Neuropathology Flashcards

1
Q

How do microorganisms gain entry into the CNS?

A

Direct spread

  • Middle ear infection
  • Base of skull fracture

Blood-borne

  • Sepsis
  • Infective endocarditis

Latrogenic

  • V-P shunt
  • Surgery
  • Lumbar puncture
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2
Q

What is meningitis?

A

Inflammation of the leptomeninges (the inner two meninges)

Variously classified:

  • Acute vs chronic
  • Bacterial vs non-bacterial

With or without septicaemia

Prompt diagnosis and treatment is life saving

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3
Q

What are the causative organisms of meningitis?

A

Different depending on age

Neonates:

  • E. Coli
  • L. monocytogenes

2-5 years
- H. influenzae type B (HiB)

5-30 years
- N. Meningitides (types)

Over 30 years
- S. pneumonia

Varies in immunocompromised

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4
Q

Tell me what happens in chronic meningitis.

A

Chronic clinical course

M. tuberculosis

  • Granulomatous inflammation
  • Fibrosis of meninges
  • Nerve entrapment
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5
Q

What are the complications of meningitis?

A
Local:
Death (swelling>RICP)
Cerebral infarction > neurological deficit
Cerebral abscess
Subdural empyema
Epilepsy

Systemic (if associated with septicaemia)

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6
Q

What is encephalitis?

A

Classically viral not bacterial

Infection of parenchyma not meninges

Neuronal cell death by virus
- Inclusion bodies

Temporal lobe
- Herpes virus

Spinal cord motor neurons
- Polio

Brain stem
- Rabies

Lymphocytic inflammatory reaction
- Perivascular cuffing with lymphocytes

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7
Q

What are prions?

A

They are prion proteins (PrP), a normal constituent of synapse

But they can be mutated
These then interact with normal PrP to undergo a post translational conformational change

These proteins then form extremely stable aggregates

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8
Q

What is prion disease?

A

PrP aggregates > neuronal death and “holes” in grey matter

Results in:
Spongiform encephalopathy's:
- Scrapie in sheep
- BSE in cows
- Kuru in tribes of New Guinea
- Varient Creutzfeld-Jacob disease
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9
Q

What is dementia?

A

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

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10
Q

What happens in Alzheimer’s Disease?

A

Exaggerated aging process

Loss of cortical neurones

  • \/ brain weight
  • Cortical atrophy

Due to /\ neuronal damage:

  • Neurofibrillary
  • Senile plaques
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11
Q

What are neurofibrillary tangles?

A

Intracellular twisted filaments of Tau protein
Tau normally binds and stabilises microtubules
Tau becomes hyperphosphorylated in AD
Tauopathy

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12
Q

What are senile plaques?

A

Foci of enlarged axons, synaptic terminals and dendrites

Amyloid deposition in vessels in centre of plaque

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13
Q

What different types of brain herniation’s are there?

A

Subfalcine

Tentorial

Tonsilar

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14
Q

What is a subfalcine herniation?

A

Same side as mass

Cingulate gyrus pushed under the free edge of the falx cerebri

Ischaemia of medial parts of the frontal and parietal lobe and corpus callosum due to compression of anterior cerebral artery > infarction

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15
Q

What is a tentorial herniation?

A

Uncus/medial part of parahippocampal gyrus through the tentorial notch

  • Damage to the occulomotor nerve on the same side
  • Occlusion of blood flow in posterior cerebral and superior cerebellar arteries

Frequently fatal because of secondary haemorrhage into the brainstem > Duret haemorrhage

Common mode of death in those with large brain tumours and intracranial haemorrhage

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16
Q

What is a cerebella herniation?

A

Cerebellar tonsils pushed into the foramen magnum compressing the brainstem

17
Q

What are the clinical consequences of RICP and herniation?

A

Prodromal phase

  • Headache
  • Vomiting
  • Papilloedema

Acute phase

  • Occulomotor nerve compression = dilation of pupil
  • Compression of the brain stem = coma

Compression of the cerebral peduncles
- Hemiparesis

Further herniation produces apnoea and cardiac arrest due to compression of vital brainstem structures

18
Q

Tell me a little about tumours of the CNS.

A

RARE!!!!!!!!!!!

Benign
- Meningeal origin > meningioma

Malignant

  • Astrocyte origin > astrocytoma
  • Spread along nerve tracts and through sub arachnoid space often presents with a spinal secondary

Others

  • Neurofibroma
  • Ependymoma
  • Neuronal e.g. medulloblastoma

Tumours from non-CNS tissues

  • Lymphoma
  • Metastasis (the most common)
19
Q

What are the two phases of head injury?

A

Primary damage

  • Due to force causing the injury
  • Secondary damage
  • Reaction to the primary damage itself worsening the injury
20
Q

What are the two categories of primary damage of head trauma?

A

Focal damage

  • Bruising and laceration of the brain as it hits the inner surface of the skull
  • Tearing of blood vessels and nerves as the brain moves > haemorrhage

Diffuse

  • Direct tearing to axons
  • Diffuse axonal injury (DAI)
21
Q

Tell me about diffuse axonal injury.

A

Micro-tears to axons at sites of differing densities of brain substance
- e.g. junction of white and grey matter
Tearing of nerves and small vessels
Tearing of the pituitary stalk
Severity proportional to the degree of force (especially rotational), often persistent vegetative state
Heals by gliotic scarring

22
Q

What is a subdural haemotoma?

A

Bridging veins from surface of cerebral hemispheres connect with vessels in the dura
Vessels susceptible to tearing as they pass through the subdural space
Brain floats freely within CSF but vessels are fixed
Sudden brain movement will tear the bridging veins
Elderly and alcohol-related