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Pathology > Trauma, Demyelination + Neurodegenerative Disease > Flashcards

Trauma, Demyelination + Neurodegenerative Disease Flashcards

1
Q

How can head injury mechanisms be divided?

A

Primary events

  • neural
  • vascular

Secondary events

  • ischaemia
  • raised ICP
  • infection
  • post-traumatic epilepsy
  • chronic traumatic encephalopathy
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2
Q

What are the different types of neural damage associated with trauma?

A

Contusional damage

Traumatic axonal injury

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3
Q

What causes contusional damage and what are the consequences?

A

Causes: (leads to swelling around brain)

  • burst lobe due to parenchymal breath through
  • intracerebral haemorrhage

Consequences:

  • Focal symptoms= specific to site of injury
  • Contre-coup injury i.e. injury to opposite side to origin of trauma
  • post traumatic epilepsy
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4
Q

What is a TAI and what causes it? What are the clinical and histological consequences of TAI?

A

Traumatic axonal injury occurs when injury causes stretching and damage to axons

Cause:
-high velocity acceleration and deceleration with torsion

Clinical consequences:
- post-traumatic PSV

Histological

  • Axonal bulbs form w/i 24hrs i.e. appears very eosinophilic
  • beta-APP i.e. released from damaged axons w/i 2-3 hrs
  • Petechiae in WM tracts in corpus callosum and brainstem
  • Gliding contusions= haemorrhage in parasagittal WM
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5
Q

What type of brain injury is a diffuse axonal injury? What is the prognosis?

A

Traumatic axonal injury

Not compatible with life

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6
Q

What are the 3 different causes of traumatic vascular damage?

A

Diffuse vascular damage= Petechial haemorrhages

Damage to arteries (neck or intracranial)

Intracranial haemorrhage

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7
Q

What are the 4 types of traumatic intracranial haemorrhage? Which vessels are they associated with?

A

Extradural

  • arterial
  • lucid interval present

Subdural

  • acute =damage to underlying brain or bridging veins
  • chronic= bridging veins

Subarachnoid
-damage to vertebral arteries
-shearing of intracranial arteries
NOTE: associated with thunderclap headache

Intracerebral:
-delayed intracranial haemorrhage often due to contusions

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8
Q

What is the role of protein misfolding in neurodegenerative disease? Why do inert fibrils form?

A
  • Intra or extracellular insoluble fibrils form inclusions
  • Incorrect polypeptide folding leads to loss of tertiary structure which means that the protein will be resistant to catalytic enzyme which means these proteins are inert
  • prefibrillar intermediate forms also form which cause toxicity associated with Huntington’s
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9
Q

Why does protein misfolding occur?

A

Endoplasmic reticulum dysfunction which can occur due to ER stress

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10
Q

What are the common causes of dementia?

A

Neurodegenerative disease (Alzheimer’s disease) i.e. neurone is primary factor

Vascular disease i.e atheroma, vasculitis or small vessel disease

Alcohol

Hydrocephalus

Metabolic i.e. hepatic or thyroid disease or B12 deficiency, anaemia and hypoxia

Cerebra tumours

AI limbic encephalitis

Chronic traumatic encephalopathy

MS

Infections i.e. Herpes Simplex Encephalitis, HIV/AIDs, Neurosyphilis

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11
Q

What is the pathological process behind Alzheimer’s disease?

A

Cerebral atrophy due to reduced dendritic branching:
Atrophy occurs due to:
-neuritic plaques (NPs)
-Neurofibrillary tangles (NFTs)
-Amyloid angioplasty (AA)
-Basal nuclei affected= loss of cholinerfgic input to cortex

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12
Q

Which parts of the cerebral cortex are most commonly effected by Alzheimers?

A

Front and temporal lobes

Sometimes parietal

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13
Q

How are the ventricles affected in Alzheimers and why?

A

Ventricles become dilated

Due to shrinkage and death of surrounding brain tissue which leads to ventricles appearing enlarged

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14
Q

What proteins are associated with Alzheimer’s disease? Can these proteins be used to definitively diagnose AD?

A

Neurofibrillary tangles (NFT)= correlate to degree of dementia

Neuritic plaques (NP)

Amyloid angiopathy (AA)

No because NFT are associated with other disorders and NPs are also associated with normal ageing and Lewy body dementia (LBD)

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15
Q

What are risk factors for alzheimers?

A

Age
Head injury
Low educational status

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16
Q

What factors reduce the risk of Alzheimer’s?

A 
Cardioprotective lifestyle 
Statin therapy 
Active and socially integrated lifestyle 
Arthritis 
IBD
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17
Q

What are the risk factors for a subdural haemorrhage?

A

Cerebral atrophy i.e age or dementia

Coagulation dysfunction

Anticoagulation therapy

Alcoholism

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18
Q

What are the secondary events which can lead to head injury?

A

Ischaemia

Raised ICP

Infection

Post-traumatic epilepsy

Chronic traumatic encephalopathy

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19
Q

What 4 factors can lead to development of cerebral ischaemia and therefore act to cause brain injury?

A
  1. Damage brain more sensitive to hypoxia and hypercapnia
  2. Reduced circulation due to hypotension/hypovolaemia/RICP
  3. Hypoxia due to obstructed airways or chest injuries
  4. Infarction due to damage to intracranial or extracranial arteries
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20
Q

What are the 2 main causes of raised intracranial pressure?

A

Cerebral oedema due to:

  • perfusion problems
  • reaction to haematoma
  • direct reaction to rapid deceleration

Mass effect of haematoma

21
Q

What are the 2 major causes of infections causing brain injury and by what route can they occur?

A

Meningitis
Cerebral abscess

Routes: i.e. enables passage of bacteria into intra-cranial cavity

  • compound depressed fracture of skull
  • fracture of base of skull i.e. air sinuses or middle ear
22
Q

What types of brain injury increase the risk of post traumatic epilepsy occurring? How can post-traumatic epilepsy lead to TBI?

A

Intracranial haematomas
Contusional damage
Depressed fractures

PTE can lead to further damage of brain occurring further down the line to original trauma which brought about the PTE

23
Q

What is chronic traumatic encephalopathy? How is it distinct from Alzheimer’s disease?

A

Neurodegenerative disease associate with repetitive brain trauma which occurs during contact sports and has a delayed onset

Associated with tau proteins rather than beta-amyloid
Associated with frontotemporal atrophy where as Alzheimers associated with entorhinal cortex and hippocampus damage

24
Q

What are the histological features associated with Alzheimer’s disease?

A

Neuritic plaques

Amyloid angiopathy

Neurofibrillary tangle i.e. filament accumulation

25
Q

What is considered the possible primary event for AD?

A

Production of beta amyloid protein from beta amyloid precusor protein (BAPP) which is then involved in the production of NPs and AAs

26
Q

What genetic factors can increase the risk of developing Alzheimer’s disease?

A

Down’s syndrome

AD mutations in genes affecting processing of BAPP

  • BAPP gene
  • presenilin 1 gene
  • Presenilin 2 gene
27
Q

What protein aggregates in Alzheimer’s disease and what causes this accumulation?

A

Beta-amyloid polypeptide

Beta secretase is pathologically active which leads to aggregation of protein

28
Q

What are the possible treatment options for Alzheimer’s disease?

A

Donezepil (anticholinergic agent)

Immunisation against amyloid beta peptide but only acts to reduce the plaques rather than having clinical influence

29
Q

What conditions can apolipoprotein E be a risk factor for?

A

Increased risk of dementia i.e 3x for those with 1 E4 allele and 8x for homozygotes
-associated with AD because apolipoprotein is involved in the processing of BAPP
MI
Poorer outcomes after heart surgery and head injury etc

30
Q

What are the 2 main examples of Lewy body disorders? Where are the Lewy bodies located in each of the disorders?

A

Parkinson’s
-substantia nigra= leads to loss of dopaminergic input to basal ganglia which presents as pallor in the substania nigra

Lewy body dementia or Dementia with Lewy body
-cortical Lewy bodies
-lewy bodies contain alpha-synuclein
NOTE: 90% of people also have Parkinson’s

31
Q

What is the aetiology of vascular dementia? Where is the damage seen?

A

Small vessel disease associated with hypertensive changes
Multiple infarcts leads to accumulation of damage

Dominant hemisphere or bilaterally

32
Q

What is the difference between small and large vessel disease in terms of which part of the brain it preferentially affects?

A

Small= periventricular white matter

Large= grey matter

33
Q

What are examples of small vessel disease which can lead to development of vascular dementia?

A

Vasculitis= associated with vasculitis
Beta-amyloid angiitis
Arteriolosclerosis

34
Q

What are the different types of dementia?

A

Alzheimers
Vascular
Lewy body
Fronto-temporal dementias

35
Q

What are the 3 different variants of fronto-temporal dementia (FTDs)? What is the difference between them?

A

Semantic-variant primary progressive aphasia
-disorder of semantic knowledge and naming i.e. loss of meanings of words

Non-fluent variant primary progressive aphasia
-gradual loss of ability to speak (i.e. pronounce), understand, read and write

Behavioural variant
-changes in personality, behaviour, insight, disinhibition, inflexibility

36
Q

What are the pathological classifications of fronts-temporal dementia?

A

Pick’s disease
-pick bodies found in neurones

Ubiquitin positive proteinopathies

  • i.e dementia in MND
  • due to depositions

Frontotemporal degeneration w/o specific histology

37
Q

What structural effect does FTD have on the brain?

A

Causes knife edge gyri and increased depth of sulci

38
Q

What are the 3 different types of MND?

A

Primary lateral sclerosis

Progressive muscular atrophy

Progressive bulbar palsy

39
Q

What is the pathology associated with MND?

A

Ubiquitinated inclusions in MN nuclei which can be TDP43 in some cases
I.e. damage to the anterior horn leading to anterior horn atrophy

40
Q

What type of dementia can motor neurone disease be associated with?

A

FTD (non-picks disease type)

41
Q

What are 2 examples of trinucleotide repeat disorders and where are the repeat expansion found?

A

Huntington’s disease: (AD)
-CAG repeats in EXON= causes abnormal variant protein to form

Friedereichs Ataxia: (AR)
-INTRON= leads to reduced level of protein forming

42
Q

What are the 3 main forms of human prion disease?

A

Kuru

Creutzfeldt-Jakob disease

  • sporadic (main type)
  • iatrogenic
  • variant

Fatal familial insomnia (affects the thalamus)

43
Q

What pathological changes occur in prion disease?

A

Spongiform changes
Neuronal loss
Gliosis= reactive astrocytic response to brain injury
Amyloid plaque formation in cerebellum mostly
NOTE: vCJD has amyloid plaques in the cerebral cortex

44
Q

Which type of prion is associated with TSEs?

A

Protease resistant form of prions which leads to switch from PrP form to PrPsc production
PrPsc are resistant to sterilisation and may form amyloid

45
Q

What is another way of classifying prion disorders?

A

Transmissible spongiform encephalopathies (TSEs)

46
Q

What is MS and what is the pathology behind the disease?

A

Relapsing condition with gradual accumulation of neurological deficit

Loss of myelin sheaths with relative preservation of axons
Inflammation and gliosis

47
Q

What structures are affected in MS and what are the commonly associated signs?

A 
Optic nerves 
Periventricular white matter= leads to formation of periventricular plaques  
Cerebellum 
Brainstem 
Spinal cord

Symptoms:

  • optic neuritis
  • spinal cord syndrome
  • ataxia
  • depression
  • cognitive problems
48
Q

What is thought to be the cause of MS?

A

T-cell mediated immune response to myelin antigens
OR
Oligondendrocyte apoptosis

49
Q

What is the cause of neuromyelitis optics?

A

Aquaporin 4 IgG antibodies which leads to damage to the spinal cord and optic nerve

I.e. optic neuritis and transverse myelitis (inflammation of both sides of one part of spinal cord)

Pathology (12 decks)

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