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Neurology > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

What can cells of the CNS be damaged by?

A 
Lack of oxygen (hypoxia/anoxia)
 Trauma
 Toxic insult
 Metabolic abnormalities
 Nutritional deficiencies
 Infections
 Ageing
 Genetic abnormalities
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2
Q

What occurs in hypoxia damage to CNS?

A

Neurones are most vulnerable-have selective vulnerability
Activation of glutamate receptors-results in uncontrolled calcium entry into the cell
Neurones can’t use anaerobic glycolysis

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3
Q

What is an axonal reaction?

A

A reaction within the cell body that is associated with axonal injury

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4
Q

What is the response to axonal injury in neuronal degeneration?

A 
Increase RNA and protein synthesis
Swelling of cell body
Peripheral displacement of nucleus 
Enlargement of nucleolus
Central chromatolysis
Anterograde degeneration of axons occurs distal to site of injury
Breakdown of myelin sheath
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5
Q

What occurs in damage to astrocytes?

A

Reactive response associated with proliferation (gliosis)

Leads to cell death or degeneration

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6
Q

What occurs in gliosis?

A

Astrocytes undergo hyperplasia and hypertrophy
Nucleus enlarges, becomes vesicular and nucleolus is prominent
Cytoplasmic expansion with extension of ramifying processes

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7
Q

What is the most important histopathological indicator of CNS injury regardless of cause?

A

Gliosis

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8
Q

What happens to old lesions in gliosis?

A

Nuclei become small and dark and lie in a dense net of processes (glial fibrils)

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9
Q

What is injury to oligodendrocytes a feature of?

A

Demyelinating disorders

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10
Q

What do ependymal cells line?

A

The ventricular system

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11
Q

What is disruption to ependymal cells associated with?

A

A local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations

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12
Q

How do microglia respond to injury by?

A

Proliferating
Developing elongated nuclei (rod cells)
Forming aggregates about small foci of tissue necrosis (microglial nodules)
Congregate around portions of dying neurons (neuronophagia)

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13
Q

How is blood supplied to the brain?

A

Via branches of the internal carotid and vertebral arteries which forms the anterior and posterior circulations

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14
Q

What occurs in anterior cerebral artery pathology?

A

Frontal lobe dysfunction
Contralateral sensory loss in foot and leg
Paresis of arm and foot, relative sparing of thigh and face

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15
Q

What occurs in middle cerebral artery pathology?

A 
Dominant vs non-dominant effects
Hemiparesis
Hemisensory loss
Aphasia/dysphagia 
Apraxia
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16
Q

What does the posterior vertebrobasilar artery supply?

A

Brain stem
Cerebellum
Occipital lobe

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17
Q

What can damage to the brainstem due to ischaemia cause?

A

Midbrain- Weber’s syndrome
Pons- Medial & lateral inferior pontine syndromes
Medulla- Lateral medullary syndrome

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18
Q

What can ischaemia to the occipital lobe cause?

A

Homonymous hemianopia with macular sparing

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19
Q

What is more vulnerable to hypoxic ischaemic damage, neurons or glial?

A

Neurons

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20
Q

What are watershed areas?

A

Junctions of arterial territories (arterial border zones)- they are first to be deprived of blood supply during hypotensive episodes

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21
Q

What are some of the watershed areas?

A

Superior cerebral convexities at the junctions of the anterior and middle cerebral arteries, and the posterior aspects of the cerebellar hemispheres at the junction of the territories supplied by the superior and posterior inferior cerebellar arteries.

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22
Q

What is the definition of a stroke?

A

Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hrs

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23
Q

What is the most common type of stroke?

A

Thrombotic infarction

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24
Q

What are the two types of strokes?

A

Infarction-Thrombotic, Embolic

Haemorrhage- Intracerebral, subarachnoid, bleeding into infarct

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25
Q

What is the most common type of haemorrhage stroke?

A

Intracerebral

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26
Q

Where does a thrombotic stroke most commonly occur?

A

At the bifurcation of the common carotids or in basilar artery

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27
Q

Where does an emboli causing an embolic stroke usually originate?

A

From the heart of atherosclerotic plaque in more proximal arterial segments

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28
Q

Where do most embolic occlusions occur?

A

In the branches of the middle cerebral arteries

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29
Q

What are the RFs for a stroke?

A 
Atheroma
Hypertension
Serum lipids, obesity, diet
Diabetes mellitus
Heart disease
Diseases of neck arteries
Drugs
Smoking
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30
Q

What is the morphology of a cerebral infarction?

A

4-12hrs: Brain may appear normal
15-20hrs: Ischaemic neuronal changes develop, defined margin between ischaemic and normal brain
24-36hrs: Inflammatory reaction, extravasation of RBCs. Activation of astrocytes and microglia
36-48hrs: Necrotic area visible macroscopically, becomes swollen and softer
Day 3: Macrophages infiltrate into area
1-2wkes: Liquefaction of tissue and gliosis
Months: Cavitation and completion of glial scar

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31
Q

What is the most common cause of an SA haemorrhage?

A

Rupture of a saccular aneurysm (Berry aneurysm)

90% arise as arterial bifurcations near internal carotid artery. 10% in vertebra-basilar circulation

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32
Q

What occurs in a Berry aneurysm?

A

Rupture may result in bleeding into SAS
May also get intracerebral haematomas adjacent to aneuryms
Infarcts of brain parenchyma may also develop due to arterial spasm, mass effect of haematoma and raised ICP

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33
Q

What are Berry aneuryms associated with?

A

Severe headache
Vomiting
Loss of consciousness

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34
Q

What is the onset of a Berry aneurysm?

A

Abrupt

Usually no history of precipitating factor

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35
Q

What changes occur in the brain due to HT?

A

Increased amount of atheroma
Hyaline arteriosclerosis
Microaneurysms
Altered response of cerebral blood vessels to chronic hypertension with a shift of the autoregulatory curve to the right.

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36
Q

What pathologies can occur in the brain due to HT?

A

Lacunar infarcts
Intracerebral haemorrhage and haematoma formation – ruptured aneurysms
Multi-infarct dementia
Hypertensive encephalopathy

37
Q

What is demyelination?

A

Preferential destruction of myelin sheath around axon

Relative preservation of axons themselves

38
Q

What is a cause of primary demyelination?

A

MS

39
Q

What is a cause of secondary demyelination?

A 
Central pintine myelinosis
Progressive multifocal leukoencephalopathy (inborn)
Sub-acute sclerosing panencephalitis
AIDS
Axonal degeneration
40
Q

What are some other causes of demyelination?

A

Metabolic

Toxic- cyanide, CO, solvents

41
Q

What is the M:F ratio of MS?

A

1:2

42
Q

What is the morphology of MS?

A

External appearance of brain and spinal cord usually normal
If surface cut- multiple areas of demyelination seen, termed plaques
Well-demarcated plaques in white matter (acute soft/pink, older firmer/pearly grey)
Non-anatomical distribution

43
Q

Where does MS commonly occur?

A

CNII, periventricular white matter, corpus callosum, brain stem and spinal cord

44
Q

What can MS act as?

A

SOL

45
Q

What are some types of MS plaques?

A

Acute active
Chronic (inactive)
Chronic active
Shadow

46
Q

Describe acute active plaques in MS

A

Demyelinated plaques are yellow/brown, with an ill-defined edge which blends into surrounding white matter

47
Q

Describe chronic plaques in MS

A

Chronic multiple sclerosis plaques – well-demarcated grey/brown lesions in white matter, classically situated around lateral ventricles

48
Q

What are the main features of a MS plaque?

A

Demyelination
Inflammation
Gliosis

49
Q

How is dementia defined?

A

An impairment of previously acquired occupational or social functioning due to development of acquired and persistent memory impairment associated with impairment of intellectual function in the presence of normal consciousness

50
Q

What are the primary dementias?

A

Alzheimer’s
Diffuse Lewy body diseae
HD
Pick’s disease

51
Q

What are the secondary dementias?

A

Other disorders resulting in secondary changes in the CNS resulting in dementia such as; vascular, metabolic, infection and trauma

52
Q

What is the macroscopic pathology of Alzheimer’s?

A

Decreased size and weight of brain (cortical atrophy)
Widening of sulci
Narrowing of gyri
Compensatory dilatation ventricles, 2’ hydropcephalus
Frontal, temporal and parietal lobes affected
Brainstem and cerebellum normal

53
Q

What are the microscopic/histological features of Alzheimer’s?

A

Intracytoplasmic neurofibrillary tangles
A-beta amyloid plaques (extracellular senile or neuritic plaques, polymerised beta pleted sheet, EM 10-12nm fibrils)
Amyloid angiopathy
Extensive neuronal loss with astrocytosis

54
Q

What are the pathological features of dementia with Lewy bodies?

A

Degeneration of the substantia nigra (as seen in Parkinson’s disease).
Remaining nerve cells contain abnormal structures called Lewy bodies (pathological hallmark).
Degeneration of the cortical areas of the brain with many or all of the features seen in Alzheimer’s disease
Degeneration of the cortical areas of the brain with formation of cortical Lewy bodies which can be detected by immunochemical staining for the protein ubiquitin.

55
Q

What is the microscopic/histological appearance of HD?

A

Loss of neurons in caudate nucleus and cerebral cortex accompanied by reactive fibrillary gliosis

56
Q

What is Pick’s disease?

A

A progressive dementia commencing in middle life (usually between 50 and 60 years) characterised by slowly progressing changes in character and social deterioration leading to impairment of intellect, memory and language

57
Q

What occurs pathologically in Pick’s?

A

Extreme atrophy of cerebral cortex in frontal and temporal lobes
Brain weight

58
Q

What are the symptoms of Pick’s disease?

A

Personality and behavioural change
Speech and communication problems
Changes in eating habits
Reduced attention span

59
Q

What is multi-infarct dementia?

A

Disorder involving a deterioration in mental functioning due to changes or damage to the brain tissue from hypoxia or anoxia (lack of oxygen) as a result of multiple blood clots within the blood vessels supplying the brain.

60
Q

Are sufferer of multi-infarct dementia aware of their deficits?

A

Yes- prone to depression and anxiety

61
Q

What criteria suggest multi-infarct dementia instead of Alzheimer’s?

A

Abrupt onset
Stepwise progression
History of HT or stroke
Evidence of stroke will be seen on CT/MRI

62
Q

What are some examples of non-missile primary damage to the head?

A 
Scalp lesions
Skull fractures
Surface contusions or lacerations
Diffuse axonal injury
Diffuse vascular injury
63
Q

Name some types of skull fracture

A

Fissure fracture- linear fracture of vault extending from occiput, across coronal suture towards frontal region
Depressed
Compound (associated with scalp lacerations)
Higher incidence of Intracranial bleeding/haematomas
Base of skull fractures

64
Q

What are coup and contracoup injuries?

A

Coup- at point of impact
Contracoup- diametrically opposite point of impact.
Contracoup more serious than Coup

65
Q

Describe diffuse axonal injury

A

Occurs at moment of injury
Can cause coma
Can lead to vegetative state
Grades of increasing severity-correlate with patient’s clinical state

66
Q

What is the morphology of diffuse axonal injury?

A 
2-4hrs: Focal axonal accumulation of APP
12-24hrs: Axonal varicosity
24hrs-2m: Axonal swelling
2wks-5m: Glial reaction
2m-Years: Degeneration and loss of myelinated fibres
67
Q

What is the most common intracranial haematoma?

A

Intradural

68
Q

What are extradural haematomas usually a complication of?

A

Fracture in temparoparietal region that involves middle meningeal artery

69
Q

What occurs if an extradural haematoma is untreated?

A

Midline shift- compression and herniation

70
Q

Is there associated brain damage with extradural haematoma?

A

Often minimal

71
Q

What can raised ICP cause?

A 
Focal lesion in brain (SOL)
Diffuse lesion in brain (e.g. oedema)
Increased CSF (hydrocephalus)
Increased venous volume
Physiological (hypoxia, hypercapnia, pain)
72
Q

What are the effects of raised ICP?

A

Intracranial shifts and herniations
Distortion and pressure on cranial nerves and vital neuro changes
Reduced level of consciousness
Impaired blood flow

73
Q

What are some types of herniations?

A

Falcine
Uncal
Cerebellar
Transcalvarium

74
Q

What are some clinical signs of raised ICP?

A

Papilloedema
Nausea and vomiting
Headache
Neck stiffness

75
Q

What are some examples of SOLs?

A

Tumours-primary, metastases
Abscess-single/multiple
Haematoma
Localised brain swelling e.g. swelling and oedema around cerebral infarct

76
Q

Describe single abscesses

A

Usually have focal cause; otitis media, sinusitis, nasal, facial and dental infections, skull fracture, penetrating injury, neurosurgical procedures

77
Q

Describe multiple abscesses

A

Usually result from septicaemia; acute bacterial endocarditis, bronchiectasis and lung abscess, cyanotic heart disease, IV drug abuse

78
Q

What is focal oedema?

A

Localised oedema which is present as a result of other pathological lesions, such as infarcts, can also lead to an increase in ICP

79
Q

What is generalised cerebral oedema?

A

Increased water content of the brain

80
Q

What are the various types of cerebral oedema?

A 
Vasogenic
Cytotoxic
Hydrostatic
Interstitial
Hypo-osmotic
81
Q

What are extradural haemorrhage’s usually due to?

A

Rupture of meningeal arteries and associated with skull fractures

82
Q

What do extradural haemorrhages compress?

A

Subjacent dura and flatten gyral crests of underlying brain

Leading to uncal gyral/cerebellar tonsillar herniation, brainstem compression and death

83
Q

What is a subdural haemorrhage caused by?

A

Caused by disruption of bridging veins that extend from the surface of the brain into subdural space

84
Q

Where do subdural haemorrhages occur?

A

Most often over cerebral hemispheres
Vary in size
Acute (clotted) or chronic (Liquefied blood clot)

85
Q

Describe an acute subdural haemorrhage

A

Clear history of trauma
Unilateral or bilateral
Associated with other traumatic lesions
Gyral contours preserved – pressure evenly distributed
Swelling of cerebrum on side of haematoma
Mass effect

86
Q

What is a chronic subdural haemorrhage associated with?

A

Brain atrophy

87
Q

What is a chronic subdural haemorrhage composed of?

A

Liquefied blood/yellow-tinged fluid separated from inner surface of dura mater and underlying brain by “neomembrane”

88
Q

What are some clinical symptoms of chronic subdural haemorrhage?

A

Altered mental status

Focal neurological deficits

Neurology (27 decks)

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