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
What is the mechanism of lacunar infarct in HTN?
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
What are the symptoms of hypertensive encephalopathy?
- Headaches - Vomiting - Confusion - Seizure
27
What types of intracranial haemorrhages are considered primary hypertensive bleeds?
Intraparenchymal Subarachnoid
28
Other than HTN, what other factors can contribute to spontaneous intraparenchymal haemorrhage?
Coagulopathy Neoplasm Vasculitis Aneurysm Vascular malformations
29
What are the different routes of CNS infection?
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
What is meningitis? How is it classified?
Inflammation of the leptomeninges and CSF within subarachnoid space. Acute pyogenic (bacterial) Aseptic (viral) Chronic (TB, cryptococcus)
31
What are causative organisms in acute pyogenic meningitis in neonates?
E. coli Group B strep S. aureus
32
What are causative organisms in acute pyogenic meningitis in infants?
Haemophilus influenzae Strep pneumoniae
33
What are causative organisms in acute pyogenic meningitis in adolescents?
N. meningitidis
34
What are causative organisms in acute pyogenic meningitis in elderly?
Strep pneumoniae Listeria monocytogenes
35
What are the characteristic CSF findings of bacterial meningitis?
High neutrophil count High protein count Low glucose
36
What are common causative organisms in aseptic meningitis? What about encephalitis?
Meningitis = Enterovirus, measles, influenzae Encephalitis = HSV 1 and 2, CMV, HIV
37
What is the CSF characteristics of viral meningitis?
elevated lymphocytes moderate protein normal glucose
38
What is the most common CNS tumour < 15 years?
Astrocytoma < 15 more commonly infratentorial > 15 = 80 % supratentorial tumours
39
What is the clinical triad of Parkinson's disease?
Bradykinesia Rigidity Tremor
40
What is the pathogenesis of Parkinson's disease?
Loss of dopaminergic neurons in substantial Nigra = functional decrease in dopamine content
41
What other neurocognitive/autonomic symptoms accompany Parkinson's disease?
Autonomic: postural hypotension, urinary and faecal incontinence Cognitive: dementia, hallucinations
42
What is Guillain-Barre Syndrome?
Disease of PNS, characterised by ascending neuropathy
43
What is the pathogenesis of Guillian Barre?
Acute onset immune mediated de-myelinating neuropathy - Type II hypersensitivity reaction. Usually after recovering from an acute, influenza like illness
44
What are organisms are implicated in Guillian barre?
Campylobacter CMV EBV Mycoplasma pneumoniae
45
What is the clinical presentation of Gillian barre?
Ascending paralysis Loss of deep tendon reflexes CSF: high protein, low pleocytosis/cell count
46
What is Wernicke's syndrome?
Alcohol induced amnesic disorder characterised by lack of Thiamine (B1) resulting in necrotic lesions in thalamus, brainstem
47
What is the triad of Wernicke's syndrome?
1. Nystagmus 2. Ataxia 3. Confusion **Acute and reversible process
48
What is Korsakoff's?
chronic, only partially reversible disease of EtOH with anterograde amnesia, confabulation, persisting beyond intoxication and withdrawal.