LAUNCH NEUROLOGY TORONTO provides training for neurology OSCE and theory examinations. Thie course is sponsored by Neurosearch Center, Toronto (Ontario Business Registration Number: 261076657)

Resident doctors spend lots of time searching for answers and to update thier knowledge. Here, LAUNCH NEUROLOGY TORONTO has done this for the residents so that you can use your time studying. The idea behind this material is to make sure that you know answers to all the possible questions. This is a unique preparation course material for the Royal College Adult Neurology theory and OSCE exams in Canada. The examination pattern has changed since 2019. Candidates have to pass the theory and OSCE exam with minimum of 70% average. There is a minimum pass mark for each section.

Course material for LAUNCH NEUROLGY TORONTO is prepared to bring the study material in one place that will help candidates to prepare for the examination easily. This material is prepared to assist those who are in need of organized material in one place especially for the OSCE exam. Large number of unique case scenarios are included. More emphasis is given to OSCE material. Cases are explained under different topics. Theory is divided into Adult neurology & Pediatric neurology topics.

About the Editor: Kunjumon I. Vadakkan completed his neurology residency from University of Manitoba and Cognitive Neurology fellowship from the University of Toronto. Author cannot reveal questions from the Royal College exams that he appeared. Author has tried his level best to frame questions from all the Neurology topics and has provided latest knowledge that are expected from the examinees. Like any other examination, Royal College exam will consist of representative questions from different topics to test the knowledge of the candidates. Author sincerely hopes that along with helping the candidates to score excellent marks in both the theory and OSCE type of questions, this material will provide practical knowledge that can be used in neurology practise. He has authored an OSCE book for MDs to prepare for QE part 2 exam with the title “Objective Structured Medicine” in 2005.

Course Fee: A fee is charged to cover the cost of material preparation. Since the number of copies of the material that can be sold are limited, we are forced to charge the following fees. Fee for course material is 2000$ (postal charges included). No refunds will be provided. Author is raising this fund to support his own research work that you can view at

Course material will be mailed by post only
OSCE material will be available by 1st of October 2019
Theory material will be available by 1st of November 2019
OSCE training via Skype: This is not included in the course fee. Fees can be decided based on your need.
Contact Email Address for LAUNCH NEUROLOGY TORONTO: Email:

Sample Material

1. Behavioral neurology

a) How do you test for calculation?
b) Name two prefrontal lobe tests?
c) How do you test for apraxia? How is apraxia of left frontal lobe lesions different from that of left parietal lobe lesions?

2. Epilepsy

a) Define Drug resistance and Epilepsy remission and Seizure freedom?

b) What advise will you give a patient to prepare for a sleep deprived EEG?

c) What is hemolytic disease of the newborn? How do you prevent it?

d) 20 female with a seizure
1) What questions will you ask to identify the type of seizure disorder?
2) Patient has symptoms of both myoclonic and absence seizures. What investigation will you do?
3) Patient insists for the best medication. What will you give?
4) When you described the issues with VPA with pregnancy, she is asking for an alternative. What will you give? How will you prescribe it?
5) You started her on LTG. If the patient wants to become pregnant and if patient agrees with a prescription of LTG, what all things you would like   to discuss?
6) What is the mechanism behind the need for increased dose of LTG?
7) “If we keep the concentration appropriate, will LTG cause any seizures doctor?”
8) You prescribed LTG. Patient cannot sleep well at night. How do you manage?
9) After delivery she stated to take is on OCP. How does that affect LTG?

3. Headache

a) How will you treat severe headache in pregnancy?
b) What are the FDA drug categories?
c) What are the features of aura in Migraine with aura?
d) How do you treat acute SUNCT in ER? What prophylaxis can you prescribe?

4. Internal Medicine

a) Patient with history of chronic alcoholism. Now has double vision for the last 1 week. What is the most common diagnosis? How do you manage?

1) What typical questionnaire you will administer?
2) Where will you refer this patient?
3) How do you manage if this patient become delirious in the hospital after 2 days?
4) What is the typical doze of diazepam for alcohol withdrawal delirium?
5) How do you manage post-operative delirium?

b) List viruses causing predominantly encephalitis and meningitis

c) 60 Male with acute onset seizures once at home. H/o HTN, smoking. History & exam. Cough, loss of weight, bone pain, mild unilateral weakness & lesion on CT brain at the gray-white junction with edema. How do you manage?

5. Movement disorder
a) Palatal tremor
1) Palatal tremor (Watch a video) Where is the lesion?
2) What are the types of palatal tremors?
3) How do you treat palatal tremor?
4) What is common accompanying change in the eyes?

b) Examine a person with parkinsonian features

c) DBS how do you select a candidate for DBS and what locations will you select?

6. MS/Inflammatory

a) What are the relapse rates of MS during pregnancy and post-partum periods compared to the normal?
b) What are the differential diagnosis for very large white matter lesions?
c) What are the diagnostic criteria for NMO spectrum disorders?

7. Neuromuscular

a) What are the three typical features of ICU myopathy and explain why?
b) How do you differentiate between pseudobulbar palsy from bulbar palsy?
c) What special history and examination will you carry out in a case of myopathy?
d) How to you test myotomes of upper and lower limbs? What muscles will you test for L5 myotome?

8. Neuro-Ophthalmology

a) Name nuclei associated with horizontal and vertical eye movements?
b) 48 F has diplopia. O/E abnormal lid elevation with any ocular movements for more than a few months. What is the name of the condition? What are the different types? What investigations will you order?
c) A patient has nystagmus. How do you differentiate between central and peripheral nystagmus?

9. Pediatric Neurology

a) Name three neurological disorders that has high chances to appear sporadically and mention the percentage chances? What other mode of transmission do each one of them have?
b) A patient diagnosed with Neurofibromatosis type 2 does not have any vestibular schwanoma. Can this be correct? Yes or No. Substantiate your answer.
c) A child with mild mental impairment show neck extension, nodding, some features of spasmodic torticollis that last only for a few minutes. What specific history do you want to ask? Is it occurring while eating?
d) Differentiate between Typical v/s Atypical absence seizures?
e) Write a list of diseases affected by AD, AR, XD and XR pattern of inheritance?

10. Stroke
a) What conditions give number needed to treat (NNT) values 8, 6, 4 and 2?
b) Name four conditions that can cause Moyamoya disease?
c) What investigations will you do for stroke in a young patient?
d) Patient on warfarin. Now INR is high. How do you manage?

11. Telemedicine
a) Name three neurological disorders where NSAIDs are contraindicated?

b) GBS-like ascending paralysis is seen in which electrolyte abnormality?

c) Relapse rates in MS
1. MS patient who don’t want to take any medications
2. MS patient who is taking disease modifying drugs
3. MS during 3rd trimester
4. MS during postpartum period


1. Behavioral neurology

a) Ask patient to calculate 6+8-7. Note that simple addition or subtraction are not enough.

b) Prefrontal lobe tests
1) Wisconsin Card Sorting Test: Color, form, number - challenges the subject to shift cognitive sets without warning. Poor cognitive flexibility & perseveration will show up.
2) Stroop test (Read the print of the name of a color printed with a different color)

c) Praxis testing
Check for handedness
“I will make sure that vision, hearing, attention and orientation are normal before testing for apraxia” Hearing or vision problem – Yes/No questions; 3 step command
Test 1 proximal & 1 distal group muscles in each limb
Gross coordination – FNF; Fine coordination: pick up a pen
Balance – stand up on one leg for a couple of seconds
Sensation: Close your eyes – which hand am I touching now?
I am looking to see if the person is using correct body parts, making correct movements in correct spatial orientation & with correct speed & repetition of movement where relevant

Ideomotor – Left parietal
Upper limb- meaningless gesture, pantomime a salute (show it), Show how you brush your teeth with your right hand, Use it wrongly & ask to command.
How do you use this correctly – act to me? How you really use it?
Lower limb – kick a ball
Whole body – stand like a boxer
Bucco-facial apraxia – stick out your tongue, blow a kiss, blow out a match, drink using a straw
Apraxia of speech – pa, ta, ka, pataka, pataka, Repeat pencil 3 times,
Hopeful-hopefully, Spagatti, Episcopalian
Constructional tasks – copy a cross, triangle with a triangle, draw a flowerpot, design blocks
Gait apraxia – ask to walk

Only left hand affected – Anterior corpus callosum – Geshwind
Ideomotor (Only motor) Left parietal lesion - has anosognosia & left frontal lesion - can recognize the defect

Ideational – Entire left hemisphere
Fold a letter, put it in an envelope, seal, stamp, address & mail 2) Light a candle
Ideational (Planning): Entire left hemisphere. Can’t do sequence (Can’t make a sandwich)
Imitation problem – Right hemisphere

Limb Kinetic Apraxia – Cannot unbutton the shirt. Cannot pick a coin from the table

2. Epilepsy

a) Definitions
1) Drug resistance = failure of adequate trials of 2 appropriately chosen, tolerated & administered anti-seizure drugs (whether as monotherapy/ in combination) to achieve seizure freedom
2) Epilepsy remission: 10 years seizure free with last 5 years off AEDs + passed the age of epilepsy syndromes
3) Seizure freedom: "Rule of 3": Seizure free after an intervention period = 3x the largest pre-intervention inter-seizure interval or 12 months, whichever is longer

b) Reduce sleep by one hour both at the beginning and at the time of getting up.

c) Hemorrhagic disease of the newborn is due to the side effect of enzyme inducing anti-seizure medications that the mother is taking during pregnancy. It can be prevented by prescribing Vitamin K 10mg OD PO during last trimester to the mother and by giving the newborn a one time injection of 1 mg vitamin K

d) 19 year old female with seizures
1) Ask for symptoms of myoclonic (exaggerated with reduced sleep and alcohol), atypical absences (see pediatric question 9d), generalized tonic clonic seizure and other types of seizures
2) EEG routine with photic stimulation & hyperventilation and sleep deprived EEG
3) Valproic acid is the best medication for both myoclonic and absences
4) LTG. Start 25 BID x 1week, slowly increase to 100 BID (over 6 weeks) (Max 150/200 BID). Get a blood level, if seizure not controlled after 100 BID to further increase doze
5) Check blood levels of LTG before becoming pregnant and it will become necessary to increase the dose of LTG during pregnancy to maintain same blood level. Follow up this during the postpartum period
6) Mechanism: Increased estrogen especially during third trimester activates uridine glucuronyl transferase (UGT) & lowers LTG
7) LTG may worsen myoclonus in some patients: tell this to your patient
8) LTG has some stimulating effect. So give the last dose of the day before 4 pm
9) Same as the answer to 6). This time it is due to oestrogen in the pill. Patient may again need more LTG. Maintain the pre-pregnancy level

3. Headache

a) Severe headache in pregnancy Rx: Metoclopromide, Tynelol, Hydration if needed. [Tryptan in pregnancy: Not recommonded normally; But can be given. No teratogenic effects are reported. Commonest side effect is atonia of uterus and so increased bleeding. If needed during lactation; Bottle feed the baby for several hours after taking tryptan]

b) FDA drug categories
A: Human studies failed to show any defect in the 1st trimester
B: Animal studies – no defect – Clopidogrel
C: Animal studies – defect – ASA
D: Human fetal risk: VPA (but has to compare risk & benefit when treated)
X: Humans or animals bad

c) Features of aura in Migraine with aura

1/< of fully reversible symptoms: Visual, Retinal, Sensory, Motor, Speech & /language, Brain stem
At least two of following 4 characteristics
1. At least 1 aura symptom spreads gradually over 5 min &/or 1/ more symptoms occur in succession.
2. Each individual aura symptom lasts 5–60 min.
3. At least 1 aura symptom is unilateral.
4. Aura is accompanied/ followed within 60 min, by headache (any type). Not better accounted for by another ICHD-3 diagnosis & TIA has been excluded

d) Acute SUNCT Rx and prophylaxis

IV Lidocaine 1.3-3.3mg/kg/h. It has 100% cure rate
Prophylaxis by either Topiramate or LTG

4. Internal Medicine

1) Wernicke’s encephalopathy. IV Thiamine 100 to 500 mg IV stat. Then daily x 3 days

2) CAGE questions
Have you ever thought of cutting down?
Have people annoyed you by criticizing your drinking?
Have you ever felt guilty?
Do you need an eye opener in the morning hours?

3) Alcoholic Anonymous

4) Diazepam IV

College of Family Physicians of Canada Rx recommondations:
Day 1: Day2: Day 3: Day 4
If patient is rigid: 10 mg four times daily:10 mg three times daily: 10 mg twice daily: 10 mg at bedtime
If patient is flexible: 10 mg every 4–6 hours as needed based on symptoms to a maximum of 60 mg/day: 10 mg every 6–8 hours as needed: 10 mg every 12 hours as needed: 10 mg at bedtime as needed
As per UpToDate: 5 to 10 mg IV every 5 to 10 minutes, until the appropriate level of sedation is achieved. Studies have shown large efficacy of the loading dose method corresponding to substantial reduction of the psychosis duration.

5) Rx: Haloperidol

Encephalitis (enveloped viruses)

HSV-1 Rx: Acyclovir
Arbovirus – Flavi (Culex) – JBE (Extrapyramidal, Flacid paralysis, Rhombencephalitis), West Nile (Back pain, tremor, flaccid paralysis), St. Louis, Western Equine


HSV-2 (Mollaret’s) Aseptic meningitis, Entero – Coxackie, Echo, Polio
VZV (+ ASA = Rey’s syndrome)
LCM (lymphocytic choreomeningitis)

c) ABCs; Oxygen-IV-Monitor; CXR, CT head, EEG
Labs: Na 120
At this stage, I want to know vitals & blood sugar. Serum osmolality, Urine Na (24 hr urine), volume status (I/O chart)
Serum electrolytes, serum osmolarity, Blood glucose, protein, EKG, urine lytes

SIADH: Na <135; Blood osmolarity <275 mosm/kg; urine osmolarity ~ 100mos; Urine Na >40 meq/L. (Note: Urine 24 hr total volume osmolality 500-800; Random urine osmolality vary between 50-1200; Normal urine Na = 20 meq/L)

SIADH has euvolemia & hyponatremia: Rx: Treat SIADH by water restriction
No AED even though Na is low. When patient’s sodium is very low and if patent start seizures then sodium level has to be corrected using hypertonic saline

Regarding rate of hypertonic solution (3% NaCl; Normal saline is 0.9% NaCl)
Never let sodium level increase more than 10 meq in 24 hours
Calculate how many meq of NaCl is required to increase Na concentration up to 130 meq/L & give that volume of 3% NaCl in 24 hours. (3% NaCl = 513 meq/L)
Body wt (60) x (130-120) x 50% (% lean body weight in men) = 60x10x0.5 = 300 meq
3% NaCl = 513 meq/L. Therefore, need 585 mL – give in 24 hours (so ~22 ml/hour)

Where is sodium balance sensed in the brain? Organum vasculosum of lamina terminalis (OVLT) (no BBB)

How do you approach to hyponatremia? Na < 135 mmol/L
Is it acute or chronic? (Only acute is worrisome)
If patient is seizing, are seizures due to hyponatremia or something else?
What important additional lab values you want to have?
Plasma osmolality (Normal: 275 – 295 mOsm/kg)
Urine Na concentration (look for values <20 mmol/L or >20 mmol/L)

If development of hyponatremia occurred within 48 hours, then the brain cells have not had time to develop idiogenic osmoles. Commonly occurs in hospitalized patients who receive hypotonic fluids postoperatively

Can Rx the hyponatremia more aggressively- Chance of osmotic demyelination syndrome namely Central pontine myelinolysis (CPM) is there
If not seizing, use Normal saline to correct Na + salt tablets
Raise serum Na+ no more than 0.5 to 1.0 mmol/L/hr & by less than 10-12 mmol/L in 24 hrs
Check lytes q 2 h - until Na+ reach ~ 125 mmol/L
If seizing use (hypertonic saline) 3% saline solution
Na+ should not be ?more than 10-12 mmol/L over the first 24 hours
A loop diuretic may be added to enhance water excretion if urine osmol is greater than 300 mOsm/kg
Rx with hypertonic saline solution is advocated only for patients with severe hyponatremia who have profound neurologic symptoms

What is your approach in a case of high serum osmolality?
If hyperglycemia or hyperglycinemia: Rx these to Rx hypoNa & Rx Sz
If glucose & glycine are normal & has hyperlipidemia/ hyperproteinemia: pseudo-hyponatremia
If glucose, glycine, lipids, protein are normal: true hyponatremia

For example, hyperosmolality, due to hyperglycemia, can result in continuous partial seizures. Seizures will respond to lowering the glucose

Urine Na >20mmol/L

Hypovolemia: Renal loss-diuretics, Addison, salt losing nephritis, Osmotic diuresis – glucose, urea

Euvolemia: HypoT4, Low cortisol, Acute water overload – Stress, post Sx, polydypsia

 Hypervolemia: Renal failure

Urine Na <20mmol/L

Hypovolemia: Extra-renal loss, Vomiting, diarrhea, skin loss

Euvolemia: SIADH Rxed with fluid restriction, fluid depletion

Hypervolemia: Renal Na retention – cirrhosis, CHF, nephrotic syndrome

Hypovolemic: Symptomatic give 3% saline; asymptomatic - normal saline
Euvolemic: Symptomatic give 3% saline judiciously + furosemide; asymptomatic - normal saline + oral salt tablets
Hypovolemic: Normal saline + furosemide; asymptomatic-furosemide

If seizing patient in ER: Tumor, stroke, SDH, head injury, HSV, CVST, hemorrhage into tumor, hypo Na or hypo Mg

If patient also has elevated CK. How to manage high CK? Minor degree of CK normalizes after seizure cessation. If levels are high, forced diuresis can be used

Also look for signs of stroke, headaches, history of falls, constitutional symptoms, cognitive changes?

Rx: General: DVT prophylaxis. Discuss palliative option with the patient or family regarding palliation. Poor prognosis is associated cerebral mets from lung cancer
Palliative medicine consult for comfort measures
Seizures will be treated as any other complications

5. Movement disorder

a) Palatal tremor
1) Inferior Olivary N. The lesion may be very small and therefore, it may not be seen in a MRI scan immediately. However, after 6 months, there will be pseudo-hypertrophy at the Inferior Olivary nucleus visible in MRI (see a MRI)

Primary (Essential)
27% m=f
Age of onset 30 (M=F); eyelids affected
Ear click present Absent
Tensor veli palatine affected

Secondary (Symptomatic) (After a stroke)
HARD TO DIAGNOSE – NEED A MRI! 73% M>F; Age of onset 45; eyelids not affected
Levator veli palatini affected; Present in sleep - mostly
Olivary pseudo-hypertrophy (after 6 months)
Asso. with CNS signs, ataxia

3) Rx: Clonazepam 1mg HS

4) Has pendular nystagmus of 1Hz (watch a video)

b) Parkinsonian features
General examination: Postural BP changes: Check pulse and BP simultaneous at 3 postures measured between 3 minutes between each of them.
Write name (micrographia), Draw a circling spiral
Parkinson’s Unified Parkinson disease rating scale (UPDRS) has 3 components:

1) Cognitive: mentation, behavior & mood, thought disorder, depression, motivation/initiative
2) ADLs + IADLs: Speech, salivation, swallowing, handwriting, cutting food/handling utensils, dressing, hygiene, turning in bed/adjusting bed clothes, freezing when walking, falling unrelated to freezing, tremor, sensory complaints related to PD
3) Motor Exam: speech, facial expression, tremor at rest (4 limbs), if not seen, ask to name months backwards, action or postural tremor (4 limbs), look fro re-emergent tremor, rigidity (4 limbs), finger taps (upper limbs), hand movements (open & close) (upper limbs: rapid alternating movements (pronate & supinate), (lower limbs: leg agility (tap on ground 3 inch), rise from chair with hands folded in front, posture when standing up, gait, body bradykinesia/ hypokinesia, postural stability (Retropulsion test: 2 steps backwards are normal). Always stand against a wall to prevent falls.

Specific care:
Medical Alert Bracelet
Power of attorney (health directives)
Referral to OT/PT for fall prevention, hypersalivation,
Driving (Clinical Dementia Rating scores 0.5, 1, 1.5, 2), inform MOT if needed

c) DBS

1) PD with good response to levodopa,
Severe motor fluctuations, dyskinesia, painful dystonia, side effect of meds, N/V, psychiatric
Age <75, interested in DBS,
No cognitive decline, can lie down for a MRI without any phobia
DBS – will improve dopamine sensitive motor symptoms

2) Locations for DBS
Ventral intermediate nucleus of the thalamus (VIN) for tremor
Globus Pallidus (GPi) for dystonia
STN (for tremor, rigidity, akinesia, postural istability) (TRAP for PD)

6. MS/Inflammatory

Normal: 1%
3rd trimester: 0.2
Postpartum: 1.2 (high relapse) – Note lactation can help slightly. So advise breast feeding
Disease modifying drugs: 0.5%

b) Differential for very large white matter lesions
1. Celiac disease: Anti-gliadin antibody; Tissue trans glutaminase (TTG)
2. Paraneoplastic: X-ray chest, Antibodies
3. CADASIL (AD): Notch 3 gene defect
4. Fatty acid oxidation & organic acid metabolism: Acyl carnitine profile (free & total)
5. Abetalipoproteinemia: Abetalipoprotein
6. Fabry’s: Alpha 1 galactosidase
7. SCA 1,3: CAG repeats
8. Metachromatic leukodystrophy MRI: All brain; Butterfly + Tiger skin pattern: Blood arylsulfatase A + Urine sulphatide
9. Adrenoleukodystrophy (posterior brain) XR, Defect in ABCD1 gene, Diagnosis by assay in skin fibroblast/ mutation analysis; Nerve Bx: demyelination + axonopathy; Rx: Steorids+Lorenzo oil+Gene therapy Plasma ?VLCFA (defect in its beta oxidation); Na low, K high, high ACTH (adrenal problem); Has peripheral neuropathy + UMN signs (In old age ALD; if in young – D/d: Friedereick’s); Sural N: Demyelination+Axon damage, onion bulb
10.Leigh’s syndrome (SNE – subacute necrotising encephalitis), MELAS Mitochondrial disease tests

c) NMO spectrum disorders

I. The diagnosis of NMOSD with AQP4-IgG antibodies requires all the 3
1. At least one core clinical characteristic
2. A positive test for AQP4-IgG using the best available detection method (cell-based assay strongly recommended)
3. Exclusion of alternative diagnoses

6 core criterial includes
1. Optic neuritis
2. Acute myelitis
3. Area postrema syndrome: episode of hiccups or nausea and vomiting
4. Acute brainstem syndrome
5. Symptomatic narcolepsy or acute diencephalic clinical syndrome with NMOSD-typical diencephalic MRI lesions
6. Symptomatic cerebral syndrome with NMOSD-typical brain lesions

II. Criteria for NMOSD with negative or unknown AQP4-IgG antibody status
1. At least two core clinical characteristics occurring as a result of one or more clinical attacks and meeting all of the following requirements:
• At least 1 core clinical characteristic must be optic neuritis, acute myelitis with LETM, or area postrema syndrome
• Dissemination in space (2/ more different core clinical characteristics)
2. Negative tests for AQP4-IgG (NMO-IgG) using best available detection method
3. Exclusion of alternative diagnoses

7. Neuromuscular

EMG will be normal. EMG examines Type 1 fibers (moves when patient moves a muscle). Steroid myopathy affect type 2 fibers. So EMG will be normal

CK will be normal. This is because in steroid myopathy cell membranes are not leaky to CK. So CK cannot escape from muscle to blood stream

Muscle biopsy shows loss of myosin. Steroid will cause myosin to lose from muscle

Pseudobulbar (UMN): Bulbar (LMN)
1. Affect mainly 5, 7, (but also 10, 11,12): Affect only 10, 11, 12
2. Affect cortico-bulbar tracts above the nucleus. Usually supply bilaterally: At or below nucleus
3. Increased GAG: Reduced GAG
4. Spastic tongue without atrophy :Fasciculation & wasting of tongue
5. Increased jaw jerk. Affect mastication & facial expression: Jaw jerk normal (because 5 & 7 are not affected)
6. Speech - spastic dysarthria: If unilateral - raspy voice, Get MRI/MRA/CTA; If affect both sides – nasal speech, when try to swallow water, it will come through the nose.
7. Emotions - labile: Normal
8. Cause: Bilateral CVA affecting bilateral IC (genu), MS, high brainstem tumors, head injury: MND - ALS, Syringobulbia, GBS, Polio, subacute meningitis (carcinoma, lymphoma), neurosyphilis, brainstem CVA

c) Muscle weakness special history and exam

Cola colored urine? myoglobinuria
Worsen with exercise? MG or periodic paralysis
Is there any myotonia? Difficulty in relaxing after a hand shake?
Proximal muscle weakness: Difficulty rising from chairs, getting out of the bathtub, climbing stairs, and/or shaving or combing the hair
Weakness of distal muscles: Weak grasp, handwriting problems, walking difficulties, trip over

Exam: Ask patient to change into a gown to examine the pattern of muscle wasting
Upper limb: Shoulder Extension, Flexion, External Rotation, Finger flexion
Lower limb: Abduction, adduction
Neck flexion
Always do: Myotonia percussion
Examine for calf hypertrophy, scapular winging
Test for hand grip and finger flexion
Functional testing: Running, stand up, squatting
Palpate for muscle tenderness
Test for myotonia? Percuss (fairly hard) on the muscle belly (not tendon) with knee hammer

d) Myotome testing
1) Testing myotomes of upper and lower limbs
C5 Elbow flexion L2 Hip flexion
C6 Wrist extension L3 Knee extension
C7 Elbow extension L4 Ankle dorsiflexion (stand on heel)
C8 Distal finger IP joint flexion L5 Big toe dorsiflexion
T1 Little finger abduction S1 Ankle plantar flexion (stand on toes)

2) L5 myotome testing = Test all L5 muscles: TA, TP, PL, GM, BF (long & short head), ST, SM

8. Neuro-Ophthalmology

a) Nuclei
Horizontal eye movement: Nucleus prepositus hypoglossi & medial vestibular nucleus
Vertical movement: Interstitial nucleus of Cajal, Ri MLF, Posterior commissure

b) Lid elevation with ocular movements
If the eyelid shows abnormal elevation with any ocular movements, it means aberrant regeneration. This condition is called synkinesis.
Types a) Muscle to lid: IR to lid - lid close when look down; SR to lid - lid close when look up; MR to LPS; SR to LPS b) Muscle to pupil - Pupil constrict when that muscle is used
It is necessary to rule out tumor immediately. MRI Brain, MRI sella (to see parasellar masses – giant aneurysms, pituitary adenoma, meningioma, craniopharyngioma) and MRI orbit

c) Differentiating between Central & peripheral nystagmus
It is carried out doing HiNTs test

Hi: Head impulse (Halmagyi head shake test). Sit in front of the patient. At the same head level. Make sure that there is no rheumatoid arthritis or cervical spine problems. Explain to patient what you are going to do. Hold the head using your hands on either side of the head. Ask the patient to keep looking at your nose. First make sure that the neck can move laterally for sufficient range by passive motion. Then, suddenly move the head for nearly 30 degrees. Usually, the eyeballs suddenly re-fixates to your nose. But in peripheral lesions, eyeball overshoots, then re-fixates slowly
N: Nystagmus. In central – spontaneous vertical or direction changing
Ts: Test of skew: Do cover cross-cover test. Vertical misalignment of two eyeballs. i. e. One eye up & other eye down (central)

In peripheral, only Hi (PHi) is abnormal!

Additional information
Peripheral has a long incubation period of ~20s compared to central origin nystagmus
Peripheral vision has fatigue (reduced intensity by repetition)
Peripheral nystagmus has habituation (reduce intensity by afternoon)
Peripheral can be dampened by visual fixation – so can use Frenzel glasses to prevent visual fixation and reduce its intensity
Central nystagmus is usually from a brain parenchymal lesion e.g. stroke – therefore look for signs of brainstem or posterior fossa stroke symptoms

9. Pediatric Neurology

Tuberous sclerosis 60% sporadic; 40% others AD
Neurofibromatosis 50% sporacid; 50% others AD
Muscular dystrophies 30% XR 70% others

b) There is no need to have a vestibular schwanoma to diagnose NF2! Refer to the criteria.
c) Sandifer syndrome has GERD and neuro features (watch a video). Occur when tries to eat food. Child is mentally impaired, Features – spasmodic torticollis & dystonia, nodding and rotation of head, neck extension, gurgling, writhing movements of limbs, severe hypotonia, lasts for 1 to 3 minutes, occur 10 times per day, Diagnosis by history of occurrence while eating + movement disorder features.

d) Typical absence seizure is seen in childhood absence seizure – Here it is 3 Hz, IQ is normal, prognosis is good and lasts for 5 to 20s.
Atypical absence – This is seen in juvenile absence seizure. <3Hz, IQ is reduced, poor prognosis, last <1 minute to several minutes, hyperventilation does not induce it, photic stimulation rarely induce it.
Autosomal dominant: HD (HTT gene) DM (both DM), NF, TS, VHL, SCA, Tourett’s, JME incomplete penetrance, Episodic ataxia I,I,                              Dystonias – DYT1, Alexander, FSH, DRPLA, Emery Dreifuss –Lamin A&C (LMNA gene), APP, PS1, PS2, Familiar FTD+PD

Autosomal recessive: Wilson’s, ARSACS, Ataxia Tielangiectasia, SMA (floppy baby), PME, Neuroacanthocytosis (high CK)
Friedereix ataxia, Congenital Muscular Dystrophy, DYT1, PKAN, LGMD                                                              

X-linked dominant: Aicardi (female child dies), Rett, Fragile X, Periventricular nodular heterotopia (Filamin 1). CMT-X, Incontinenta pigmenti

X-linked recessive: DMD (30% sporadic) & Becker muscular dystrophy, Fabry, Kennedy (spino-bulbo muscular atrophy) - Fasciculations + sensory neuropathy. ALD (adreno leukodystrphy), DYT1, DYT3, Emery Dreifuss -Emerin

10. Stroke

a) Number needed to treat (NNT): (8:6:4:2)
tPA after 3 hours: 8
Endovascular treatment: 4%
Anterior temporal lobectomy for temporal lobe epilepsy: 2%

b) Sickle cell disease, Down’s syndrome, Radiation, and Neurofibromatosis

c) Stroke work up in a young patient

Hematologic factors that lead to coagulation:
Low Protein C, S, Antithrombin III, APC (activated (by thrombin) protein C) that inhibits factor V
High Fibrinogen (Factor I), Plasminogen (Factor II), factor V Leiden (not inhibited by APC)
Hb electrophoresis (HbS & others), homocystine
Infection: RPR (Rapid plasma reagin), FTA-ABS (Florescent antibody-absorption test)
Immunological: For antiphospholipid antibody syndrome: 1) anti-lupus antibody, 2) beta 2 microglobulin antibody, 3) anti-cardiolipin antibody; ANA
Cardiac: Bubble study for cryptogenic stroke, suspect pulmonary AVM, if everything else fails

d) High INR on warfarin

>10: Hold warfarin + vitamin K 10 mg IV inD5W in 30 minutes
5-10: Hold warfarin + vitamin K 1-2.5 mg IV. Rpt q 12 hours if needed
<5: Omit 1 doze + Continue with a reduced dose
Always investigate the cause: Infection, heart failure, dosing error, liver disease, cancer, poor nutrition
If actively bleeding: Give fresh frozen plasma. Consult hematology. Consider starting Octaplex (prothrombin complex concentrate)

11. Telemedicine

a) No NSAIDS in vasculitis, CVST and pseudoxanthoma elasticum

b) GBS-like ascending paralysis is seen in hypophosphatemia

c) Relapse rates in MS

1) MS patient who don’t want to take any medications: 1%
2) MS patient who is taking disease modifying drugs: 0.5%
3) MS during 3rd trimester: 0.2 (very low relapse)
4) MS during postpartum period: 1.2 (high relapse)
Note lactating baby can help reduce this rate slightly. So can advise breast feeding

Sample Material pdf: Launch Neurology Toronto

                  LAUNCH NEUROLOGY TORONTO - Neurology OSCE and THEORY training. Last updated 12th September, 2019