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Yr 4 - CCC > Corrections - Neurology > Flashcards

Corrections - Neurology Flashcards

1
Q

Where do the pontine arteries radiate from?

What do they supply?

A

From the basilar artery on the brainstem.

They supply the pons.

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2
Q

Presentation of a pontine haemorrhage?

A

1) Pinpoint pupils: thought to be caused by irritation and stimulation of parasympathetic pathways in the pons

2) Paralysis: due to motor tracts in the pons that descend to supply the limbs

3) Low GCS

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3
Q

What structures are within the lateral medulla?

How does this explain features of a posterior inferior cerebellar artery lesion (i.e. lateral medullary syndrome)?

A

1) sympathetic tract: hence ipsilateral Horner’s syndrome

2) inferior cerebellar peduncle (connects medulla to cerebrum): ipsilateral ataxia

3) part of the trigeminal nerve nucleus: ipsilateral facial numbness

4) spinothalamic tract: contralateral body numbness

5) nucleus ambiguus (which gives rise to some vagus nerve and glossopharyngeal motor fibres): dysphonia and dysphagia

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4
Q

What should all TIA patients have?

A

an urgent carotid doppler unless they are not a candidate for carotid endarterectomy

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5
Q

What can be taken for 2ary prevention of stroke if clopidogrel is contraindicated?

A

Aspirin + dipyridamole

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6
Q

Role of dipyridamole in 2ary prevention of stroke?

A

Dipyridamole works synergistically with aspirin by inhibiting platelet activation and adhesion, as well as having vasodilatory effects.

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7
Q

How long should aspirin + dipyridamole be continued in 2ary prevention of ischaemic stroke?

A

lifelong

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8
Q

Causes of a brain abscess?

A

1) ascending infection from middle ear or from facial sinuses

2) trauma or surgery to the scalp

3) penetrating head injuries

4) embolic events from endocarditis

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9
Q

Presentation of brain abscess?

A

1) headache: often dull, persistent

2) fever: may be absent and usually NOT the swinging pyrexia seen with abscesses at other sites

3) focus neurology e.g. oculomotor nerve palsy or abducens nerve palsy 2ary to raised intracranial pressure

4) other features consistent with raised intracranial pressure e.g. nause, papilloedema, seizures

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10
Q

Management of brain abscess?

A

1) surgery: craniotomy

2) IV antibiotics: IV 3rd-generation cephalosporin + metronidazole

3) intracranial pressure management: e.g. dexamethasone

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11
Q

What can rapid correction of hyponatraemia cause?

A

Osmotic demyelination syndrome (central pontine myelinolysis)

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12
Q

Symptoms of osmotic demyelination syndrome?

How soon after correction of hyponatraemia do they occur?

A

Typically after 2 days.

Symptoms: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, locked in syndrome, confusion, and coma.

These are usually IRREVERSIBLE.

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13
Q

Acute vs chronic management of migraine?

A

Acute: triptan + NSAID/paracetamol

Chronic: propanolol or topiramate

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14
Q

Features of a medication overuse headache?

A
  • present for 15 days or more per month
  • developed or worsened whilst taking regular symptomatic medication
  • patients using opioids and triptans are at most risk
  • may be psychiatric co-morbidity
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15
Q

Management of medication overuse headache?

A

simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)

opioid analgesics should be gradually withdrawn

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16
Q

What 2 classes of drugs are at most risk of causing medication overuse headache?

A

triptans & opioids

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17
Q

What class of drug is metoclopramide?

A

Dopamine antagonist: blocking dopamine receptors in the chemoreceptor trigger zone of the CNS.

This can decrease N&V but increase EPSEs.

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18
Q

What is a Valsalva maneuver?

A

Performed by a forceful attempt of exhalation against a closed airway, usually done by closing one’s mouth and pinching one’s nose shut while expelling air out as if blowing up a balloon.

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19
Q

What do headaches that are worsened by alsalva manoeuvres associated with?

A

Raised ICP until proven otherwise

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20
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21
Q
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22
Q

Most common side effect of lumbar puncture?

A

Post-lumbar puncture headache (1/3 patients)

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23
Q

UKMEC 4 conditions for COCP?

A

1) more than 35 years old and smoking more than 15 cigarettes/day

2) migraine with aura

3) history of stroke or ischaemic heart disease

4) history of thromboembolic disease or thrombogenic mutation e.g. Factor V Leiden

5) breastfeeding <6 weeks postpartum

6) uncontrolled HTN

7) active breast cancer

8) major surgery with prolonged immobilisation

9) positive antiphospholipid antibodies (e.g. in SLE)

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24
Q

Most common side effects of sildenafil?

A

1) headache

2) visual disturbances: blue discolouration (The blue pill (viagra) causes blue discolouration of vision)

3) nasal congestion

4) flushing

5) GI side effects

6) priapsim

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25
Q

What is a prolactinoma?

A

Prolactinomas are a type of pituitary adenoma, a benign tumour of the pituitary gland.

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26
Q

Features of a prolactinoma?

A
  • amenorrhoea
  • galactorrhoea
  • infertility
  • osteoporosis
  • loss of libido
  • headache
  • visual changes: bitemporal hemianopia (‘tunnel vision’)
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27
Q

What condition can give a falsely low HbA1c reading?

A

Sickle cell anaemia (and other haemoglobinopathies) due to decreased lifespan of RBCs.

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28
Q

Acute management of cluster headache?

A

High flow O2 and subcutaneous triptan

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29
Q

How should triptans be given in acute cluster headache?

A

SC

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30
Q

What is paroxysmal hemicrania (PH)?

A

Defined by attacks of severe, unilateral headache, usually in the orbital, supraorbital or temporal region.

Features:
- Often associated with autonomic features e.g. tearing, nasal congestion
- Usually last less than 30 minutes and can occur multiple times a day.

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31
Q

What is paroxysmal hemicrania (PH) completely responsive to?

A

indomethacin (NSAID)

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32
Q

Presenation of acute closed angle glaucoma?

A

1) Severe pain: may be ocular or headache

2) decreased visual acuity

3) symptoms worse with mydriasis (e.g. watching TV in a dark room)

4) hard, red-eye

5) haloes around lights

6) semi-dilated non-reacting pupil

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33
Q

What is acute closed angle glaucoma?

A

There is a rise in IOP secondary to an impairment of aqueous outflow.

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34
Q

Who are triptans contraindicated in?

A

Patients with coronary artery disease as they can cause coronary vasospasm.

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35
Q

What are the 3 options for migraine prophylaxis?

A

1) propanolol
2) topiramate
3) amitriptlyine

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36
Q

What is preferred for prophylaxis of migraines in women of childbearing age?

A

Propanolol

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37
Q

Can topiramate be used for the prophylaxis of migraines in women of reproductive age?

Why?

A

No
1) it may be teratogenic
2) it can reduce the effectiveness of hormonal contraceptives

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38
Q

Causes of Horner’s syndrome can be differentiated according to the LOCATION of anhidrosis.

Give some causes of Horner’s with anhidrosis of the face only

A

Caused by pre-ganglionic lesions:

1) Pancoast’s tumours
2) Thyroidectomy
3) Trauma
4) Cervical rib

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39
Q

Give some causes of Horner’s with anhidrosis of the face, arm and leg

A

Caused by central lesions:

1) Stroke
2) MS
3) Tumour
4) Encephalitis
5) Syringomyelia

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40
Q

Give some causes of Horner’s where there is NO anhidrosis

A

Caused by post-ganglionic lesions:

1) Carotid artery dissection
2) Carotid aneurysm
3) Cavernous sinus thrombosis
4) Cluster headache

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41
Q

Presentation of a carotid artery dissection?

A

1) Headache (60-75%): usually severe, unilateral, gradual onset

2) Partial Horner’s syndrome (58%): ptosis & miosis if a haematoma of the artery compresses sympathetic nerve fibres to the eye that run along the carotid sheath

3) Pulsatile tinnitus (27%)

4) Unilateral neck pain (25%)

5) Transient monocular blindness (25%)

6) Cranial nerve palsy (12%): most commonly cranial nerves IX to XII

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42
Q

If there is the present of sweating in Horner’s syndrome, where is the lesion?

A

Post-ganglionic

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43
Q

Give some differentials for facial pain

A

1) Trigeminal neuralgia: Severe lancinating facial pain along one or more branches of the trigeminal nerve.

2) Sinusitis: Facial pain accompanied by symptoms such as nasal discharge or congestion suggests sinusitis.

3) Dental problems: Dental caries or abscesses can cause localised facial pain.

4) Tension type headache: Band-like pressure around the forehead that can extend into facial regions.

5) Migraine: Unilateral throbbing head and face pain associated with nausea, vomiting or photophobia.

6) Giant cell arteritis: In older patients, new onset facial pain may be a sign of this condition, which can threaten vision.

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44
Q

What is chronic cough 2ary to in sinusitis?

A

Post-nasal drip

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45
Q

How is pain of cluster headaches often described?

A

Intense, sharp, stabbing pain around eye

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46
Q

Describe eye in cluster headache

A
  • Redness, lacrimation & lid swelling
  • Miosis and ptosis in a minority
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47
Q

Features of temporal arteritis?

A
  • typically >60y
  • usually rapid onset (e.g. < 1 month)
  • headache (found in 85%)
  • jaw claudication (65%)
  • tender, palpable temporal artery
  • around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)
  • lethargy, depression, low-grade fever, anorexia, night sweats
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48
Q

What condition does temporal arteritis have an overlap with?

A

Polymyalgia rheumatica (50%)

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49
Q

Management of trigeminal neuralgia?

A

High-dose prednisolone as well as urgent referral for assessment by a specialist.

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50
Q

How can smoking affect carboxyhaemoglobin levels?

A

Smokers may normally have carboxyhaemoglobin levels of up to 10% (normal 0.5-2.5)

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51
Q

What is the most common complication following bacterial meningitis?

A

Sensorineural hearing loss

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52
Q

What is benign rolandic epilepsy?

A

a form of childhood epilepsy that typically occurs between the age of 4 and 12 years.

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53
Q

Features of benign rolandic epilepsy?

A

1) seizures characteristically occur at night

2) seizures are typically partial (e.g. paraesthesia affecting the face) but secondary generalisation may occur (i.e. parents may only report tonic-clonic movements)

3) the child is otherwise normal

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54
Q

When do seizures typically occur in benign rolandic epilepsy?

A

At night

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55
Q

What does an EEG characteristically show in benign rolandic epilepsy?

A

Centrotemporal spikes

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56
Q

Prognosis of benign rolandic epilepsy?

A

Excellent - seizures stopping by adolescence

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57
Q

Can cocaine toxicity cause seizures?

A

Yes

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58
Q

CVS effects of cocaine?

A

1) coronary artery spasm –> myocardial ischaemia/infarction

2) both tachycardia and bradycardia may occur

3) hypertension

4) QRS widening and QT prolongation

5) aortic dissection

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59
Q

When should parents call an ambulance in febrile convulsions?

A

Lasting >5 minutes

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60
Q

Person suddenly falls to the ground then lays motionless - what type of seizure?

A

Atonic

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61
Q

What are 2 important causes to rule out in status epilepticus?

A

1) hypoxia
2) hypoglycaemia

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62
Q

When is is juvenile myoclonic epilepsy (Janz syndrome) typically seen?

A

typical onset is in the teenage years, more common in girls

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63
Q

Features of juvenile myoclonic epilepsy?

A

1) infrequent generalized seizures, often in morning//following sleep deprivation

2) daytime absences

3) sudden, shock-like myoclonic seizure (these may develop before seizures)

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64
Q

When are genralised seizures often seen in juvenile myoclonic epilepsy?

A

often in morning//following sleep deprivation

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65
Q

Management of juvenile myoclonic epilepsy?

A

usually good response to sodium valproate

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66
Q

What is Chagas’ disease?

A

caused by the protozoan Trypanosoma cruzi.

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67
Q

What is the most frequent and most severe manifestation of chronic Chagas’ disease?

A

Cardiomyopathy

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68
Q

What is used to prevent seizures in patients with severe pre-eclampsia and treat seizures once they develop?

A

Magnesium sulphate

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69
Q

What do psychogenic non-epileptic seizures tend to mimic?

A

Generalised tonic-clonic seizures and generally last longer.

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70
Q

Patient has episodes of olfactory hallucinations while retaining consciousness throughout - what is most likely diagnosis?

A

Focal aware seizure

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71
Q

The following 2 groups of patients are at an increased risk of developing hepatotoxicity following a paracetamol overdose:

A

1) patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)

2) malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days

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72
Q

Describe effect of alcohol on liver in paracetamol overdose

A

Interestingly, acute alcohol intake, as opposed to chronic alcohol excess, is not associated with an increased risk of developing hepatotoxicity and may actually be protective.

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73
Q

The EEG feature hypsarrhythmia is seen in what condition?

A

West’s syndrome (infantile spasms)

74
Q

Seizures located in the temporal lobe features:

A

1) May occur with or without impairment of consciousness or awareness

2) Aura occurs in most patients:
a) typically a rising epigastric sensation
b) psychic or experiential phenomena, such as déjà vu, jamais vu
c) less commonly hallucinations (auditory/gustatory/olfactory)

3) Seizures typically last around one minute

4) Automatisms (e.g. lip smacking/grabbing/plucking) are common

75
Q

Seizures located in the frontal lobe features:

A

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

76
Q

Seizures located in the parietal lobe features:

A

Paraesthesia

77
Q

Seizures located in the occipital lobe features:

A

Floaters/flashes

78
Q

What methods of contraception are all women taking an enzyme-inducing drug (EID) (e.g. carbamazepine) advised to use?

A

Reliable contraceptive that is unaffected by EIDs:
1) Copper intrauterine device (usually preferred)
2) Progesterone injection (Depo-provera)
3) Mirena intrauterine system

79
Q

A seizure causing post-ictal dysphasia is associated with what lobe?

A

Temporal

80
Q

What type of seizures typically are febrile convulsions?

A

Tonic clonic

81
Q

In a ‘simple’ febrile convulsion, how long is recovery period?

A

<1 hour

If >1 hour - refer to paediatrics

82
Q

How long does a simple febrile convulsion last?

A

<15 minutes

83
Q

How long does a ‘complex’ febrile convulsion last?

A

15-30 mins

84
Q

What type of seizure is a ‘complex’ febrile convulsion?

A

Focal seizure

85
Q

Do regular antipyretics reduce the chance of a febrile seizure occurring?

A

no

86
Q

What is the risk of further febrile convulsion?

A

1 in 3

87
Q

What are risk factors for a further febrile convulsion?

A

a) age of onset < 18 months
b) fever < 39ºC
c) shorter duration of fever before the seizure
d) a family history of febrile convulsions

88
Q

What diet may help in Lennox Gastuaut syndrome (which may be extension of infantile spasms)?

A

Ketogenic diet (if antiepilpetics not effective)

89
Q

What dose of rectal diazepam is given in adult status epilepticus?

A

10-20 mg (max 30mg)

90
Q

A seizure affecting which lobe can cause post-ictal weakness (Todd’s paresis)?

A

Frontal lobe

91
Q

What is UKMEC for COCP and POP for women taking phenytoin, carbamazepine, barbiturates & topiramates?

A

UKMEC 3

92
Q

What is UKMEC for IUD and IUS for women taking phenytoin, carbamazepine, barbiturates & topiramates?

A

UKMEC 1

93
Q

Suitable antiemetics in pregnancy?

A
  • cyclizine
  • metoclopramide
  • prochlorperazine
  • promethazine
  • chlorpromazine
  • domperidone
  • ondansetron
94
Q

What is preferred drug for treatment of hyperthyroidism in pregnancy?

A

Propylthiouracil (less likely to cross the placenta than carbimazole)

95
Q

What are the 2 safest antiepileptics in pregnancy?

A

Lamotrigine & carbamazepine

96
Q

What 2 medications are used in the management of absence seizures?

A

1) ethoxuximide
2) valproic acid

97
Q

Give some factors that would favour a pseudoseizure over a seizure

A

1) pelvic thrusting
2) family member with epilepsy
3) much more common in females
4) crying after seizure
5) don’t occur when alone
6) gradual onset

98
Q

Prolactin level in seizure?

A

Raised

99
Q

What is bupropion?

A

An atypical antidepressant used for smoking cessation.

It is a norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist.

100
Q

Contraindication of burpropion?

A

1) Epilepsy: lowers seizure threshold

2) Pregnancy & breastfeeding

101
Q

What type of seizure does a short, transient episode of olfactory hallucination (e.g. smelling roses when there are none) indicate?

A

Focal (often aware) seizure

102
Q

What is score measures disability or dependence in activities of daily living in stroke patients?

A

Barthal index

103
Q

What score categorises patients into levels of frailty according to their function?

A

Rockwood frailty scale

104
Q

If a patient is on warfarin/a DOAC/ or has a bleeding disorder and they are suspected of having a TIA, what is immediate next step?

A

Admit immediately for CT head to rule out haemorrhage.

105
Q

2ary prevention of ischaemic stroke?

A

1) Clopidogrel
(or aspirin and dipyridamole if clopdiogrel is contraindicated)

2) Statin (if cholesterol is >3.5 mmol/l)

106
Q

What is the preferred imaging modality in patients with suspected TIA?

A

MRI brain with diffusion-weighted imaging

107
Q

What is polycythaemia vera?

A

A rare blood disorder in which there are an increase in all blood cells, particularly RBCs.

108
Q

Complications of polycythaemia vera?

A

Can increase the risk of thrombotic events e.g. MI, stroke

109
Q

Management of polycythemia vera?

A

1) Low dose aspirin - can help to reduce the risk, whilst not increasing the risk of haemorrhage.

2) Venesection (1st line treatment)

3) Chemotherapy

110
Q

How does a pontine haemorrhage present?

A

1) Reduced GCS
2) Quadriplegia
3) Miosis
4) Absent horizontal eye movements

111
Q

What is autonomic dysreflexia?

A

A clinical syndrome that occurs in patients who have had a spinal cord injury at, or above T6 spinal level.

112
Q

What happens in autonomic dysreflexia?

A

1) Briefly, afferent signals, most commonly triggered by faecal impaction or urinary retention (but many other triggers have been reported) cause a sympathetic spinal reflex via thoracolumbar outflow.

2) The usual, centrally mediated, parasympathetic response however is prevented by the cord lesion.

3) The result is an unbalanced physiological response

113
Q

At what spinal level does autonomic dysreflexia occur?

A

At or above T6 spinal level

114
Q

Clinical features of autonomic dysreflexia?

A
  • Extreme HTN
  • Flushing
  • Sweating above the level of the cord lesion
  • Agitation
115
Q

What can autonomic dysreflexia lead to?

A

Complications of extreme HTN e.g. haemorrhagic stroke

116
Q

What is the best assessment tool for differentiating between stroke and stroke mimics?

A

The Recognition of Stroke in the Emergency Room (ROSIER) scale

117
Q

Describe the levels of T4 and TSH in subclinical hyperthyroidism

A

Normal T3/T4

Low TSH

118
Q

What complications is subclinical hyperthyroidism associated with?

A

AF, osteoporosis, dementia

119
Q

After an ischaemic stroke, how long should the patient receive 300mg aspirin daily for?

A

14 days

120
Q

What artery is affected: contralateral homonymous hemianopia with macular sparing and visual agnosia?

A

posterior cerebral artery

121
Q

How is carotid artery stenosis diagnosed?

A

Duplex US

122
Q

Give some examples of dopamine receptor agonists

A
  • Bromocriptine
  • Ropinirole
  • Cabergoline
  • Apomorphine
123
Q

What type of dopamine receptor agonists are most associated with pulmonary, retroperitoneal & cardiac fibrosis?

A

ergot-derived dopamine receptor agonists (bromocriptine, cabergoline)

124
Q

what are the ergot-derived receptor agonists?

A

Bromocriptine & cabergoline

125
Q

What is a feature of Parkinson’s disease that is a result of autonomic dysfunction?

A

Postural hypotension (no compensatory tachycardia)

126
Q

Onset of motor symptoms in LBD vs Parkinson’s disease?

A

LBD: dementia starts before or within 1 year of the onset of the parkinsonian symptoms

PD: more likely if dementia occurs around 4-5 years after motor symptoms (or at very least 1 year after)

127
Q

Is Cabergoline or Ropinirole more associated with pulmonary fibrosis (dopamine agonists)?

A

Cabergoline - as is an ergot-dervied dopamine receptor agonist

128
Q

What type of dementia is MND most associated with?

A

Frontotemporal dementia

129
Q

What 2 types of dementia is Parkinson’s disease associated with?

A

1) parkinson’s dementia
2) LBD

130
Q

What triad of symptoms is seen in normal pressure hydrocephalus?

A

1) urinary incontinence

2) gait abnormality (may be similiar to Parkinson’s)

3) dementia

131
Q

What are the 4 causes of postural hypotension with compensatory tachycardia? (4 D’s)

A

Deconditioning

Dysfunctional heart: aortic stenosis

Dehydration

Drugs: anti-anginals, anti-parkinsonian medications (levodopa), antidepressants, antipsychotics, anti–benign prostatic hyperplasia drugs (tamsulosin).

132
Q

What are the features of multiple system atrophy?

A

1) parkinsonism

2) autonomic disturbance:
- erectile dysfunction (often an early feature)
- postural hypotension
- atonic bladder

3) cerebellar signs

133
Q

What feature can help distinguish between idiopathic PD and drug indiced Parkinsonism?

A

Idiopathic PD –> asymmetrical tremor

Drug induced –> symmetrical tremor

134
Q

Cause of bilateral vs unilateral foot drop?

A

Bilateral –> peripheral neuroapthy

Unilateral –> common peroneal nerve lesion

135
Q

What gait feature does foot drop cause?

A

High stepping gate (to compensate for foot drop)

136
Q

What can acute withdrawal of levodopa precipitate?

A

Neuroleptic malignant syndrome

137
Q

What are the features of progressive supranuclear palsy?

A

1) postural instability & falls

2) impairment of vertical gaze (e.g. descending stairs, reading)

3) parkinsonism (bradykinesia is prominent)

4) front lobe dysfunction

138
Q

Does progressive supranuclear palsy respond to levadopa?

A

No

139
Q

What class of drug is metoclopramide?

A

D2 receptor antagonist

140
Q

Main indication of metoclopramide?

A

Antiemetic

Others:
- GORD
- Prokinetic action useful in gastroparesis secondary to diabetic neuropathy

141
Q

Adverse effects of metoclopramide?

A

1) EPSEs:
- acute dystonia e.g. oculogyric crisis

2) diarrhoea

3) hyperprolactinaemia

4) tardive dyskinesia

5) parkinsonism

142
Q

Does domperidone exacerbate Parkinson’s symptoms?

A

No - does not cross BBB

143
Q

What is preferred antiemetic in Parkinson’s disease?

A

Domperidone

144
Q

Is diplopia common in Parkinson’s disease?

A

No - suggest alternative diagnosis

145
Q

Is autonomic instability an early or late symptom in Parkinson’s disease?

A

Late

146
Q

What is Uhthoff ’s phenomenon?

A

Where neurological symptoms are exacerbated by increases in body temperature is typically associated with multiple sclerosis.

Often affecting the eyes of multiple sclerosis (MS) patients.

Patients commonly report symptoms following exercise or hot showers/baths, which last for under 24 hours.

147
Q

Is MRI with or without contrast best to view demyelinating lesions in MS?

A

With contrast

148
Q

What drug has the strongest evidence base for reducing relapse in multiple sclerosis?

A

Monoclonal antibodies such as natalizumab

149
Q

Proximal muscle weakness + raised CK + no rash?

A

Polymyositis

150
Q

What is the most common presentation of neonatal sepsis?

A

Grunting and other signs of respiratory distress

151
Q

Where do seizures in benign rolandic epilepsy typically occur?

A

At night

152
Q

Describe seizures typically seen in benign rolandic epilepsy

A

seizures are typically partial (e.g. paraesthesia affecting the face) but secondary generalisation may occur (i.e. parents may only report tonic-clonic movements)

153
Q

What is the anterior circulation in the brain responsible for supypling?

A

1) cerebrum

2) opthalmic artery

154
Q

At what level to the R and L common carotid arteries bifurcate?

What do they bifurcate to give off?

A

Bifurcate at C3/C4 to give off the internal carotid arteries (ICA) within the carotid sheath.

155
Q

How do the internal carotid arteries enter the cranial cavity?

A

They proceed through the respective carotid canal, within the petrous portion of the temporal bone.

156
Q

Once in the cranial cavity, where do the internal carotid arteries pass?

A

They pass anteriorly through the cavernous sinus.

157
Q

Once the internal carotid arteries are distal to the cavernous sinus, what branches does each give rise to?

A

1) Ophthalmic artery

2) Posterior communicating artery

3) Anterior cerebral artery

The internal carotid arteries then continue as the middle cerebral arteries.

158
Q

What does the ophthalmic artery supply?

A

It supplies all the structures in the orbit and some in the nose, face and meninges.

159
Q

What does the posterior communicating artery communicate with anteriorly and posteriorly?

A

Anteriorly: Connects to the internal carotid artery before the terminal bifurcation of the ICA into the anterior cerebral artery and middle cerebral artery.

Posteriorly: Communicates with the posterior cerebral artery.

160
Q

What do the middle cererbral arteries supply?

A

The lateral cerebral cortex, anterior temporal lobes and the insular cortices.

161
Q

What 3 areas is the posterior circulation in the brain responsible for supplying?

A

1) occipital lobes
2) cerebellum
3) brainstem

162
Q

What do the vertebral arteries arise from?

A

Subclavian arteries

163
Q

How do the vertebral arteries enter the spine and then the cranial vault?

A

They enter the transverse foramina of the spine at level C6 and continue superiorly.

After passing through the transverse foramen of C1, the arteries traverse the foramen magnum.

164
Q

Once inside the cranial vault, what branches doe the vertebral arteries give off?

A

1) Posterior inferior cerebellar artery (PICA)

2) Anterior and posterior meningeal arteries

3) Anterior and posterior spinal arteries

165
Q

What is the largest branch of the vertebral artery?

A

PICA: this is one of the main arteries supplying the cerebellum.

166
Q

What do the anterior and posterior meningeal arteries supply?

A

The dura mater

167
Q

What do the anterior and posterior spinal arteries supply?

A

They supply the spinal cord along its entire length

168
Q

What do the vertebral arteries converge to form?

A

The basilar artery at the base of the pons

169
Q

Where does the basilar artery run?

A

It runs superiorly within the central groove of the pons.

170
Q

What branches does the basilar artery give off?

A

Pontine arteries

171
Q

What do the pontine arteries supply?

A

The pons

172
Q

What does the basilar artery eventually anastomose with?

A

The circle of Willis via the posterior cerebral arteries and posterior communicating arteries.

173
Q

What infarcts can cause locked in syndrome?

A

Pontine infarcts

174
Q

What is locked in syndrome?

A

Pontine infarcts cause an interruption in the myriad of neuronal pathways enabling communication between the cerebrum, cerebellum and spinal cord.

This can result in complete paralysis of all voluntary muscle groups, sparing those controlling the eyes.

Individuals suffering from damage to the pons are fully conscious and cognitively intact.

175
Q

What is the circle of Willis formed by?

A

The terminal branches of the anterior and posterior circulation form an anastomosis to create a ring-like vascular structure known as the circle of Willis, within the base of the cranium.

This is formed by:

1) Internal carotid arteries continue as the MCA after each giving off a branch to supply the anterior cerebral arteries (ACA).

2) The anterior communicating artery links the two anterior cerebral arteries together

3) The internal carotid arteries also give off the posterior communicating arteries (PCoA) –> this links the MCA with the posterior cerebral artery

176
Q

What links the 2 anterior cerebral arteries together?

A

Anterior communicating artery

177
Q

What does the posterior communicating artery link?

A

The posterior cerebral artery with the middle cererbal artery.

178
Q

Where do saccular or ‘berry‘, aneurysms occur most frequently?

A

Within the circle of Willis

179
Q

What is the most common cause of non-traumatic SAH?

A

Saccular/berry aneurysms the most com

180
Q

Management of saccular/berry aneurysms?

A

Treatment involves urgent neurosurgical referral and subsequent endovascular coiling or inserting a surgical clip to occlude flow to an aneurysm.

181
Q

What nerve is commonly affected by aneurysms in the circle of Willis (particularly those involving the posterior communicating artery due to its close anatomical relationship)?

A

The 3rd cranial nerve (oculomotor nerve).

182
Q

How can a ‘surgical’ 3rd nerve palsy be differentiated from a ‘medical’ 3rd nerve palsy?

A

If there is pupillary involvement.

183
Q

Pupillary involvement in medical vs surgical 3rd nerve palsy?

A

Surgical:
- external compression of the 3rd nerve affects parasympathetic fibres surrounding the outermost region of the third nerve
- this compression results in an inability to constrict the pupil: fixed and dilated (‘blown pupil’)

Medical:
- results from involvement of the vaso vasorum, which is involved in supplying the central area of the third cranial nerve
- pupillary involvement arises much later

184
Q

Give 2 common causes of medical 3rd nerve palsy

A

Conditions affecting microvasculature, such as diabetes and atherosclerosis:
1) diabetes
2) atherosclerosis

185
Q
A

Yr 4 - CCC (54 decks)

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