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High Yield Review: Phase II MEQ Pros > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

List a few risk factors for ischemic stroke.

A
  • Older (>65 years old)
  • Male sex
  • History of transient ischemic attack
  • Atherosclerosis
  • Systemic Arterial Hypertension
  • Cardiovascular heart disease
  • Hypercoagulable states (e.g. pregnancy, hyperhomocysteinemia, protein C and S deficiency, cancer or malignancy)
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2
Q

How does atrial fibrillation increases the risk of stroke?

A

During atrial fibrillation, the blood becomes stagnant, this promotes blood clotting (Virchow’s Triad), and blood clot is formed in the left atrial appendage. This blood clot then embolism into the cerebral circulation / blood vessels towards the brain, resulting in ischemic stroke.

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3
Q

Name 3 common sites of thrombotic stroke.

A

Carotid bifurcation
Basilar artery
Origin of middle cerebral artery

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4
Q

Name 4 clinical features you will see in MCA infarcts?

A

Contralateral hemipararesis and loss of sensation in the lower half of the face and upper limbs

Contralateral homonymous hemianopia without macular sparing

Eye gaze to the side of lesion (ipsilateral)

Aphasia

Broca’s Area (left inferior anterior gyrus)
Wernicke’s Area (left superior temporal gyrus)

Contralateral hemineglect

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5
Q

How do you quantify the severity of stroke?

A

Using the National Institute of Health (NIH) Stroke Scale

Normal: 0
Mild: 1-6
Moderate: 7-12
Severe: >12
Max: 42
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6
Q

How do you know imaging is highly suggestive of stroke instead of tumour or lesions?

A

When there is a straight line boundaries, which is indicative of the vascular boundaries.

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7
Q

Name the first line imaging modality used for detecting stroke.

A

Head CT (computed tomography) without contrast

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8
Q

Are Head CT with contrast contraindicated in stroke? What is the other contraindication?

A

Yes, they are contraindicated in patients with stroke, and intracranial haemorrhage.

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9
Q

What would you see on neuroimaging from MCA infarcts?

A

Hyperdense (brighter) MCA dot sign (usually after 90 mins)

Hypodense (darker) brain tissue (can be due to oedema)

Loss of “insular ribbon sign” (loss of grey-white matter differentiation)

Obscuration of lentiform nucleus (loss of basal ganglia)

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10
Q

What are the advantages of Head CT over MRI?

A

Faster / quick to perform, so to shorten the time before administrating thrombolytic drugs

Easier to obtain compared to MRI (logistically)

More affordable (MRI is more expensive)

Able to detect haemorrhage better than MRI

Can be performed by anyone

Reproducible

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11
Q

What are the criteria (indications) for thrombolytic therapy (e.g. tissue plasminogen activator, tPA)?

A

Dagnosis of acute stroke
Age > or equal to 18 years old
Onset of symptoms < 4.5 hours before tPA administration (best is <3 hours)
Head CT confirming no contraindications (e.g. haemorrhage and large stroke)

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12
Q

What are the contraindications for thrombolytic therapy (e.g. tissue plasminogen activator, tPA)?

A 
Recent head trauma
Large stroke
Intracranal haemorrhage
Bleeding Diathesis
Recent surgery or procedure
Recent MI 
Recent GI bleed / malignancy
Pregnancy
Improving symptoms
Seizure at onset
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13
Q

What is the necrosis that occurs with infarction of brain tissue?

A

Liquefactive necrosis

Note: coagulative necrosis are seen after infraction in other organs.

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14
Q

What are the causes of subarachnoid haemorrhage?

A

Traumatic: head trauma

Non-traumatic: rupture cerebral (saccular, berry) aneurysm

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15
Q

Name 3 risk factors for subarachnoid haemorrhage.

A

Hypertension
Smoking
Positive Family History

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16
Q

Describe the clinical features of subarachnoid haemorrhage.

A

Thunderclap headache: often described as the worst headache in patients’ lives

Impaired consciousness

Mass effect

Meningeal signs

Prodromal symptoms

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17
Q

What would you see on CT without contrast for subarachnoid haemorrhage?

A

Hyperdense (whitish, brighter, blood) lesion in the subarachnoid space

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18
Q

Briefly describe the 3 classification of subdural haemorrhage.

A

Acute SDH: symptoms onset <3 days

Subacute SDH: symptoms onset 4-20 days

Chronic SDH: symptoms onset >21 days

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19
Q

What are the causes of SDH?

A

Rupture or tear of the bridging veins which can occur secondary to any of the following:

Head trauma
Shaken baby syndrome
Acceleration-deceleration injury
Cerebral atrophy
Alcohol use disorder
Advanced age and very young
Hyponatremia
20
Q

Why are elderly has an increased risk of subdural haemorrhage?

A

Elderly (advanced age) are prone to cerebral atrophy. When there is cerebral atrophy, there is an enlargement of the subdural space, which results in an increased length that bridging vein has to transverse. The bridging veins are more vulnerable to shearing force

21
Q

Why does alcohol abuse increase the risk of subdural haemorrhage?

A

Alcohol -> thins the veins and increased risk for thrombocytopenia, easier to rupture.

22
Q

Describe how a SDH would appear in Head CT without contrasts.

A

Crescent-shaped (concave) hyperdense (blood) lesion

Cross the suture line

Does not cross the midline (due to the presence of flax cerebri)

Ventricular and sulcal effacement

If the mass is large enough, it can cause a midline shift to the contralateral side due to mass effect

Radiodensity of the lesion on CT depends on the timeline of SDH.

Acute: usually hyperdense
Subacute: isodense
Chronic: hypodense

23
Q

What is the cause of epidural haemorrhage?

A

Rupture or tear to the middle meningeal artery (branch of maxillary artery)

24
Q

Where is the most common site of rupture? Explain why.

A

The pterion is the most common site of rupture, as it is the thinnest part of the skull, and where the middle meningeal artery lies in close proximity to the skull\

25
Q

Which region of the brain does blood usually pool in EDH?

A

Temporal or tempo-parietal region

26
Q

What kind of herniation does EDH result in? Why does it occur?

A

Transtentorial uncal herniation. Due to increased intracranial pressure.

27
Q

Describe the classical presentation of EDH.

A
  1. Initial sudden loss of consciousness
  2. Lucid interval: temporary restoration of consciousness with normal or near-normal neurological function
  3. Renewed decline in neurological status and onset of symptoms due to hematoma (e.g. mass effect)
28
Q

Explain why there is a period of restoration of consciousness with normal or near-normal neurological function.

A

Due to the venous shunting of blood out from the epidural space.

29
Q

Describe how EDH would appear in Head CT without contrast

A

Lenticular-shaped (biconvex) hyperdense (typically) lesion

Does not cross the suture lines

Crosses the midline (EDH can cross the dural attachment sites)

Ventricular and sulcal effacement

If the mass is large enough, it will cause a midline shift to the contralateral side (mass effect)

30
Q

What are the red flags of Headache?

A

Mnemonics: SNOOPP

S: Systemic signs & symptoms (fever, weight loss)
N: neurological deficits/dysfunction (altered mental status, seizure)
O: onset of headache is abrupt
O: older age (>50y/o) with new or progressive headache
P: papilloedema, and other signs of increased intracranial pressure
P: progressive headache

31
Q

What are the indication for brain imaging in headache?

A

Mnemomics: I WARN P

I: incapacitating headache

W: worst headache in patient’s life
A: abrupt onset
R: recent onset in patients > 50 years old
N: new onset of nocturnal headache

P: papilloedema, pattern change in headache, post-traumatic headache, pituitary dysfunction, elevated pressure in eye or intracranially

32
Q

Describe the pathophysiological mechanism contributing to Alzheimer Disease.

A

Enzymatic cleavage of transmembrane amyloid precursor protein (APP) by beta-secretase and gamma-secretase, results in the formation of insoluble beta-amyloid monomers. Beta-amyloid monomers aggregates to form beta-amyloid plaques, which deposits outside the neuron

Extracellular beta-amyloid initiate the activation of intracellular kinase, which results in the phosphorylation of tau protein in the microtubule. Hyperphosphorylate tau protein results in the formation of neurofibrillary tangles in the neuron, which damages the microtubules via apoptosis, and result in Alzheimer Disease.

33
Q

Name the 3 genetic factors that predispose to Alzheimer Disease.

A
  • Amyloid Precursor Protein (APP) gene on Chromosome 21. People with trisomy 21 have an overpression of APP gene, predisposing them to Alzheimer Disease.
  • Apo ε gene on chromosome 19. Apo ε breaks down beta-amyloid. The lack of ApoE, predispose individuals to Alzheimer Disease.
  • Presenilin-1 and -2 (PSEN-1 and PSEN-2) gene, on chromosome 14 and chromosome 1, respectively. PSEN gene mutation results in gamma secretes to change location, forming plaques.
34
Q

Describe the microscope findings of the brain in Alzheimer Disease.

A
  • pink or red beta-amyloid plaques in the interneuronal space of the brain under Congo Red stain
  • green birefringent of beta-amyloid plaques under polarised light
  • Gallyas stain of neurofibrillary tangles (aggregated of hyperphosphorylated tau protein)
35
Q

Name 3 complications of Alzheimer Disease

A

Infection: aspiration pneumonia
Malnourishment/dehydration
Intracerebral haemorrhage (due to increased risk of cerebral amyloid angiopathy)

36
Q

Parkinson disease primarily affects individual of which age?

A

> 45 years old

37
Q

Name a contributing genetic factor to Parkinson Disease

A

α-Synuclein (SNCA) gene, which results in the accumulation of lewy bodies

38
Q

Describe the pathophysiology of Parkinson Disease.

A

α-Synuclein (SNCA) gene -> accumulation of lewy bodies -> progressive dopaminergic neuron degeneration in the substantia nigra (part of the basal ganglia) -> decrease dopaminergic neuron -> dopamine deficiency -> movement disorder

39
Q

Describe the clinical features of Parkinson Disease

A

Triad of Parkinsonism

  1. Bradykinesia (slow movement)
  2. Resting tremor (pill-rolling tremor)
  3. Rigidity (Cogwheel rigidity)
40
Q

Describe how the brain will look like grossly in Parkinson Disease.

A

The loss of pigmentation in the substantia nigra

41
Q

Describe the microscopic findings of the brain in Parkinson DIsease

A

Lewy bodies (aggregates of misfolded α-Synuclein (SNCA) in the neural cell bodies of substantia nigra

42
Q

Describe the genetic factor of Hutington disease

A

Mutation of hutington gene on chromosome 4

Autosomal dominant

43
Q

Describe the pathogenesis of Hutington disease.

A

Mutation of hutington gene on chromosome 4 -> increased CAG trinucleotide repeats -> increased glutamine -> increased Hutington protein -> accumulation of Hutington protein which aggregates in the neuronal cells of dorsal striatum (cudate & putamen) -> over activation of NMDA receptors -> atrophy and neuronal cell death -> increased dopamine, decreased GABA and acetylcholine -> movement disorder

44
Q

Describe the clinical features of Hutington disease.

A

Early stage:

  • hyperkinesia
  • chorea (involuntary, sudden, irregular, nonrepetitive arrhythmic movments of the limbs, neck, head, and/or face)

Late stage:

  • Hypokinetic (dystonia, rigidity, bradykinesia)
  • Akinetic (inability to move or speak)
  • Cognitive decline and behaviour/personality changes
45
Q

Why does subsequent generation have an earlier onset and more severe presentation of Hutington disease?

A

Hutington disease can be due to the autosomal dominant mutation of hutington gene.

Because of “anticipation” genetic phenomenon, there is an increased in the number of CAG repeats (repeat expansion) in subsequent generation

High Yield Review: Phase II MEQ Pros (10 decks)

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