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Baz Y2 Semester 1 > Week 4 Neurology > Flashcards

Week 4 Neurology Flashcards

1
Q

Describe the parts of the brain supplied by the anterior, middle and posterior cerebral arteries?

A
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2
Q

What is the difference between the anterior circulation and the anterior cerebral artery?

A

The anterior circulation is everything going to the aterior brain and includes both the anterior cerebral artery and middle cerebral artery.

For example an occlusion in the internal corotid artery would affect the anterior circulation whereas if it was higher up in the anterior cerebral artery it would just be the anterior cerebral artery

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3
Q

What are the effects of a stroke depending which cerebral artery is affected?

A
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4
Q

What is the bamford classification of strokes? What are the four strokes and what defines them?

A
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5
Q

Thinking of the anatomy what is brainstem syndrome based on the part of the brain stem affected?

A

Generally: Contralateral motor and sensory symptoms for parts innervated by spinal nerves with ipsilateral cranial nerve problems with cranial nerves asscosiated with that area.

  1. Weber’s Syndrome
    Location: Midbrain.
    Symptoms:
    Ipsilateral oculomotor nerve palsy (drooping eyelid, dilated pupil, and inability to move the eye).
    Contralateral hemiparesis (weakness of the opposite side of the body).
  2. Locked-In Syndrome
    Location: Pons.
    Symptoms:
    Complete paralysis of voluntary muscles except for the eyes (blinking and vertical eye movements may remain intact).
    Preserved consciousness and cognitive function.
  3. Medial Medullary Syndrome
    Location: Medulla.
    Symptoms:
    Contralateral limb weakness.
    Contralateral loss of proprioception and vibration sense.
    Ipsilateral tongue weakness (tongue deviates toward the affected side).

All have effects on motor and sensory below. Pons is total as lesion is often bilateral. They have localised effects on the corresponding cranial nerves.

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6
Q

What is a TIA?

A

Symptoms of ischemic stroke but resolved in 24h

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7
Q

First thing you do with a stroke?

A

CT scan without contrast to differentiate between haemorrhagic and ischaemic stroke

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8
Q

First line of treatment for an ischaemic stroke?

A

Perform/ Do/ Give/ Administer/ Gift / Enforce/ Oversee Thrombolysis - Usually alteplase.

Within 4.5h of symptoms

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9
Q

What are the contraindications to thrombolysis?

A

Basically anything that increases risk of bleeding.

Contraindications:
recent surgery
recent trauma to the head
taking anti-coagulant
systolic bp >185
Raised INR

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10
Q

What is the treatment for ischaemic stroke if it is 6-24h after symptom onset?

A

Mechanical thrombectomy

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11
Q

Mid length treatment for ischaemic stroke between 24h-2weeks?

A

Aspirin

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12
Q

Long term treatment after an ischaemic stroke >2weeks

A
  • Clopidogrel 75mg daily (patient with AF requires warfarin or DOAC, this is initiated 2 weeks after stroke)
  • Statin (atorvastatin 20-80mg daily)
  • Lifestyle modification (diet, physical activity, alcohol intake, smoking)
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13
Q

Treatment for a haemorrhagic stroke?

A

Surgical intervention to releive cranial pressure if needed.

Aim to decrease BP to 120-139 systolic after 24h and maintain for 7 days

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14
Q

What layers of the brain will blood fill in between in a subarachnoid haemorrhage?

A

Underneath the arachnoid mater.

Above the pia mater.

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15
Q

What is the presentation of a subarachnoid haemorrhage?

A

Thunderclap headache (sudden onset and “worst headache they’ve ever had”)

Other symptoms may include reduced consciousness, seizures, focal neurological signs, meningism

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16
Q

Diagnosis of a sub arachnoid haemorrhage?

A

Most are visible on a CT, however this diminishes after 12h.

If appropriate history for SAH and negative CT brain, lumbar puncture (LP) performed to test for evidence of bleeding into CSF space: xanthochromia.
Need to do this 12 hours after onset (allows time for blood breakdown products)

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17
Q

If using a lumber puncture to detect SAH what are you looking for?

A

Xanthochromia: a medical condition that causes cerebrospinal fluid (CSF) to appear yellow

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18
Q

Order of management of a SAH

A
  1. Acute supportive care:
    - basic resuscitation measures (e.g. airway support, ventilation)
    - management of complications (e.g. seizures, intracranial pressure)
  2. Nimodipine: prevents development of delayed cerebral ischaemia (which increases mortality) by preventing arterial vasospasm
  3. Secure aneurysm
    - typically coiling (via endovascular procedure) or clipping (neurosurgical)
  4. Ongoing rehabilitation and long-term care (including psychological support)
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19
Q

What drug might you use in SAH?

A

Nimodipine: prevents development of delayed cerebral ischaemia (which increases mortality) by preventing arterial vasospasm

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20
Q

What is the definition of meningitis?

A

Invasion of bacteria intot he meninges

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21
Q

What is the pathophysiology of meningitis?

A
  • Invasion by bacteria leads to inflammation - Immune reaction; neutrophils (pus)
  • Elevated intracranial pressure
  • Inflammation and thrombosis in arteries
  • can lead to ischaemia/stroke
  • Damage to cranial nerves
  • can lead to deficits (e.g. deafness)
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22
Q

3 most common microbial causes of meningitis?

A

1.Neisseria meningitidis (‘meningococcus’)
- Epidemic outbreaks (e.g. student halls)

  1. Streptococcus pneumonia (‘pneumococcus’)
  2. Haemophilus influenza
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23
Q

If there is an outbreak of meningitis in somewhre like student halls what is it likely to be caused by?

A

Neisseria meningitidis (‘meningococcus’)

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24
Q

If there is trauma what microbe might cause the meningitis?

A

Staphylococcus aureas (skull fractures)

Common environmental microbe.

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25
Q

Clinical features of meningitis?

A
  • Acute headache – typically developing over hours
  • Meningism: neck stiffness, photophobia
  • Fever
  • Non-blanching rash (meningococcus)
  • Confusion, reduced consciousness
  • Sometimes seizures

Exam:
Stiff neck
Kernig’s & Brudzinski’s
These lack sensitivity; often not be present

Think meningitis in anyone with fever and headache tbh

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26
Q

How to diagnose meningitis?

A

Do a LP to send ot microbiology

27
Q

If you think someone has meningitis when you should you not perform a lumber puncture?

A

If they present with loss of conciousness and focal features make sure to do a CT first.

If there is a mass lesion a LP can result in brain herniation

28
Q

What differences would you expect to see in a lumber puncter between bacterial nd viral meningitis

A
29
Q

Management of meningitis?

A

Antibiotics!

Ideally after lumber puncture/ ct however osmetimes given earlier to increase chance of survival

Supportative treatment depending on specifics e.g. surgery to remove abscess or life support.

If meningococcus should do a prophylactic single dose of ciprofloxacin to contacts

30
Q

What is encephalitis?

What type of encephalitis are we covering this module?

A

Encephalitis: inflammation (-itis) of brain parenchyma (gray and white mater).
Contrast to meningitis which is the meninges.

It can be autoimmune/ paraneoplastic but we will focus on viral.

31
Q

Most common cause of viral encephalitis in the UK?

A

Herpes.

HSV1:90%
HSV2:10%

32
Q

Seconds most important cause of viral encephalitis?

A

Varicella zoster (VZV) aka chicken pox and shingles

33
Q

Main differences between encephalitis caused by herpes or varicella zoster?

A

Herpes:

  • Invades via olfactory nerves
  • Affects the temporal lobes

Varicella zoster:

  • Invades via retrograde transport. e.g. up the trigeminal in the case of opthalmic rash.
  • Sometimes get haemorrhage
  • Sometimes occurs with a rash across the opthalmic dermatome
34
Q

Common encephelitis clinical features

A

May include some/all of:
- Headache - Fever - Seizures
- Confusion - Decreased consciousness
- Focal deficits (e.g. dysphasia, weakness)

Meningism not typical

Rapid progression – decreasing consciousness.

35
Q

What should I think if I see this rash combined with encephalitis symptoms?

A

Encaphalitis caused by varicella zosta.

The rash covers the opthalmic dermatome.

36
Q

What is the pathophysiology of the clinical features of viral encephalitis?

Aka what is the form of brain damage?

A

Inflamation and necrosis

37
Q

What would I expect to find in a csf sample form a patient with viral encephalitis?

A

Elevated lymphocytes and protein. Normal glucose (low glucos indicates bacteria as they feed on it)

PCR would find a specific virus

38
Q

What antiviral would you use for encephalitis?

A

Aciclovir IV

39
Q

Define these terms for muscle disorders:

Myopathy

Myositis

Myalgia

Muscular dystrophy

A

Myopathy: disease of muscle

Myositis: inflammation of muscle

Myalgia: pain arising from muscles

Muscular dystrophy: a large group of hereditary disorders featuring abnormal muscle development and function

40
Q

What is Gower’s sign?

A

Gowers’ sign

  • Sign of proximal muscles weakness in a child
  • Use of arms to provide support while standing
  • Indicates weakness of pelvic girdle
  • Typical in congenital muscular dystrophies such as Duchenne’s
41
Q

Where is the weakness typically observed in muscle disorders?

A

Proximal weakness

42
Q

Summary of Duchenne’s?

A
  • X-linked - Mutation in dystrophin gene
  • Type of muscle dystrophy
  • Very common! About 1/3500 male births
  • Manifestations typically emerge age 3-6
  • Initial pelvic girdle weakness then shoulder, trunk, arms ; scoliosis develops
  • Characteristic calf pseudohypertrophy – muscle infiltration by fat
43
Q

What gnen is mutated in Duchenne’s?

A

Dystrophin

Can remember because Duchennes full name is Duchenne’s muscle dystrophy

44
Q

What is Polymyositis?

A

Acquired inflammatory muscle disorder
Progressive proximal weakness
Subacute tempo (arising over weeks)
Associated muscle pain

CK elevated
Inflammatory pattern on muscle biopsy

45
Q

What is elevated CK a biomarker of?

A

Muscle damage

Creatine Kinase

46
Q

Common drug cause of myalgia?

A

Statins

47
Q

Causes of myalgia?

A
  • Drugs
  • Infection (e.g. flu, COVID)
  • Inflammatory disorders (e.g. polymyalgia rheumatic)
  • After strenuous exertion
48
Q

What is the pathophysiology behind Rhabdomyolysis?

A
  • Massive breakdown of muscle fibres
  • Leakage of myoglobin
  • Accumulation in renal tubules leading to acute renal failure
49
Q

What protein when leaked from muscle injury in large ammounts can cause kidney failure?

A

Myoglobin

50
Q

What are common causes of Rhabdomyolysis?

A
  • drug toxicity
  • infection
  • crush injuries, burns, genetic muscle disorders (e.g. metabolic pathway enzyme deficiencies) - and sustained exertion in healthy people
51
Q

How does alcohol cause neuropaphy?

A

Through B1 deficiency

52
Q

What might you use a nerve conduction test for?

A

To distinguish between axonal and demyelinating neuropathy

53
Q

Why can hypothyroidism lead to carpel tunnel syndrome?

A

It causes fluid retention and swelling leading to compression of the median nerve. The carpel tunnel is one of the first areas to get affected.

54
Q

What parts of the body does neuropathy affect first?

A

Distal nerves

55
Q

What could this be?

42 year old man
Recent diarrhoeal illness, confirmed Campylobacter jejuni on stool culture

5 days of progressive numbness and weakness
– initially causing difficulty walking, progressing: now difficulty standing, weakness in hands
- weak areas have also lost sensation
- also developing bilateral facial weakness

Examination: extensive distal (ankles, hands) weakness, milder proximal weakness, bilateral lower-motor neuron VII palsies

A

Guillian Barre Syndrome

56
Q

What is Guillian Barre?

A

Acute polyneuropathy caused by an autoimmune response following an infection normally Campylobacter jejuni

57
Q

Guillian Barre treatment and prognosis?

A

supportive measures and IVIg or plasma exchange.

good chance of full or partial neurological recovery over months

58
Q

What is the common bacteria resonsible for Guillian Barre syndrome?

A

Campylobacter jejuni

Hint: Guillian Barre was barred from the inn (peripheral nervous system) now she has to camp

59
Q

What is Charcot-Marie-Tooth disease?

A

An inherited disease causing gradually progressive poly neuropathy.

Hint: I might inherit the shark tooth, which I could accidently cut my nerve with

60
Q

Explain the pathophisiology of locked in syndrome?

A

It is a bilateral lesion of the ventral pons.

Result is complete paralysis except for blinking and vertical eye movements.

Consciousness is spared because the reticular activating system in above in the midbrain.

Both occipital lobes knocked out resulting in blindness.

It is bilateral because it often due to thrombosis of the basiller artery which is just the one artery so will knock out both sides.

This completely knocks out motor (corticospinal and corticobulbar) and sensory pathways on both sides and knocks out both cranial nerves V-VII hence the only movement spared is blinking and vertical eye movements.

61
Q

Why in brainstem lesions does the effects of the cranial nerve getting knocked out dominate that of the contralateral cortico bulbar tracts?

A

Because a lot of the cortico bulbar tracts fibres are bilateral and even those that aren’t the fibres appear rather diffuse so many are spared resulting in minimal weakness.

62
Q

What is another cause of meningitis that only see in old people, immunocompromised diabetic patients and pregnent people?

A

Listeria Monocytogenes

63
Q

Which cause of meningitis commonly affects young children?

A

Haemophilus influenzae type b (Hib)

64
Q

Which cause of meningitis has the worst prognosis?

A

Streptococcus pneumoniae

Baz Y2 Semester 1 (17 decks)

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