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ED Primary Exam > Week 7 - CNS Pathology > Flashcards

Week 7 - CNS Pathology Flashcards

1
Q

In relation to the dura, where do dural arteries run?

A

Above the dura mater

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2
Q

What are the major differences between extradural and subdural haemorrhage?

A

Subdural = bridging veins between arachnoid and dura mater, drain into venous sinuses. Bleeds from tears in subdural space. Dura intact.

Extradural = dural arteries (i.e. middle meningeal artery) torn by traumatic fracture –> blood under arterial pressure and causing dura to separate from periosteum of skull

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3
Q

What are the 3 different mechanisms of stroke?

A

1) Thrombosis
2) Embolism
3) Haemorrhage

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4
Q

What % of CO and O2 consumption is the brain responsible for?

A

15% CO
20% O2 consumption

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5
Q

What are different ways in which hypoxia of brain tissue can occur?

A

Decreased partial pressure of O2
Reduced O2 carrying capacity of blood
Inhibition of O2 utilisation in tissue
Ischaemia

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6
Q

How does ischaemia lead to injury in CNS?

A

Reduction in ATP can lead to inappropriate release of excitatory amino acids (glutamate) and cell damage via excessive Ca2+ influx into cells (free radical generation and mitochondrial injury)

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7
Q

What is penumbra?

A

At risk tissue surrounding core necrotic area, which can undergo recovery with restoration of blood flow, or may progress to apoptosis if injury too severe/non reversible

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8
Q

Where does watershed ischaemic impact the brain?

A

Most distal aspects of arterial supply - in cerebral hemispheres this is between anterior and middle cerebral artery distributions

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9
Q

What pathological process is responsible for the majority of thrombosis related stroke?

A

Atherosclerosis

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10
Q

What are the most common sites of primary thrombosis in CNS?

A

Carotid bifurcation
Origin of MCA
Either end of basilar artery

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11
Q

What distribution do EMBOLIC phenomena usually affect?

A

MCA

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12
Q

What is the clinical presentation of MCA stroke?

A

Contralateral weakness and sensory loss of face and arms
IF left hemisphere, dysphasia, motor aphasia, receptive aphasia
IF right hemisphere, heme-neglect

**Eye deviation towards side of lesion and away from weak side

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13
Q

What is clinical presentation of ACA stroke?

A

Contralateral leg paresis and sensory loss

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14
Q

What is clinical presentation of PCA stroke?

A

Contralateral hemianopia or quadrantanopia
CN III and IV palsy

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15
Q

What are neurological symptoms suggestive of anterior circulation occlusion/TIA?

A

Amaurosis fugax
Aphasia
Hemiparesis
Hemisensory loss
Hemianopia visual loss

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16
Q

What are neurological symptoms associated with posterior circulation occlusion/TIA?

A

Diplopia
Vertigo
Vomiting
Choking/dysarthria
Ataxia
Transient global amnesia

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17
Q

What is subfalcine herniation? What symptoms can it cause?

A

Below falx cerebri —> causes herniation of singular gyrus below the fall and compresses anterior cerebral artery

Can cause gait/motor disturbance

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18
Q

What is uncle herniation and what symptoms does it cause?

A

Uncus = part of temporal lobe

Herniation is uncut through tentorium cerebelli

Can cause compression of oculomotor nerve, and post ganglionic parasympathetic fibres –> causing ‘down and out’ appearance of eye due to compression of sympathetic supply to the eye –> mydriasis

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19
Q

What is tonsillar herniation? What does this cause?

A

Cerebellar tonsils herniate through foramen magnum (coning)

Cardiorespiratory centres compressed –> arrest

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20
Q

What is the most common subtype of aneurysm?

A

Berry/Saccular

21
Q

Where are aneurysms most commonly found?

A

Major arterial branch points of anterior circulation (i.e. junction of anterior cerebral artery and anterior communicating artery

22
Q

Are aneurysms congenital?

A

No - but can be genetically predisposed or have environmental risk factors

  • Genetic: PCKD, Ehler’s Danlos, Marfans, NF
  • Environmental: HTN, Smoking
23
Q

What space do aneurysms bleed into when ruptured?

A

Subarachnoid space

24
Q

What are the acute CNS pathologies linked to acute hypertension?

A
  1. Lacunar infarct
  2. Slit haemorrhage
  3. Hypertensive encephalopathy
  4. Intracranial haemorrhage
25
Q

What is the mechanism of lacunar infarct in HTN?

A

Deep penetrating arteries to the basal ganglia can develop arteriolar stenosis and become occluded, leading to small cavity infarcts/lacunae. Occur in thalamus, internal capsule, caudate nucleus and pons.

26
Q

What are the symptoms of hypertensive encephalopathy?

A
  • Headaches
  • Vomiting
  • Confusion
  • Seizure
27
Q

What types of intracranial haemorrhages are considered primary hypertensive bleeds?

A

Intraparenchymal
Subarachnoid

28
Q

Other than HTN, what other factors can contribute to spontaneous intraparenchymal haemorrhage?

A

Coagulopathy
Neoplasm
Vasculitis
Aneurysm
Vascular malformations

29
Q

What are the different routes of CNS infection?

A

1) Haematogenous spread
2) Direct implantation (trauma, surgery)
3) Local extension (sinuses, nasal cavity, teeth, cranial OM)
4) Transport along peripheral nervous system (rabies, VZV)

30
Q

What is meningitis? How is it classified?

A

Inflammation of the leptomeninges and CSF within subarachnoid space.

Acute pyogenic (bacterial)
Aseptic (viral)
Chronic (TB, cryptococcus)

31
Q

What are causative organisms in acute pyogenic meningitis in neonates?

A

E. coli
Group B strep
S. aureus

32
Q

What are causative organisms in acute pyogenic meningitis in infants?

A

Haemophilus influenzae
Strep pneumoniae

33
Q

What are causative organisms in acute pyogenic meningitis in adolescents?

A

N. meningitidis

34
Q

What are causative organisms in acute pyogenic meningitis in elderly?

A

Strep pneumoniae
Listeria monocytogenes

35
Q

What are the characteristic CSF findings of bacterial meningitis?

A

High neutrophil count
High protein count
Low glucose

36
Q

What are common causative organisms in aseptic meningitis?

What about encephalitis?

A

Meningitis = Enterovirus, measles, influenzae

Encephalitis = HSV 1 and 2, CMV, HIV

37
Q

What is the CSF characteristics of viral meningitis?

A

elevated lymphocytes
moderate protein
normal glucose

38
Q

What is the most common CNS tumour < 15 years?

A

Astrocytoma

< 15 more commonly infratentorial
> 15 = 80 % supratentorial tumours

39
Q

What is the clinical triad of Parkinson’s disease?

A

Bradykinesia
Rigidity
Tremor

40
Q

What is the pathogenesis of Parkinson’s disease?

A

Loss of dopaminergic neurons in substantial Nigra = functional decrease in dopamine content

41
Q

What other neurocognitive/autonomic symptoms accompany Parkinson’s disease?

A

Autonomic: postural hypotension, urinary and faecal incontinence

Cognitive: dementia, hallucinations

42
Q

What is Guillain-Barre Syndrome?

A

Disease of PNS, characterised by ascending neuropathy

43
Q

What is the pathogenesis of Guillian Barre?

A

Acute onset immune mediated de-myelinating neuropathy - Type II hypersensitivity reaction.

Usually after recovering from an acute, influenza like illness

44
Q

What are organisms are implicated in Guillian barre?

A

Campylobacter
CMV
EBV
Mycoplasma pneumoniae

45
Q

What is the clinical presentation of Gillian barre?

A

Ascending paralysis
Loss of deep tendon reflexes
CSF: high protein, low pleocytosis/cell count

46
Q

What is Wernicke’s syndrome?

A

Alcohol induced amnesic disorder characterised by lack of Thiamine (B1) resulting in necrotic lesions in thalamus, brainstem

47
Q

What is the triad of Wernicke’s syndrome?

A
  1. Nystagmus
  2. Ataxia
  3. Confusion

**Acute and reversible process

48
Q

What is Korsakoff’s?

A

chronic, only partially reversible disease of EtOH with anterograde amnesia, confabulation, persisting beyond intoxication and withdrawal.

ED Primary Exam (46 decks)

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