoplegia), Botulism

166
Q

Differentiate conus medullaris from cauda equina

A

Conus: UMN, bilateral, hyper reflexia
Cauda: LMN, unilateral, hypo reflexia
Both: saddle anesthesia, urinary retention, reduced rectal tone

167
Q

List 3 mechanisms of neuromuscular junction disorders and an example of each

A

Block of receptors i.e. myasthenia gravis
Decreased Ach released i.e. botulism
Inactivation of Ach by irreversible binding i.e. organophosphate poisoning

168
Q

How can you differentiate myasthenia gravis from botulism toxicity? What is the underlying pathophsiology?

A

Botulism toxicity will have anti-cholinergic effects (ex. Confusion, urinary retention, flushed skin)
This is because botulism affects the release of Ach (at both nicotinic and muscarinic receptors) vs. myasthenia only affects the nicotinic receptors

169
Q

What organism causes botulism

A

Clostridium botulinum

170
Q

What is the mechanisms of action of botulism

A

Neurotoxins bins to the presynaptic nerve membrane and inhibit the release of acetylcholine causing paralysis

171
Q

List 5 types of botulism

A

Food born: ex. Home canned foods that contain preformed toxins
Baby botulism: usually <6 mo of age, due to the ingestion of spores in honey. Causes floppy baby syndrome
Wound botulism: esp in IVDU
Unclassified botulism: adult version of infant botulism
Inadvertent: ex. Iatrogenic from cosmetic and therapeutic uses

172
Q

What is the clinical presentation of botulism

A

Descending symmetric paralysis
Cranial nerve palsies: diplopia, blurred vision, dysphonia, dysphagia, ptosis
Anti-cholinergic toxidrome
No pain. No sensory deficits. Reflexes are normal. Mental status is normal

173
Q

What is the treatment of botulism

A

Botulism antiglobulin (from horses)
Baby BIG for infants (from human pooled plasma)

174
Q

What is the pathophysiology of myasthenia gravis

A

Auto antibodies attack the acetylcholine receptors on the post synaptic cell. This blocks the receptors. With repeated stimulation, fewer and fewer receptor sites are available for Ach and fatigue develops

175
Q

What are the symptoms of myasthenia gravis

A

Fatigue and muscle weakness. Symptoms worsen as the day progresses and improves with rest
Proximal muscle weakness of the neck, facial, and bulbar (ex. dysarthria, dysphagia). Often first presents with ptosis and diplopia/ocular weakness
No anticholinergic symptoms. No mental status changes

176
Q

List 3 ways to diagnose myasthenia

A

Edrophonium test: 1-2mg IV boluses looking for a change in ptosis
Ice bag test on eyelids
Serum testing for Ach receptor antibodies

177
Q

List 2 treatments for myasthenia crisis, and 2 treatments for the long term management of myasthenia

A

Acute: plasma exchange, IVIG
Long term: acetylcholinesterase inhibitors ex. Neostigmine, steroids and immunosuppressant drugs, thymectomy

178
Q

How would you modify your intubation of a patient with myasthenia

A

Try to avoid succ; but if using will need to increase dose 2mg/kg
Decrease dose of roc to 0.6 mg/kg

179
Q

Other than medications, list 3 causes of myasthenia crisis

A

Infection, surgery, pregnancy,

180
Q

What is Lambert-Eaton syndrome? What is it associated with?

A

Auto antibodies affect the pre synaptic cell and prevent release of acetylcholine. Presents with weakness that IMPROVES with muscle use. This is due to increased Ach in the cleft with related stimulation. Associated with small cell carcinoma of the lung

181
Q

List 5 causes of myopathies

A

Inflammatory ex. dermatomyositis, polymyositis
Toxic-metabolic ex. electrolyte abnormalities, thyroid disorder, periodic paralysis

182
Q

List 3 causes of polymyositis

A

idiopathic, infectious (viral, bacterial), inflammatory (sarcoidosis, hypereosinophilic syndrome), neoplastic

183
Q

List 5 metabolic disorders that can cause myopathy

A

Electrolyte
- Hypokalemia, hyperkalemia
- Hypocalcemia, hypercalcemia
- Hypomagnesemia
- Hypophosphatemia
Endocrine
- Thyroid, parathyroid
- Adrenal

184
Q

What is periodic paralysis

A

Rare hereditary disorders of ion channels resulting in intermittent attacks of flaccid extremity weakness. Occurs with both hypokalemia and hyperkalemia (hypo more common), thyrotoxic periodic paralysis. Often resolves spontaneously. Supportive care only.

185
Q

*What % of patients suffer post LP headache

A

10-30% as per UTD

186
Q

*How to improve LP success

A
  • Different position
  • Different operator
  • Different interspace
  • Different approach (e.g. paramedian)
  • Use ultrasound
  • Use fluoroscopy
187
Q

*What are methods to decrease incidence of post-LP headache

A
  • Orient needle bevel parallel to longitudinal axis of spine
  • Use of non-cutting spinal needle
  • Use of smaller-diameter needle (typically 20- to 22-gauge)
  • Replace stylet prior to spinal needle withdrawal
  • Limit number of lumbar puncture attempts
  • Early ambulation
188
Q

*5 contraindications to LP

A
  • Focal neurological deficit
  • Signs of herniation
    Unilateral third nerve palsy
    Seizures
    Papilledema
  • Platelets < 50
189
Q

*5 indications to CT before LP

A
  • clinical concern for a CNS abscess, bleed or mass lesion:
  • History of trauma
  • Known tumor or history of cancer
  • History of immune compromise
  • Focal neurological deficit
  • Focal seizures
  • aLOC
  • Clinical features of raised ICP (papilledema, severe headache, irritability, decreased HR)
190
Q

*Where does the conus medullaris end

191
Q

*Gram stain findings (LP) for
- Streptococcus pneumoniae
- Neisseria meningitidis
- Listeria monocytogenes
- Hemophilus influenzae

A
  • Streptococcus pneumoniae: Gram-positive cocci, paired diplococci
  • Neisseria meningitidis: Gram-negative cocci, paired diplococci
  • Listeria monocytogenes: Gram-positive rods, single or chains
  • Hemophilus influenzae: Gram-negative coccobacilli - pleiomorphic
192
Q

List 10 risk factors for meningitis

A

Ongoing infections esp. sinusitis, pneumonia
Immunosuppression, alcoholism, advanced or early age, unvaccinated, splenectomy, sickle cell disease, diabetes, IVDU, malignancy
Recent neurosurgical procedure or indwelling device, dural defect, VP shunt
Low socioeconomic status, crowding (ex. military)

193
Q

List 3 bacteria that can cause meningitis

A

strep pneumo (58%), group B strep (18.1%), Neisseria meningitides (13.9%), haemophilus influenza (6.7%), listeria (3.4%)

194
Q

What type of bacterial may cause meningitis in a patient with a splenectomy

A

Encapsulated organisms in patients with splenectomy”
Some Nasty Killers Have Serious Capsule Protection: Strep (pneumo and group B), Neisseria, Klebsiella, Haemophilus, Salmonella, Cryptococcus, Pseudomonas

195
Q

List 10 causes of aseptic (culture negative) meningitis

A

Viral: enterovirus, coxsackie, HSV, varicella-zoster, cytomegalovirus, adenovirus, HIV
Fungal: cryptococcus, histoplasma, aspergillus, candida, Lyme
Noninfectious
- Post infectious and post vaccination ex. rubella, varicella, rabies, pertussis
- Drugs: NSAIDs, Septra, Azathioprine, Isoniazid, intrathecal medications, Allopurinol, Carbamazepine, Sulfasalazine
- Systemic disease, lupus, RA, sarcoidosis, Bechet’s disease
Neoplastic

196
Q

List common bacterial and preferred treatment for meningitis in each of the following age groups:
1. infants < 1 mo
2. children 1 mo - 2 years
3. children and adults 2-50 years
4. older adults and immunocompromised hosts
5. patients with basilar skull fracture
6. patients with penetrating trauma, post neurosurgery, or VP shunt

A
  1. Group B strep, Listeria, E coli. Ampicillin + Cefotaxime
  2. Strep pneumo, Neisseria meningitidis, Hemophilus influenza. Vanco + Ceftriaxone
  3. Neisseria meningitidis, Strep pneumo. Vanco + Ceftriaxone
  4. Neisseria meningitidis, Strep pneumo, Listeria. Vanco + Ceftriaxone + Ampicillin
  5. Strep pneumo, H influenza, Group B strep. Vanco + Ceftriaxone
  6. Staph aureus, Strep, Vanco + Cefepime
197
Q

List 5 immediate and 5 delayed complications of meningitis

A

Immediate: coma, loss of airway reflexes, seizures, cerebral edema, DIC, respiratory arrest, pericardial effusion, death
Delayed: seizure disorder, paralysis, subdural effusion, intellectual deficits, sensorineural hearing loss, ataxia, blindness, bilateral adrenal hemorrhage, CVST, death

198
Q

What is normal CSF opening pressure

A

5-20 cmH20

199
Q

How can you adjust the CSF for a traumatic tap

A

subtract 1 WBC for every 700 RBCs and 10 mg/L of protein for each 1000 RBCs

200
Q

Describe the appearance of each of the following CSF:
1. Normal
2. Bacterial meningitis
3. Viral meningitis
4. SAH
5. MS
6. GBS

A
  1. Clear and colourless, WBC <5, RBC 0-10, normal protein, normal glucose
  2. Cloudy and turbid, WBC >500 (neutrophils), RBC normal, increased protein, low glucose
  3. Clear and colourless, WBC 10-1000 (lymphocytes), RBC normal, normal/decreased protein, normal glucose
  4. Blood stained or xanthochromia, WBC normal, RBC high, high protein, normal glucose
  5. Clear and colourless, WBC high, RBC normal, high protein, normal glucose
  6. Clear anc colourless, normal WBC, RBC normal, high protein, normal glucose
201
Q

What is the dose for empiric antibiotics in an adult patient suspected to have meningitis

A

Ceftriaxone 2g IV and vancomycin 15mg/kg IV
- Consider ampicillin if history of Listeria
- Consider acyclovir 10mg/kg if HSV is suspected

202
Q

What are the indications for chemoprophylaxis in meningitis

A

Individuals for have been exposed to patients diagnoses with Neisseria meningitidis and H influenza (not for pneumococcal). Close contact include housemates, individuals exposures to secretions (shared utensils), incubators
- Rifampin 600mg PO q12 x 4 doses or Cipro 500mg PO once or CTX 250mg IM once

203
Q

List 5 contraindications for LP

A

Suspicion of mass lesion: focal neurologic deficits, new seizure, papilledema, immunocompromised states, malignancy, hx of CNS disease, age >60
Elevated INR >1.5, decreased platelets <50, hemophilia, von Willebrand’s
Hemodynamically unstable, uncooperative patient, lack of consent
Local skin infection

204
Q

List 5 non neurological causes of weakness

A

Dehydration, hypoglycemia, electrolyte abnormalities, anemia
ACS, shock, increased metabolic demand i.e. sepsis
Tox

205
Q

List 5 critical causes of neuromuscular weakness

A

Stroke, spinal cord compression, acute demyelination (Guillain Barre), myasthenic crisis, botulism, tick paralysis, organophosphate poisoning

206
Q

Localize the lesion in the following scenarios:
1. Unilateral weakness with ipsilateral facial involvement
2. Unilateral weakness with contralateral facial involvement
3. Unilateral weakness of upper and lower extremity with no facial involvement
4. Unilateral weakness of a single extremity
5. Bilateral upper extremity weakness
6. Bilateral lower extremity weakness
7. All extremity weakness
8. Proximal extremities only
9. Distal extremities only

A
  1. Contralateral lesion of the cerebral cortex or internal capsule
  2. Brainstem lesion
  3. Brown Sequard hemi cord syndrome or lesion in cerebral cortex
  4. Plexopathy or neuropathy
  5. Central cord syndrome
  6. Anterior cord syndrome, Cauda equina, Guillain Barre
  7. Anterior cord syndrome, Guillain Barre
  8. Myositis, rhabdomyolysis, NMJ disorder
  9. Polyneuropathy
207
Q

List 5 critical causes of coma

A

Metabolic: hypoglycemia, sepsis, adrenal crisis, hypoxia, hypercarbia
Tox: opioids, CO, methemoglobinemia
Structural: SAH, stoke, elevated ICP

208
Q

Describe the components of the GCS

A

see photo - GCS

209
Q

List 3 ways to test for brainstem reflexes

A

Oculocephalic reflex (doll’s eyes), oculovestibular reflex (cold caloric testing), corneal reflex, gag reflex

210
Q

List 5 principles of neuroprotective resuscitation

A

[Box 13.1]
Elevate head of bed to 30 degrees
Remove any constricting ties or collars
Avoid hypoxia or hyperoxia
Maintain EtCO2 35
Avoid hypotension
Avoid hyperthermia
Prevent and treat seizures

211
Q

List 10 seizure mimics

A

Cardiac: syncope
Neurologic: TIA, migraine, movement disorders, mass lesions, tetanus, CNS infections
Tox: intoxication, oversedation, extrapyramidal symptoms
Metabolic: hypo or hyperglycemia, thyrotoxicosis, delirium tremens
Psych: pseudoseizure, panic attacks cataplexy

212
Q

List 5 ways to differentiate pseudoseizure from seizure

A

pseudoseizures last longer, brief or no postictal period, patient can recall events during the seizure, pelvic trusting, head movements, avoidance of noxious stimuli or gaze deviation away from examiner, no metabolic acidosis

213
Q

*Two accepted definitions of status epilepticus

A

Serial seizure activity without recovery in between, or
Prolonged, continuous seizure activity (> 5 min)

214
Q

*Two non-IV treatments in seizure

A
  1. Intranasal midazolam, PR diazepam
  2. O2
215
Q

*Ideal first line treatment for seizure if IV in place

A
  • Ativan 2mg IV
216
Q

*What is the second line agent in status epilepticus: MDMA OD

A

***hyponatremia so give hypertonic saline

217
Q

*What is the second line agent in status epilepticus: patient with recent positive TB skin test

A

pyridoxine (for presumed INH induced seizures)

218
Q

*What is the second line agent in status epilepticus: eclampsia

A

Magnesium sulfate (4-6g IV over 20 mins)

219
Q

(What is the second line agent in status epilepticus: patient with Hx schizophrenia and psychogenic polydipsia

A

Hypertonic saline

220
Q

*7 toxicologic causes of seizures (excluding EtOH and withdrawal states) (looking for categories of drugs)

A
  • Amphetamines,
  • anticholinergics,
  • cocaine,
  • isoniazid,
  • organophosphates,
  • phenothiazines,
  • TCA,
  • salicylates,
  • lithium
221
Q

*5 causes of seizure other than toxic ingestion

A
  • Metabolic (e.g. hepatic encephalopathy, hypoCa, hypo- or hyperglycemia, hypoNa, uremia)
  • Infectious processes (e.g. CNS abscess, encephalitis, meningitis)
  • Withdrawal syndromes (e.g. alcohol, anti-epileptic drugs, baclofen, barbiturates, benzodiazepines)
  • CNS lesions (e.g. hydrocephalus, anoxic insult, AV malformation, brain metastases, CVA, eclampsia, head trauma, ICH, neoplasm)
222
Q

*What is the treatment for seizures caused by hyponatremia?

A

Hypertonic saline

223
Q

Which patients with a seizure should get a CT head?

A

New focal deficits, persistent altered mental status, fever, recent trauma, persistent headache, hx of CA, hx of AIDs, anticoagulant use, age >40, partial seizures

224
Q

*FILL IN TABLE: BPPV, Meniere’s, Labyrinthitis, Vestibular Neuronitis, Acoustic Neuroma with Tinnitus, Hearing Loss, Ataxia

A

Tinnitus Hearing loss Ataxia
BPPV - - +
Meniere’s + + +
Labyrinthitis +. + +
Vestibular neuritis - - +
Acoustic neuroma + + +/-

225
Q

*Which side is affected in positive Dix Hallpike? Which semicircular canal? Which direct do you roll the patient to resolve the symptoms?

A

Direction of roll/looking is affected side. Posterior canal. Opposite

226
Q

*Which canal is affected in supine roll test?

A

Horizontal

227
Q

*Causes of acute vestibular syndrome

A

Acute vestibular syndrome is used to describe a clinical condition in which dizziness develops acutely, is constant, persists longer than a day, and is accompanied by nausea or vomiting, unsteady goat, nystagmus, and intolerance to head motion
Causes:
- Vestibular neuritis: often viral due to inflammation of CN8, no hearing loss
- Labyrinthitis: due to infection of the labyrinth, hx of ear infections, with hearing loss

228
Q

*Describe each step of HINTS exam and what it means

A

HINTS (Head Impulse test, Nystagmus, Test of Skew)
- Head impulse test: A corrective saccade indicates a positive test and is more reassuring for vestibular neuritis
- Nystagmus: Unidirectional, horizontal nystagmus suggests a peripheral lesion - Test of Skew: Lack of eye movement in uncovered eye reassuring

INFARCT:
1. head I-impulse is N-ormal
2. F-ast-phase A-alternating (or bidirectional) nystagmus 3. The eye moves to R-efixate during C-over T-est

229
Q

*5 characteristics suggestive of peripheral vertigo.

A

Hearing loss
Tinnitus
Episodic/resolves
Head position may worsen
No associated neuro findings

230
Q

*3 medication classes that may be helpful in peripheral vertigo to relieve symptoms

A

promethazine (vestibular suppressant)
ondansetron (anti-emetic)
lorazepam (benzo)

231
Q

Briefly describe the details of one non-pharmacologic intervention for BPPV

A

Various maneuvers to dislodge otolith
Epley’s: With the head held beneath the plane of the bed at 45 degrees, continue to turn the head in 90 degree increments until the dizziness has resolved. Then sit the patient upright

232
Q

*What does the corrective saccade mean in the HINTS exam

A

There is a peripheral cause to the vertigo; acute vestibular syndrome i.e. labyrinthitis or vestibular neuritis

233
Q

W*hat is the cause of vertigo after URTI

A

Labyrinthitis

234
Q

*Compare peripheral vs central vertigo - duration, onset, severity of symptoms, and associated neuro findings

A

Peripheral: sudden onset, initial severe but decreasing over time, variable duration based on etiology, nystagmus is usually torsional and upbeat, change in symptoms with head position, no neurologic findings, associated with auditory findings

Central: gradual or sudden onset, mild in most cases, variable duration depending on etiology, nystagmus is usually purely vertical, direction changing or torsional, associated with neurologic findings, no auditory findings

235
Q

List 5 causes of peripheral vertigo and 5 causes of central vertigo

A

[Box 16.1] see photo

236
Q

What is an INO and what does it signify?

A

INO: on eye movement the adducting eye shows little to no movement but the abducting eye moves normally. Eyes are in normal position on straight-ahead gaze
Symptom of MS

237
Q

List 2 vertigo mimics

A

Dysequilibrium - )I feel like a need to fall, vs vertigo which is I feel like I am moving)
Near syncope

238
Q

List 3 causes of constant vertigo and 3 causes of intermittent vertigo

A

Constant: vestibular neuritis or labyrinthitis, stroke, MS
Intermittent: BPPV, migraines, Meniere’s, TIA

239
Q

List 5 drugs that can cause ototoxicity

A

aminoglycosides, ASA, anticonvulsants, quinine, quinidine, minocycline, furosemide

240
Q

What is Wallenberg syndrome

A

occlusion of the posterior inferior cerebellar artery causing vertigo, loss of pain and temperature on the face ipsilateral to the lesion and on the body contralateral to the lesion, Horner’s syndrome, paralysis of the palate, pharynx, and larynx

241
Q

What kinds of nystagmus suggest a central cause

A

purely vertical, torsional, downbeating, non fatigable, direction changing

242
Q

Describe the Dix Hallpix test

A

Turn the head to 45 degrees and then quickly move the patient from an upright seated position to a supine position. Make sure the head is brought 20 degrees below the examining table. Rotary orupbeatingnystagmus within 30 seconds is considered a positive test. Side with the symptoms is the side with the lesion; in general only one side is positive

243
Q

How can you differentiate between posterior and horizontal canal otoliths

A

BPPV for posterior
Supine roll test for horizontal

244
Q

Exclusion criteria SAH rule

A

prior anneursym, prior SAH, known tumor, new focal deficit and chronic reccurent (more than 3 in last 6 months)

245
Q

What is HINTS+ what does it pick up?

A

Add on hearing each side. if HINTs peripheral and loss of hearing think of labrynth infarct or pontine

246
Q

Ascending and descending paralysis differential

A

Ascending - GBS, tick bite, Rabies, Polio, Heavy metal, Etoh, vitamin defeciency

Descrneding - Miller fischer varient GBS, MG, lambert eaton, tick bite on head, diptheria, botulism, organophosphastes, pontine infarct

KChan Saves the World (24 decks)

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