KC Neuro Flashcards
(246 cards)
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
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.
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.
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.
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
6
Q
*Biggest risk factor for spontaneous bleed
A
Hypertension
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
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
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
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
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
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
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
14
Q
*What are 5 causes for this patient’s presentation other than stroke?
A
Hypoglycemia
Seizure
Migraine
Hyponatremia
Encephalitis
Wernicke’s
Intoxication
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
- Acute ischemic stroke (can still have a normal plain CT brain in this case)
- Migraine
- Todd’s paralysis
- Internal carotid artery dissection
- GCA
- Aortic dissection
- CVT
- 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)
16
Q
*6 reasons to decrease BP in this patient?
A
- If you’re going to thrombolyse them (ie, ischemic stroke inside the window)
- If they’re having an aortic dissection
- Reduce risk of intracranial hemorrhage
- Signs of raised ICP
- Acute myocardial infarction
- Hypertensive encephalopathy (10-15% reduction)
- Severe left ventricular heart failure
- Should slowly reduce BP over 24h even in ischemic stroke not getting tPA (15-25%)
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)
18
Q
*tPA airway complication? One thing
A
Angioedema
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
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
21
Q
*What is the range over which CPP is auto-regulated.
A
50-160
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
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
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
25
*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
1. Cerebellar or brainstem ischemia
2. Cerebellar or brainstem hemorrhage
3. Vertebral artery dissection
4. brainstem met
26
*4 therapies you would initiate in the emergency department for acute ischemic stroke?
- 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
27
*What is Broca’s aphasia?
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
28
*22-year-old presents with facial droop and hemiplegia. What is on the differential for other than stroke in this patient?
- Seizure/Todd's paralysis
- Tumour
- Complicated migraine
- Alcohol intoxication
- Psychiatric (e.g. conversion disorder)
- Drug toxicity
- Bell's palsy
29
*What are CT features of an MCA stroke?
- Hyperdense MCA sign
- Parenchymal hypoattenuation
- swelling of the grey-white matter junction
- Mass effect
30
*What causes strokes in young people?
- 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
31
*5 stroke mimics
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
32
*4 features of a high risk TIA
(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
33
*Define TIA
A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.
34
What are BP targets for hemorrhagic strokes?
140-160 in the first 24-48 hours as per Canadian Stroke Guidelines
35
List 5 factors associated with hemorrhagic strokes
Vascular malformations, aneurysms, hypertension, alcohol use, cocaine use, cerebral amyloid angiopathy
36
List 3 clinical tools that can be used to assess stroke
NIHSS, FAST (facial droop, arm weakness, slurred speech, time <24 hours), VAN (vision, aphasia, neglect)
37
List 5 components of the NIHSS
LOC, gaze, visual fields, facial droop, motor arms, motor legs, ataxia, sensory, language, dysarthria
38
List 5 findings on non contrast CT that suggest stroke
Dense MCA, loss grey-white differentiation, loss deep nuclei, sulcal or gyral effacement, insular ribbons, hemorrhage, mass effect
39
List 5 findings from stroke that can be seen on CTA
Posterior circulation better visualized, intravascular thrombi, intraluminal narrowing, dissection, AVM
40
What is a high risk TIA
aphasia, unilateral weakness, amaurosis fugax
41
What imaging is required for a stroke in the 0-4.5 hour window. What interventions are possible
CT head (CAEP). Most get CTA
TPA +/- thrombectomy
42
What imaging is required for a stroke in the 4.5-6 hour window. What interventions are possible
CT head + CTA
CT perfusion if +ve VAN or NIHSS >6
Thrombectomy
43
What imaging is required for a stroke in the >6 window. What interventions are possible
CT. CTA + CT perfusion if +ve VAN or NIHSS >10
Thrombectomy
44
What are blood pressure targets in acute stroke
<185/110 if planning to give tPA. Otherwise permissive hypertension up to 220/120, lowering 15% in the first 24 hours
45
List 5 features of a primary stroke centre
Continuous monitoring capability
Emergency physician
24 hour access to CT + CTA
Telehealth equipment for stroke consultation
TPA capability
## Footnote
Think of this one as Joe Brant
46
List 5 additional features of a comprehensive stroke centre
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
47
What is the dose of TPA
0.9mg/kg IV alteplase max dose 90mg, 10% of dose as a bolus over 1 minute
48
Patient with a high risk TIA is being discharged. What medications should be prescribed
If ABCD >4
ASA 160mg PO load then 81mg daily
Plavix 300mg PO load then 75 mg PO OD
49
*Two accepted definitions of status epilepticus
Seizure lasting longer than greater than 5 minutes duration, or
recurrent seizure activity without intervening return to baseline mental status
50
*Two NON IV treatments of status epilepticus
Midaz (IM, IN, buccal, IO)
Diazepam (IO, PR)
51
*Ideal first line treatment for status epilepticus, if have IV?
Lorazepam 2mg IV
52
*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. Hypertonic saline 100mL
b. Pyridoxine max dose 5g (for presumed INH induced seizures)
c. Mag sulf 4g
d. Hypertonic saline 100mL
53
Describe the two main classification of seizures
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
54
List 10 potential etiologies of seizure
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
55
List 3 options for first line agents to use in seizure
Lorazepam 0.1mg/kg IV, max 4mg
Midazolam 0.2mg/kg IV, max 10mg IM
Diazepam 0.5mg/kg PR
56
List 3 options for second line agents to use in seizure
Fosphenytoin or phenytoin 20mg/kg IV
Phenobarbital 20mg/kg IV
Valproic acid 40mg/kg IV
Levetiracetam 60mg/kg IV (usually 1g)
Others: ketamine, propofol
57
*Patients who is a young female (22). You suspect idiopathic intracranial hypertension.
What are 4 medication causes of IIH?
Vit A
Retinoids
Tetracycline
HGH
58
*What are three neurologic findings of IIH on exam?
Papilledema
Visual field defect/visual loss
Sixth nerve palsy
59
*What is one medication you can give for this? What are two alternatives?
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.
60
*What are two non-medical treatment options for IIH if medical treatment fails?
CSF shunting
Optic nerve sheath decompression
61
*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:
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
62
*5 causes of unilateral facial weakness besides Bell’s palsy
- Stroke
- Ramsay Hunt syndrome
- Lyme disease
- Bacterial infection (e.g. complicated otitis media/externa)
- Trauma
- Tumor
63
*6 indications for urgent CT in workup for atraumatic headache
1. Fever
2. AMS
3. Lateralizing signs
4. Thunderclap
5. Recent neurosurgery
6. Signs of uncal herniation
64
*6 parenteral therapies for migraine
Ketorolac, stemetil, metoclopramide, ondansetron, IV fluids, morphine, dexamethasone, dihydroergotamine
65
*1 treatment specific to cluster headache
High flow O2
66
*What diagnosis must be ruled out in patients with mydriasis and CN 3 palsy?
Pcomm aneurysm
67
*What are the 6 criteria as part of the SAH rule by Perry?
Age>40
Neck pain / stiffness
Thunderclap headache
Loss of consciousness
Exertional onset
Flexion of neck limited on exam
| ANT LEaF
68
*What is the diagnostic gold standard used in the paper (SAH rule by Perry) (3 things)?
SAH on CT
Xanthochromia on CSF
Presence of RBC with >1x106 on CSF with aneurysm or AVM on CTA
69
*What is the sensitivity and specificity of the SAH rule by Perry?
Sensitivity 100%, specificity 13.6%
70
*Take home message from Perry's SAH
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
71
*The sensitivity and specificity of CT overall for SAH
sensitivity 93%, specificity 100%
72
*Sensitivity and specificity of the patients scanned within 6 hrs of headache onset
Sensitivity 100%, specificity 100%
73
*4 Inclusion criteria Perry's SAH
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
74
*% post LP headache
10-30% as per UTD
75
*How to improve LP success
- 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
76
*5 contraindications to LP vs CT first?
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
77
*What are methods to decrease incidence of post-LP headache
- 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
78
*5 indications to CT before LP
- 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)
79
*6 indications for urgent CT in workup for atraumatic headache
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
80
*Acute, atraumatic headache, list EIGHT historical features that suggest a potentially serious etiology.
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
81
*LP interpretation in SAH
In short, increased WBC, protein and decreased glucose = infection
82
What is the diagnostic criteria of migraine without aura
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
83
What is the diagnostic criteria of migraine with aura
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
84
What is the presentation of a tension headache
Gradual onset, band-like, bilateral often with associated neck and scalp muscle pain
85
What is the presentation of a cluster headache
Sudden unilateral retro orbital pain that occurs in clusters. May have ipsilateral autonomic symptoms ex. Ptosis, miosis
86
List 10 causes of secondary headaches
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
87
List 5 risk factors for the development of CVST
OCP use, antiphospholipid syndrome lupus, protein C and S deficiency, factor V Leiden mutation, thrombophilia, sickle cell anesthesia, pregnancy
88
What is the diagnostic criteria of idiopathic intracranial hypertension
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
89
What are risk factors for SAH
Age, hypertension, smoking, alcohol consumption, sympathomimetic drugs, family hx of aneurysms, family hx of polycystic kidney disease, Marfan or connective tissue disorder
90
What is the components of the Ottawa SAH rule
ANT LEaF: Age>40, Neck pain, Thunderclap onset, LOC, Exertional onset, Flexion decreased
100% sensitive if no factors are present
91
What is the Hunt and Hess clinical grading scale for SAH
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
92
What is the blood pressure target in SAH
<140-160
93
What specific therapy is indicated in SAH to reduce vasospasm
Nimodipine
94
What is the clinical presentation of carotid artery dissection
Unilateral headache or neck pain, ipsilateral partial Horner's syndrome (ptosis, miosis, anhidrosis), blindness or contralateral motor deficits caused by cerebral ischemia
95
What is the clinical presentation of vertebral artery dissection
posterior headache with rapidly progressive neurologic cerebellar deficits ex. vertigo, severe vomiting, ataxia, diplopia, hemiparesis, tinnitus
96
What is the diagnostic criteria for delirium
1. Acute onset with fluctuating course
2. Disturbs attention and awareness (inattention)
3. Disturbed Perception
4. NOT better explained by another neurocognitive disorder
## Footnote
FAPE'N
97
What are the 4 components of the CAM screen
1. Acute onset and fluctuating course
2. Inattention
3. Disorganized thinking OR
4. Altered Level of consciousness
| A TIA
98
List 10 causes of dementia
See photo - causes of dementia
99
List 3 bedside tests that can be used in the assessment of delirium
CAM, MMSE, clock drawing test, short portable mental status questionnaire, cognitive capacity screening examination
100
What is the definition of dementia
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
## Footnote
CIDE + LEAM
101
Contrast delirium and dementia
Delirium: acute, fluctuating, reversible, decreased awareness/attention, disorganized thoughts
Dementia: chronic, gradual, progressive, permanent, normal consciousness, disinhibited thoughts
102
What is the clinical presentation of Parkinson's
TRAP Presentation: tremor, rigidity (cog-wheeling), akinesia (slow and small movements), postural instability. Also shuffling gait, masked facies.
103
List the ADLs and IADLs
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
*What are 5 causes of facial nerve injury (not idiopathic)?
Trauma
Tumor
Otitis media
Lyme disease
EBV
HSV
105
*What is treatment for a mild case of Bell’s palsy (Name, Dose, Route, Frequency, Duration) [5 marks]
Prednisolone 50-60mg PO daily x10 days
106
*What are 3 physical exam signs of SEVERE facial nerve paralysis (3 points)?
Inability to close eyes
Asymmetry at rest
No perceptible movement
107
*Patients can get corneal scarring because they can’t close their eyes; what are 3 interventions to prevent this over short- or long-term?
Patching
Goggles
Ointment/artificial tears
Referral to ophtho
108
*Visual stim: eye down and out. What is the diagnosis?
Most emergent diagnosis (cause)
5 other diagnoses that could cause this
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
*Vesicular rash anterior to ear, CN involved and eponymous syndrome
CN VII - Ramsay Hunt
110
*Bitemporal vision loss (mechanism and common cause)
Lesion at optic chiasm eg. pituitary adenoma
111
What nerve is affected in trigeminal neuralgia
CN5
112
What medication can be used in the treatment of trigeminal neuralgia
Carbamazepine 100mg PO BID
113
List all the cranial nerves and specific findings associated with CN palsies
see photo
114
List 6 ddx for CN 7 palsy
Bell's palsy, Ramsay hunt, lyme disease, OM
Guillain Barre, HIV infection
Tumor compression, stroke
115
How can a central vs. peripheral cause of facial droop be differentiated?
Peripheral CN7 palsy INVOLVES the forehead (ex. Bell's palsy)
Central cause SPARES the forehead (ex. Stroke)
116
What are the clinical features of optic neuritis
acute or subacute vision, unilateral eye pain, +RAPD
117
*Non traumatic ddx of cauda equina
Malignancy / path fracture
Epidural abscess
Epidural Hematoma
Spinal SAH
Potts disease
118
*What are the 3 most common malignancies that can metastasize to spine?
Breast
Lung
Lymphoma
119
*ED management of cauda equina
Dexamethasone 10mg IV edema decompression
Neurosurgery
120
*MRI shows lytic lesion and spinal compression with elevated Cr, calcium with anemia. What is your presumed Dx and next lab test?
MM
SPEP
121
*5 diagnoses requiring urgent spinal MRI in the ED
Transverse osteomyelitis
Cauda equina or conus medullaris syndromes
Epidural abscess
Epidural compression
Epidural hematoma
122
*What are 3 physical exam findings suggestive of cauda equina in the ED
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
*Describe 2 differences between neurogenic and vascular claudication.
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
*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
- Neurologic deficit/suspected cauda equina syndrome
- Disabling pain despite 12 weeks conservative therapy
125
*Table with L3-S1 dermatomes, muscular function and reflexes
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
*Most sensitive finding of Cauda Equina
Urinary retention
127
*Most common organism for spinal epidural abscess
Staph aureus
128
*Most urgent treatment for SEA
Abx (ceftri vanco) and surgical decompression - unsure which they are asking for here
129
*List diagnosis, mechanism/most common cause
1. Vibration/position sens maintained; Motor & temp/pain impaired
2. Unilateral facial & body sensory deficit
1. Anterior cord syndrome - forced flexion or injury to anterior spinal artery
2. Hemibody syndrome - functional
130
Describe the tracts of the spinal cord
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
Describe the clinical findings of a complete spinal cord lesion
Total loss of motor and sensation distal to the injury. Absolutely no signs of sparing (ex. No rectal tone)
132
Describe the mechanism and clinical findings of a central cord lesion
See photo
133
Describe the mechanism and clinical findings of a Brown Sequard lesion
See photo
134
Describe the mechanism and clinical findings of an anterior cord lesion
See photo
135
Describe the grading of neuromuscular weakness
See photo
136
List 10 non traumatic causes of spinal cord dysfunction
Compressive lesions: hematoma, abscess, diskitis, cancer
Non compressive: MS, transverse myelitis, spinal subarachnoid hemorrhage, syringomyelia, HIV myelopathy, other myelopathies, spinal cord infarction
137
Describe the dermatomes associated with: C5, C7, L1, L4, S1, S2
See photo - dermatomes
138
Describe the myotomes associated with: C5, C7, L1, L4, S1, S2
See photo - myotomes
139
What is transverse myelitis
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
What is Syringomyelia? What makes it worse? How does it present similarly to?
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
What is diskitis
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
*List diagnosis, mechanism/most common cause: Weak dorsiflexion; sens 1st web space decreased
Deep peroneal nerve compression - habitual leg crossing
143
How many peripheral spinal nerves are there?
12 cranial nerves and 31 spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal)
144
List 10 causes of emergent weakness
Autoimmune: GBS, myasthenia gravis
Toxic: botulism, tick paralysis, metals, paralytic shellfish toxin
Metabolic: dyskalemia, hypophosphatemia, hypermagnesemia, porphyria
Infectious: poliomyelitis, diphtheria
145
Which peripheral nerve disorder presents with purely motor symptoms
ALS
146
Which peripheral nerve disorder presents with purely sensory symptoms
Gangliopathy
147
Which peripheral nerve disorders present with symmetrical symptoms
Demyelinating (ex. GBS), distal polyneuropathy (ex. Diabetes)
148
List 7 categories of peripheral nerve disorders and an example of each
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
List 5 causes of demyelinating polyneuropathy
GBS, Miller-Fischer variant, CIDP, HIV, Diphtheria, buckthorn, malignancy
150
List 5 causes of distal polyneuropathy
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
List 3 plexopathies
Brachial plexus, lumbar plexus, conus medullaris
152
List 5 isolated mononeuropathies
Radial, median, ulnar, sciatic, femoral, peroneal, facial
153
List 3 causes of mononeuropathies multiplex
Diabetes, lyme, vasculitis, HIV, neoplastic
154
List 5 causes of ganglionopathies
Pyridoxine, HSV, VZV, heavy metals, paraneoplastic
155
What is the clinical presentation of Miller Fischer syndrome
ophthalmoplegia, ataxia, and areflexia
156
List 3 triggers of GBS
Post infectious campylobacter (30%), mycoplasma, CMV, EBV
Vaccinations
157
Describe the clinical symptoms of GBS
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
What measurements can be used to predict the need for intubation in a GBS patient
Vital capacity should be >20 cc/kg; MIP >30 ccH20; MEP >40 ccH2O
159
What are the CSF findings of GBS
high protein and a low/normal cell count; albuminocytologic dissociation
160
What two therapies can be used in the management of GBS
IVIG, plasmapheresis
161
Which ulnar neuropathies will have sensory symptoms
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
List 4 diseases associated with carpal tunnel
acromegaly, amyloid, diabetes, hypothyroid, obesity, pregnancy, renal failure, rheumatoid arthritis
163
List signs of UMN vs LMN disease
UMN: Increased reflexes, increased muscle tone, +ve Babinski. No muscle wasting
LMN: Decreased reflexes, decreased muscle tone, -ve Babinski. Muscle wasting and fasciculations
164
List 5 drugs that can precipitate a myasthenia crisis
See photo
165
List 2 causes of ascending paralysis and 2 causes of descending paralysis
Ascending paralysis: Polio, GBS, Tick paralysis, Periodic (hypoK)
Descending paralysis: Miller Fischer (variant of GBS - starts with ophthalmoplegia), Botulism
166
Differentiate conus medullaris from cauda equina
Conus: UMN, bilateral, hyper reflexia
Cauda: LMN, unilateral, hypo reflexia
Both: saddle anesthesia, urinary retention, reduced rectal tone
167
List 3 mechanisms of neuromuscular junction disorders and an example of each
Block of receptors i.e. myasthenia gravis
Decreased Ach released i.e. botulism
Inactivation of Ach by irreversible binding i.e. organophosphate poisoning
168
How can you differentiate myasthenia gravis from botulism toxicity? What is the underlying pathophsiology?
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
What organism causes botulism
Clostridium botulinum
170
What is the mechanisms of action of botulism
Neurotoxins bins to the presynaptic nerve membrane and inhibit the release of acetylcholine causing paralysis
171
List 5 types of botulism
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
What is the clinical presentation of botulism
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
What is the treatment of botulism
Botulism antiglobulin (from horses)
Baby BIG for infants (from human pooled plasma)
174
What is the pathophysiology of myasthenia gravis
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
What are the symptoms of myasthenia gravis
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
List 3 ways to diagnose myasthenia
Edrophonium test: 1-2mg IV boluses looking for a change in ptosis
Ice bag test on eyelids
Serum testing for Ach receptor antibodies
177
List 2 treatments for myasthenia crisis, and 2 treatments for the long term management of myasthenia
Acute: plasma exchange, IVIG
Long term: acetylcholinesterase inhibitors ex. Neostigmine, steroids and immunosuppressant drugs, thymectomy
178
How would you modify your intubation of a patient with myasthenia
Try to avoid succ; but if using will need to increase dose 2mg/kg
Decrease dose of roc to 0.6 mg/kg
179
Other than medications, list 3 causes of myasthenia crisis
Infection, surgery, pregnancy,
180
What is Lambert-Eaton syndrome? What is it associated with?
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
List 5 causes of myopathies
Inflammatory ex. dermatomyositis, polymyositis
Toxic-metabolic ex. electrolyte abnormalities, thyroid disorder, periodic paralysis
182
List 3 causes of polymyositis
idiopathic, infectious (viral, bacterial), inflammatory (sarcoidosis, hypereosinophilic syndrome), neoplastic
183
List 5 metabolic disorders that can cause myopathy
Electrolyte
- Hypokalemia, hyperkalemia
- Hypocalcemia, hypercalcemia
- Hypomagnesemia
- Hypophosphatemia
Endocrine
- Thyroid, parathyroid
- Adrenal
184
What is periodic paralysis
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
*What % of patients suffer post LP headache
10-30% as per UTD
186
*How to improve LP success
- Different position
- Different operator
- Different interspace
- Different approach (e.g. paramedian)
- Use ultrasound
- Use fluoroscopy
187
*What are methods to decrease incidence of post-LP headache
- 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
*5 contraindications to LP
- Focal neurological deficit
- Signs of herniation
Unilateral third nerve palsy
Seizures
Papilledema
- Platelets < 50
189
*5 indications to CT before LP
- 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
*Where does the conus medullaris end
L1-L2
191
*Gram stain findings (LP) for
- Streptococcus pneumoniae
- Neisseria meningitidis
- Listeria monocytogenes
- Hemophilus influenzae
- 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
List 10 risk factors for meningitis
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
List 3 bacteria that can cause meningitis
strep pneumo (58%), group B strep (18.1%), Neisseria meningitides (13.9%), haemophilus influenza (6.7%), listeria (3.4%)
194
What type of bacterial may cause meningitis in a patient with a splenectomy
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
List 10 causes of aseptic (culture negative) meningitis
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
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
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
List 5 immediate and 5 delayed complications of meningitis
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
What is normal CSF opening pressure
5-20 cmH20
199
How can you adjust the CSF for a traumatic tap
subtract 1 WBC for every 700 RBCs and 10 mg/L of protein for each 1000 RBCs
200
Describe the appearance of each of the following CSF:
1. Normal
2. Bacterial meningitis
3. Viral meningitis
4. SAH
5. MS
6. GBS
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
What is the dose for empiric antibiotics in an adult patient suspected to have meningitis
Ceftriaxone 2g IV and vancomycin 15mg/kg IV
- Consider ampicillin if history of Listeria
- Consider acyclovir 10mg/kg if HSV is suspected
202
What are the indications for chemoprophylaxis in meningitis
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
List 5 contraindications for LP
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
List 5 non neurological causes of weakness
Dehydration, hypoglycemia, electrolyte abnormalities, anemia
ACS, shock, increased metabolic demand i.e. sepsis
Tox
205
List 5 critical causes of neuromuscular weakness
Stroke, spinal cord compression, acute demyelination (Guillain Barre), myasthenic crisis, botulism, tick paralysis, organophosphate poisoning
206
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
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
List 5 critical causes of coma
Metabolic: hypoglycemia, sepsis, adrenal crisis, hypoxia, hypercarbia
Tox: opioids, CO, methemoglobinemia
Structural: SAH, stoke, elevated ICP
208
Describe the components of the GCS
see photo - GCS
209
List 3 ways to test for brainstem reflexes
Oculocephalic reflex (doll's eyes), oculovestibular reflex (cold caloric testing), corneal reflex, gag reflex
210
List 5 principles of neuroprotective resuscitation
[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
List 10 seizure mimics
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
List 5 ways to differentiate pseudoseizure from seizure
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
*Two accepted definitions of status epilepticus
Serial seizure activity without recovery in between, or
Prolonged, continuous seizure activity (> 5 min)
214
*Two non-IV treatments in seizure
1. Intranasal midazolam, PR diazepam
2. O2
215
*Ideal first line treatment for seizure if IV in place
- Ativan 2mg IV
216
*What is the second line agent in status epilepticus: MDMA OD
***hyponatremia so give hypertonic saline
217
*What is the second line agent in status epilepticus: patient with recent positive TB skin test
pyridoxine (for presumed INH induced seizures)
218
*What is the second line agent in status epilepticus: eclampsia
Magnesium sulfate (4-6g IV over 20 mins)
219
(What is the second line agent in status epilepticus: patient with Hx schizophrenia and psychogenic polydipsia
Hypertonic saline
220
*7 toxicologic causes of seizures (excluding EtOH and withdrawal states) (looking for categories of drugs)
- Amphetamines,
- anticholinergics,
- cocaine,
- isoniazid,
- organophosphates,
- phenothiazines,
- TCA,
- salicylates,
- lithium
221
*5 causes of seizure other than toxic ingestion
- 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
*What is the treatment for seizures caused by hyponatremia?
Hypertonic saline
223
Which patients with a seizure should get a CT head?
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
*FILL IN TABLE: BPPV, Meniere's, Labyrinthitis, Vestibular Neuronitis, Acoustic Neuroma with Tinnitus, Hearing Loss, Ataxia
Tinnitus Hearing loss Ataxia
BPPV - - +
Meniere’s + + +
Labyrinthitis +. + +
Vestibular neuritis - - +
Acoustic neuroma + + +/-
225
*Which side is affected in positive Dix Hallpike? Which semicircular canal? Which direct do you roll the patient to resolve the symptoms?
Direction of roll/looking is affected side. Posterior canal. Opposite
226
*Which canal is affected in supine roll test?
Horizontal
227
*Causes of acute vestibular syndrome
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
*Describe each step of HINTS exam and what it means
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
*5 characteristics suggestive of peripheral vertigo.
Hearing loss
Tinnitus
Episodic/resolves
Head position may worsen
No associated neuro findings
230
*3 medication classes that may be helpful in peripheral vertigo to relieve symptoms
promethazine (vestibular suppressant)
ondansetron (anti-emetic)
lorazepam (benzo)
231
Briefly describe the details of one non-pharmacologic intervention for BPPV
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
*What does the corrective saccade mean in the HINTS exam
There is a peripheral cause to the vertigo; acute vestibular syndrome i.e. labyrinthitis or vestibular neuritis
233
W*hat is the cause of vertigo after URTI
Labyrinthitis
234
*Compare peripheral vs central vertigo - duration, onset, severity of symptoms, and associated neuro findings
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
List 5 causes of peripheral vertigo and 5 causes of central vertigo
[Box 16.1] see photo
236
What is an INO and what does it signify?
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
List 2 vertigo mimics
Dysequilibrium - )I feel like a need to fall, vs vertigo which is I feel like I am moving)
Near syncope
238
List 3 causes of constant vertigo and 3 causes of intermittent vertigo
Constant: vestibular neuritis or labyrinthitis, stroke, MS
Intermittent: BPPV, migraines, Meniere's, TIA
239
List 5 drugs that can cause ototoxicity
aminoglycosides, ASA, anticonvulsants, quinine, quinidine, minocycline, furosemide
240
What is Wallenberg syndrome
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
What kinds of nystagmus suggest a central cause
purely vertical, torsional, downbeating, non fatigable, direction changing
242
Describe the Dix Hallpix test
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 or upbeating nystagmus 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
How can you differentiate between posterior and horizontal canal otoliths
BPPV for posterior
Supine roll test for horizontal
244
Exclusion criteria SAH rule
prior anneursym, prior SAH, known tumor, new focal deficit and chronic reccurent (more than 3 in last 6 months)
245
What is HINTS+ what does it pick up?
Add on hearing each side. if HINTs peripheral and loss of hearing think of labrynth infarct or pontine
246
Ascending and descending paralysis differential
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
