let’s break this down

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Let’s break this down Neuroscience: 20/180 Geriatrics + Ethics + immunology: 60/180 Faster to learn Straightforward What is 1 MEQ then? 20/180 =0.11 0.11/2*100 = 5.56 (assuming MEQ is 50%) 5.56*60/100 = 3.33 MARKS for THEORY MD2140

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Let’s break this down. Neuroscience: 20/180 Geriatrics + Ethics + immunology: 60/180 Faster to learn Straightforward What is 1 MEQ then? 20/180 =0.11 0.11/2*100 = 5.56 (assuming MEQ is 50%) 5.56*60/100 = 3.33 MARKS for THEORY MD2140. So…. - PowerPoint PPT Presentation

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Page 1: Let’s break this down

Let’s break this down

Neuroscience: 20/180

Geriatrics + Ethics + immunology: 60/180 Faster to learn Straightforward

What is 1 MEQ then? 20/180 =0.11 0.11/2*100 = 5.56 (assuming MEQ is 50%) 5.56*60/100 = 3.33 MARKS for THEORY MD2140

Page 2: Let’s break this down

So….

If you haven’t finish stuff like systemic patho or pharmaco, and have no time to do neuroscience

Ditch it

Or just study stroke and hope you luck out

Go learn why old people are prone to falls

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However… If you got spare time and are already ethical

Neuroscience is FUN

It’s more understanding and less memorizing If you are memorizing more than you understand, you

are doing it wrong I’m NOT talking about the ‘HOW DO YOU _____’ lectures

It forms the corner-stone of every neuro-exam you gonna have in clinical years.

It’s gonna be super important in future. But maybe not for M2 pros.

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Drugs Used in CNS

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Pharma Qns

Mode of Action

Indications

Side Effects

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Drug Types

Anxiolytic + hypnotic

Anti-depressant

Anti-psychotic

Examples?

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Anxiolytic + Hypnotic

Benzodiazepine (BZD) Short acting: Midazolam Intermediate acting: Lorazepam, Alprazolam Long Acting: Diazepam

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Benzodiazepine (BZD)

Mode of Action?

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Benzodiazepine (BZD)

Mode of Action Binds to specific BZD sites in the CNS and potentiates

GABA (an inhibitory neurotransmitter) action by increasing frequency of chloride channel opening

Increase Cl- Influx

Increase neuron hyperpolarization

Sedation

Drug action dependent on GABA OD doesn’t kill

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Benzodiazepine (BZD)

Indications? Think of 3

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Benzodiazepine (BZD)

Indications Convulsion, seizure (IV) Anxiety disorder Insomnia

‘Date-rape’

karina ng
Date Rape
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Benzodiazepine (BZD)

Side Effect? Think of 3 classes and some examples

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Benzodiazepine (BZD) Side Effect

CNS: increase sedation decrease motor skills slower reaction time Anterograde Amnesia (esp with IV)

CVS Decrease BP, decrease respiration rate

Paradoxical symptoms Hallucination, irritability, violent tendency, excitement

Floppy Child syndrome (contra-indicated in pregnancy)

TOLERANCE, DEPENDENCE, WITHDRAWAL

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Non-BZD hypnotics

Zolpidem, Zopiclone

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Depression

Theory for Depression: Deficiency in monoamines in the synaptic cleft Deficiency of neurotransmitters to effect it’s action

on the post synaptic membrane

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Anti-depressants

2 types?

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SSRI

MOA? Related to the name

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SSRI

MOA: Binds to serotonin reuptake transporter in the

presynaptic cell membrane Increase concentration of serotonin in the synaptic

cleft

Name: Fluoxetine, escitalopram

OD WILL NOT DIE!!!

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SSRI

Adverse Effect? Think of 3

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SSRI

Adverse Effect: Anxiety Weight loss/gain Headache Sexual dysfunction

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TCA –amitriptyline, imipramine TCA blocks both serotonin reuptake transporter

and norepinephrine reuptake transporter

Gold standard treatment

BUT OD can lead to death Depressed people tend to want to die more Easy way to commit suicide

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TCA

Side Effect: Cardiac rhythm: Tachycardia, arrhythmia Postural hypotension Anticholinergic effects CNS: sedation, fatigue

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Antipsychotics

Broad classes?

Mode of action?

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Antipsychotic - Haloperidol

Typical antipsychotic

Blocks: Dopaminergic receptors Serotonic receptors Histaminic receptors Cholinergic receptors Alpha adrenergic

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Haloperidol

Side effects?

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Haloperidol

Side effect: Extrapyramidal side effects:

Acute dystonia Parkinsonism Akathisia Malignant syndrome Tardive dyskinesia

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CNS Pathology

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Quick Start

What’s the mean ICP? 7 to 15 mmHg

How much blood does the brain need? 150ml/100g/min

What can cause acute rise in ICP? (think of 2) Hemorrhagic stroke, Intracranial Hemorrhage

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Quick Start

What can cause gradual focal deficits and also increase in ICP? (Think of 2) Tumor, infection

What are the 2 different types of hydrocephalus? Name 2 etiology of each. Non-communicating vs communicating NC: SOL(medulloblastoma), meningitis (TB meningitis, scarring),

congenital (Arnold Chiari malformation) C: Subarachnoid hemorrhage, NPH, meningitis

What are the presentations and complications of raised ICP? Papilloedema, headache, nausea, HERNIATION (most dangerous

form of herniation is?)

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Keep going… What are the 4 most common tumors in children? Where are

they found? Medulloblastoma (posterior fossa/infratentorial) Pilocytic Astrocytoma (Glioma, anywhere in the brain

parenchyma) Ependymoma (para/intra-ventricular) Germ Cell tumor (Mid-line)

What are the presentation of a slow-growing Meningioma? SOL Focal deficits and raised ICP

What type of CNS tumor (that we’ve learned) cross the midline and forms a butterfly shape lesion? What grade is it? Glioblastoma Multiforme (Grade IV)

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Keep going… What must you suspect if you find primary lymphoma in

the brain? HIV Immunosuppression

What can be the possible diagnoses when there are multiple SOL in the brain? Lymphoma, Abscess, METASTASIS

What are the acute, chronic, and pregnant complications of drinking alcohol? (Name 1 each) Acute: Respiratory depression -> Death Chronic: cerebellar atrophy, cortical atrophy, Wernicke’s

encephalopathy, Korsakoff syndrome Pregnant: fetal alcohol syndrome (growth retardation)

karina ng
might wanna add under Chronic:Korsakoff psychosis
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Almost there… What histological changes of the brain can you see in

Alzheimer’s disease? Amyloid plagues / Neurofibrillary tangles (tau protein in

neurons) These cannot be digested. Leads to reactive gliosis and

neuronal damage and progressive cognitive decline

Which lobe is most affect in AD – Smaller, atrophied brain? Temporal Lobe

What are the clinical features of Parkinson’s Disease? TRAP – asymmetric Mask-like face Gait abnormality Respond to Levo Dopa (for 5 to 7 years)

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Almost there… What are the 2 broad groups of meningitis?

Bacterial vs Aseptic What’s the difference in Cell/Glucose/Protein?

What are the top 3 cause of meningitis in neonates? E coli, Listeria monocytogenes, Streptococcal agalactiae

What are the other few bacteria that cause meningitis in pediatrics? (young children) Nisseria meningitidis, Streptococcal pneumonia, Hemophilus

influenza type B THEY ALL HAVE CAPSULE!!!!!!!!!

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HYPERTENSION AND IT’S ASSOCIATED HYPERTENSIVE CEREBRAL VASCULAR DISEASE IS IMPORTANT!!!!!!!

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Localising Lesions

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Revision DCML

Spino-thalamic

Corticospinal

Spino-cerebellar

General route, Decussation, Function?

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UMN VS LMN

What is UMN and LMN?

How does it help in localizing the level of the lesion? Understand: Inverted supinator jerk and Inverted

knee jerk Where is the level of the lesion?

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UMN vs LMN

Inverted Supinator Jerk Weak biceps jerk (C5, 6) Weak brachioradialis jerk (C5,6) Brisk triceps Jerk (C7, 8) (Brisk flexion of the fingers)

Will this guy be able to breathe?

Inverted Knee Jerk Weak knee jerk (L3) Brisk ankle jerk (S1)

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What’s wrong with this guy?

karina ng
Take away the diagnosis from the title?
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Brown Sequard Syndrome

Where is the Lesion? T2 to L2

How to narrow down further? Strength of Hip Flexion Cremasteric reflex Superficial Abdominal Reflex

What are the OTHER clinical signs? UMN signs… WHICH SIDE? Loss of proprioception and touch… WHICH SIDE?

karina ng
Lesion should be above L3 - We cannot be sure if there is weakness of hip flexion; if there isnt, the lesion can be at L1 or L2Lesion should be below T1. If T1 is affected. Upper limbs will not be normal. Suggested level of lesion - T2 - L2How to narrow down further: What you mentioned + Strength of hip flexion *My two cents worth. But I guess it's really how you argue.
karina ng
I feel that you should be more specific. =)UMN sign in the Left Leg: Babinski sign, Ankle Clonus, Increased ToneLoss of Proprioception and Fine Touch/Vibration in the LEFT Leg
Page 42: Let’s break this down

Brown Sequard Syndrome

Hemisection of the spinal cord

What are some SOL in the spinal cord that can cause hemicord syndrome? Tumor (meningioma, lymphoma), Abscess

Can syringomyelia/hydromyelia cause brown sequard?

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Revision

What is somatotopy? Of the Brain Of the Spinal Cord

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Ascending weakness

What are the causes of ascending weakness? Guillain-Barre syndrome Myelopathy (compression, vascular, inflammation)

What are some microbes that can cause Guillain-Barre syndrome? Campylobacter jejuni CMV Influenza Varicella

How will a syringomyelia present? (usually grows laterally and anteriorly)

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Stroke

What are the 2 different type of infarct? “An artery can either _____ or ______.”

What are the risk factors for each? (name at least 5)

What are the etiologies? (at least 2 for each)

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Stroke Ischemic infarct vs hemorrhagic infarct

What are the risk factors? Hypertension, Diabetes, hyperlipidemia, TIA,

Hypercoagulable state, Atrial Fibrillation, RHD, Vascular malformations (Berry aneurysm, Charcot-Bouchard Aneurysm, AVM, moya-moya)

What are the etiologies? Ischemic: Shock, acute plague change, thromboembolism Hemorrhagic: Rupture of aneurysm, trauma, tumor,

malignant hypertension

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Revision

What clinically important areas does the superior branch of the middle cerebral artery supply?

How about the inferior branch of the MCA?

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MCA Superior

Frontal Lobe: Broca(left), FEF, Primary Motor Cortex(UL and Face) Parietal lobe: Somatosensory cortex (UL and Face)

Inferior Parietal lobe: Wernicke’s Area(left), Somatosensory cortex(UL and Face) Parietal and Temporal Lobe: Optic Radiation(contralateral homonymous

hemianopia)

Internal Capsule (lenticulostriate arteries, LL and lots of other stuff)

What about the PCA and ACA?

karina ng
might want to talk about leticulostriate arteries. They are responsible for the lower limb weakness in MCA territory stroke
Page 50: Let’s break this down
karina ng
You wanna add in the answers?
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UMN VS LMN

What are 6 things to look out for when testing for UMN vs LMN?

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UMN vs LMN

Tone Atrophy Fasiculations Deep tendon reflex Clonus Plantar reflex

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THE EYES!

What is the difference between a destructive and irritative lesion involving the FEF?

What side does the eye gaze in a left sided pontine lesion? (PPRF lesion)

What is internuclear opthalmoplegia?

What is a possible clinical presentation of the eye in an Uncal lesion?

Which motor nerve to the eye has the longest course between the brainstem and the eye?

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The MyoNeuro-axis Muscle NMJ Peripheral nerves Plexus Roots Spinal cord Brain stem Brain

Cerebellar Basal ganglia Extra-pyramidal Cranial nerves

What are their hallmarks?

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Muscle Proximal weakness Gower’s sign Muscular dystrophy

Creatinine kinase, rhabdomyolysis

NMJ Severe fatigability, especially in muscles that usually does

not gets tired Gets better with rest Gets better with ice Gets better with Acetylcholinesterase inhibitor (tensilon

test)

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Peripheral Nerves/Diffuse polyneuropathy Glove and stocking deficits (distal weakness) Length dependent Usually a systemic problem (bilaterally affected) Weakness and wasting (Pes Cavus), Sensory abnormality Denervated muscles become completely dead in 18 month

Mononeuropathy (nerve entrapment) Patchy sensory abnormality Motor and sensory loss follows specific nerve innervation

pattern

What disease affects peripheral nerve?

karina ng
Term here should be mononeuropathy - refering to damage of one nerveMononeuritis multiplex is a painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas. Multiple nerves in random areas of the body can be affected. As the condition worsens, it becomes less multifocal and more symmetrical.
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Plexopathy Involvement of multiple areas supplied by different

nerves, but distribution fits into the supply from trunks/cords of the plexus

Weakness + wasting + sensory deficits (patchy) Somewhat like a peripheral nerve problem, but

more extensive, and NOT length dependent

Radiculopathy Deficits will present in a myotomal/dermatomal

pattern No longer length dependent

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Anterior Horn Cell Non-length dependent pattern of weakness Wasting FASCICULATIONS

“Dramatic dying of the cell body, crying and screaming, anyhow firing”

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Spinal Cord

UMN vs LMN signs

What test can you do to localize the level of the lesion?

karina ng
In this case, the defect can be anywhere from the pon and above. You might want to be more specific in your symptoms. E.g. Midbrain lesion - Ipsilateral III palsy and contralateral hemiparesis with spastic dysarthriaPontine lesion - ipsilateral VII palsy with contralateral hemiparesis and spastic dysarthria
Page 60: Let’s break this down

If patient has a hemiplegia + speech defect, where is the level of the lesion?

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Brain Stem and the Rule of 4

Rule of 4 – What is this?

Speech deficits What’s the difference between bulbar and pseudobulbar

palsy?

Facial droop (UMN VS LMN) What other cranial nerve is unilaterally supplied? Half face paralysis + contralateral hemiparesis – Level?

Ocular muscle weakness What happens in a 3rd nerve palsy? 3rd Nerve palsy + contralateral hemiparesis – Level?

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Brain

When is the lesion LEAST LIKELY to be in the brain?

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Brain

When is the lesion LEAST LIKELY to be in the brain? Bilaterally affected (tetraplegia) Ascending weakness Glove and Stocking deficits NO UMN signs

What about a guy with just a unilateral LL weakness?

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Explain the following….

Sudden right Hemiparesis Expressive aphasia Ipsilateral gaze shift towards the lesion

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Seizure

Reactive Gliosis -> Glial Scar -> predispose to uncoordinated firing of neurons

Destructive lesion vs Irritative lesion of the FEF

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Harlem Shake?

No….. Definitely Ballismus