Neurology Flashcards

1
Q

Subarachnoid Haemorrhage

2023.1 OSCE Station:
42y F with sudden onset severe headache
- Discuss investigations (CT, LP, CTA)
- Interpret CT scan
- GCS drops to 5. Outline your management

ASSESSMENT:
HISTORY:
- thunderclap
- loss of consciousness/syncope
- neck stiffness
- onset on exertion/sex
- vomiting
- eye pain

Sentinel bleed - headache in the preceding days/weeks

Risk factors:
- hypertension
- smoking
- heavy alcohol
- sympathomimetic use - cocaine
- personal history of cerebral
- aneurysm
- polycystic kidney disease
- connective tissue disease - ehlers danlos

EXAMINATION:
Temp - may have low grade temperature
Hypertension - will need to be reduced

Neck stiffness/meningism

Eyes:
- optic fundi (subhyaloid haemorrhage)
- IOP (glaucoma)
- unequal pupils, diplopia, disconjugate gaze (cranial nerve 3,4,6 palsy)
POCUS - optic sheath diametre (raised ICP/hydrocephalus)

Gross neurological examination:
- GCS
- motor function
- speech
- vision

INVESTIGATIONS:
BSL - rule out hypoglycemia as mimic
Hb - anaemia more difficult to detect SAH on CT
ECG - deep ST depression and T wave inversion in praecordial leads

Non-contrast CT
- 99.7% sensitive within 6hrs of headache onset if modern CT scanner and interpreted by radiologist
- sensitivity declines with time

LUMBAR PUNCTURE:
- indicated if negative CT beyond 6hrs
- increase ED length of stay (wait 12hrs for xanthochromia)

Contraindications to LP
- anticoagulation
- spinal metal hardware in situ
- cellulitis overlying the lumbar spine

Complications
- post LP headache
- traumatic tap
- increase ED length of stay

Pro’s
- can diagnose meningitis
- cost effective
- may avoid need for CTA which comes with radiation dose and contrast load

CT angiography
- higher radiation dose
- can’t detect microaneurysms <3mm
- incidental finding of aneurysm 2.5% of population may lead to unnecessary invasive intervention

COMPLICATIONS:
- hydrocephalus - RBCs block arachnoid villi and CSF drainage - need for VP shunt
- rebleeding
- vasospasm - nimodipine
- infarction/ischemia (careful BP management to maintain CPP)
- raised intracranial pressure and brain herniation

MANAGEMENT:
prevent secondary brain injury

*prevent raised ICP - head of bed up
*prevent hypoxia - oxygen
*prevent hypercarbia
*BP control - esmolol target SBP 140
*maintain CPP - keep SBP 140 with noradrenaline infusion
*reverse anticoagulation
*seizure prophylaxis - levitiracetam 60mg/kg
manage ICP - 3% hypertonic saline
prevent vasospasm - nimodipine 60mg q4h

DEFINITIVE MANAGEMENT:

manage hydrocephalus with external ventricular drain

A

Differential diagnosis for THUNDERCLAP HEADACHE
“severe headache with maximal intensity within 1hr of onset”

  • subarachnoid haemorrhage
  • carotid/vertebral artery dissection
  • pituitary apoplexy
  • reversible cerebral vasoconstriction syndrome
  • PRES (posterior reversible encephalopathy syndrome)
  • intracerebral haemorrhage
  • acute closed angle glaucoma
  • cerebral venous sinus thrombosis

CAUSES SAH:
Traumatic - most common cause

Spontaneous atraumatic:
- aneurysm (85%)
- AV malformation
- CVST
- RCVS
- amyloid angiopathy

RISK FACTORS:
- hypertension
- age >50
- smoking
- heavy alcohol or sympathomimetic use
- known aneurysm >5mm or in posterior circulation
- family history aneurysms
- connective tissue disorder (ehlers danlos)
- polycystic kidney disease

Increase likelihood ratio:
- thunderclap headache plus
+ vomiting
+ neck stiffness
+ syncope/loc
+ similar recent headache indicative of sentinel bleed

SAH can be ruled out with 100% sensitivity with the OTTAWA SAH RULE F0R HEADACHE evaluation.
- < 40 years of age
- without neck pain or stiffness
- without a witnessed loss of consciousness
- without onset during exertion
- without a thunderclap headache
- and without limited neck flexion

INVESTIGATIONS:
“Less likely to see SAH on CT if patient is anaemic”

Modern Non-contrast CT within 6 hours
- 99.7% sensitive
- >99.5% specific
sensitivity decreases with time therefore a SAH cannot be excluded with a normal CT after 6hrs

“a normal head CT within 6 hours of headache onset is extremely sensitive in ruling out aneurysmal subarachnoid haemorrhage”

CT 6-12hrs
- 98% sensitive

91-93% at 24hrs
50% at 7days

Ref: Tintinalli’s

If CT is performed beyond 6hrs and is negative for SAH. Need to proceed to LP.

CSF for xanthochromia (bilirubin released from RBC)
Takes 12hrs for xanthochromia to develop.

CSF RBC count in the 3rd and 4th tube.

Comparison RBC counts between consecutive tubes or between tubes 1 and 4 can be used to differentiate SAH from a traumatic lumbar puncture

Unfortunately, no agreed threshold number of RBCs needed in the CSF to diagnose SAH.

CT angiography for those who refuse LP, LP is contraindicated or have failed LP
- can’t see micro aneurysms
- incidental finding of aneurysms leading on unnecessary intervention

Negative CT, no xanthochromia, and zero or <5 RBCs in tube 4 CSF exclude SAH.

Negative CT with xanthrochromia or elevated RBC count in tube 4 is diagnostic for SAH.

CAUSES FOR DROP IN GCS:
- seizure
- hydrocephalus
- re-bleed
- vasospasm with ischemia
- iatrogenic - excessive opioids/sedation
- hypercapnoeic respiratory failure

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2
Q

Intracranial Haemorrhage

A

Greatest predictor of haemorrhagic extension and poor outcomes:
- intraventicular extension
- anticoagulation
- spot sign (contrast extravasion)
- swirl sign
- volume of blood on initial scan

Prevent secondary brain injury:

Reverse anticoagulation
Control BP (aim SBP 140)

CPP = MAP - ICP

NEUROPROTECTIVE INTUBATION:

POSITION:
elevate head of bed 30 deg
tragus in line with sternal notch
face parallel with ceiling

PREOXYGENATION:
100% oxygen with 15L NRBM and NP

PREMEDICATION with fentanyl 100mcg iv (blunt sympathetic response with laryngeal manipulation)

SEDATION with ketamine 1-2mg/kg iv (haemodynamically stable)

PARALYSIS with rocuronium 1.2mg/kg iv

Apnoeic BVM - Prevent hypoxia and hypercapnoea
Post intubation sedation with propofol and fentanyl

Treat hypertension - esmolol aim SBP 140-160

BP support with noradrenaline 0.1-0.2mcg/kg/min titrate to SBP 120-160

Invasive blood pressure monitoring - arterial line

Prevent raised ICP:
- Elevate head of bed 30 degrees
- Loose neck ties

Aim for normal physiological parametres:
- normotensive SBP 110-140
- normal CO2 PCO2 35-40
- normal glucose 4-10mmol/L
- normal temperature 36-37

Seizure prophylaxis
- Levitiracetam 60mg/kg iv

Regularly evaluate for signs of raised ICP and brain herniation
- unilateral blown pupil
- focal neurological deficit (hemiparesis)
- cushings reflex (bradycardia, hypertension)
- increased tone, upgoing babinski, decorticate posturing

Repeat CT scan

Urgent neurosurgical consult

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3
Q

Meningitis

EM Rapid Bombs ep 62,

Meningococcemia: a form of DIC
due to N. meningitidis.
-Diffuse purpuric rash (10-25%)
-Signs of distributive shock
-Waterhouse-Friderichsen
syndrome (adrenal hemorrhage
and failure)

0-2months:
- *Group B strep (Strep aglactiae)
- E. coli
- Listeria monocytogenes

2months - 50yrs:
*Strep pneumoniae
E. coli
H. influenza type B (rare with vaccinations)
N. meningitidis (rare with vaccinations)

> 50yrs -
*Strep pneumoniae
E. coli
H. influenzae
N. meningitidis
*need cover for Listeria monocytogenes

A

History:
headache
fever
photophobia
neck stiffness
petechial rash
prodrome - flu like illness

VP shunt in situ?
vaccinations (haemophilus infuenzae, neisseria meningitidis)

Examination:
nuchal rigidity - inability to touch the chin to the chest
kernigs - hips flexed at 90 degrees. inability to extend knees

Investigations:

Management:
0-2months:
dexamethasone 0.15mg/kg IV
benzylpenicillin 60mg/kg IV +
cefotaxime 50mg/kg IV

2month - 50yrs:
Dexamethasone 10mg (0.15mg/kg) IV Q6h 4 days

Ceftriaxone 2g (50mg/kg) IV
- E. coli
- N. meningitidis
- H. influenza

Vancomycin 30mg/kg IV
- Strep pneumoniae

Benzylpenicillin 2.4g (60mg/kg) IV Q4h
- Listeria monocytogenes
- Group B strep

Antibiotics for VP shunt meningitis:
- vancomycin 30mg/kg
- cefepime 2g IV q8h

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4
Q

Headache in Pregnancy

2021.2 History taking station

  • Take the history
  • Relevant differential diagnoses
  • Further investigation and management

Medical Expertise: History taking and differential diagnosis – 50%
* Seeks evidence of time critical diagnoses when performing assessment
* Generates a relevant list of differential diagnoses
* Elicits a focused, relevant history de novo
* Identifies important historical details (red flags) diagnostic of the conditions

Medical Expertise: Plan for further assessment – 20%
* Creates a focused investigation plan that confirms or excludes time critical diagnoses
* Explains the reasons for selecting those tests in that investigation plan
* States the theoretical accuracy of an investigation for confirming a diagnosis
Communication – 30%
* Introduces self and purpose, establishes rapport, demonstrates a professional and respectful
approach
* Uses appropriate non-verbal skills e.g. body language, space between doctor and patient, eye
contact
* Uses language appropriate to the patient’s level of understanding / avoids jargon/ explains
medical terms
* Actively listens e.g. paraphrases and clarifies what has been said

A

Wash hands
Introduce
Gain permission

Start with Open Ended Questions:

“What’s brought you in to the ED today?”
“Tell me about the issues you’ve been experiencing.”

“Ok, can you tell me more about that?”
“Can you explain what that pain was like?”

SOCRATES:

SITE:
“Where is the headache?”
“Can you point to where you experience the headache?”

ONSET:
“Did the headache come on suddenly or gradually?”
“When did the headache first start?”
“How long have you been experiencing the headache?”

thunderclap headache, reaching maximum intensity within 5 min = SAH

CHARACTER:
“How would you describe the headache?”
- ‘aching’, ‘throbbing’, ‘pounding’, ‘pulsating’, ‘pressure’, ‘pins and needles’ and ‘stabbing’.

RADIATION:
“Does the headache spread elsewhere?”
- neck (meningitis, SAH)
- face (trigeminal neuralgia)
- eyes (acute angle closure glaucoma)

ASSOCIATED SYMPTOMS:
“Are there any other symptoms that seem associated with the headache?”

TIME COURSE:
“How has the headache changed over time?”
“Is the headache worse at a particular time of day?”

EXACERBATING OR RELIEVING FACTORS:
“Does anything seem to trigger or make the headaches worse?”
“Does anything make the headaches better?”

Triggers - caffeine, excessive codeine use, stress, coughing, lying flat, physical exertion, sex

Relieving factors - analgesia

SEVERITY:
“On a scale of 0-10, how severe is the headache, if 0 is no pain and 10 is the worst pain you’ve ever experienced?”

KEY SYMPTOMS:
- Nausea & Vomiting
- Visual disturbance (flashing lights, reduced vision, blind spots, blurred vision)
- Photophobia
- Neck stiffness or pain
- Rash
- Fever
- Weakness, numbness, tingling in arms or legs
- Tender temples, tender scalp, pain in jaw with chewing (GCA)

RED FLAGS:
- thunderclap headache = pain at least 7/10 in less than 1min
- head trauma
- physical exertion
- fever, purpuric rash, neck stiffness
- altered mental status or LOC
- new focal neurological deficit
- seizure
- visual disturbance
- malignancy
- pregnancy
- connective tissue disorder (marfans, ehler danlos)
- anti-coagulation
- immune suppression

SYSTEMS REVIEW:
- Viral URTI symptoms (headache occurs in 60%)
- ENT pain suggestive of otitis media or sinusitis

PAST MEDICAL HISTORY:
- Hypertension
- Malignancy (Metastases)
- Connective tissue disorders (carotid/vertebral artery dissections)
- Thrombophilia (cerebral venous sinus thrombosis)
- Bleeding disorders
- Immune compromise (intracranial infections)
- Head trauma (bleeds)
- CSF shunt device (blocked or kinked)

FAMILY HISTORY:
- Aneurysms or sudden death
- Polycystic kidney disease

MEDICATIONS:
- Analgesics (analgesia overuse headache)
- nitrites
- Anticoagulation (bleeds)
- OCP (cerebral venous sinus thrombosis)

ALLERGIES:

SOCIAL:
- alcohol abuse (increases risk of ICH due to falls and liver dysfunction with prolong coagulation times and thrombocytopenia)
- drugs (cocaine, amphetamines increase risk of ICH and PRES)
- occupation (occupational exposure to carbon monoxide)
- stress (tension headache)
- affects daily living?
- Domestic violence (increased in pregnancy)

EXAMINATION:
General:
- Fever
- Hypertension
- Cough, coryza
- Photophobic
- Mental status/level of consciousness

Head/Neck:
- Meningism (Kernigs)
- ENT exam (otitis media/sinusitis)
- Palpate temples and scalp for tenderness (GCA)

EYES:

  • Visual acuity
  • Visual fields
  • Pupils and eyelids for Horner’s syndrome
  • measure IOP with tonometer

FUNDOSCOPY assess for papilloedema
- optic disc oedema with cotton wool spots
- optic cupping (optic disc ration of 0.8) - normal is 0.8
- spontaneous venous pulsations

POCUS - EYE
- 90% sensitive for detecting raised ICP
- no universal cut off level for the diameter of the optic sheath
- optic sheath diameter <5mm considered normal, >6mm is abnormal
- use linear probe
- lots of gel to avoid applying pressure to the eye ball
- can see bump that represents papilloedema
- measure diameter of optic sheath > 6mm

DIFFERENTIAL DIAGNOSIS OF HEADACHE IN PREGNANCY:

  • Pre eclampsia
  • Cerebral venous sinus thrombosis
  • Posterior reversible encephalopathy syndrome
  • Pituitary apoplexy

MIGRAINE:
- starts unilateral
- pulsatile/throbbing
- may have aura
- familiar triggers
- history of migraines with multiple previous episodes that feels similar
- nausea/vomiting
- photophobia/phonophobia
- lasts 4-72hrs

CLUSTER HEADACHE:
- severe (patient distressed or restless)
- unilateral
- lasts 15-180mins
Ispilateral symptoms:
- lacrimation
- eyelid swelling
- ptosis or miosis
- conjunctival injection
- nasal congestion
- sweating of forehead
Rx:
- 100% oxygen with 15L/min NRBM 20min
- sumatriptan 20mg IN or 6mg sc

TENSION HEADACHE:

MEDICATION OVERUSE HEADACHE:
- overuse of triptans/opioids leading to rebound headache

HYPERTENSION HEADACHE:

INTRACRANIAL HYPOTENSION:
- post LP or epidural
- worse when sitting upright or standing
- better when lying down
Rx epidural blood patch

IDIOPATHIC INTRACRANIAL HYPERTENSION:
- obese women aged 20-45yrs
- associated blurred vision and vision loss
- can lead to permanent vision loss if not treated
- papilloedema with opening pressures >25cmH2O

  • LP in lateral decubitus position
  • no sedation (hypercapnoea can give false reading)
  • base of the manometer should be at the level of the right atrium
  • tell patient to avoid valsalva
  • opening pressures of >25cmH2O is diagnostic
  • can removal 1ml aliquots of CSF (1ml of CSF removal will lower ICP by 1cmH2O - aim for 15-20cmH2O)

Rx oral acetazolamide 250mg bd
Ventricular Peritoneal Shunt
Optic nerve sheath fenestration
Weight loss

CAROTID/VERTEBRAL ARTERY DISSECTION:

SUBARACHNOID HAEMORRHAGE:

SUBDURAL HAEMORRHAGE:

INTRACEREBRAL HAEMORRHAGE:

MENINGITIS/ENCEPHALITIS:

CEREBRAL VENOUS SINUS THROMBOSIS:

POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME:

MALIGNANCY:

OCCIPITAL NEURALGIA:
- electric shocks and hypersensitivity in the distribution of the nerve

Rx occipital nerve block

GIANT CELL ARTERITIS:

ACUTE ANGLE CLOSURE GLAUCOMA
- decreased visual acuity
- fixed dilated pupil
- hazy cornea
- IOP > 30mmHg

CARBON MONOXIDE EXPOSURE:
- smoke inhalation
- engine exhaust
- heating sources with inadequate ventilation

PITUITARY APOPLEXY:
- spontaneous haemorrhage or infarction of the pituitary gland
- retro-orbital, bifrontal headache
- associated ophthalmoplegia, reduced visual acuity, visual field defects

THIRD VENTRICLE COLLOID CYST:
- intermittent obstruction of CSF drainage at the foramina of Monro causing sharp increases in ICP

VALSALVA HEADACHE
COITAL HEADACHE

INVESTIGATIONS for Pre-eclampsia

FBC/EUC/LFT/LDH
- low haemoglobin with haemolysis
- high LDH with haemolysis
- elevated liver enzymes (ALT & AST)
- low platelets
- high haematocrit

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5
Q

Headache with Vision Impairment

A

DIFFERENTIAL DIAGNOSIS
- Acute closure angle glaucoma
- Giant cell arteritis
- Idiopathic intracranial hypertension
- Pituitary apoplexy
- Migraine with aura
- Optic neuritis
- Herpes zoster ophthalmicus
- Stroke (ischemic & haemorrhagic)
- Orbital cellulitis

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6
Q

Ischemic Stroke

2022.2 History and Examination

Causes:
- thromboembolism (carotid atheroma)
- cardioembolic (AF, endocarditis)
- small vessel ischemia (lacunar infarcts)
- carotid/vertebral artery dissection
- Cerebral venous sinus thrombosis

A

Clinical Assessment:

**Rule out Stroke Mimics

  • hypoglycemia
  • hyponatraemia
  • post ictal paralysis (todds paralysis)
  • bells palsy
  • complex migraine
  • intracerebral haemorrhage (hypertensive, amyloid angiopathy)
  • subdural haematoma
  • subarachnoid haemorrhage
  • brain tumours/abscess

**Confirm diagnosis
**Determine cause for stroke
**Eligibility for reperfusion therapy

HISTORY:
symptoms -
onset - last seen well

PMHx:
- hypertension
- diabetes
- dyslipidemia
- atherosclerosis
- atrial fibrillation
- seizures/epilepsy

Medications:
- anticoagulation
- oral hypoglycemics
-

Allergies:

Social: (Modified Rankin Score)

IVDU (endocarditis)

PHYSICAL EXAMINATION:
GCS & glucose
Airway patent
Breathing spontaneously - RR, SaO2%
Circulation - BP (avoid hypertension - aim 185/110 or lower), HR

Fever - aspiration, meningitis, brain abscess

Carotid bruit

Auscultate heart:
- irregularly irregular in AF
- murmur in endocarditis

Pupils

Fundoscopy - papilloedema

NIH Stroke Scale

Speech
Facial droop
Weakness

INVESTIGATIONS:
*BSL
*Electrolytes (hyponatremia, hypercalcemia)
*FBC - polycythemia, thrombocytopenia (when thrombolytics are being considered)
*Coagulation profile (when thrombolytics are being considered)

ECG - atrial fibrillation (as cause)

Non-contrast CT - intracranial haemorrhage, can see early signs of infarction and hyperdense MCA sign

MRI is more sensitive at assessing for ischemia.
- CT is more readily available and more cost effective

CT angiography - large vessel occlusion and dissection

CT perfusion - shows potentially salvageable brain tissue

Urgent review of imaging by stroke neurologist or neuroradiologist

MANAGEMENT:
Attach cardiac monitoring and pulse oximetry

Address immediate life threats

seek and treat hypoglycemia

detect hypoxia (SaO2 < 90%) give oxygen 2L NP to maintain SaO2 >94%

Treat hypertension aim <185/110

IV access

Nil by mouth - to protect against aspiration

Discuss with stroke neurologist
Admission to a dedicated stroke unit
- reduces mortality
- reduces dependency
- increases the likelihood of discharge to home

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7
Q

Acute Stroke

2022.2 History and Examination Station

assessment and examination of a patient who has presented with a suspected stroke.

A

Who is going to benefit from endovascular clot retrieval?
- stroke patients with large vessel occlusion i.e. cortical strokes
- MCA
- proximal ICA
- basilar artery
A NIHSS 5 or more has traditionally been used to predict a cortical stroke. However this score is complicated and time consuming for the ED provider and ideally requires specific
training to use it.
VAN tool has been shown in a pilot
study to have a 100% sensitivity and 90% specificity for detecting cortical strokes.

VAN Tool to identify large vessel cortical strokes
Patient must have weakness plus one or all of the V, A, or N to be VAN
positive.

Step 1: Weakness
Weakness – ask the patient to raise both arms up for 10 seconds and
assess for drift, weakness or paralysis; if any of these are present
proceed to step 2

Step 2: V or A or N

Visual disturbance – field cut, diplopia or blindness

Aphasia – expressive (repeat and name 2 objects) or receptive (unable
to follow commands – close eyes or make a fist)

Neglect – inability to track to one side, ignoring one side, unable to feel
both sides at the same time or unable to identify own arm

History:

Examination:
BP

ACEM statement on thrombolysis in acute stroke

  • evidence is controversial
  • experts who have reviewed the trial data have different interpretations
  • some say the studies are not as robust as initially thought
  • need to discuss the risks and benefits with patient so they can make informed decision

IV thrombolysis given within 3 hours acute stroke in SELECTED patients

  • may improve functional outcomes
    NNT 10 (for every 10 patients who have this treatment, only 1 may have a good functional outcome at 30 days)
  • won’t reduce your risk of dying
  • moderate risk of intracranial haemorrhage
    NNH 42 (for every 42 patients who have this treatment, 1 will go onto have an intracranial haemorrhage)
  • moderate risk of dying from that intracranial haemorrhage
    NNH 122 (for every 122 patients who are treated with this medication, 1 patient will die from an intracranial haemorrhage)
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8
Q

Ataxia

2021.1 Examination station

Adult with unsteady GAIT (cerebellar dysfunction)

list differential diagnoses
perform the cerebellar neurological exam
outline investigations with explanation

A

Watch Geeky medics cerebellar exam video

DIFFERENTIAL DIAGNOSES:
- cerebellar stroke (ischemic or haemorrhagic)
- wernickes encephalopathy
- hydrocephalus
- parkinson’s disease

Toxins + altered mentation:
- acute alcohol intoxication
- sedatives (benzodiazepines)

Toxins but patient is alert:
- carbamazepine
- sodium valproate
- phenytoin

Metabolic:
- hyponatremia
- wernicke’s encephalopathy

EXAMINATION:

Level of alertness
Essential tremors

TRUNCAL ATAXIA:
- observe in sitting position
- do they sway or need help sitting upright

STANDING BALANCE:
- observe stance and balance
- feet together

GAIT ASSESSMENT:
- walk, turn around and walk back
- walk on heels and toes
? broad based GAIT

TANDEM GAIT ASSESSMENT:

ROMBERG’S TEST: proprioception rather than cerebellar function

CO-ORDINATION:

FINGER NOSE TEST:
?dysmetria
?intention tremor
past pointing in cerebellar disease

DYSDIADOCHOKINESIA
- impaired rapid alternating movements

REBOUND PHENOMENA

HEEL SHIN TEST:
?lower limb dysmetria

SPEECH:
- Ataxic dysarthria or slurred staccato speech
“baby hippopotamus”

NYSTAGMUS
- gaze provoked nystagmus

TONE:
- hypotonia in cerebellar disease

REFLEXES:
- hyporeflexia in cerebellar disease

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9
Q

Ischemic Stroke

A

INDICATIONS FOR CLOT RETRIEVAL:

Onset of stroke symptoms <24hrs

No intracranial haemorrhage on CT

Large vessel occlusion on CTA (MCA, proximal ICA, basilar artery)

Ischemic stroke on CT perfusion
- with significant volume of salvageable tissue
(small ischemic core & large ischemic penumbra)

  • Substantial neurological deficit NIHSS 5 or more
  • Functionally independent prior to stroke (Modified Rankin score 0-2)

Needs to be discussed with stroke neurologist for endovascular clot retrieval

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10
Q

Stroke Thrombolysis

A

INDICATIONS

Consider for acute ischaemic CVA within 3 hours of onset after exclusion of haemorrhage
Most appropriately used in a stroke center or as part of a randomised controlled trial
Used up to 4.5 hours in some centers based on ECASS-III

7% risk of ICH (3% are fatal haemorrhages)

No overall mortality benefit
Small but significant chance of improved neurologic outcomes at 90days

Overall this treatment reduces dependency but is associated with a risk of potentially fatal intracranial haemorrhage.

Current ACEM position, March 2014 (Statement S129)

“ACEM recognises intravenous thrombolysis as a potentially beneficial intervention for acute ischaemic stroke. There is however, conflicting evidence such that the administration of stroke thrombolysis by ED staff is a controversial area and cannot currently be considered a ‘standard of care’”

CONTRAINDICATIONS:

Last known well time >4.5 hours
Acute ICH

*Previous ICH

*Brain tumour

*Ischaemic stroke <3months

*Intracranial/intraspinal surgery within 3 months

*Current active bleeding

*GI bleeding within 21 days

*Pretreatment systolic blood pressure >185 mm Hg or diastolic blood pressure >110 mm Hg despite therapy

*Thrombocytopenia <100

*Major surgery last 14 days i.e. CABG

DOSE:

0.9mg/kg alteplase (r-TPA) (maximum 90mg) over 60 minutes (10% given as a bolus)

BLEEDING MANAGEMENT:
stop alteplase infusion
IV TXA 1g IV
IV Cryoprecipitate 10units
Blood transfusion to replace volume – 10mls/kg packed cells to SBP >100/MAP >65

SHARED DECISION MAKING DISCUSSION:

  • There is a treatment we sometimes use for stroke that is supposed to break down the clot causing the stroke.

The treatment is controversial

The issue is that out of 12 major trials, only 2 have shown benefit, and both of those trials have some problems, and they were both paid for by the people who make the drug.

There are some risks that we’re certain about: about 1 in 12 patients will have severe bleeding resulting in worse neurologic outcome.

Despite that risk, in the best case scenario, about 1 in 10 people given this drug early will have a noticeable improvement in their function after 3 months.

Unfortunately, it isn’t clear how reliable the science has been, and we don’t know which patients have the greatest chance at benefit or harm. The choice to receive this medication remains up to each individual patient.”

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11
Q

Cerebellar Stroke

EM Board Bombs ep 225

Full neurological exam
HINTS exam

INVESTIGATIONS:
non-con CT brain
CT angiography
CT perfusion

Admit for MRI

A

vertebral artery dissection
cerebral venous sinus thrombosis

Vertigo
Ataxia
Dysmetria
Diplopia
Dysarthria
Dysphagia
Nystagmus

Complications:
- brain herniation
- obstructive hydrocephalus

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12
Q

Altered Mental Status

2022.1 CBD station

Assessment and
management a post-partum female presenting with erratic behaviour

List differential diagnoses

Describes how medico-legal frameworks and principles are applied in the following situations:
- Assessment of capacity to make decisions
- Mental health assessment and treatment
- Mandatory notification.

eTG:
Post partum psychosis is a rare but dangerous diagnosis
- significant risk of suicide and infanticide

A

DIFFERENTIAL DIAGNOSES:

Psychiatric:
- post partum psychosis

Endocrine:
- thyroid storm

Toxicological:
- recreational drug use (cocaine, methamphetamines)
- alcohol intoxication
- anticolinergic syndrome
- serotonin syndrome
- drug or alcohol withdrawal

Neurological:
- seizures (post partum eclampsia)
- brain tumour

Trauma:
- domestic violence (head injury)

Metabolic derrangements:
- hyponatremia
- hypoglycemia

Infection
- meningitis/encephalitis

MENTAL STATUS EXAMINATION

Appearance - dischevelled, eye contact
Motor - psychomotor agitation, catatonia
Speech - pressured, coherent, flight of ideas, tangential
Affect -
Thought content - Suicidal ideation, death wishes, homicidal ideation, depressive cognitions, obsessions, ruminations, phobias, ideas of reference, paranoid ideation, magical ideation, delusions, overvalued ideas, worries, hypochondriasis
Thought form -
Perceptual disturbance - hallucinations
Insight -
Judgement -

RESPECT FOR PATIENT AUTONOMY
- every competent patient has the moral right to choose what happens to their body
- therefore patients have the right to freely accept or reject a physicians recommendations

ASSESSMENT OF CAPACITY:

  • Cognitive ability to understand and retain information in regards to their medical situation
  • Compare the treatment options and understand the consequences of each
  • Engage in rational deliberation about the proposed treatment plan
  • Maintain and communicate a choice

DUTY OF CARE:
Doctors have a ‘duty of care’ to their patients that includes acting in the patients best interests if the patient is not competent to consent to or refuse treatment.

If a patient is suffering from a
- mental health disorders or organic illness that renders them incompetent
- poses a risk to themselves or others
- not willing to accept treatment
- we have a duty of care to act in the best interest of the patient and treat against their wishes

MANAGEMENT:
- need to involve paediatrics and social work
- admit under paediatrics to allow sufficient time for social work to evaluate the social circumstances fully

Detain under the mental health act

eTG:
PHARMACOLOGICAL MANAGEMENT OF AGITATION:
Oral regimens:
- lorazepam 1-2mg PO (6mg max)
- olanzapine 5-10mg PO (30mg max)

IM regimens:
- droperidol 10mg IM (20mg max)
- olanzapine 10mg IM (30mg max)
- midazolam 5-10mg IM (20mg max)

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13
Q

Vertigo

2023.2 Examination station

Perform a focussed exam on a patient with vertigo

Medical Expertise: Examination (50%)
- Perform a focused and relevant physical examination.
- Perform a proficient examination technique to elicit physical signs.
- Describe expected physical signs for a diagnosis.
- Differentiate expected physical signs for different conditions.

Medical Expertise: Diagnosis and Management (30%)
- Generate a relevant list of differential diagnoses after synthesising clinical information found on initial assessment.
- Formulate a provisional diagnosis to match the immediate issues.

Prioritisation and Decision Making (20%)
- Provide a rationale to explain decisions about ongoing assessment.

Candidates were required to interact with the role player and the examiner and their tasks were to:
- Demonstrate a relevant, focused examination, and provide explanation as you go.
- Provide your diagnosis, a differential and management.
- Answer any further questions

PERIPHERAL VERTIGO:

  • Benign paroxysmal positional
    vertigo
  • Vestibular neuritis
  • Labyrinthitis
  • Ménière’s disease
  • Vestibular schwannoma

CENTRAL VERTIGO:

  • Vestibular migraine
  • Cerebellar/brainstem stroke
  • Posterior circulation transient ischemic stroke.
  • Cerebellar haemorrhage

IMAGING:
Non-contrast CT brain - intracranial haemorrhage
CT angiography arch cow - vertebral artery dissection
CT brain post contrast - cerebellar tumour
MRI - cerebellar ischemia

A

Examination video on HINTS PLUS exam plus others

Geeky medics osce station on HINTS PLUS

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14
Q

Facial Palsy - unilateral facial paralysis

2023.2 Examination station

Medical Expertise: Assessment and Diagnosis (50%)
- Generate a relevant list of differential diagnoses.
- Perform a proficient examination to elicit physical signs.
- Describe expected physical signs for a diagnosis.

Prioritisation and Decision Making (20%)
- Create a focused investigation plan that confirms or excludes time critical diagnoses.

Medical Expertise: Management – (30%)
- Initiate treatments specific to identified neurological pathologies.
- Create a safe and clear discharge plan for a patient.

Candidates were required to interact with the examiner and their tasks were to:
- Outline the potential causes of a unilateral facial weakness to the examiner.
- Demonstrate the focused examination you would perform.
- Discuss any investigations and management required for such patients.

Bell’s palsy:
Isolated cranial nerve 7 palsy - no other cranial nerves should be affected

  • loss of motor function to face
    (unable to wrinkle forehead, raise eyebrows, close eye, loss of naso labial fold and mouth droop)
  • loss of parasympathetic innervation to lacrimal and salivary glands
  • loss oftaste to anterior 2/3 tongue

may have change in taste sensation, ispilateral ear pain, changes to tearing and salivation

No sensory deficits (CN 5 trigeminal is intact)

No pupil abnormality
No extra-ocular muscle palsy

PRESENTATION:
- acute onset, usually overnight, patient wakes with facial droop
- symptoms peak at 72hrs
- no other neurological symptoms should be present

INVESTIGATIONS:
none
Bell’s palsy is a clinical diagnosis

Advanced imaging is required if there are red flags:
- sparing of forehead
- other cranial nerve palsy or neurological deficits
- prolonged facial palsy >4months
- slow progression of symptoms beyond 72hrs

To rule out
- parotid tumour
- brain tumour
- stroke
- stroke of CN 7 nucleus

An MRI is the modality of choice as it can detect if there is any
- facial nerve inflammation
- the presence of a schwannoma, hemangioma or any other space-occupying lesion.

MANAGEMENT:
Steroids
- improve recovery
- start within 72hrs of onset
- Prednisone 1mg/kg up to 75mg daily for 5 days

Antivirals
- Add acyclovir for Ramsay hunt syndrome

Eye care
Inability to completely close the eyelid
Chlorsig ointment
Polytears - eye lubricants
Tape the eye at night to prevent abrasions

PROGNOSIS:
Overall good. 85% regain function in 3 weeks with steroid therapy.

Those who do not have good outcomes usually will present with
- complete paralysis
- age > 60
- have decreased salivation or taste on the ipsilateral side.

The longer the recovery, the more likely that residual sequelae may develop.

Recurrence is not uncommon, occurring in up to 15%.

A

DIFFERENTIAL DIAGNOSES:

Idiopathic

Vascular:
- stroke (sparing of forehead)

*The rule that strokes never involve the unaffected upper facial muscles is not 100% true. Rarely, ipsilateral pontine strokes or masses can lead to a lower motor neuron pattern of facial weakness.

*However, in this case, there is dysfunction of the ipsilateral abducens nerve resulting in a lateral gaze palsy. This can help differentiate between Bell’s palsy and stroke.

Infection:
- Suppurative Otitis Media
- Ramsay hunt syndrome (Varicella zoster reactivation)
- HSV reactivation
- EBV

Neoplasm:
- brain malignancy (ispilateral pontine)
- parotid tumour

Autoimmune:
- Guillaine Barre

Trauma:
- fracture of ispilateral temporal bone
- facial laceration

RISK FACTORS: (immunecompromise)
- diabetes
- HIV
- Pregnancy (particularly 3rd trimester)

EXAMINATION:

Facial nerve examination:
Sparing of the forehead muscles is suggestive of a central (upper motor neuron) lesion

EAR EXAMINATION:
Painful vesicles in the ispilateral ear canal in Ramsay Hunt Syndrome

EXAMINE PAROTID GLAND:
- Tumours

CRANIAL NERVE EXAM:

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15
Q

Status Epilepticus

Tips:
- use max benzo doses early

  • the longer status continues, the harder it is to terminate

Airway management
- difficult intubation because it’s difficult to do an airway assessment before intubation
- medications given cause hypotension which will be exacerbated on induction
- oxygen consumption and CO2 production is high
- quick time to desaturation

2x NPA’s
nasal prongs + NRBM

fluid resuscitate
push dose pressors
noradrenaline infusion

MANAGEMENT:

25ml 50% dextrose IV for hypoglycemia

100ml 3% hypertonic saline over 10min for hyponatremia (raise serum Na+ no more than 6mmol)

Antibiotics to cover for bacterial meningitis

dexamethasone 10mg IV + ceftriaxone 2g IV

A

DIFFERENTIAL DIAGNOSES:

Eclamptic seizures in females

Primary seizure disorder - not compliant with medication

Alcohol withdrawal
Drug withdrawal

Toxicological - TCA’s

Metabolic:
- hypoglycemia
- hyponatremia

Trauma - head injury

Infection - meningitis, encephalitis

Autoimmune encephalitis

Malignancy - primary of metastatic

Vascular - Stroke

Hypertensive encephalopathy

Hydrocephalus

MANAGEMENT:

HYPOGLYCEMIA:
check BSL
25ml of 50% dextrose

Airway - OPA & NPA, chin lift & jaw thrust
high flow oxygen 15L NRBM

Place in lateral decubitus

2x IV cannula

eTG:
FIRST LINE:
- use max benzo doses early
- the longer status continues, the harder it is to terminate

  • Midazolam 10mg IM/IV (0.2mg/kg)
  • Diazepam 10mg IV over 2-5 mins (0.3mg/kg)
  • Clonazepam 1mg IV

Give second dose while drawing up second line agents

SECOND LINE:

  • Levetiracetam 60mg/kg up to 4.5g IV
  • Sodium valproate 40mg/kg up to 3g followed by infusion (avoid in pregnancy)
  • Phenytoin (20mg/kg) - need cardiac monitoring and BP monitoring, don’t give this in toxicological status, contraindicated in pregnancy

*second line agents effective in approximately 70% of cases
-if seizures not controlled, give a different second line agent

THIRD LINE

RSI & Intubate

Induction will be dangerous as all of the medications given will cause hypotension. This will be exacerbated with induction medications.

FLUID RESUSCITATION
- 20ml/kg NS IV - Assess IVC

VASOPRESSORS:
- noradrenaline infusion 0.5mcg/kg/hr

Sedative - propofol 2mg/kg IV
Paralysis - suxamethonium 1.5mg/kg

Use rocuronium 1.2mg/kg IV and then reversal with sugamadex 16mg/kg IV - to be able to observe for seizure activity

EEG - subclinical seizures

POST INTUBATION SEDATION: Propofol 3-5mg/kg/hr
Continue noradrenaline infusion for hypotension

EEG monitoring

ASSESSMENT:

Collateral history:
- primary seizure disorder
- pregnancy/post partum
- drug use/alcoholic
- drug overdose

BSL - hypoglycemia
VBG - Na+
Bhcg ?eclamptic seizure, phenytoin contraindicated
POCUS - > 20wk gestation
CK - rhabdomyolysis
UEC - Na+
CMP - hypocalcemia
CRP - infection

CXR - aspiration, non-cardiogenic pulmonary oedema

CT brain - bleed, stroke, mass, CVT,
LP

DISPOSITION:
ICU with neurologist input

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16
Q

Motor Weakness

2022.2 RMO interaction

advise a junior doctor on the assessment of a patient who has presented with weakness

A
17
Q

Motor Weakness

2023.2 Examination

Focused upper limb neurology
examination.

Provide a list of differential diagnosis and formulate an investigation and
management plan for the patient.

A

MYASTHENIA GRAVIS
- Autoimmune

Fluctuating, fatiguable, descending paralysis without loss of sensation

Bulbar symptoms:
- dysphagia
- dysarthria
- dysphonia

Ocular symptoms:
- ptosis
- diplopia

Progresses distallay
Can progress to respiratory failure

Associated autonomic dysfunction
- swings of tachycardia/bradycardia
- swings of hypotension/hypertension

There is a bimodal peak age of presentation;
- females in their 20-30s
- male in their 70-80s

2 F’s of Myasthenia gravis
fatigability - with repeated muscle us
fluctuates - fine in the morning, worse at night

  • extraocular muscles (diplopia & ptosis)
  • muscles of mastication (difficulty chewing by the end of a meal)
  • phonation (voice weakens by the end of a conversation)
  • proximal muscles weakness in the limbs

EXAMINATION:
provocative testing

Prolonged upward gaze test:
- ask the patient to gaze at the ceiling for 30s
- this should induce ptosis and diplopia

Ice pack test:
- place ice pack on orbit
- the cold temperature inhibit acetylcholinesterase
- this should resolve ptosis and diplopia

Diagnosis is confirmed with tensilon test:
- give acetylcholine esterase inhibitor IV endrophonium and observe for improved ptosis and diplopia

EMG testing may support
the diagnosis as well.

Clinical pearl: Sensation, reflexes and pupillary reflexes are all spared in
patients with myasthenia gravis

TREATMENT:
Physostigmine
Immunesuppressants
IV immunoglobulins
Plasma exchange

LAMBERT EATEN SYNDROME:
- Autoimmune
- Antibodies that target the presynaptic calcium channels which
results in decreased calcium influx and prevent acetylcholine release.

Usually elderly
May have an underlying malignancy
– usually small cell lung cancer.
Motor weakness is fluctuating but power improves with repeated use

BOTULISM

18
Q

Motor Weakness

2022.2 Examination

Adult presents with bilateral lower limb weakness

Focussed lower limb neurological examination.

Provide a list of differential diagnosis and formulate an investigation and
management plan for the patient.

A
19
Q

Motor Weakness

2021.2 Examination

focused examination of a 50 year old woman who presents with one week of progressive bilateral lower limb weakness.

Provide a list of differential diagnosis and formulate an investigation and
management plan for the patient.

IMPENDING RESPIRATORY FAILURE:

*Tachypnea

*Weak neck flexion - patient unable to lift head off bed (neck flexion has shared innervation with the diaphragm)

“20/30/40 rule”

can bridge with HFNP or Bipap

A

Guillain-Barre Syndrome:
- Autoimmune disorder
- Relatively common

Preceeding infection
- *Campylobacter jejuni (most common)
- Mycoplasma pneumoniae
- Influenza
- Covid 19
- HIV

Starts with parasthesia in the feet
Ascending flaccid paralysis.
Symmetrical.
Progressively gets worse

25% will develop respiratory failure and required intubation

Cranial nerve involvement is common
- facial weakness
- ophalmoplegia, diplopia
- dysphagia

May have autonomic dysfunction
- labile blood pressure
- gastroparesis or illeus
- urinary retention

EXAMINATION:

*Complete loss of reflexes in an ascending order
*Loss of muscle power that is symmetrical
*Sensation testing is intact

INVESTIGATIONS:
LP - CSF analysis
*Albuminocytologic dissociation (elevated protein, despite normal WBC count)
HIV serology to excluse as cause for GBS

TREATMENT:

*Early treatment is important to prevent autonomic dysfunction and respiratory failure

*IV immunoglobulin

*Plasma exchange

*Intubation and mechanical ventilation for respiratory failure

Prolonged admission to hospital

TRANSVERSE MYELITIS:
- inflammation of the spinal cord
- rare

bilateral lower leg weakness
*distinct sensory level deficit
*back pain is a typical feature
*reflexes are present
*parasthesia may be asymmetric
*bowel and bladder dysfunction
*Associated autonomic dysfunction

INVESTIGATION:
*diagnosed on MRI - increased T2 signal
*LP and CSF analysis
- pleiocytosis (elevated WBC count)