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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
What is the most common type of haemorrhage stroke?
Intracerebral
26
Where does a thrombotic stroke most commonly occur?
At the bifurcation of the common carotids or in basilar artery
27
Where does an emboli causing an embolic stroke usually originate?
From the heart of atherosclerotic plaque in more proximal arterial segments
28
Where do most embolic occlusions occur?
In the branches of the middle cerebral arteries
29
What are the RFs for a stroke?
``` Atheroma Hypertension Serum lipids, obesity, diet Diabetes mellitus Heart disease Diseases of neck arteries Drugs Smoking ```
30
What is the morphology of a cerebral infarction?
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
31
What is the most common cause of an SA haemorrhage?
Rupture of a saccular aneurysm (Berry aneurysm) | 90% arise as arterial bifurcations near internal carotid artery. 10% in vertebra-basilar circulation
32
What occurs in a Berry aneurysm?
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
33
What are Berry aneuryms associated with?
Severe headache Vomiting Loss of consciousness
34
What is the onset of a Berry aneurysm?
Abrupt | Usually no history of precipitating factor
35
What changes occur in the brain due to HT?
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.
36
What pathologies can occur in the brain due to HT?
Lacunar infarcts Intracerebral haemorrhage and haematoma formation – ruptured aneurysms Multi-infarct dementia Hypertensive encephalopathy
37
What is demyelination?
Preferential destruction of myelin sheath around axon | Relative preservation of axons themselves
38
What is a cause of primary demyelination?
MS
39
What is a cause of secondary demyelination?
``` Central pintine myelinosis Progressive multifocal leukoencephalopathy (inborn) Sub-acute sclerosing panencephalitis AIDS Axonal degeneration ```
40
What are some other causes of demyelination?
Metabolic | Toxic- cyanide, CO, solvents
41
What is the M:F ratio of MS?
1:2
42
What is the morphology of MS?
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
Where does MS commonly occur?
CNII, periventricular white matter, corpus callosum, brain stem and spinal cord
44
What can MS act as?
SOL
45
What are some types of MS plaques?
Acute active Chronic (inactive) Chronic active Shadow
46
Describe acute active plaques in MS
Demyelinated plaques are yellow/brown, with an ill-defined edge which blends into surrounding white matter
47
Describe chronic plaques in MS
Chronic multiple sclerosis plaques – well-demarcated grey/brown lesions in white matter, classically situated around lateral ventricles
48
What are the main features of a MS plaque?
Demyelination Inflammation Gliosis
49
How is dementia defined?
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
What are the primary dementias?
Alzheimer's Diffuse Lewy body diseae HD Pick's disease
51
What are the secondary dementias?
Other disorders resulting in secondary changes in the CNS resulting in dementia such as; vascular, metabolic, infection and trauma
52
What is the macroscopic pathology of Alzheimer's?
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
What are the microscopic/histological features of Alzheimer's?
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
What are the pathological features of dementia with Lewy bodies?
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
What is the microscopic/histological appearance of HD?
Loss of neurons in caudate nucleus and cerebral cortex accompanied by reactive fibrillary gliosis
56
What is Pick's disease?
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
What occurs pathologically in Pick's?
Extreme atrophy of cerebral cortex in frontal and temporal lobes Brain weight
58
What are the symptoms of Pick's disease?
Personality and behavioural change Speech and communication problems Changes in eating habits Reduced attention span
59
What is multi-infarct dementia?
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
Are sufferer of multi-infarct dementia aware of their deficits?
Yes- prone to depression and anxiety
61
What criteria suggest multi-infarct dementia instead of Alzheimer's?
Abrupt onset Stepwise progression History of HT or stroke Evidence of stroke will be seen on CT/MRI
62
What are some examples of non-missile primary damage to the head?
``` Scalp lesions Skull fractures Surface contusions or lacerations Diffuse axonal injury Diffuse vascular injury ```
63
Name some types of skull fracture
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
What are coup and contracoup injuries?
Coup- at point of impact Contracoup- diametrically opposite point of impact. Contracoup more serious than Coup
65
Describe diffuse axonal injury
Occurs at moment of injury Can cause coma Can lead to vegetative state Grades of increasing severity-correlate with patient's clinical state
66
What is the morphology of diffuse axonal injury?
``` 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
What is the most common intracranial haematoma?
Intradural
68
What are extradural haematomas usually a complication of?
Fracture in temparoparietal region that involves middle meningeal artery
69
What occurs if an extradural haematoma is untreated?
Midline shift- compression and herniation
70
Is there associated brain damage with extradural haematoma?
Often minimal
71
What can raised ICP cause?
``` Focal lesion in brain (SOL) Diffuse lesion in brain (e.g. oedema) Increased CSF (hydrocephalus) Increased venous volume Physiological (hypoxia, hypercapnia, pain) ```
72
What are the effects of raised ICP?
Intracranial shifts and herniations Distortion and pressure on cranial nerves and vital neuro changes Reduced level of consciousness Impaired blood flow
73
What are some types of herniations?
Falcine Uncal Cerebellar Transcalvarium
74
What are some clinical signs of raised ICP?
Papilloedema Nausea and vomiting Headache Neck stiffness
75
What are some examples of SOLs?
Tumours-primary, metastases Abscess-single/multiple Haematoma Localised brain swelling e.g. swelling and oedema around cerebral infarct
76
Describe single abscesses
Usually have focal cause; otitis media, sinusitis, nasal, facial and dental infections, skull fracture, penetrating injury, neurosurgical procedures
77
Describe multiple abscesses
Usually result from septicaemia; acute bacterial endocarditis, bronchiectasis and lung abscess, cyanotic heart disease, IV drug abuse
78
What is focal oedema?
Localised oedema which is present as a result of other pathological lesions, such as infarcts, can also lead to an increase in ICP
79
What is generalised cerebral oedema?
Increased water content of the brain
80
What are the various types of cerebral oedema?
``` Vasogenic Cytotoxic Hydrostatic Interstitial Hypo-osmotic ```
81
What are extradural haemorrhage's usually due to?
Rupture of meningeal arteries and associated with skull fractures
82
What do extradural haemorrhages compress?
Subjacent dura and flatten gyral crests of underlying brain | Leading to uncal gyral/cerebellar tonsillar herniation, brainstem compression and death
83
What is a subdural haemorrhage caused by?
Caused by disruption of bridging veins that extend from the surface of the brain into subdural space
84
Where do subdural haemorrhages occur?
Most often over cerebral hemispheres Vary in size Acute (clotted) or chronic (Liquefied blood clot)
85
Describe an acute subdural haemorrhage
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
What is a chronic subdural haemorrhage associated with?
Brain atrophy
87
What is a chronic subdural haemorrhage composed of?
Liquefied blood/yellow-tinged fluid separated from inner surface of dura mater and underlying brain by “neomembrane”
88
What are some clinical symptoms of chronic subdural haemorrhage?
Altered mental status | Focal neurological deficits

Neurology (27 decks)

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