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NEURO > 8.3 brain Pathology > Flashcards

8.3 brain Pathology Flashcards

1
Q

3 ways microorganisms can gain entry into CNS?

A
  • DIRECT spread : middle ear, basilar skull fracture
  • BLOOD-borne : sepsis, infective endocarditis
  • IATROGENIC : ventriculoperitoneal shunt, post neurosurgery , lumbar puncture
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2
Q

What is meningitis

A

Inflammation of the leptomeninges ( pia and arachnoid)

+/- septicaemia

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3
Q

What is the non-blanching rash a sign of ?

A

Meningococcal septicaemia

NOT meningitis itself

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4
Q

Causative organism of meningitis in

  • neonates
  • 2-5yrs
  • 5-30yrs
  • > 30yrs
A
  • E.coli, L.monocytogenes
  • h.infleunza type b
  • n.meningitidis
  • S.penumoniae
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5
Q

Causes of chronic meningitis and features

A
  • M.tuberculosis
  • granulomatous inflammation
  • fibrosis of meninges
  • cranial nerve entrapment
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6
Q

What is a complication of chronic meningitis and name of syndrome

A

Bilateral adrenal haemmorhage

Waterhouse Friederichsen syndrome

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7
Q

5 local complications of meningitis

A
  • Death due to raised ICP from swelling
  • cerebral infarction (stroke) can -> neuro deficit
  • cerebral abscess
  • subdural empyema (= collection of pus in subdural space )
  • epilepsy ( due to direct irritation of brain )
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8
Q

Systemic complication of meningitis are caused by ?

A

Result from septicaemia

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9
Q

What is Encephalitis

A

Inflammation of the brain parenchyma

not the meninges - but Can occur as a complication of meningitis

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10
Q

What is the usual cause of encephalitis

A

Usually VIRAL rather than bacterial

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11
Q

What is a typical feature of encephalitis

A

Viruses kill neurones
Causing inflammation and
Presence of INTRACELLULAR VIRAL INCLUSIONS.

LYMPHOCYTIC INFILTRATE typical.

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12
Q

3 typical organisms affecting the temporal lobe, spinal cord, and brainstem to cause encephalitis

A

Temporal lobe - herpes viruses (most common )

Brainstem - rabies ( v rare )

Spinal cord - polio ( now eradicated !)

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13
Q

What is the pathophysiology of Prion Diseases

A

Prion protein (PrP) transforms into PrPsc
- PrPsc causes damage by forming aggregates, which destroys neurones & causes the brain to take on a spongiform appearance
causes holes in grey matter

Microscopy pic

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14
Q

What is PrPsc

How does PrP transform into it

A

Abnormal form of the prion protein

  • sporadic mutation
  • familial inheritance of mutated gene
  • ingestion of PrPsc
  • protein-protein interactions between PrPsc and normal form
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15
Q

Why is PrPsc able to survive

A
  • ecteely stable as it is resistant to disinfectants and irradiation
  • is not susceptible to immune attack as it is essentially a self - antigen
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16
Q

4 examples of spongiform encephalopathies

A 
o  Scrapie in sheep 
o  BSE in cows (‘mad cow’ disease) 
o  Kuru in New Guinean tribes (due to cannibalism and ingestion of PrPsc) 
o  Creutzfeld Jacob disease (CJD)
   - Variant CJD (vCJD)
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17
Q

Difference between CJD and vCJD

A

Table in notes

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18
Q

Define Dementia

A

Acquired , global impairment Of intellect, reason and personality without impairment of consciousness

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19
Q

Most common type of dementia

A

Alzheimer’s disease 50% cases )

Then vascular dementia (20%)

Dementia with lewy bodies
Pick’s disease

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20
Q

Pahtophysiology in Alzheimer’s disease

A

Exaggerated aging process , due to
- loss of cortical neurones
= less brain weight, cortical atrophy

  • increased neuronal damage
    Due to : - neurofibrillary tangles
    - senile plaques
21
Q

What are neurofibrillary tangles

A

Intracellular twisted filaments of Tau proteins
(Normally bind to microtubules )
Thought to be caused by Tau protein hyperphosphorylation

22
Q

What are senile plaques

A

Foci of enlarged axons, synaptic terminals and dendrites

amyloid deposition in centre of plaques associated with vessel s

23
Q

What is central to the pathogenesis of Alzheimer’s disease ?

Name one condition that is therefore associated with early onset AD

A

Amyloid deposition

  • Down’s syndrome
    Trisomy 21
    Mutation of 3 genes on chromosome 21 - APP gene and PS Genoese 1 & 2
    Leads to amyloid deposition
24
Q

What is normal intracranial pressure

A

0-10mmHg

Coughing and straining can increase it to 20, but only significant if continued for several mins

25
What are 3 compensatory mechanisms for raised ICP
- reduce blood volume - reduce CSF volume - brain atrophy ( is chronically elevated )
26
Cerebral blood flow can be maintained as long as ICP is less than
60 mmHg
27
What 3 things can space occupying lesions result in
- damage or destroys surrounding brain - displace midline structures - Brain herniation ! = part of brain protrudes through wall that normally contains it
28
What Happens in a subfalcine herniation
Cingulate gyrus is pushed under the free edge of falx cerebri
29
How can subfalcine herniation - herniated brain become ischaemic ?
Compression of the ACA | normally loops up around corpus callosum and can ge toicnhed
30
What happens in a tentorial herniation
Medial temporal lobe (usually uncus) is pushed down through tentorial notch
31
What 2 things can can a tentorial herniation compress and therefor cause
ipsilateral oculomotor nerve - ipsilateral CNIII palsy ipsilateral cerebral peduncle - contralateral UMN signs in limbs
32
What can tentorial herniation be complicated by
Secondary brainstem haemorrhage (Duret haemorrhage ) | Often fatal
33
.
Tentorial herniation is usually the mode of death for those with large brain tumours or severe intracranial haemorrhages
34
What happens in a tonsilar herniation and what does it compress
Cerebellar tonsils are pushed through the Foramen magnum | Compresses brainstem
35
Name of benign tumour of meningeal origin
Meningioma
36
``` Malignant tumour originating in astrocytes Features - name if high grade - how is it direct spread - how can it spread distantly CNS ```
Astrocytoma - low grade, slow growing , but difficult to remove - high grade = glioblastoma multiforme Direct spread along white matter pathways Can spread to distant parts of CNS via CSF
37
Where does neurofibroma originate
Schwann cells of peripheral or cranial nerves
38
Ependymoma origin
Ependymal cells lining ventricular system
39
Neuronal tumour
From neurones | V rare
40
2 types of cancers from non-CNS tissues
- lymphoma | - metastases - most common of all Brain tumours
41
What is a stroke
Sudden event Producing disturbance of CNS function Due to VASCULAR event
42
4 risk factors for stroke
- hypertension - hyperlipidaemia - smoking - diabetes
43
Pathogenesis of stroke
``` - most commonly EMBOLISM Sources include - heart (due to AF, mural thrombus) - atheromatous debris (carotid atheroma) - thrombus over ruptured atheromatous plaque - aneurysms ``` - Thrombosis - over atheromatous plaque
44
What are the 2 broad categories of stroke
- Cerebral infarction (85%cases) - regional : in territory of named cerebral artery - lacunar - cerebral haemorrhage (15%) Usually spontaneous
45
What is a lacunar cerebral infarction
Small Less than 1cm area affected Associated with hypertension Commonly affects basal ganglia and internal capsule
46
Features of intracerebral haemorrhage
Associated with - increasing age, hypertensive vessel damage, amyloid deposition in vessels Charcot-Bouchard aneurysms are seen Produces SOL
47
How is SAH usually caused
Rupture of berry aneurysms, usually found at points in circle of Willis Blood in subarachnoid space can cause secondary spasms of cerebral arteries Associations - Male , hypertension, atherosclerosis , other disease e,g, connective tissue disorders
48
How does. SAH present
- THUNDERCLAP headache - sudden , severe - May be preceded by a sentinel headache - LOC - often fatal

NEURO (2 decks)

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