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- Y6 Neurology > Acute Neurological Presentations > Flashcards

Acute Neurological Presentations Flashcards

1
Q

Describe the epidemiology of headache.

A

Common problem

  • –4.4% per year consult GP for headache
  • –1-3% of all hospital admission
  • –24% of acute admissions to acute neurology service
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2
Q

What are the common causes of headache?

A
  • 13% primary headache
  • »2.5 % CNS infections
  • »1% SAH
  • »0.2% Head injury
  • »7.3% other
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3
Q

Does the brain have sensation?

A

Brain tissue is insensate

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4
Q

How do you assess headache?

A
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5
Q

How is headache classified?

A
  1. Primary headache (no causative disorder)
  2. Secondary headache (causative disorder)
  3. Cranial neuralgias
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6
Q

List some primary causes of headaches.

A
  • Migraine
  • Tension Type
  • Cluster Headache
  • Other primary head aches
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7
Q

What are the secondary causes of headache?

A
  • Head or neck trauma
  • Vascular disorder
  • CNS Infection
  • Intracranial Pressure disorder
  • Metabolic disorders
  • Drug withdrawal disorders
  • Headache psychiatric disorder
  • Dental, ENT or ocular problem
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8
Q

What are the headache “red flags”?

A
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9
Q

What is the most uncomfortable posture if you have increased inracranial pressure?

A

Lying supine

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10
Q

Sudden onset, thunderclap headache in a young patient. What is a good differential?

A

Subarachnoid haemorrhage

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11
Q

How does subarahcnoid haemorrhage present in A&E?

A
  • 1/3 present with acute onset severe headache as the only symptom
  • 5 to 11 % misdiagnosed (most commonly as migraine)
  • Headache onset- Abrupt, sudden, acute, thunderclap (over seconds or minutes)
  • Excruciating headache may only last 1-2 hours (reason went to the ER). HEADACHE may last 3 to 8d
  • About 50% pts have warning symptoms prior to major SAH – minor leak or expansion – “unusual headache – some TCH
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12
Q

What are some common pitfalls when diagnosing SAH?

A

Perceived presentations

  • “no neck stiffness”
  • “looked too well for SAH”
  • “got better with NSAIDS or Triptans”
  • “only lasted 4 hours”

1/3 present with acute onset severe headache as the only symptom

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13
Q

Describe CT diagnosis in SAH.

A

Sensitivity to detect SAH on CT decreases with time.

  • 12 hours from headache - 98%
  • 3 days - 80%
  • 1 week - 50%
  • After 3 weeks - 0%
  • Even if done 12 hours from headache onset 2% will have SAH with normal scan.

SO CT HEAD ASAP

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14
Q

Describe LP abnormality in SAH.

A

LP may be negative less than 2 hours after the bleed;

  • most sensitive at 12 hours after symptom onset.
  • Xanthochromia (yellow-to-pink CSF supernatant) usually is seen by 12 hours

At 2 hours need to use spectrophotometry (oxyhemoglobin)

  • Xanthochromia results from lysis of RBCs with release of oxyhemoglobin, methhemoglobin and bili ( up to 2 weeks)
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15
Q

List some causes of thunderclap headache.

A
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16
Q

Which secondary headache conditions can have a normal CT head scan?

A
  • •Meningitis
  • •SAH
  • •Ischaemic stroke
  • •Cerebral venous thrombosis
  • •Cervical arterial dissection
  • •Reversible Cerebral Vasoconstriction Syndrome (RCVS)
  • •Cerebral vasculitis and Temporal arteritis
  • •Pituitary apoplexy
  • •Malignant hypertension
  • •Others
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17
Q

Describe the peripheral and central vestibular system.

A
18
Q

Name 3 peripheral causes of vestibular symptoms.

A
  • BPPV
  • Meniere’s
  • Vestibular Neuritis
19
Q

Which maneouvre is diagnostic for peripheral vestibular symptoms?

A

Hallpike?

20
Q

How do you assess diplopia?

A
  • Onset
  • Character - is it more horizontal than vertical?
  • Duration
  • Associated symptoms
  • Triggers/alleviators

Double vision = diplopia

21
Q

How does CN III palsy present?

A
  • Ptosis (70% of L paplebrae by Parasympathetic III fibres) – may be complete
  • Mydriasis with decreased direct and consensual constriction
  • Inferio-lateral deviation of eye in primary position
  • Diplopia on upwards and inwards gaze
  • Loss of accomodation
22
Q

How does CN VI palsy present?

A
  • Normal eye position in primary position.
  • Diplopia and strasbismus on lateral gaze towards the side of the lesion.
  • True horizontal diplopia.
  • Often the strabismus is not appreciable; check the diplopia is true (disappears when you test one eye) the direction of maximal diplopia, and the eye responsible for the outermost image.
23
Q

What is the cause of palsy in pupillary sparing with sudden onset?

A

Sudden infarction of nerve

24
Q

What is a common cause of fatiguability on one side of face?

A

Myasthenia gravis - NMJ problem causes fatiguability

25
Q

When do you get a monoocular nystagmus?

A

Most nystagmuses are biocular unless in a medial pontine stroke, where the unilateral medial longitudinal fasciculus is affected. Patient will present with contralateral internuclear opthalmoplegia (INO).

26
Q

Desccribe the aetiology of INO.

A
  • Most nystagmuses are biocular unless in a medial pontine stroke, where the unilateral medial longitudinal fasciculus is affected.
  • Patient will present with contralateral internuclear opthalmoplegia (INO).
  • If the right medial longitudinal fasciculus is damaged, and patient is instructed to look to the left, the right eye will not look to the left (fails to adduct) while the left eye has horizontal nystagmus.
  • This is because the medial longitudinal fasciculus function is for concurrence contraction of medial rectus muscle and lateral rectus muscle on adduction gaze.
  • Any lesion that damages the unilateral medial longitudinal fasciculus can produce INO.
27
Q

Describe Horner’s syndrome.

A
  • Mild ptosis
  • Moisis
  • Anhdrosis
  • Enophalmos
28
Q

When do you get forehead sparing?

A

UMN lesion - still getting some innervation to frontalis muscle on the contralateral side.

In LMN you get total face paralysis on one side

29
Q

Bell’s palsy

A

Subnuclear

Bell’s sign - on affected side eye won’t close properly which can have many complications such as irritation of eye.

???

30
Q

What is bright on a CT head scan?

A

Fresh blood

Calcium (often found in choroid plexus)

Metal

31
Q

What are the effects of haemorhage on brain tissue?

A

Diplaces parenchyma increasing pressure

Blood also irritates brain tissue (causing oedema)

32
Q

What are the causes of haemorrhage?

A
  • HTN
  • Rupture of aneurysm or AVN
  • Haemorrhagic necrosis (e.g. tumour, infection[infective endocarditis - pyrogenic matter, splinters and embolises in small artery in brain and this causes a myocotic aneurysm as it eats away on the vessel)
  • CVT (venous outflow obstruction)
  • Trauma
  • Altered haemostasis (tendency to bleed)
33
Q

Describe the epidemiology of stroke.

A
  • 1 in 10 deaths is caused by a stroke
  • 3rd most common cause of death
  • World wide 15m people suffer a stroke each year 1/3 die & 1/3 disabled
  • Estimated cost in US $73.7billion
  • Estimated cost in EU E 64.1 billion
  • WHO predict disability adjusted life years (DALYs) lost to stroke to rise from 38mil in 1990 to 61 mil in 2020
34
Q

Why does the brain become dark on CT where damage has occurred? Describe the pathophysiology.

A

Density of the brain where ischaemic damage has occurred decreases.Hypoattenuated because density is like fluid.

Ischaemic cascade - if deprived of oxygen for long enough then cell death will occur. Cells expand and burst. Inflammation recruits macrophages and clears this away.

35
Q

How does an ischaemic penumbra form?

A
  • Ischemic zone surrounds a central core of infarction
  • Viability of brain tissue is preserved if perfusion is restored within a critical time period.
  • Tissue surrounding the infarct that is salvageable, but at risk.
36
Q

List 3 types of large artery atherosclerosis. What are the risk factors?

A
  • Intracranial stenosis
  • Carotid stenosis
  • Aortic Arch Plaque
  • HT
  • DM
  • Smoking
  • Chol
  • BMI
  • CAD
  • FMHx
  • Age
37
Q

How do you assess someone’s risk of stroke if they have AF?

A
38
Q

How do you prevent risk of stroke in AF?

A

Oral anticoagulants

Oral anticoagulation (OAC) is more effective than aspirin(antiplatelets) for secondary prevention and at risk patients

39
Q
A
40
Q

What is used for thrombolysis?

A

rt-PA/alteplase

41
Q

What is the therapeutic window for thrombolysis?

A

Up tp 4.5 hours after onset of symptoms only

NICE 2012 indication - Adults aged 18-80 years with acute ischaemic stroke (AIS) within 3 to 4.5 hours of symptom onset, after prior exclusion of intracranial haemorrhage by brain scan

42
Q

What are the advantages of multi-modal imaging in stroke?

A

Multi-modal brain imaging - CT and MRI - allows us to treat patients up to 24 hours of onset of symptoms.

- Y6 Neurology (29 decks)

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