NEUROLOGY > Neuropathology > Flashcards

Neuropathology Flashcards

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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
Intranuclear and cytoplasmic inclusions are seen in?
Viral infections affecting the brain.
26
What do astrocytes look like?
- Star-shaped. | - Multipolar cytoplasmic processes.
27
Where are astrocytes located?
Throughout the CNS.
28
What is the function of astrocytic processes?
- Envelop synaptic plates. | - Wrap around vessels and capillaries within the brain.
29
What is the role of astrocytes?
- Ionic, metabolic and nutritional homeostasis. - Work alongside endothelial cells to maintain BBB. - Main cell involved in repair and scar formation (lack of fibroblasts).
30
Astrocytes perform anaerobic glycolysis to produce what and why?
Lactate to be transferred to neurons for use as a metabolite in the production of ATP. Astrocytes are therefore metabolically coupled to neurones.
31
How is synaptic function of neurones coupled to astrocytes?
Astrocytes envelop synaptic plates where they take up Glutamate from synapse and recycle it to neurons.
32
How do astrocytes regulate the BBB and cerebral blood flow?
They have foot processes entirely enveloping intracerebral small vessels and capillaries. They respond to neuronal signals.
33
What is the most important histopathological indicator of CNS injury, regardless of cause?
Gliosis (an astrocytic response).
34
What is gliosis?
- Astrocytes undergo hyperplasia and hypertrophy (more and larger). - Develop enlarged vesicuar nuclei and prominent nucleoli. - Cytoplasmic expansion with extension of ramifying processes.
35
What do old lesions of gliosis look like?
- Nuclei become small, dark and lie in a dense net of processes (glial fibrils).
36
Describe gliotic tissue and its function.
- Translucent and firm. | - Limiting barrier to sites of tissue damage.
37
What is the function of oligodendrocytes?
Wrap around axons to form myelin sheath.
38
What is the CNS equivalent of a Schwann cell?
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.
39
What is the (relatively limited) reaction to injury of oligodendrocytes?
- Variable patterns of demyelination. - Variable degrees of demyelination. - Apoptosis.
40
Oligodendrocytes are sensitive to what type of damage?
Oxidative damage.
41
Oligodendrocyte damage is a feature of which disorders?
Demyelinating disorders.
42
Myelin insulation allows for what?
- Saltatory conduction (nodes of Ranvier). - Contain depolarisation locally (prevents leakage to adjacent axons). - Provides barrier to injury.
43
What is Wallerian degeneration?
Axonal damage causing antegrade degeneration of the axon to the nearest node.
44
Why are oligodendrocytes sensitive to oxidative damage?
Low anti-oxidant reserves and high intracellular iron. They will die in response to significant hypoxic injury.
45
Disruption of the myelin sheath is characterised by?
Abnormalities in neuronal conduction.
46
Axonal loss is generally irreversible in the CNS why?
Oligodendrocytes do not have the same reparative ability as Schwann cells of the PNS.
47
Ependymal cell function?
Line the ventricular system.
48
Ependymal cell reaction to injury?
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.
49
Disruption of ependymal cells can cause what?
- Local reactive proliferation of sub-ependymal astrocytes to produce small irregularities on ventricular surfaces: Ependymal granulations.
50
What may produce changes in ependymal cells?
Infectious agents and viruses.
51
Ependymal cells can form tumours causing what?
Due to position in ventricular system, they can obstruct CSF flow - pathological consequences.
52
What are microglia?
Embryologically derived cells that function as a macrophage system using phagocytosis. The "CNS immune cell".
53
How do microglia respond to injury?
- Proliferation. - Recruited through inflammatory mediators. - Form aggregates around areas of necrotic and damaged tissues.
54
Microglia are important mediators in acute nervous system injury, describe their role.
- M2: anti-inflammatory, phagocytic, more acute. | - M1: pro-inflammatory, more chronic.
55
Describe M1 type microglia.
- 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.
56
What causes of hypoxia damage the brain?
- Cerebral ischaemia. - Cerebral infarct. - Haemorrhages. - Trauma. - Cardiac arrest. - Cerebral palsy.
57
The brain consumes what percentage of total body resting oxygen consumption?
20%.
58
What is the maximum that cerebral blood flow can increase to maintain oxygen delivery in ischaemia?
- Two fold.
59
After ischaemia onset in the brain, mitochondrial inhibition of ATP synthesis leads to?
- Consumption of ATP reserves within minutes.
60
What CNS cells are most vulnerable to hypoxia?
Neurones.
61
Why are neurones the most vulnerable CNS cells to hypoxia?
They are metabolically dependant on oxidative phosphorylation.
62
What is the principle mechanism through which hypoxia exerts its toxic influence?
Energy failure of neurones, accumulating injurious oxidative stress and excitotoxicity.
63
What are the most important mechanisms in excitotoxicity?
Glutamate and Oxygen free radical formation causing Calcium influx.
64
Activation of glutamate receptors in excitotoxicity causes?
Uncontrolled calcium entry into cell.
65
Uncontrolled calcium entry into cells during excitotoxicity triggers?
- Protease activation. - Mitochondrial dysfunction. - Oxidative stress. - Apoptosis and necrosis.
66
Energy failure prevents glutamate recycling through astrocytes, enhancing?
Glutamate accumulation and excitotoxicity.
67
What is cytotoxic oedema?
Pre-morbid process in which dying cells accumulate water as osmotically active ions (Na+ and Cl-) move into cells, bringing water with them.
68
Cytotoxic oedema can enhance what?
Ionic and vasogenic oedema.
69
What may cause cytotoxic oedema?
- Intoxication. - Reye's. - Severe hypothermia.
70
What is the first dysfunction of the blood brain barrier?
Ionic oedema.
71
What are the causes of ionic oedema?
- Hyponatraemia. | - Excess water intake e.g. SIADH.
72
How does ionic oedema occur?
- 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.
73
Vasogenic oedema occurs with?
- 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.
74
How does haemorrhagic conversion occur?
- When endothelial integrity is lost and blood is allowed to enter the extracellular space. - Extravasation of RBCs occur in 30-40% of ischaemic strokes.
75
The anterior carotid arteries are paired blood vessels, supplying oxygenated blood to what?
Most midline portions of frontal and superior medial parietal lobes.
76
The middle cerebral artery arises from what?
The internal carotid.
77
The middle cerebral artery arises from internal carotid and continues where?
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.
78
What supplies oxygenated blood to posterior aspect of brain - the occipital lobe?
The posterior cerebral arteries.
79
Disruption of blood supply to the following area will result in which symptoms? - Anterior cerebral artery territory.
- Sensory and motor abnormalities of the the trunk and legs. - Frontal lobe dysfunction. - Higher cognitive dysfunction.
80
Disruption of blood supply to the following area will result in what? - Middle cerebral artery territory.
- Deficits of the majority of the sensory and motor cortex.
81
Disruption of blood supply to the following area will result in which symptoms? - Posterior cerebral artery territory.
- Occipital lobes: homonymous hemianopia with visual field defect in both eyes on the same side as the lesion.
82
The brain requires what?
Active aerobic metabolism of glucose.
83
Autoregulatory mechanisms of the brain help to maintain what?
Blood flow at a constant rate by dilatation and constriction of cerebral vessels.
84
What is cerebrovascular disease?
Any abnormality of the brain caused by a pathological process of blood vessels.
85
Give an example of Cerebrovascular disease.
- Brain ischaemia and infarction. - Haemorrhage. - Vascular malformation. - Aneurysm.
86
Cerebrovascular disease involves what general processes?
- 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.
87
What may cause global hypoxic ischaemic cerebral damage?
- Generalised reduction in blood flow/oxygenation. - Cardiac arrest. - Severe hypotension e.g. trauma with hypovolaemic shock.
88
What may cause focal cerebral ischaemia?
Vascular obstruction.
89
What is global hypoxic ischaemic cerebral damage?
When systemic circulation compromise cannot be compensated for by CNS auto-regulatory mechanisms,
90
What is focal cerebral ischaemia?
Restriction of blood flow to a localised area of the brain. | - Typically due to vascular obstruction.
91
What may a cause generalised reduction in cerebral perfusion?
- Cardiac arrest. - Shock/severe hypotension. - Trauma. Where autoregulatory mechanisms cannot compensate.
92
Which "watershed" areas of the brain are particularly sensitive to global hypoxic ischaemic damage?
Zones between two arterial territories e.g. parieto-occipital.
93
Which neurons are more sensitive than the others to global hypoxic ischaemic damage?
- 3rd and 5th layer neurones of Neocortex. - CA1 neurones of Hippocampus. - Purkinje cells of cerebellum.
94
At what mean arterial pressure is there a generalised reduction of cerebral perfusion?
<50mmHg. | The point at which autoregulatory mechanisms cannot sufficiently compensate.
95
Why are "watershed" areas particularly sensitive to hypoxia?
- At the periphery of vascular territories, most distant from the heart and least well-supplied.
96
Define stroke.
Sudden disturbance of cerebral function of vascular origin that either causes death or lasts over 24 hours.
97
Stroke is classified clinically into what three categories?
- Completed strokes. - Evolving strokes. - Transient ischaemic attacks.
98
Completed strokes result in what?
Irreversible tissue loss due to local arrest or severe reduction in cerebral blood flow.
99
Epidemiological evidence suggest that what percent of strokes are due to infarction?
- 84% (of which 53% are thrombotic).
100
What causes cerebral infarction?
- Interruption of cerebral blood flow due to thrombosis or emboli.
101
Peak age of cerebral infarction incidence?
>70 years.
102
In which sex is cerebral infarction most likely?
Men.
103
Thrombotic cerebral infarctions are due to what?
Thrombosis in an atherosclerotic segment, most commonly the middle cerebral artery territory.
104
Thrombotic cerebral infarctions most commonly occur in which territory?
Middle cerebral artery.
105
Embolic cerebral infarctions are due to what?
Atheroma originating from the internal carotid, aortic arch or the heart.
106
Embolic cerebral infarctions most commonly occur where?
Branches of the middle cerebral arteries.
107
Name a rare cause of cerebral infarction.
- Osteophytes compromising vertebral circulation. | - Vasculitis.
108
What are risk factors for cerebral infarction?
- Atheroma (intra- and extra-cranial vessels). - Hypertension. - Serum lipids, obesity, smoking, drugs, diet. - Diabetes mellitus, heart disease. - Diseases of neck arteries.
109
Atheroma can affect all the main cerebral arteries, but which one in general is more commonly affected?
The basilar artery.
110
In cerebral infarction, the location, distribution and extend of parenchymal damage is determined by?
- Arterial territory of affected artery. - Timescale of occlusion. - Extent of collateral circulatory relief (anastomoses/ collaterals). - Systemic perfusion pressure.
111
After 48 hours following cerebral infarction, what becomes visible macroscopically?
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.
112
After 48 hours following cerebral infarction, what becomes visible microscopically?
- ^ neutrophils. - Extravasation of RBCs (haemorrhagic conversion). - Activation of astrocytes and microglia.
113
Following cerebral infarction, at what point time does neutrophil infiltration drop off histologically?
- After 48 hours.
114
Following cerebral infarction, neutrophils do what?
Phagocytose necrotic debris inc. myelin, which results in sharper demarcation at site of infarct.
115
A week after cerebral infarction, what process begins?
Reactive gliosis.
116
What is reactive gliosis?
Astrocytes increase in number and size following cerebral infarction.
117
A few weeks after cerebral infarction, what forms?
A cavity lined by a gliotic scar, characterised by astrocytes with abundant fine cytoplasmic processes.
118
As the gliotic scar desists, what remains as a permanent marker of infarction?
A cystic gap.
119
Haemorrhagic infarct occurs for what two main reasons?
- 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.
120
Carotid artery disease leading to cerebral infarction results in what symptoms?
- Contralateral weakness or sensory loss. | - If dominant hemisphere affected there may be aphasia or apraxia.
121
What is apraxia?
Difficulty performing motor movements when asked despite having the ability to perform them, and difficulty speaking.
122
Middle cerebral artery disease leading to cerebral infarction results in what symptoms?
- Weakness predominantly in the contralateral face and arm.
123
Anterior cerebral artery disease leading to cerebral infarction results in what symptoms?
- Weakness and sensory loss in the contralateral leg.
124
Vertebro-basilar artery disease leading to cerebral infarction results in what symptoms?
- Vertigo. - Ataxia. - Dysarthria. - Dysphasia. Complex "brain stem syndromes".
125
Hyaline arteriolosclerosis results in?
Thinning and weakening of small vessel walls, making them more prone to occlusion and to rupture.
126
Chronic hypertension is associated with the development of?
Micro-aneurysms (Charcot-Bouchard).
127
Where do micro-aneurysms occur within the brain?
Commonly in small middle cerebral arteries - most commonly within the basal ganglia.
128
Rupture of micro-aneurysms within the brain lead to?
Intracerebral haemorrhage.
129
What are lacunar infarcts?
"Lake-like" infarcts of <15mm maximum in diameter.
130
Where do lacunar infarcts occur?
Where there is occlusion of a small penetrating vessel e.g. occlusion of part of a lenticulostriate artery.
131
In whom does hypertensive encephalopathy occur?
- Severe hypertension. - Upper limit of autoregulatory mechanism overwhelmed. - BBB is incapable of resisting plasma protein and water movement leading to vasogenic oedema.
132
Symptoms of hypertensive encephalopathy?
Raised ICP: - Headache. - Vomiting. - Fits. - Confusion. - Coma.
133
Pathology shows what in hypertensive encephalopathy?
- Cerebral oedema. - Herniations (tentorial and tonsillar). - Petechiae. - Arteriolar wall necrosis.
134
Clinical outcome of a lacunar infarct?
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.
135
Give an example of a spontaneous intracranial haemorrhage.
- Intracerebral haemorrhage. - Subarachnoid haemorrhage. - Haemorrhagic infarct.
136
Give an example of a traumatic intracranial haemorrhage.
- Extra-dural haematoma. - Sub-dural haematoma. - Contusion (surface bruising). - Intracerebral haemorrhage. - Sub-arachnoid haemorrhage.
137
Why is hypertension an important factor in both subarachnoid and intracerebral haemorrhages?
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.
138
In addition to hypertension, what are other contributing factors in intracerebral haemorrhage?
- Aneurysms. - Systemic coagulation disorders. - Anti-coagulation. - Vascular malformations. - Amyloid deposits (cerebral amyloid angiopathy). - Open heart surgery. - Neoplasms. - Vasculitis (infec. and non-infec.).
139
Where does intracerebral haemorrhage occur?
Most commonly in basal ganglia. | - Also thalamus, cerebral white matter and the cerebellum.
140
In intracerebral haemorrhage, what morphology is observed on the cut surface?
- 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.
141
Amyloid angiopathy occurs in what disease?
- Alzheimer's. | - Ageing.
142
What is amyloid angiopathy?
- 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.
143
What are the two most important vascular malformations in terms of brain haemorrhage?
- Arteriovenous malformations. | - Cavernous angiomas.
144
Why are anastomoses between an artery and vein (arteriovenous malformation) prone to rupture?
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.
145
What is an arteriovenous malformation?
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.
146
In addition to bleeding, vascular malformations in the brain may also cause what symptoms?
- Headaches. - Seizures. - Focal neurological deficits.
147
What is the most common congenital vascular abnormality of the brain?
Arteriovenous malformations.
148
Arteriovenous malformations are most common where?
In cerebral hemispheres of the middle cerebral artery territory.
149
Most common cause of subarachnoid haemorrhages?
- Rupture of a saccular aneurysm (Berry aneurysm).
150
Berry aneurysms are present in what percentage of the population?
1%.
151
Berry aneurysms arise where?
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
Saccular aneurysms enlarge with time, and are at great risk of rupture when they reach a diameter of?
6-10mm.
153
Describe the effect of saccular aneurysms >25mm diameter.
- Risk of rupture decreases. | - Symptoms due to mass effect predominate.
154
Following subarachnoid haemorrhage due to aneurysm rupture, what may be seen?
- 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
Risk factors of subarachnoid haemorrhage?
- Smoking. - Hypertension. - Kidney disease.
156
Subarachnoid haemorrhage is associated with which features?
- Abrupt symptom onset. - Severe headache. - Vomiting. - Loss of consciousness.
157
Subarachnoid haemorrhages are most common in which sex?
Females.
158
Subarachnoid haemorrhage has higher incidence in patient with which diseases?
- Polycystic kidneys. - Fibromuscular dysplasia. - Coarctation of aorta. - AVMs of the brain. - Developmental abnormality in collagen type 3. + smoking and hypertension.
159
Symptoms of raised ICP?
- Meningeal signs e.g. neck rigidity. - Visual symptoms. - Severe headache. - Loss of conscious.
160
What are acute complications of subarachnoid haemorrhage?
- Cerebral infarcts (4-9 days). - Acute hydrocephalus. - Herniation.
161
What percentage of patients die within several days of subarachnoid haemorrhage onset?
50%.
162
Demyelination is characterised by?
Defects in rate and consistency of neuronal conduction.
163
Oligodendrocyte damage disrupts what?
Neuronal conduction.
164
Demyelination causes what to myelin sheath?
Preferential damage to the myelin sheath.
165
Give an example of a primary demyelinating disorder.
- Multiple sclerosis. - Acute disseminated encephalomyelitis. - Acute haemorrhagic leukoencephalitis.
166
Give an example of a secondary demyelinating disorder.
- Viral: Progressive multifocal leukoencephalopathy (PML). - Metabolic: e.g. central pontine myelinosis. - Toxic: CO, organic solvents, cyanide.
167
Briefly describe acute disseminated encephalomyelitis.
- Primary demyelinating disorder. - Post-infectious auto-immune disorder. - Self-limited disorder most commonly affecting children.
168
Briefly describe acute haemorrhagic leukoencephalitis.
- Primary demyelinating disorder. - Post-infectious auto-immune disorder. - Rapidly fatal disease primarily affecting adults.
169
When does central pontine myelinosis (secondary metabolic demyelination) occur?
In over-rapid therapeutic correction of hyponatraemia, triggering oligodendrocyte death and resultant demyelination.
170
Why do organic solvents cause secondary demyelination?
- 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
What is the most common demyelinating disease?
Multiple sclerosis.
172
Peak incidence of multiple sclerosis?
20-30 years old.
173
Multiple sclerosis is more common in which sex?
Females.
174
What is multiple sclerosis?
- 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
How is a clinical diagnosis of multiple sclerosis made?
- 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
What investigations are supportive of a diagnosis of multiple sclerosis?
- Visual evoked potentials (evidence of slowed conduction) during conduction studies. - Presence of 2 or more IgG oligoclonal bands in CSF.
177
Multiple sclerosis often presents with a focal neurological deficit. How would an optic nerve lesion i.e. optic neuritis, present?
Unilateral visual impairment.
178
Multiple sclerosis often presents with a focal neurological deficit. How would a spinal cord lesion present?
- Motor or sensory deficit in trunk and limbs. - Spasticity. - Bladder dysfunction.
179
Multiple sclerosis often presents with a focal neurological deficit. How would a brain stem lesion present?
- CN signs. - Ataxia. - Nystagmus. - Internuclear ophthalmoplegia.
180
Describe the clinical pattern of symptoms in MS?
- Acute or insidious onset. - Relapsing and remitting. - Later becomes progressive.
181
On T2 weighted MRI scans, in areas corresponding to white matter, demyelination shows up as?
Hyperintense regions.
182
Multiple sclerosis is principally a disease of what?
White matter (where myelinated axons are concentrated).
183
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?
Plaques.
184
What are plaques in the brain?
- Various sized lesions which are well circumscribed and well demarcated. - Irregularly shaped. - Glassy, almost translucent appearance. - Non-anatomical distribution.
185
Although plaques may occur at any site in the CNS, where are they commonly found?
- CN II (optic). - Periventricular white matter. - Corpus callosum. - Brainstem. - Spinal cord.
186
Describe the histology of active plaques in the CNS.
- Perivascular inflammatory cells. - Microglia. - Ongoing demyelination.
187
Describe the histology of inactive plaques in the CNS.
- Gliosis. - Little remaining myelinated axons. - Oligodendrocytes and axons reduced in number.
188
What are shadow plaques?
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
Describe the macroscopic appearance of acute active plaques.
Demyelinating plaques are yellow/brown with an ill-defined edge blending into surrounding white matter.
190
Plaques tend to centre around what?
Small vessels.
191
Describe the macroscopic appearance of inactive chronic plaques.
- Well-demarcated grey/brown lesions in white matter. | - Classically situated around lateral ventricles.
192
If inactive chronic plaques are large enough, they may be seen on the cut surface of the brain as?
Translucent brownish areas of gliotic scarring.
193
What environmental factors are thought to contribute to MS?
- Association with latitude, the further north the higher the incidence. - Vit. D deficiency: sunlight exposure?? - Hypothetical viral trigger e.g. EBV.
194
What genetic factors are thought to contribute to MS?
- 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
Why is MS an immune mediated disease?
- Lymphocytic infiltration in histology. - Oligoclonal IgG bands in CSF. - Genetic linkage to HLA DRB1.
196
Why are humoral factors/ antibody mediated immunity important in the cause of MS?
- Oligoclonal IgG bands in CSF are seen in MS. | - Anti-B cell therapy, Rituximab is effective in reducing relapse severity and frequency.
197
Give an example of a degenerative disease affecting the cerebral cortex.
- Alzheimer's. - Pick's disease. - Creutzfeld-Jakob disease (CJD).
198
Give an example of a degenerative disease affecting the basal ganglia and brain stem.
- Parkinson's. - Progressive supranuclear palsy. - Multiples system atrophy. - Huntington's disease.
199
Give an example of a degenerative disease affecting the spinocerebellar tract.
- Spinocerebellar ataxias e.g. Friedreich Ataxia.
200
Give an example of a degenerative disease affecting the motor neurones.
Motor neuron disease.
201
Degenerative diseases are pathologically characterised by?
Simple neuronal atrophy and subsequent gliosis.
202
Define dementia.
Acquired and persistent general disturbance of higher mental functions in an otherwise fully alert person.
203
Neurodegenerative diseases are characterised by?
- Progressive loss of neurons typically affecting funtionally related neuronal groups. - Often symmetrical involvement.
204
Is dementia part of the normal ageing process?
No, it is always pathological.
205
What are the two groups of dementia classification?
- Primary dementia. | - Secondary dementia.
206
How do primary and secondary dementias differ?
- Primary arises of their own accord. | - Secondary arise from another underlying disorder e.g. trauma.
207
Give an example of a primary dementia.
- Alzheimer's (60-75%). - Lewy body dementia. - Pick's disease (fronto-temporal dementia). - Huntington's disease.
208
Name a cause of secondary dementia.
- 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
What is the most common cause of dementia in the elderly?
- Alzheimer's disease.
210
How do symptoms tend to present with increasing age at presentation of Alzheimer's?
The later the onset, the more severe and rapid changes tend to be.
211
Is alzheimer's more common in men or women?
F:M is 2:1.
212
Although Alzheimer's is a generally sporadic condition, what percent of cases are familial?
1%.
213
There is an increased incidence of Alzheimer's disease in those with which chromosome abnormality?
Trisomy 21 (amyloid precursor protein).
214
How does Alzheimer's disease present?
Insidious impairment of higher intellectual function with alterations in mood and behaviour.
215
What are the later stages of Alzheimer's disease?
- Progressive disorientation. - Memory loss and aphasia indicating severe cortical dysfunction. - Profound disability, muteness and immobility.
216
Death in Alzheimer's usually occurs due to what?
A secondary cause e.g. bronchopneumonia.
217
Macroscopic pathology of Alzheimer's?
- 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
Microscopic features of Alzheimer's?
- Extensive neuronal loss with astrocyte proliferation i.e. lost neurones replaced with astrocyte gliosis. - Neurofibrillary tangles. - Neuritic plaques. - Amyloid angiopathy.
219
What are neurofibrillary tangles?
Bundles of insoluble microtubules in neuron cytoplasm.
220
What dysregulated protein is a major component in Alzheimer's?
Tau protein.
221
What are neuritic plaques?
Focal, spherical collections of dilated tortuous neuritic processes of neurons surrounding a central amyloid core.
222
Amyloid Aβ is produced by?
Cleavage of amyloid precursor protein (APP).
223
What is the central element of neuritic plaques?
Aβ amyloid.
224
Why is Down's syndrome (Trisomy 21) associated with early onset of Alzheimer's?
Amyloid precursor protein is on Chromosome 21.
225
What is the most common familial cause of Alzheimer's?
Apolipoprotein E - allele e4. | - Dysregulates APP.
226
Which feature seen in Alzheimer's brains shows polymerised β-pleated sheets formed by Aβ?
Amyloid angiopathy.
227
Amyloid angiopathy disrupts the BBB, causing what?
- Serum leakage. - Local oedema. - Local hypoxia. - Exacerbation of oxidative stress, excitotoxicity and neuronal injury.
228
Amyloid angiopathy stains with what?
Congo red.
229
What may be seen microscopically in amyloid angiopathy?
- Extracellular eosinophilic accumulation. | - Polymerised β-pleated sheets formed by Aβ.
230
What is a Lewy body dementia?
3rd most common dementia. Progressive + hallucinations + fluctuating levels of attention/cognition. Some overlap with Alzheimer's but memory is affected later.
231
Features of Parkinsonism present when in Lewy Body Dementia?
At onset or shortly after.
232
How may Parkinsonism display clinically?
- Loss of facial expression, stooping, shuffling gait, slow initiation of movements, stiffness and pill rolling tremor.
233
Parkinsonism is seen in conditions affecting which pathway?
- Nigro-striatal dopaminergic pathways.
234
Pathological features of Lewy Body dementia?
Degeneration of substantia nigra (seen in Parkinson's).
235
Macroscopic features of Lewy Bodies Dementia?
- Pallor in substantia nigra (where pigmented dopaminergic neurons run).
236
Microscopic features of Lewy Body Dementia?
- Loss of pigmented neurons. - Reactive gliosis, microglial accumulation. - Remaining neurons may show lewy bodies. - Fewer cortical Lewy bodies.
237
What are Lewy bodies?
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
What is Huntington's disease?
Relentlessly progressive neuropsychiatric disorder inherited by autosomal dominance.
239
Clinical features of Huntington's disease?
Emotional , cognitive and motor disturbances.
240
Symptoms of Huntington's disease?
- Chorea. - Myoclous. - Clumsiness. - Slurred speech. - Depression. - Irritability. - Apathy. - Dementia.
241
Huntington's is inherited by which pattern?
Autosomal dominant.
242
The Huntingtin gene is found on which chromosome?
4p.
243
What causes Huntington's Disease?
Mutation of Huntingtin gene on chromosome 4p causing additional CAG repeats.
244
How many CAG repeats must there be to cause Huntington's disease?
Disease penetrant when >35 repeats occur. <28 is still normal.
245
How many years from symptom onset to death in Huntington's disease?
Typically 15 years.
246
Macroscopic pathological features of Huntington's?
- Atrophy of basal ganglia, caudate nucleus and putamen. | - Later cortical atrophy.
247
Microscopic pathological features of Huntington's?
- Simple neuronal atrophy of striatal neurones of the basal ganglia, most severely in caudate nucleus. - Pronounced astrocytic gliosis.
248
What is another name for fronto-temporal dementia?
Pick's disease.
249
What is fronto-temporal dementia (Pick's disease)?
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
Symptoms of fronto-temporal dementia (Pick's disease)?
- Personality and behavioural change. - Speech and communication problems. - Changes in eating habits. - Reduced attention span.
251
Describe progression of fronto-temporal dementia (Pick's disease).
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
What causes fronto-temporal dementia (Pick's disease)?
Extreme atrophy of cerebal cortex and later in the temporal lobes.
253
What does the brain weigh in fronto-temporal dementia (Pick's disease)?
Often <1kg implying loss of 300-400g.
254
Microscopic pathology of fronto-temporal dementia (Pick's disease)?
- Neuronal loss, gliosis. - Pick's cells (swollen neurons). - Intracytoplasmic filamentous inclusions - Pick's bodies.
255
Pick's bodies are enriched in what?
Tau protein.
256
What is multi-infarct dementia?
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
How do multiple infarcts cause dementia?
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
Are men or women more commonly affected by multi-infarct dementia?
Men.
259
Multi-infarct dementia becomes more common after which age?
60. | - Also seen in middle-age hypertensives.
260
Sufferers of multi-infarct dementia who are aware of mental deficits are prone to?
Depression and anxiety.
261
What clues may suggest multi-infarct dementia rather than Alzheimer's disease?
- Abrupt onset. - Stepwise progression. - Hx of hypertension or stroke. - Evidence of stroke on CT or MRI.
262
What type of infarct is more common in multi-infarct dementia?
- Large vessel infarcts. - Scattered throughout hemispheres. - Atheroma of large cerebral arteries which provoke thromboembolism.
263
Describe the rarer infarcts causing multi-infarct dementia?
- Small vessel (lacunar) infarcts. - Central, subcortical distribution. - Hx of lonstanding hypertension and arteriosclerosis of small vessels.
264
What separates cerebral hemispheres?
Falx cerebri.
265
What overlies the cerebellum?
Tentorium cerebelli.
266
If the brain swells, what must happen?
- Blood +/- CSF must leave the cranial vault to prevent rising pressure.
267
If reduction in blood and CSF can no longer compensate for increasing brain swelling, what happens?
Rapid increases in ICP. - Flattened venous sinuses. - Little or no CSF.
268
What may cause raised ICP?
- Increased CSF. - Focal brain lesion. - Diffuse brain lesion. - Increased venous volume. - Physiological mechanisms (hypoxia, pain, hypercapnia).
269
Define hydrocephalus.
Excess accumulation of CSF within the ventricular system of the brain.
270
CSF is produced by?
Choroid plexus in lateral and fourth ventricles.
271
CSF is absorbed by?
Arachnoid granulations.
272
What causes hydrocephalus?
- Obstructed CSF flow e.g. inflammation, pus and tumours. - Decreased CSF resorption (post SAH or meningitis). - CSF overproduction (very rare - choroid plexus tumours).
273
What is non-communicating hydrocephalus?
Obstruction to CSF flow occurs within ventricular system.
274
What is communicating hydrocephalus?
Obstruction CSF flow occurs outside of ventricular system e.g. in subarachnoid space or at arachnoid granulations.
275
Give a cause of communicating hydrocephalus.
- Post SAH, infective bacterial meningitis.
276
Give a cause of non-communicating hydrocephalus.
- Arnold chiari malformations.
277
If hydrocephalus occurs before the closure of cranial sutures, what happens?
Cranial enlargement.
278
If hydrocephalus occurs after suture closure, what happens?
Ventricle expansion and increased ICP. - Flattening of gyri and fullness of sulci.
279
What is hydrocephalus ex vacuo?
Hydrocephalus due to loss of brain parenchyma. Ventricles expand and CSF pool grows to account for change in intracranial volume.
280
In which diseases does hydrocephalus ex vacuo occur?
- Any disease that causes atrophy e.g. Alzheimer's.
281
What are the effects of raised ICP?
- Intracranial shifts and herniations - "coning". - Midline shift. - Distortion and pressure on CNs and vital neurological centres. - Impaired blood flow. - Reduced level of consciousness.
282
What are the three most common forms of brain herniation?
- Subfalcine. - Tentorial. - Tonsillar.
283
Describe subfalcine herniation.
Unilateral or asymmetric expansion of cerebral hemisphere displaces the cingulate gyrus under the falx cerebri.
284
Subfalcine herniation is associated with compression of which structure?
Anterior cerebral artery.
285
How does compression of the anterior cerebral artery manifest in subfalcine herniation?
- Weakness and/ or sensory loss in leg, because of ischaemia to primary motor and/ or sensory cortex in these areas.
286
Describe tentorial herniation.
Medial aspect of temporal lobe (hippocampal uncus and parahippocampal gyrus) herniates over tentorium cerebelli.
287
Tentorial herniation is associated with compression of what and how does this manifest?
- Ipsilateral CN III and its parasympathetic fibres. | - Manifests as pupillary dilation and impaired ocular movements on the side of the lesion.
288
Describe tonsillar herniation.
Displacement of cerebellar tonsils through foramen magnum.
289
Why is tonsillar herniation life threatening?
Causes brainstem compression and compromises vital respiratory centres in medulla oblongata.
290
What is transcalvarial herniation?
Swollen brain will herniate through any defect in the dura and skull.
291
What are symptoms of brain herniation?
- Reduced level of consciousness. - Dilated pupil on same side as mass lesion. - Bradycardia, increased pulse pressure and increased MAP. - Cheyne-Stokes respiration.
292
What clinical signs suggest raised ICP?
- Papilloedema. - Headache. - Nausea and vomiting. - Neck stiffness.
293
What features of a headache suggest raised ICP?
Worse on lying down, coughing, sneezing, straining.
294
What causes neck stiffness in raised ICP?
Pressure on dura around cerebellum and brainste,.
295
Why does nausea and vomiting occur in raised ICP?
Pressure on vomiting centres in pons and medulla.
296
Give an example of a space occupying lesion.
- Tumour. - Abscess[es]. - Haematoma[s]. - Localised brain swelling. - Infection. - Haemorrhage.
297
The majority of brain tumours present as?
Focal neurological symptoms and headache that is worse in mornings.
298
Brain tumours in children are generally found where?
Below tentorium cerebelli.
299
Brain tumours in adults are generally found where?
Above tentorium cerebelli.
300
Are brain metastases or primary tumours more common?
Metastases.
301
Cancers which most commonly metastasise to the brain?
- Breast, bronchus, kidney, thyroid and colon carcinomas. | - Malignant melanoma.
302
Brain metastases are often found where?
At the boundaries between grey and white matter.
303
The presence of multiple intracerebral tumours is indicative that their origin is?
Metastatic. Solitary tumours are more likely to be primary.
304
Why is the distinction between benign and malignant tumours not so relevant in the brain?
High grade tumours may not metastasise and benign lesions can kill simply due to their location in the brain.
305
CNS tumours are classified according to what?
Presumed cell of origin.
306
Most common subtype of primary brain tumour in adults?
Astrocytoma. | - Also meningiomas are common.
307
Most common subtype of primary brain tumour in children?
Medulloblastoma. | - Also low grade astrocytoma are common.
308
Describe Grade I pilocytic astrocytoma.
Distinct childhood tumour that do not progress to become higher grade. - Benign behaving, long hair like processes, cystic areas.
309
Well differentiated Grade II astrocytomas have an average survival of?
approx. 5 years.
310
What happens to well differentiated grade II astrocytomas with time?
They become more poorly differentiated and more anaplastic, thus becoming more clinically aggressive.
311
Grade IV glioblastomas have an average survival time of what, following diagnosis?
10 months.
312
Grade IV glioblastomas may occur secondary to?
Well differentiated or anaplastic astrocytoma. They may also occur de novo or as a primary form.
313
What leads to neoangiogenesis (increased vascularity) in high grade brain lesions?
VEFG secretion by tumour.
314
Medulloblastoma accounts for what percentage of paediatric CNS neoplasms?
20%.
315
Describe medulloblastomas.
- Poorly differentiated/embryonal (resemble primitive undifferentiated embryonal cells). - Occurs in midline of cerebellum.
316
Untreated medulloblastoma have poor prognosis, but fortunately they are extremely sensitive to?
Radiotherapy.
317
What is the 5 year survival rate of medulloblastoma with resection and radiotherapy?
75%.
318
Medulloblastomas tend to occur where?
Below tentorium cerebelli in the midline.
319
A single abscess in the brain may arise due to?
- 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
Multiple brain abscesses may arise due to?
- 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
Symptoms of brain abscess?
- Fever, raised ICP. | - Symptomsof underlying cause.
322
How is a brain abscess diagnosed?
CT or MRI.
323
How are brain abscess treated?
Aspiration of pus for culture and treatment.
324
Brain abscess is associated with significant mortality and thus requires what?
Weeks of antibiotics.
325
What is bacterial meningits?
Inflammation of leptomeninges and CSF within subarachnoid space due to bacterial infection.
326
What can be seen in CSF of bacterial meningitis?
- Many polymorphs. | - Reduced glucose.
327
Resolution of bacterial meningitis may be followed by?
- Arachnoiditis. - Obliteration of subarachnoid space. - Obstructive hydrocephalus.
328
Arachnoiditis may cause?
- Lack of CSF absorption. - Hydrocephalus. - Raised ICP.
329
E. Coli gram stain?
Gram negative rods.
330
H. Influenzae gram stain?
Gram negative cocco-bacilli.
331
N. Meningitidis gram stain?
Gram negative diplococci.
332
S. Pneumoniae gram stain?
Gram positive cocci in chains.
333
L. Monocytogenes gram stain?
Gram positive rods.
334
In pathology, head injury is classifed into?
- Missile (penetrating). | - Non-missile (blunt).
335
Describe penetrating/ missile injury to the head.
- Focal damage. - Lacerations in the region of brain damage. - Haemorrhage. - High vs low velocity impacts.
336
If the penetrating missile in head injury exits the skull, is this a bad or good for clinical outcome?
Bad - indicated high velocity nature in whichinjury extent can be far greater.
337
what is non-missile/ blunt injury of the head?
- Sudden acceleration and/or deceleration. e.g. being hit with a bat or falling on your head.
338
What is primary brain injury?
- Damage to the brain at time of injury. | - Currently irreversible.
339
What is secondary brain injury?
- Potentially treatable. | - Haemorrhage, oedema.
340
What is a linear skull fracture?
Straight, sharp fracture line that may cross sutures (diastatic fracture).
341
What is a compound skull fracture?
Associated with full thickness scalp lacerations.
342
The presence of a linear fracture greatly increases the chance of what?
Presence or likelihood of emerging clinically important haematoma.
343
What is a depressed skull fracture?
Break in cranial bone with depression of the bone in toward the brain.
344
Base of skull fractures are always regarded as compound or open given high probability of what?
e.g. that the adjacent paranasal sinuses have also been torn and the fracture is therefore open to outside world.
345
What are surface contusions of the brain?
Usually asymmetrical bruises caused by tissue damage following severe compressive strains.
346
With time, what happens to contusions of the brain?
They become brown shrunken scars.
347
Coup tends to occur where?
To the brain at the side/ point of impact.
348
Contracoup occurs where?
Diametrically opposite the point of impact.
349
Which are often worse, coup or contracoup injuries?
Contracoup.
350
Coup and contracoup injuries tend to cause compressive strains and thus cause?
Contusion and laceration.
351
When does diffuse axonal injury occur?
Occurs at moment of injury, and affects central areas. Due to shearing strains.
352
What results from diffuse axonal injury?
- Reduced consciousness and coma. | - Possibly lead to vegetative state.
353
What happens to cerebral metabolism in head injury?
It is decreased.
354
What is cytotoxic oedema?
A pre-morbid process where dying cells accumulate water as ions move into cells bringing water with them.
355
When does cytotoxic oedema occur?
Intoxication, Reye's and severe hypothermia.
356
what is ionic oedema?
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
What is vasogenic oedema?
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
What is haemorrhagic conversion?
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
Describe location of traumatic haematomas.
Most are supratentorial, unilateral and intradural.
360
What is a burst lobe?
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
Traumatic extradural haematomas are usually a complication of what?
Fracture in tempero-parietal region often involving middle meningeal artery. Immediate brain damage is often minimal.
362
If a traumatic extradural haematoma goes untreated, what happens?
Midline shift of brain due to compression and herniation.
363
Extradural haematomas require what?
Prompt evacuation by surgery.
364
What are subdural haematomas?
Collections of blood between internal surface of dura and arachnoid tending to occur over cerebral convexities.
365
What causes acute subdural haematomas?
Disruption of bridging veins that extend from brain surface into subdural space perforating the dura.
366
What causes disruption of bridging veins and subsequent acute sub-dural haematoma?
Injury associated with rapid change in head velocity.
367
Why are gyral contours preserved in acute sub-dural haematoma?
Pressure is evenly distributed.
368
What happens to cerebrum on the side of the haematoma in acute sub-dural haematoma?
Cerebrum swells.
369
What happens to non-treated, non fatal acute sub-dural haematoma?
They become liquified and form a yellowish neomembrane.
370
Acute sub-dural haematoma has a mortality of?
>60%.
371
Chronic subdural haemorrhages are less frequently associated with what, and more often associated with what?
- Less often ass. with well-defined traumatic insult. | - More often ass. with brain atrophy.
372
Chronic subdural haemorrhages are composed of what?
Liquiefied blood/yellow tinged fluid separated from the inner surface of dura and underlying brain by a neomembrane.
373
Blood vessels within the neomembrane are abnormally permable, leading to what in Chronic Subdural haemorrhage?
Continuous accumulation of fluid and recurrent haematomas.
NEUROLOGY
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