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CNS CLERKSHIP > Neuropathology > Flashcards

Neuropathology Flashcards

1
Q

Give examples of glial cells.

A
  • Astrocytes.
  • Oligodendrocytes.
  • Ependymal cells.
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2
Q

Glial cells are derived from?

A

Neuroectoderm.

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3
Q

Function of astrocytes?

A

Provide brain with a fixed 3D grid-structure, within which the other CNS cells are supported. Functionally, they are closely coupled with neurones.

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4
Q

Function of oligodendrocytes?

A

Wrap around axons to form myelin sheath.

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5
Q

Function of ependymal cells?

A

Line the ventricular system.

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6
Q

What are microglia?

A

Mesoderm-derived cells originating in bone marrow, serving as a fixed macrophage system.

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7
Q

What is hypoxia?

A

Anoxia (absence) or lack of oxygen.

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8
Q

Why does hypoxia injure CNS?

A

Results in energy failure of cells of the brain parenchyma.

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9
Q

Damage to nerve cells and/or their processes can lead to?

A
  • Rapid necrosis with sudden acute functional failure e.g. stroke.
  • Slow atrophy with gradually increasing dysfunction e.g. age-related cerebral atrophy.
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10
Q

When does acute neuronal injury (Red neuron) occur?

A

In the context of hypoxia/ischaemia.

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11
Q

When can acute neuronal injury be seen?

A

Typically visible 12-24 hours after an irreversible “insult” to the cell.

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12
Q

Acute neuronal injury results in what?

A

Neuronal cell death.

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13
Q

What pattern is seen in acute neuronal injury?

A
  • Shrinking and angulation of nuclei.
  • Loss of nucleus.
  • Intense eosinophilia/ redness of cytoplasm.
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14
Q

Acute neuronal injury represents a lethal injury to the neuron typically caused by?

A

Ischaemia or hypoxia e.g. strokes.

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15
Q

What are the responses to injury/ disease of neurones?

A
  • Acute neuronal injury.
  • Axonal reactions.
  • Simple neuronal atrophy (chronic degradation).
  • Sub-cellular alterations (inculsions).
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16
Q

What is axonal reaction?

A

A neuronal cell body reaction associated with axonal injury.

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17
Q

What may be seen in an axonal reaction?

A
  • Swelling.
  • Enlarged nucleolus due to protein synthesis.
  • Chromatolysis: margination and loss of Nissl granules.
  • Degeneration of axon and myelin distal to site of injury: “Wallerian Degeneration”.
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18
Q

How do axonal reactions differ in the CNS to the PNS?

A

In the PNS there is often some myelin sheath preserved, thus allowing neural tube formation and some regeneration.

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19
Q

What can be seen in simple neuronal atrophy (chronic degeneration)?

A
  • Shrunken, angulated and lost neurones.
  • Small dark nuclei.
  • Lipofuscin pigment.
  • Reactive gliosis.
  • Though cause dependent, often affects functionally related neurons.
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20
Q

Sub-cellular alterations/ inclusions to neuronal organelles and cytoskeleton are common in?

A
  • Classically, neurofibrillary tangles in Alzheimer’s disease.
  • Lewy bodies in Lewy Body Dementia and Parkinson’s.
  • Neural inclusions in ageing.
  • Intranuclear and cytoplasmic inclusions in viral disease.
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21
Q

Simple neuronal atrophy occurs in diseases of long duration, for example?

A
  • MS.

- Alzheimer’s.

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22
Q

Neurofibrillary tangles are classically associated with which disease?

A

Alzheimer’s.

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23
Q

Lewy bodies are associated with which diseases?

A

Lewy body dementia and Parkinson’s.

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24
Q

Neural inclusions appear to accumulate with?

A

Ageing.

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25
Q

Intranuclear and cytoplasmic inclusions are seen in?

A

Viral infections affecting the brain.

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26
Q

What do astrocytes look like?

A
  • Star-shaped.

- Multipolar cytoplasmic processes.

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27
Q

Where are astrocytes located?

A

Throughout the CNS.

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28
Q

What is the function of astrocytic processes?

A
  • Envelop synaptic plates.

- Wrap around vessels and capillaries within the brain.

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29
Q

What is the role of astrocytes?

A
  • Ionic, metabolic and nutritional homeostasis.
  • Work alongside endothelial cells to maintain BBB.
  • Main cell involved in repair and scar formation (lack of fibroblasts).
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30
Q

Astrocytes perform anaerobic glycolysis to produce what and why?

A

Lactate to be transferred to neurons for use as a metabolite in the production of ATP.

Astrocytes are therefore metabolically coupled to neurones.

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31
Q

How is synaptic function of neurones coupled to astrocytes?

A

Astrocytes envelop synaptic plates where they take up Glutamate from synapse and recycle it to neurons.

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32
Q

How do astrocytes regulate the BBB and cerebral blood flow?

A

They have foot processes entirely enveloping intracerebral small vessels and capillaries. They respond to neuronal signals.

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33
Q

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

A

Gliosis (an astrocytic response).

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34
Q

What is gliosis?

A
  • Astrocytes undergo hyperplasia and hypertrophy (more and larger).
  • Develop enlarged vesicuar nuclei and prominent nucleoli.
  • Cytoplasmic expansion with extension of ramifying processes.
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35
Q

What do old lesions of gliosis look like?

A
  • Nuclei become small, dark and lie in a dense net of processes (glial fibrils).
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36
Q

Describe gliotic tissue and its function.

A
  • Translucent and firm.

- Limiting barrier to sites of tissue damage.

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37
Q

What is the function of oligodendrocytes?

A

Wrap around axons to form myelin sheath.

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38
Q

What is the CNS equivalent of a Schwann cell?

A

Oligodendrocytes.
- Wrap around axons to form myelin sheath in CNS.

Schwann cells: wrap around axons to form myelin sheath in PNS.

Both form nodes of Ranvier for saltatory conduction.

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39
Q

What is the (relatively limited) reaction to injury of oligodendrocytes?

A
  • Variable patterns of demyelination.
  • Variable degrees of demyelination.
  • Apoptosis.
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40
Q

Oligodendrocytes are sensitive to what type of damage?

A

Oxidative damage.

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41
Q

Oligodendrocyte damage is a feature of which disorders?

A

Demyelinating disorders.

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42
Q

Myelin insulation allows for what?

A
  • Saltatory conduction (nodes of Ranvier).
  • Contain depolarisation locally (prevents leakage to adjacent axons).
  • Provides barrier to injury.
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43
Q

What is Wallerian degeneration?

A

Axonal damage causing antegrade degeneration of the axon to the nearest node.

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44
Q

Why are oligodendrocytes sensitive to oxidative damage?

A

Low anti-oxidant reserves and high intracellular iron.

They will die in response to significant hypoxic injury.

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45
Q

Disruption of the myelin sheath is characterised by?

A

Abnormalities in neuronal conduction.

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46
Q

Axonal loss is generally irreversible in the CNS why?

A

Oligodendrocytes do not have the same reparative ability as Schwann cells of the PNS.

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47
Q

Ependymal cell function?

A

Line the ventricular system.

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48
Q

Ependymal cell reaction to injury?

A

Limited.
However, they are an important focus for infection as infection can pass from one set of ependymal cells to another at a distant site via CSF spread through ventricular system.

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49
Q

Disruption of ependymal cells can cause what?

A
  • Local reactive proliferation of sub-ependymal astrocytes to produce small irregularities on ventricular surfaces: Ependymal granulations.
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50
Q

What may produce changes in ependymal cells?

A

Infectious agents and viruses.

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51
Q

Ependymal cells can form tumours causing what?

A

Due to position in ventricular system, they can obstruct CSF flow - pathological consequences.

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52
Q

What are microglia?

A

Embryologically derived cells that function as a macrophage system using phagocytosis.

The “CNS immune cell”.

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53
Q

How do microglia respond to injury?

A
  • Proliferation.
  • Recruited through inflammatory mediators.
  • Form aggregates around areas of necrotic and damaged tissues.
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54
Q

Microglia are important mediators in acute nervous system injury, describe their role.

A
  • M2: anti-inflammatory, phagocytic, more acute.

- M1: pro-inflammatory, more chronic.

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55
Q

Describe M1 type microglia.

A
  • Appear after acute injury - more chronic.
  • Pro-inflammatory.
  • May exacerbate aspects of acute brain injury.
  • Important mediators in neurological injury of chronic disease e.g. Alzheimer’s and MS.
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56
Q

What causes of hypoxia damage the brain?

A
  • Cerebral ischaemia.
  • Cerebral infarct.
  • Haemorrhages.
  • Trauma.
  • Cardiac arrest.
  • Cerebral palsy.
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57
Q

The brain consumes what percentage of total body resting oxygen consumption?

A

20%.

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58
Q

What is the maximum that cerebral blood flow can increase to maintain oxygen delivery in ischaemia?

A
  • Two fold.
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59
Q

After ischaemia onset in the brain, mitochondrial inhibition of ATP synthesis leads to?

A
  • Consumption of ATP reserves within minutes.
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60
Q

What CNS cells are most vulnerable to hypoxia?

A

Neurones.

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61
Q

Why are neurones the most vulnerable CNS cells to hypoxia?

A

They are metabolically dependant on oxidative phosphorylation.

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62
Q

What is the principle mechanism through which hypoxia exerts its toxic influence?

A

Energy failure of neurones, accumulating injurious oxidative stress and excitotoxicity.

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63
Q

What are the most important mechanisms in excitotoxicity?

A

Glutamate and Oxygen free radical formation causing Calcium influx.

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64
Q

Activation of glutamate receptors in excitotoxicity causes?

A

Uncontrolled calcium entry into cell.

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65
Q

Uncontrolled calcium entry into cells during excitotoxicity triggers?

A
  • Protease activation.
  • Mitochondrial dysfunction.
  • Oxidative stress.
  • Apoptosis and necrosis.
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66
Q

Energy failure prevents glutamate recycling through astrocytes, enhancing?

A

Glutamate accumulation and excitotoxicity.

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67
Q

What is cytotoxic oedema?

A

Pre-morbid process in which dying cells accumulate water as osmotically active ions (Na+ and Cl-) move into cells, bringing water with them.

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68
Q

Cytotoxic oedema can enhance what?

A

Ionic and vasogenic oedema.

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69
Q

What may cause cytotoxic oedema?

A
  • Intoxication.
  • Reye’s.
  • Severe hypothermia.
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70
Q

What is the first dysfunction of the blood brain barrier?

A

Ionic oedema.

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71
Q

What are the causes of ionic oedema?

A
  • Hyponatraemia.

- Excess water intake e.g. SIADH.

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72
Q

How does ionic oedema occur?

A
  • Cytotoxic oedema leaves extracellular space devoid of Na+.
  • Na+ ions cross BBB and drive Cl- transport, creating osmotic gradient for water accumulation.
  • BBB is dysfunctional but maintains its integrity causing swelling.
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73
Q

Vasogenic oedema occurs with?

A
  • Deterioration and breakdown in the BBB.
  • Disruption of endothelial tight junctions allows plasma proteins e.g. albumin (potent osmotic factors) to cross into extracellular space and water follows.
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74
Q

How does haemorrhagic conversion occur?

A
  • When endothelial integrity is lost and blood is allowed to enter the extracellular space.
  • Extravasation of RBCs occur in 30-40% of ischaemic strokes.
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75
Q

The anterior carotid arteries are paired blood vessels, supplying oxygenated blood to what?

A

Most midline portions of frontal and superior medial parietal lobes.

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76
Q

The middle cerebral artery arises from what?

A

The internal carotid.

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77
Q

The middle cerebral artery arises from internal carotid and continues where?

A

Into lateral sulcus where it branches and projects to supply many parts of lateral cerebral cortex.

  • Also supplies blood to anterior temporal lobes and insular cortices.
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78
Q

What supplies oxygenated blood to posterior aspect of brain - the occipital lobe?

A

The posterior cerebral arteries.

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79
Q

Disruption of blood supply to the following area will result in which symptoms?
- Anterior cerebral artery territory.

A
  • Sensory and motor abnormalities of the the trunk and legs.
  • Frontal lobe dysfunction.
  • Higher cognitive dysfunction.
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80
Q

Disruption of blood supply to the following area will result in what?
- Middle cerebral artery territory.

A
  • Deficits of the majority of the sensory and motor cortex.
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81
Q

Disruption of blood supply to the following area will result in which symptoms?
- Posterior cerebral artery territory.

A
  • Occipital lobes: homonymous hemianopia with visual field defect in both eyes on the same side as the lesion.
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82
Q

The brain requires what?

A

Active aerobic metabolism of glucose.

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83
Q

Autoregulatory mechanisms of the brain help to maintain what?

A

Blood flow at a constant rate by dilatation and constriction of cerebral vessels.

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84
Q

What is cerebrovascular disease?

A

Any abnormality of the brain caused by a pathological process of blood vessels.

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85
Q

Give an example of Cerebrovascular disease.

A
  • Brain ischaemia and infarction.
  • Haemorrhage.
  • Vascular malformation.
  • Aneurysm.
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86
Q

Cerebrovascular disease involves what general processes?

A
  • Hypoxia, ischaemia and infarction resulting from impairment of blood supply and oxygenation of tissue.
  • Haemorrhage resulting from rupture of CNS vessels.
  • Hypertension causing hypertensive cerebrovascular disease.
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87
Q

What may cause global hypoxic ischaemic cerebral damage?

A
  • Generalised reduction in blood flow/oxygenation.
  • Cardiac arrest.
  • Severe hypotension e.g. trauma with hypovolaemic shock.
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88
Q

What may cause focal cerebral ischaemia?

A

Vascular obstruction.

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89
Q

What is global hypoxic ischaemic cerebral damage?

A

When systemic circulation compromise cannot be compensated for by CNS auto-regulatory mechanisms,

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90
Q

What is focal cerebral ischaemia?

A

Restriction of blood flow to a localised area of the brain.

- Typically due to vascular obstruction.

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91
Q

What may a cause generalised reduction in cerebral perfusion?

A
  • Cardiac arrest.
  • Shock/severe hypotension.
  • Trauma.

Where autoregulatory mechanisms cannot compensate.

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92
Q

Which “watershed” areas of the brain are particularly sensitive to global hypoxic ischaemic damage?

A

Zones between two arterial territories e.g. parieto-occipital.

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93
Q

Which neurons are more sensitive than the others to global hypoxic ischaemic damage?

A
  • 3rd and 5th layer neurones of Neocortex.
  • CA1 neurones of Hippocampus.
  • Purkinje cells of cerebellum.
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94
Q

At what mean arterial pressure is there a generalised reduction of cerebral perfusion?

A

<50mmHg.

The point at which autoregulatory mechanisms cannot sufficiently compensate.

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95
Q

Why are “watershed” areas particularly sensitive to hypoxia?

A
  • At the periphery of vascular territories, most distant from the heart and least well-supplied.
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96
Q

Define stroke.

A

Sudden disturbance of cerebral function of vascular origin that either causes death or lasts over 24 hours.

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97
Q

Stroke is classified clinically into what three categories?

A
  • Completed strokes.
  • Evolving strokes.
  • Transient ischaemic attacks.
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98
Q

Completed strokes result in what?

A

Irreversible tissue loss due to local arrest or severe reduction in cerebral blood flow.

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99
Q

Epidemiological evidence suggest that what percent of strokes are due to infarction?

A
  • 84% (of which 53% are thrombotic).
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100
Q

What causes cerebral infarction?

A
  • Interruption of cerebral blood flow due to thrombosis or emboli.
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101
Q

Peak age of cerebral infarction incidence?

A

> 70 years.

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102
Q

In which sex is cerebral infarction most likely?

A

Men.

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103
Q

Thrombotic cerebral infarctions are due to what?

A

Thrombosis in an atherosclerotic segment, most commonly the middle cerebral artery territory.

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104
Q

Thrombotic cerebral infarctions most commonly occur in which territory?

A

Middle cerebral artery.

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105
Q

Embolic cerebral infarctions are due to what?

A

Atheroma originating from the internal carotid, aortic arch or the heart.

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106
Q

Embolic cerebral infarctions most commonly occur where?

A

Branches of the middle cerebral arteries.

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107
Q

Name a rare cause of cerebral infarction.

A
  • Osteophytes compromising vertebral circulation.

- Vasculitis.

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108
Q

What are risk factors for cerebral infarction?

A
  • Atheroma (intra- and extra-cranial vessels).
  • Hypertension.
  • Serum lipids, obesity, smoking, drugs, diet.
  • Diabetes mellitus, heart disease.
  • Diseases of neck arteries.
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109
Q

Atheroma can affect all the main cerebral arteries, but which one in general is more commonly affected?

A

The basilar artery.

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110
Q

In cerebral infarction, the location, distribution and extend of parenchymal damage is determined by?

A
  • Arterial territory of affected artery.
  • Timescale of occlusion.
  • Extent of collateral circulatory relief (anastomoses/ collaterals).
  • Systemic perfusion pressure.
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111
Q

After 48 hours following cerebral infarction, what becomes visible macroscopically?

A

The necrotic area - which is more swollen and softer than its surrounding normal parenchyma. It is accentuated by loss of oedema in surrounding normal tissue.

Areas of haemorrhage may also be seen.

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112
Q

After 48 hours following cerebral infarction, what becomes visible microscopically?

A
  • ^ neutrophils.
  • Extravasation of RBCs (haemorrhagic conversion).
  • Activation of astrocytes and microglia.
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113
Q

Following cerebral infarction, at what point time does neutrophil infiltration drop off histologically?

A
  • After 48 hours.
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114
Q

Following cerebral infarction, neutrophils do what?

A

Phagocytose necrotic debris inc. myelin, which results in sharper demarcation at site of infarct.

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115
Q

A week after cerebral infarction, what process begins?

A

Reactive gliosis.

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116
Q

What is reactive gliosis?

A

Astrocytes increase in number and size following cerebral infarction.

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117
Q

A few weeks after cerebral infarction, what forms?

A

A cavity lined by a gliotic scar, characterised by astrocytes with abundant fine cytoplasmic processes.

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118
Q

As the gliotic scar desists, what remains as a permanent marker of infarction?

A

A cystic gap.

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119
Q

Haemorrhagic infarct occurs for what two main reasons?

A
  • BBB disruption/ deterioration in the context of a vasogenic oedema and ischaemia.
  • Intentional reperfusion results in haemorrhage through damaged vessels deteriorating the context of infarcted tissue.

+ Thrombolysis: vessel occlusion, usually by embolus with reperfusion and leakage through a damaged capillary bed following lysis of the embolus.

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120
Q

Carotid artery disease leading to cerebral infarction results in what symptoms?

A
  • Contralateral weakness or sensory loss.

- If dominant hemisphere affected there may be aphasia or apraxia.

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121
Q

What is apraxia?

A

Difficulty performing motor movements when asked despite having the ability to perform them, and difficulty speaking.

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122
Q

Middle cerebral artery disease leading to cerebral infarction results in what symptoms?

A
  • Weakness predominantly in the contralateral face and arm.
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123
Q

Anterior cerebral artery disease leading to cerebral infarction results in what symptoms?

A
  • Weakness and sensory loss in the contralateral leg.
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124
Q

Vertebro-basilar artery disease leading to cerebral infarction results in what symptoms?

A
  • Vertigo.
  • Ataxia.
  • Dysarthria.
  • Dysphasia.
    Complex “brain stem syndromes”.
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125
Q

Hyaline arteriolosclerosis results in?

A

Thinning and weakening of small vessel walls, making them more prone to occlusion and to rupture.

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126
Q

Chronic hypertension is associated with the development of?

A

Micro-aneurysms (Charcot-Bouchard).

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127
Q

Where do micro-aneurysms occur within the brain?

A

Commonly in small middle cerebral arteries - most commonly within the basal ganglia.

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128
Q

Rupture of micro-aneurysms within the brain lead to?

A

Intracerebral haemorrhage.

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129
Q

What are lacunar infarcts?

A

“Lake-like” infarcts of <15mm maximum in diameter.

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130
Q

Where do lacunar infarcts occur?

A

Where there is occlusion of a small penetrating vessel e.g. occlusion of part of a lenticulostriate artery.

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131
Q

In whom does hypertensive encephalopathy occur?

A
  • Severe hypertension.
  • Upper limit of autoregulatory mechanism overwhelmed.
  • BBB is incapable of resisting plasma protein and water movement leading to vasogenic oedema.
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132
Q

Symptoms of hypertensive encephalopathy?

A

Raised ICP:

  • Headache.
  • Vomiting.
  • Fits.
  • Confusion.
  • Coma.
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133
Q

Pathology shows what in hypertensive encephalopathy?

A
  • Cerebral oedema.
  • Herniations (tentorial and tonsillar).
  • Petechiae.
  • Arteriolar wall necrosis.
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134
Q

Clinical outcome of a lacunar infarct?

A

Depends entirely on area affected.

e. g. post-mortem may find infarct incidentally with no clinical correlate.
e. g. small lacunar infarct affecting internal capsule causes extensive motor weakness inc. face, arm and leg.

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135
Q

Give an example of a spontaneous intracranial haemorrhage.

A
  • Intracerebral haemorrhage.
  • Subarachnoid haemorrhage.
  • Haemorrhagic infarct.
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136
Q

Give an example of a traumatic intracranial haemorrhage.

A
  • Extra-dural haematoma.
  • Sub-dural haematoma.
  • Contusion (surface bruising).
  • Intracerebral haemorrhage.
  • Sub-arachnoid haemorrhage.
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137
Q

Why is hypertension an important factor in both subarachnoid and intracerebral haemorrhages?

A

Hyaline arteriolosclerosis of smaller vessels results in:

  • Reduced compliance thus predisposing to failure.
  • Micro-aneurysm formation.
  • Exacerbation of existing saccular aneurysms.

All of which increase chances of Subarachnoid haemorrhage.

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138
Q

In addition to hypertension, what are other contributing factors in intracerebral haemorrhage?

A
  • Aneurysms.
  • Systemic coagulation disorders.
  • Anti-coagulation.
  • Vascular malformations.
  • Amyloid deposits (cerebral amyloid angiopathy).
  • Open heart surgery.
  • Neoplasms.
  • Vasculitis (infec. and non-infec.).
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139
Q

Where does intracerebral haemorrhage occur?

A

Most commonly in basal ganglia.

- Also thalamus, cerebral white matter and the cerebellum.

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140
Q

In intracerebral haemorrhage, what morphology is observed on the cut surface?

A
  • Asymmetrical distortion (mass effect due to haematoma and oedema).
  • Various shifts and herniations.
  • Well-demarcated intra-parenchymal haematomas.
  • Softening of adjacent tissue (no necrosis - differentiates to infarct).
  • Surrounding oedema.
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141
Q

Amyloid angiopathy occurs in what disease?

A
  • Alzheimer’s.

- Ageing.

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142
Q

What is amyloid angiopathy?

A
  • Beta amyloid forms tightly packed beta-pleated sheets deposited within cerebral and meningeal vessels.
  • Vessels become less compliant and deal poorly with localised increased pressure, and may rupture as a result to form lobar intracerebral haemorrhages.
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143
Q

What are the two most important vascular malformations in terms of brain haemorrhage?

A
  • Arteriovenous malformations.

- Cavernous angiomas.

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144
Q

Why are anastomoses between an artery and vein (arteriovenous malformation) prone to rupture?

A

A vein can experience arterial pressure leading to vascular accommodation and remoulding, but the anastomosis can become a point of weakness - rupturing or forming aneurysms prone to rupture.

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145
Q

What is an arteriovenous malformation?

A

Shunting from artery to a vein that undergoes smooth muscle hypertrophy, is uncompliant and prone to rupture, also forming aneurysms which rupture.

  • Space occupying lesions which can grow and lead to focal neurological deficits.
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146
Q

In addition to bleeding, vascular malformations in the brain may also cause what symptoms?

A
  • Headaches.
  • Seizures.
  • Focal neurological deficits.
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147
Q

What is the most common congenital vascular abnormality of the brain?

A

Arteriovenous malformations.

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148
Q

Arteriovenous malformations are most common where?

A

In cerebral hemispheres of the middle cerebral artery territory.

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149
Q

Most common cause of subarachnoid haemorrhages?

A
  • Rupture of a saccular aneurysm (Berry aneurysm).
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150
Q

Berry aneurysms are present in what percentage of the population?

A

1%.

151
Q

Berry aneurysms arise where?

A

At arterial bifurcation in the territory of the internal carotid artery (90%).

Typically occurring at arterial bifurcations arising from the circle of Willis (10% in vertebro-basilar circulation).

152
Q

Saccular aneurysms enlarge with time, and are at great risk of rupture when they reach a diameter of?

A

6-10mm.

153
Q

Describe the effect of saccular aneurysms >25mm diameter.

A
  • Risk of rupture decreases.

- Symptoms due to mass effect predominate.

154
Q

Following subarachnoid haemorrhage due to aneurysm rupture, what may be seen?

A
  • Intracerebral haematomas adjacent to aneurysms.
  • Brain parenchyma infarcts (due to arterial spasm - 40% of cases).
  • Mass effect of haematoma and features of raised ICP.
155
Q

Risk factors of subarachnoid haemorrhage?

A
  • Smoking.
  • Hypertension.
  • Kidney disease.
156
Q

Subarachnoid haemorrhage is associated with which features?

A
  • Abrupt symptom onset.
  • Severe headache.
  • Vomiting.
  • Loss of consciousness.
157
Q

Subarachnoid haemorrhages are most common in which sex?

A

Females.

158
Q

Subarachnoid haemorrhage has higher incidence in patient with which diseases?

A
  • Polycystic kidneys.
  • Fibromuscular dysplasia.
  • Coarctation of aorta.
  • AVMs of the brain.
  • Developmental abnormality in collagen type 3.

+ smoking and hypertension.

159
Q

Symptoms of raised ICP?

A
  • Meningeal signs e.g. neck rigidity.
  • Visual symptoms.
  • Severe headache.
  • Loss of conscious.
160
Q

What are acute complications of subarachnoid haemorrhage?

A
  • Cerebral infarcts (4-9 days).
  • Acute hydrocephalus.
  • Herniation.
161
Q

What percentage of patients die within several days of subarachnoid haemorrhage onset?

A

50%.

162
Q

Demyelination is characterised by?

A

Defects in rate and consistency of neuronal conduction.

163
Q

Oligodendrocyte damage disrupts what?

A

Neuronal conduction.

164
Q

Demyelination causes what to myelin sheath?

A

Preferential damage to the myelin sheath.

165
Q

Give an example of a primary demyelinating disorder.

A
  • Multiple sclerosis.
  • Acute disseminated encephalomyelitis.
  • Acute haemorrhagic leukoencephalitis.
166
Q

Give an example of a secondary demyelinating disorder.

A
  • Viral: Progressive multifocal leukoencephalopathy (PML).
  • Metabolic: e.g. central pontine myelinosis.
  • Toxic: CO, organic solvents, cyanide.
167
Q

Briefly describe acute disseminated encephalomyelitis.

A
  • Primary demyelinating disorder.
  • Post-infectious auto-immune disorder.
  • Self-limited disorder most commonly affecting children.
168
Q

Briefly describe acute haemorrhagic leukoencephalitis.

A
  • Primary demyelinating disorder.
  • Post-infectious auto-immune disorder.
  • Rapidly fatal disease primarily affecting adults.
169
Q

When does central pontine myelinosis (secondary metabolic demyelination) occur?

A

In over-rapid therapeutic correction of hyponatraemia, triggering oligodendrocyte death and resultant demyelination.

170
Q

Why do organic solvents cause secondary demyelination?

A
  • Like dissolves like.

Oligodendrocytes are full of lipid and organic solvents dissolve such lipids - which is why they have ability to disrupt myelin sheath.

171
Q

What is the most common demyelinating disease?

A

Multiple sclerosis.

172
Q

Peak incidence of multiple sclerosis?

A

20-30 years old.

173
Q

Multiple sclerosis is more common in which sex?

A

Females.

174
Q

What is multiple sclerosis?

A
  • Auto-immune demyelinating disorder characterised by distinct episodes of neurological deficits, separated in time and which correspond to spatially separated foci of neurological injury.
175
Q

How is a clinical diagnosis of multiple sclerosis made?

A
  • Two distinct neurological defects occurring at different times.
  • Neurological defect implicating one neuroanatomical site and an MRI appreciated defect at another neuro-anatomical site.
  • Multiple distinct (usually white matter) CNS lesions on MRI.
176
Q

What investigations are supportive of a diagnosis of multiple sclerosis?

A
  • Visual evoked potentials (evidence of slowed conduction) during conduction studies.
  • Presence of 2 or more IgG oligoclonal bands in CSF.
177
Q

Multiple sclerosis often presents with a focal neurological deficit. How would an optic nerve lesion i.e. optic neuritis, present?

A

Unilateral visual impairment.

178
Q

Multiple sclerosis often presents with a focal neurological deficit. How would a spinal cord lesion present?

A
  • Motor or sensory deficit in trunk and limbs.
  • Spasticity.
  • Bladder dysfunction.
179
Q

Multiple sclerosis often presents with a focal neurological deficit. How would a brain stem lesion present?

A
  • CN signs.
  • Ataxia.
  • Nystagmus.
  • Internuclear ophthalmoplegia.
180
Q

Describe the clinical pattern of symptoms in MS?

A
  • Acute or insidious onset.
  • Relapsing and remitting.
  • Later becomes progressive.
181
Q

On T2 weighted MRI scans, in areas corresponding to white matter, demyelination shows up as?

A

Hyperintense regions.

182
Q

Multiple sclerosis is principally a disease of what?

A

White matter (where myelinated axons are concentrated).

183
Q

As Multiple sclerosis is principally a disease of white matter, the exterior brain surface usually appears normal. However, the cut surface of the brain shows what?

A

Plaques.

184
Q

What are plaques in the brain?

A
  • Various sized lesions which are well circumscribed and well demarcated.
  • Irregularly shaped.
  • Glassy, almost translucent appearance.
  • Non-anatomical distribution.
185
Q

Although plaques may occur at any site in the CNS, where are they commonly found?

A
  • CN II (optic).
  • Periventricular white matter.
  • Corpus callosum.
  • Brainstem.
  • Spinal cord.
186
Q

Describe the histology of active plaques in the CNS.

A
  • Perivascular inflammatory cells.
  • Microglia.
  • Ongoing demyelination.
187
Q

Describe the histology of inactive plaques in the CNS.

A
  • Gliosis.
  • Little remaining myelinated axons.
  • Oligodendrocytes and axons reduced in number.
188
Q

What are shadow plaques?

A

Inactive plaques that are less distinct and less well circumscribed than usual inactive plaques.

Due to a degree of peripheral remyelination or progressively thinning myelin sheaths.

189
Q

Describe the macroscopic appearance of acute active plaques.

A

Demyelinating plaques are yellow/brown with an ill-defined edge blending into surrounding white matter.

190
Q

Plaques tend to centre around what?

A

Small vessels.

191
Q

Describe the macroscopic appearance of inactive chronic plaques.

A
  • Well-demarcated grey/brown lesions in white matter.

- Classically situated around lateral ventricles.

192
Q

If inactive chronic plaques are large enough, they may be seen on the cut surface of the brain as?

A

Translucent brownish areas of gliotic scarring.

193
Q

What environmental factors are thought to contribute to MS?

A
  • Association with latitude, the further north the higher the incidence.
  • Vit. D deficiency: sunlight exposure??
  • Hypothetical viral trigger e.g. EBV.
194
Q

What genetic factors are thought to contribute to MS?

A
  • 15x risk if 1st degree relative has MS.
  • 150x risk with an affected monzygotic twin.
  • Genetic linkage to HLA DRB1.
  • Ass, with polymorphisms in IL-2 and IL-7.
195
Q

Why is MS an immune mediated disease?

A
  • Lymphocytic infiltration in histology.
  • Oligoclonal IgG bands in CSF.
  • Genetic linkage to HLA DRB1.
196
Q

Why are humoral factors/ antibody mediated immunity important in the cause of MS?

A
  • Oligoclonal IgG bands in CSF are seen in MS.

- Anti-B cell therapy, Rituximab is effective in reducing relapse severity and frequency.

197
Q

Give an example of a degenerative disease affecting the cerebral cortex.

A
  • Alzheimer’s.
  • Pick’s disease.
  • Creutzfeld-Jakob disease (CJD).
198
Q

Give an example of a degenerative disease affecting the basal ganglia and brain stem.

A
  • Parkinson’s.
  • Progressive supranuclear palsy.
  • Multiples system atrophy.
  • Huntington’s disease.
199
Q

Give an example of a degenerative disease affecting the spinocerebellar tract.

A
  • Spinocerebellar ataxias e.g. Friedreich Ataxia.
200
Q

Give an example of a degenerative disease affecting the motor neurones.

A

Motor neuron disease.

201
Q

Degenerative diseases are pathologically characterised by?

A

Simple neuronal atrophy and subsequent gliosis.

202
Q

Define dementia.

A

Acquired and persistent general disturbance of higher mental functions in an otherwise fully alert person.

203
Q

Neurodegenerative diseases are characterised by?

A
  • Progressive loss of neurons typically affecting funtionally related neuronal groups.
  • Often symmetrical involvement.
204
Q

Is dementia part of the normal ageing process?

A

No, it is always pathological.

205
Q

What are the two groups of dementia classification?

A
  • Primary dementia.

- Secondary dementia.

206
Q

How do primary and secondary dementias differ?

A
  • Primary arises of their own accord.

- Secondary arise from another underlying disorder e.g. trauma.

207
Q

Give an example of a primary dementia.

A
  • Alzheimer’s (60-75%).
  • Lewy body dementia.
  • Pick’s disease (fronto-temporal dementia).
  • Huntington’s disease.
208
Q

Name a cause of secondary dementia.

A
  • Multi-infarct (vascular) dementia.
  • Infection (HIV, syphilis).
  • Trauma.
  • Metabolic.
  • Drugs and toxins (alcohol).
  • Vitamin deficiencies (Vitamin B1).
  • Paraneoplastic syndromes.
  • Intracranial space occupying lesions.
  • Chronic hydrocephalus.
209
Q

What is the most common cause of dementia in the elderly?

A
  • Alzheimer’s disease.
210
Q

How do symptoms tend to present with increasing age at presentation of Alzheimer’s?

A

The later the onset, the more severe and rapid changes tend to be.

211
Q

Is alzheimer’s more common in men or women?

A

F:M is 2:1.

212
Q

Although Alzheimer’s is a generally sporadic condition, what percent of cases are familial?

A

1%.

213
Q

There is an increased incidence of Alzheimer’s disease in those with which chromosome abnormality?

A

Trisomy 21 (amyloid precursor protein).

214
Q

How does Alzheimer’s disease present?

A

Insidious impairment of higher intellectual function with alterations in mood and behaviour.

215
Q

What are the later stages of Alzheimer’s disease?

A
  • Progressive disorientation.
  • Memory loss and aphasia indicating severe cortical dysfunction.
  • Profound disability, muteness and immobility.
216
Q

Death in Alzheimer’s usually occurs due to what?

A

A secondary cause e.g. bronchopneumonia.

217
Q

Macroscopic pathology of Alzheimer’s?

A
  • Cortical atrophy esp. frontal, temporal and parietal lobe atrophy.
  • Widening of sulci.
  • Narrowing of gyri.
  • Compensatory dilatation of ventricle (2y hydrocephalus ex vacuo).
  • Sparing of occipital lobe, brainstem and cerebellum.
218
Q

Microscopic features of Alzheimer’s?

A
  • Extensive neuronal loss with astrocyte proliferation i.e. lost neurones replaced with astrocyte gliosis.
  • Neurofibrillary tangles.
  • Neuritic plaques.
  • Amyloid angiopathy.
219
Q

What are neurofibrillary tangles?

A

Bundles of insoluble microtubules in neuron cytoplasm.

220
Q

What dysregulated protein is a major component in Alzheimer’s?

A

Tau protein.

221
Q

What are neuritic plaques?

A

Focal, spherical collections of dilated tortuous neuritic processes of neurons surrounding a central amyloid core.

222
Q

Amyloid Aβ is produced by?

A

Cleavage of amyloid precursor protein (APP).

223
Q

What is the central element of neuritic plaques?

A

Aβ amyloid.

224
Q

Why is Down’s syndrome (Trisomy 21) associated with early onset of Alzheimer’s?

A

Amyloid precursor protein is on Chromosome 21.

225
Q

What is the most common familial cause of Alzheimer’s?

A

Apolipoprotein E - allele e4.

- Dysregulates APP.

226
Q

Which feature seen in Alzheimer’s brains shows polymerised β-pleated sheets formed by Aβ?

A

Amyloid angiopathy.

227
Q

Amyloid angiopathy disrupts the BBB, causing what?

A
  • Serum leakage.
  • Local oedema.
  • Local hypoxia.
  • Exacerbation of oxidative stress, excitotoxicity and neuronal injury.
228
Q

Amyloid angiopathy stains with what?

A

Congo red.

229
Q

What may be seen microscopically in amyloid angiopathy?

A
  • Extracellular eosinophilic accumulation.

- Polymerised β-pleated sheets formed by Aβ.

230
Q

What is a Lewy body dementia?

A

3rd most common dementia.

Progressive + hallucinations + fluctuating levels of attention/cognition.

Some overlap with Alzheimer’s but memory is affected later.

231
Q

Features of Parkinsonism present when in Lewy Body Dementia?

A

At onset or shortly after.

232
Q

How may Parkinsonism display clinically?

A
  • Loss of facial expression, stooping, shuffling gait, slow initiation of movements, stiffness and pill rolling tremor.
233
Q

Parkinsonism is seen in conditions affecting which pathway?

A
  • Nigro-striatal dopaminergic pathways.
234
Q

Pathological features of Lewy Body dementia?

A

Degeneration of substantia nigra (seen in Parkinson’s).

235
Q

Macroscopic features of Lewy Bodies Dementia?

A
  • Pallor in substantia nigra (where pigmented dopaminergic neurons run).
236
Q

Microscopic features of Lewy Body Dementia?

A
  • Loss of pigmented neurons.
  • Reactive gliosis, microglial accumulation.
  • Remaining neurons may show lewy bodies.
  • Fewer cortical Lewy bodies.
237
Q

What are Lewy bodies?

A

Eosinophilic intracytoplasm inclusions with a round to elongated body that have a dense core and a surrounding pale halo.

They are aggregates of a-synuclein and ubiquitin.

238
Q

What is Huntington’s disease?

A

Relentlessly progressive neuropsychiatric disorder inherited by autosomal dominance.

239
Q

Clinical features of Huntington’s disease?

A

Emotional , cognitive and motor disturbances.

240
Q

Symptoms of Huntington’s disease?

A
  • Chorea.
  • Myoclous.
  • Clumsiness.
  • Slurred speech.
  • Depression.
  • Irritability.
  • Apathy.
  • Dementia.
241
Q

Huntington’s is inherited by which pattern?

A

Autosomal dominant.

242
Q

The Huntingtin gene is found on which chromosome?

A

4p.

243
Q

What causes Huntington’s Disease?

A

Mutation of Huntingtin gene on chromosome 4p causing additional CAG repeats.

244
Q

How many CAG repeats must there be to cause Huntington’s disease?

A

Disease penetrant when >35 repeats occur.

<28 is still normal.

245
Q

How many years from symptom onset to death in Huntington’s disease?

A

Typically 15 years.

246
Q

Macroscopic pathological features of Huntington’s?

A
  • Atrophy of basal ganglia, caudate nucleus and putamen.

- Later cortical atrophy.

247
Q

Microscopic pathological features of Huntington’s?

A
  • Simple neuronal atrophy of striatal neurones of the basal ganglia, most severely in caudate nucleus.
  • Pronounced astrocytic gliosis.
248
Q

What is another name for fronto-temporal dementia?

A

Pick’s disease.

249
Q

What is fronto-temporal dementia (Pick’s disease)?

A

Progressive dementia with onset in middle life 50-60, characterised by progressive changes in character and social deterioration leading to impaired intellect, memory and language.

250
Q

Symptoms of fronto-temporal dementia (Pick’s disease)?

A
  • Personality and behavioural change.
  • Speech and communication problems.
  • Changes in eating habits.
  • Reduced attention span.
251
Q

Describe progression of fronto-temporal dementia (Pick’s disease).

A

Rapidly progressive, lasting between 2-10 years with mean length around 7 years.

Personality changes correspond with frontal lobe atrophy, language issues with temporal lobe atrophy.

252
Q

What causes fronto-temporal dementia (Pick’s disease)?

A

Extreme atrophy of cerebal cortex and later in the temporal lobes.

253
Q

What does the brain weigh in fronto-temporal dementia (Pick’s disease)?

A

Often <1kg implying loss of 300-400g.

254
Q

Microscopic pathology of fronto-temporal dementia (Pick’s disease)?

A
  • Neuronal loss, gliosis.
  • Pick’s cells (swollen neurons).
  • Intracytoplasmic filamentous inclusions - Pick’s bodies.
255
Q

Pick’s bodies are enriched in what?

A

Tau protein.

256
Q

What is multi-infarct dementia?

A

Deteriorating mental function due to cumulative damage to brain through hypoxia or anoxia due to multiple blood clots within the vessels supplying the brain.

257
Q

How do multiple infarcts cause dementia?

A

The successive, multiple cerebral infarctions cause growing areas of cell death and damage. When a sufficient portion of the brain is damaged, dementia results.

258
Q

Are men or women more commonly affected by multi-infarct dementia?

A

Men.

259
Q

Multi-infarct dementia becomes more common after which age?

A

60.

- Also seen in middle-age hypertensives.

260
Q

Sufferers of multi-infarct dementia who are aware of mental deficits are prone to?

A

Depression and anxiety.

261
Q

What clues may suggest multi-infarct dementia rather than Alzheimer’s disease?

A
  • Abrupt onset.
  • Stepwise progression.
  • Hx of hypertension or stroke.
  • Evidence of stroke on CT or MRI.
262
Q

What type of infarct is more common in multi-infarct dementia?

A
  • Large vessel infarcts.
  • Scattered throughout hemispheres.
  • Atheroma of large cerebral arteries which provoke thromboembolism.
263
Q

Describe the rarer infarcts causing multi-infarct dementia?

A
  • Small vessel (lacunar) infarcts.
  • Central, subcortical distribution.
  • Hx of lonstanding hypertension and arteriosclerosis of small vessels.
264
Q

What separates cerebral hemispheres?

A

Falx cerebri.

265
Q

What overlies the cerebellum?

A

Tentorium cerebelli.

266
Q

If the brain swells, what must happen?

A
  • Blood +/- CSF must leave the cranial vault to prevent rising pressure.
267
Q

If reduction in blood and CSF can no longer compensate for increasing brain swelling, what happens?

A

Rapid increases in ICP.

  • Flattened venous sinuses.
  • Little or no CSF.
268
Q

What may cause raised ICP?

A
  • Increased CSF.
  • Focal brain lesion.
  • Diffuse brain lesion.
  • Increased venous volume.
  • Physiological mechanisms (hypoxia, pain, hypercapnia).
269
Q

Define hydrocephalus.

A

Excess accumulation of CSF within the ventricular system of the brain.

270
Q

CSF is produced by?

A

Choroid plexus in lateral and fourth ventricles.

271
Q

CSF is absorbed by?

A

Arachnoid granulations.

272
Q

What causes hydrocephalus?

A
  • Obstructed CSF flow e.g. inflammation, pus and tumours.
  • Decreased CSF resorption (post SAH or meningitis).
  • CSF overproduction (very rare - choroid plexus tumours).
273
Q

What is non-communicating hydrocephalus?

A

Obstruction to CSF flow occurs within ventricular system.

274
Q

What is communicating hydrocephalus?

A

Obstruction CSF flow occurs outside of ventricular system e.g. in subarachnoid space or at arachnoid granulations.

275
Q

Give a cause of communicating hydrocephalus.

A
  • Post SAH, infective bacterial meningitis.
276
Q

Give a cause of non-communicating hydrocephalus.

A
  • Arnold chiari malformations.
277
Q

If hydrocephalus occurs before the closure of cranial sutures, what happens?

A

Cranial enlargement.

278
Q

If hydrocephalus occurs after suture closure, what happens?

A

Ventricle expansion and increased ICP.

  • Flattening of gyri and fullness of sulci.
279
Q

What is hydrocephalus ex vacuo?

A

Hydrocephalus due to loss of brain parenchyma. Ventricles expand and CSF pool grows to account for change in intracranial volume.

280
Q

In which diseases does hydrocephalus ex vacuo occur?

A
  • Any disease that causes atrophy e.g. Alzheimer’s.
281
Q

What are the effects of raised ICP?

A
  • Intracranial shifts and herniations - “coning”.
  • Midline shift.
  • Distortion and pressure on CNs and vital neurological centres.
  • Impaired blood flow.
  • Reduced level of consciousness.
282
Q

What are the three most common forms of brain herniation?

A
  • Subfalcine.
  • Tentorial.
  • Tonsillar.
283
Q

Describe subfalcine herniation.

A

Unilateral or asymmetric expansion of cerebral hemisphere displaces the cingulate gyrus under the falx cerebri.

284
Q

Subfalcine herniation is associated with compression of which structure?

A

Anterior cerebral artery.

285
Q

How does compression of the anterior cerebral artery manifest in subfalcine herniation?

A
  • Weakness and/ or sensory loss in leg, because of ischaemia to primary motor and/ or sensory cortex in these areas.
286
Q

Describe tentorial herniation.

A

Medial aspect of temporal lobe (hippocampal uncus and parahippocampal gyrus) herniates over tentorium cerebelli.

287
Q

Tentorial herniation is associated with compression of what and how does this manifest?

A
  • Ipsilateral CN III and its parasympathetic fibres.

- Manifests as pupillary dilation and impaired ocular movements on the side of the lesion.

288
Q

Describe tonsillar herniation.

A

Displacement of cerebellar tonsils through foramen magnum.

289
Q

Why is tonsillar herniation life threatening?

A

Causes brainstem compression and compromises vital respiratory centres in medulla oblongata.

290
Q

What is transcalvarial herniation?

A

Swollen brain will herniate through any defect in the dura and skull.

291
Q

What are symptoms of brain herniation?

A
  • Reduced level of consciousness.
  • Dilated pupil on same side as mass lesion.
  • Bradycardia, increased pulse pressure and increased MAP.
  • Cheyne-Stokes respiration.
292
Q

What clinical signs suggest raised ICP?

A
  • Papilloedema.
  • Headache.
  • Nausea and vomiting.
  • Neck stiffness.
293
Q

What features of a headache suggest raised ICP?

A

Worse on lying down, coughing, sneezing, straining.

294
Q

What causes neck stiffness in raised ICP?

A

Pressure on dura around cerebellum and brainste,.

295
Q

Why does nausea and vomiting occur in raised ICP?

A

Pressure on vomiting centres in pons and medulla.

296
Q

Give an example of a space occupying lesion.

A
  • Tumour.
  • Abscess[es].
  • Haematoma[s].
  • Localised brain swelling.
  • Infection.
  • Haemorrhage.
297
Q

The majority of brain tumours present as?

A

Focal neurological symptoms and headache that is worse in mornings.

298
Q

Brain tumours in children are generally found where?

A

Below tentorium cerebelli.

299
Q

Brain tumours in adults are generally found where?

A

Above tentorium cerebelli.

300
Q

Are brain metastases or primary tumours more common?

A

Metastases.

301
Q

Cancers which most commonly metastasise to the brain?

A
  • Breast, bronchus, kidney, thyroid and colon carcinomas.

- Malignant melanoma.

302
Q

Brain metastases are often found where?

A

At the boundaries between grey and white matter.

303
Q

The presence of multiple intracerebral tumours is indicative that their origin is?

A

Metastatic.

Solitary tumours are more likely to be primary.

304
Q

Why is the distinction between benign and malignant tumours not so relevant in the brain?

A

High grade tumours may not metastasise and benign lesions can kill simply due to their location in the brain.

305
Q

CNS tumours are classified according to what?

A

Presumed cell of origin.

306
Q

Most common subtype of primary brain tumour in adults?

A

Astrocytoma.

- Also meningiomas are common.

307
Q

Most common subtype of primary brain tumour in children?

A

Medulloblastoma.

- Also low grade astrocytoma are common.

308
Q

Describe Grade I pilocytic astrocytoma.

A

Distinct childhood tumour that do not progress to become higher grade.
- Benign behaving, long hair like processes, cystic areas.

309
Q

Well differentiated Grade II astrocytomas have an average survival of?

A

approx. 5 years.

310
Q

What happens to well differentiated grade II astrocytomas with time?

A

They become more poorly differentiated and more anaplastic, thus becoming more clinically aggressive.

311
Q

Grade IV glioblastomas have an average survival time of what, following diagnosis?

A

10 months.

312
Q

Grade IV glioblastomas may occur secondary to?

A

Well differentiated or anaplastic astrocytoma.

They may also occur de novo or as a primary form.

313
Q

What leads to neoangiogenesis (increased vascularity) in high grade brain lesions?

A

VEFG secretion by tumour.

314
Q

Medulloblastoma accounts for what percentage of paediatric CNS neoplasms?

A

20%.

315
Q

Describe medulloblastomas.

A
  • Poorly differentiated/embryonal (resemble primitive undifferentiated embryonal cells).
  • Occurs in midline of cerebellum.
316
Q

Untreated medulloblastoma have poor prognosis, but fortunately they are extremely sensitive to?

A

Radiotherapy.

317
Q

What is the 5 year survival rate of medulloblastoma with resection and radiotherapy?

A

75%.

318
Q

Medulloblastomas tend to occur where?

A

Below tentorium cerebelli in the midline.

319
Q

A single abscess in the brain may arise due to?

A
  • Local extension e.g. mastoiditis, chronic otitis media, paranasal sinusitis, nasal/facial/dental infection.
  • Direct implantation e.g. skull fracture, penetrating injury.

Tend to occur adjacent to source.

320
Q

Multiple brain abscesses may arise due to?

A
  • Haematogenous spread e.g. bronchopneumonia, bacterial endocarditi, lung abscess, congenital heart disease, IV drug use.

Tend to occur at boundary of grey and whtie matter.

321
Q

Symptoms of brain abscess?

A
  • Fever, raised ICP.

- Symptomsof underlying cause.

322
Q

How is a brain abscess diagnosed?

A

CT or MRI.

323
Q

How are brain abscess treated?

A

Aspiration of pus for culture and treatment.

324
Q

Brain abscess is associated with significant mortality and thus requires what?

A

Weeks of antibiotics.

325
Q

What is bacterial meningits?

A

Inflammation of leptomeninges and CSF within subarachnoid space due to bacterial infection.

326
Q

What can be seen in CSF of bacterial meningitis?

A
  • Many polymorphs.

- Reduced glucose.

327
Q

Resolution of bacterial meningitis may be followed by?

A
  • Arachnoiditis.
  • Obliteration of subarachnoid space.
  • Obstructive hydrocephalus.
328
Q

Arachnoiditis may cause?

A
  • Lack of CSF absorption.
  • Hydrocephalus.
  • Raised ICP.
329
Q

E. Coli gram stain?

A

Gram negative rods.

330
Q

H. Influenzae gram stain?

A

Gram negative cocco-bacilli.

331
Q

N. Meningitidis gram stain?

A

Gram negative diplococci.

332
Q

S. Pneumoniae gram stain?

A

Gram positive cocci in chains.

333
Q

L. Monocytogenes gram stain?

A

Gram positive rods.

334
Q

In pathology, head injury is classifed into?

A
  • Missile (penetrating).

- Non-missile (blunt).

335
Q

Describe penetrating/ missile injury to the head.

A
  • Focal damage.
  • Lacerations in the region of brain damage.
  • Haemorrhage.
  • High vs low velocity impacts.
336
Q

If the penetrating missile in head injury exits the skull, is this a bad or good for clinical outcome?

A

Bad - indicated high velocity nature in whichinjury extent can be far greater.

337
Q

what is non-missile/ blunt injury of the head?

A
  • Sudden acceleration and/or deceleration. e.g. being hit with a bat or falling on your head.
338
Q

What is primary brain injury?

A
  • Damage to the brain at time of injury.

- Currently irreversible.

339
Q

What is secondary brain injury?

A
  • Potentially treatable.

- Haemorrhage, oedema.

340
Q

What is a linear skull fracture?

A

Straight, sharp fracture line that may cross sutures (diastatic fracture).

341
Q

What is a compound skull fracture?

A

Associated with full thickness scalp lacerations.

342
Q

The presence of a linear fracture greatly increases the chance of what?

A

Presence or likelihood of emerging clinically important haematoma.

343
Q

What is a depressed skull fracture?

A

Break in cranial bone with depression of the bone in toward the brain.

344
Q

Base of skull fractures are always regarded as compound or open given high probability of what?

A

e.g. that the adjacent paranasal sinuses have also been torn and the fracture is therefore open to outside world.

345
Q

What are surface contusions of the brain?

A

Usually asymmetrical bruises caused by tissue damage following severe compressive strains.

346
Q

With time, what happens to contusions of the brain?

A

They become brown shrunken scars.

347
Q

Coup tends to occur where?

A

To the brain at the side/ point of impact.

348
Q

Contracoup occurs where?

A

Diametrically opposite the point of impact.

349
Q

Which are often worse, coup or contracoup injuries?

A

Contracoup.

350
Q

Coup and contracoup injuries tend to cause compressive strains and thus cause?

A

Contusion and laceration.

351
Q

When does diffuse axonal injury occur?

A

Occurs at moment of injury, and affects central areas.

Due to shearing strains.

352
Q

What results from diffuse axonal injury?

A
  • Reduced consciousness and coma.

- Possibly lead to vegetative state.

353
Q

What happens to cerebral metabolism in head injury?

A

It is decreased.

354
Q

What is cytotoxic oedema?

A

A pre-morbid process where dying cells accumulate water as ions move into cells bringing water with them.

355
Q

When does cytotoxic oedema occur?

A

Intoxication, Reye’s and severe hypothermia.

356
Q

what is ionic oedema?

A

First dysfunction of BBB. Cytotoxic oedema, leaves extracellular space devoid of Na+ so Na+ ions cross BBB and consequently drive Cl- transport creating osmotic gradient for water accumulation.

357
Q

What is vasogenic oedema?

A

Deterioration and breakdown in BBB (disruption of endothelial tight junctions) allows plasma proteins e.g. albumin to cross into extracellular space and water follows.

358
Q

What is haemorrhagic conversion?

A

Endothelial integrity is completely lost and blood can enter the extracellular space.
Extravasation of RBCs occurs in up to 30-40% of ischaemic strokes.

359
Q

Describe location of traumatic haematomas.

A

Most are supratentorial, unilateral and intradural.

360
Q

What is a burst lobe?

A

Subdural in continuity with intracerebral haematoma.T

Gross contusion disrupting much of the frontal and temporal lobes and associated with a significant degree of haemorrhage.

361
Q

Traumatic extradural haematomas are usually a complication of what?

A

Fracture in tempero-parietal region often involving middle meningeal artery.

Immediate brain damage is often minimal.

362
Q

If a traumatic extradural haematoma goes untreated, what happens?

A

Midline shift of brain due to compression and herniation.

363
Q

Extradural haematomas require what?

A

Prompt evacuation by surgery.

364
Q

What are subdural haematomas?

A

Collections of blood between internal surface of dura and arachnoid tending to occur over cerebral convexities.

365
Q

What causes acute subdural haematomas?

A

Disruption of bridging veins that extend from brain surface into subdural space perforating the dura.

366
Q

What causes disruption of bridging veins and subsequent acute sub-dural haematoma?

A

Injury associated with rapid change in head velocity.

367
Q

Why are gyral contours preserved in acute sub-dural haematoma?

A

Pressure is evenly distributed.

368
Q

What happens to cerebrum on the side of the haematoma in acute sub-dural haematoma?

A

Cerebrum swells.

369
Q

What happens to non-treated, non fatal acute sub-dural haematoma?

A

They become liquified and form a yellowish neomembrane.

370
Q

Acute sub-dural haematoma has a mortality of?

A

> 60%.

371
Q

Chronic subdural haemorrhages are less frequently associated with what, and more often associated with what?

A
  • Less often ass. with well-defined traumatic insult.

- More often ass. with brain atrophy.

372
Q

Chronic subdural haemorrhages are composed of what?

A

Liquiefied blood/yellow tinged fluid separated from the inner surface of dura and underlying brain by a neomembrane.

373
Q

Blood vessels within the neomembrane are abnormally permable, leading to what in Chronic Subdural haemorrhage?

A

Continuous accumulation of fluid and recurrent haematomas.

CNS CLERKSHIP (43 decks)

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