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Pathology > Neuro > Flashcards

Neuro Flashcards

1
Q

What do contusions involve?

A

The surface of the brain

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2
Q

2 types of contusions?

A

Coup (contusion at the site of impact)

Contrecoup (contusion at the opposite to the site of impact)

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3
Q

Common scenario for epidural haemorrhage?

A

Parietal/squamous temporal bone fracture with middle meningeal artery rupture

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4
Q

What is a ‘lucid interval’ in epidural haemorrhage?

A

initial consciousness level appears normal

progressive pain and LOC hours later

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5
Q

What causes subdural haemorrhage?

A

rupture of bridging veins causing haemorrhage into the potential space between the brain and the dura

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6
Q

Causes of subdural haemorrhage?

A

injury/impact (most common)
spontaneous or following trivial impact (coagulopathy)
chronic hydrocephalus

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7
Q

Features of chronic subdural haemorrhage?

A

weeks or months following injury
slowly progressive symptoms
older patients

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8
Q

Causes of subarachnoid haemorrhage?

A

Can be spontaneous (rupture of berry aneurysm)

can be caused by single punch (stretching and tearing of artery consequent to impact)

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9
Q

Features of intracerebral haemorrhage?

A

Usually associated with other trauma manifestations

take time to develop

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10
Q

What are deep seated haemorrhages associated with?

A

High-velocity blunt force trauma

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11
Q

What causes traumatic diffuse axonal injury (DAI)?

A

rotational forces leading to shearing of neuronal processes

patients have immediate prolonged coma

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12
Q

What is seen microscopically in DAI?

A

white matter haemorrhages
corpus callosum lesions
axonal retraction balls

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13
Q

Examples of secondary brain injury?

A 
intracranial haemorrhage may extend
brain swelling
intracranial herniation syndromes
global ischaemic brain damage
infections
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14
Q

What causes ‘ring’ haemorrhages in the brain?

A

Fat embolism

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15
Q

How does a fat embolism reach the brain?

A

if pulmonary trapping capacity is exceeded

via a v-shunt

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16
Q

Consequences of head injury?

A

post-traumatic hydrocephalus
post-traumatic epilepsy
chronic infections or late-presenting infection
chronic traumatic encephalopathy

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17
Q

3 determinants of ICP?

A

blood brain barrier
pressure volume equilibrium
cerebrovascular autoregulation

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18
Q

What is average intra-cranial volume in adults?

A

1700ml

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19
Q

What is the Monroe-Kellie doctrine?

A

ICP can only be held stable if an increase in one component is compensated for by the other two

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20
Q

What are the three components of ICP?

A

brain tissue, blood, CSF

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21
Q

What is cerebral perfusion pressure?

A

The difference between ICP and mean arterial pressure

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22
Q

What does an elevated ICP that approaches MAP mean?

A

this results in reduced cerebral perfusion pressure- ischaemic injury to cerebral tissue

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23
Q

What is the major consequence of BBB failure?

A

Cerebral oedema

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24
Q

What is cerebral oedema?

A

a state where there is a local or diffuse increase in brain water

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25
Q

Causes of cerebral oedema?

A 
Physical injury
Tumours (especially mets)
Inflammatory disease
Pseudotumor cerebri
Vascular disease
Drugs and chemicals
Metabolic disease
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26
Q

Appearance of cerebral oedema?

A

Increased brain weight and swelling

Possible discolorations

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27
Q

Where is CSF formed?

A

In the choroid plexus

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28
Q

What happens if there is increased CSF and venous pressure?

A

may be transmitted to the eye and cause venous distension and optic disc swelling

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29
Q

Herniation syndromes include?

A

subfalcine herniation
transtentorial herniation
cerebellar tonsillar herniation

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30
Q

What becomes compressed in subfalcine herniation?

A

the anterior cerebral arterty

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31
Q

What becomes compressed in transtentorial herniation?

A

CN III

posterior cerebral artery

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32
Q

What becomes compressed in cerebellar tonsillar herniation?

A

brainstem compression

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33
Q

What is a Duret haemorrhage?

A

Haemorrhage within the brainstem

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34
Q

What name is given to a haemorrhage within the brainstem?

A

Duret haemorrhage

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35
Q

Clinical manifestations of increased ICP?

A 
Headache (worse when lying down)
Nausea
Vomiting
Confusion
LOC
Localising signs due to herniation effects
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36
Q

What is a hydrocephalus?

A

accumulation of excessive CSF in the ventricular system

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37
Q

Causes of hydrocephalus?

A

overproduction due to tumour of choroid plexus (rare)

reabsorption limited by altered flow due to obstruction

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38
Q

Clinical features of hydrocephalus?

A 
headache
nausea and vomiting
drowsiness and LOC
ocular palsies and pupal dilation
papilledema
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39
Q

Outcome of hydrocephalus?

A

Acute- no time for compensation- collapse/death

Chronic- time for compensation- CSF pressure can return to normal limits

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40
Q

Where are most CNS tumours located in children?

A

Posterior fossa (70%)

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41
Q

Where are most CNS tumours located in adults?

A

Cerebral hemispheres (70%)

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42
Q

How do CNS tumours typically present?

A

with signs of increased ICP

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43
Q

Are diffuse gliomas amenable to surgical resection?

A

No- they typically infiltrate large volumes of brain tissue

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44
Q

What are the commonest primary CNS tumours in adults?

A

Diffuse Gliomas

Meningiomas

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45
Q

What are the commonest CNS tumours in children?

A 
Gliomas
Embryonal tumours (medulloblastomas)
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46
Q

What percent of primary brain tumours in adults are diffuse gliomas?

A

80%

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47
Q

What are ependymomas?

A

slow growing neoplasms that arise from an ependymal surface, usually the 4th ventricle
commonest neoplasm of the spinal cord

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48
Q

In who are ependymomas commonly seen?

A

Young children (adverse prognosis)

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49
Q

Where do medulloblastomas arise?

A

In the cerebellum in children

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50
Q

Features of medulloblastomas?

A

Present with headache and vomiting
growth rate is rapid
extensive local infiltration
spread via CSF pathways

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51
Q

Who do primary CNS lymphomas occur in?

A

middle-age

primarily in the immunosuppressed

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52
Q

Features of primary CNS lymphomas?

A

primary high grade B cell lymphomas
radiosensitive
steroid responsive

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53
Q

How common are meningiomas?

A

20% of primary brain tumours in adults

more common in women

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54
Q

Prognosis of meningiomas?

A

Usually low-grade tumours

Outcome related to completeness of surgical resection

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55
Q

Most common sites for mets to the brain?

A

breast, lung, kidney and malignant melanoma

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56
Q

Examples of familial brain tumours?

A

Turcot syndrome
Li-Fraumeni syndrome
Cowden syndrome

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57
Q

What is Turcot syndrome associated with?

A

medulloblastoma or glioblastoma

APC gene

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58
Q

What is Li-Fraumeni syndrome associated with?

A

medulloblastoma, TP53 mutations

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59
Q

What is Cowden syndrome associated with?

A

Lhermitte Duclos disease

PTEN mutations

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60
Q

What is the inheritance pattern of tuberous sclerosis?

A

Autosomal Dominance

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61
Q

What is tuberous sclerosis associated with?

A

seizures, mental retardation and autism

hamartomas and benign tumours of brain and other tissues

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62
Q

Translocation associated with tuberous sclerosis?

A

TSC1 (9q) and TSC2 (16p)

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63
Q

What does von Hippel Landau disease cause?

A

hemangioblastomas of CNS
cysts of liver, pancreas and kidneys
propensity to develop RCC and pheochromocytoma

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64
Q

Pattern of inheritance of vHL?

A

autosomal dominant

mutations of VHL 3p

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65
Q

Neurofibromatosis 1 features?

A

more common

neurofibromas of peripheral nerves, cafe au lait spots, Lisch nodules, optic nerve gliomas

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66
Q

Neurofibromatosis 2 features?

A

less common

bilateral acoustic neuromas, multiple meningiomas

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67
Q

Two major causes of CVAs?

A

Thrombosis

Haemorrhage

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68
Q

Why is it important to establish the cause of a CVA?

A

to determine treatment

thrombolysis vs anticoagulants

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69
Q

Why is treatment urgent in a CVA?

A

possibility of limiting ischaemia and secondary damage to penumbra
managing ICP

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70
Q

Causes of thrombotic CVA?

A 
atherosclerosis
antiphospholipid syndrome
arteritis
arteriopathy
coagulopathy, smoking
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71
Q

Causes of a haemorrhagic CVA?

A 
aneurysm
arterio-venous malformation
arterial HTN
anticoagulants
amyloid angiopathy
arteritis
anaplastic tumour
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72
Q

3 main sources of thromboembolism causing CVA?

A

Heart (A Fib)
Carotid bifurcation (atherosclerosis)
Aorta (spine)

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73
Q

What does occlusion result in?

A

Infarction and liquefactive necrosis

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74
Q

‘Pale’ infarct vs ‘Red’ infarct?

A

‘Pale’ infarct comes from complete infarction

‘Red’ infarct occurs when there is reperfusion

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75
Q

What causes hypoxic/ischaemic encephalopathy?

A

cardiac arrest

shock

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76
Q

Pathophysiology behind HIE?

A

glutamate release from neurons
calcium influx
free radicals and catabolic enzymes
neuronal necrosis

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77
Q

Which section of the brain is particularly vulnerable to HIE?

A

Ammon’s horn in the hippocampus

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78
Q

What is multi-infarct dementia?

A

impairment in multiple cognitive functions due to a vascular cause

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79
Q

Risk factors for multi-infarct dementia?

A

Elderly
DM
smoking
HTN

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80
Q

Where does a hypertensive haemorrhage most affect?

A

the basal ganglia and the brainstem

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81
Q

What occurs in hypertension?

A

Fibrinoid degeneration of the arteries

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82
Q

What does cerebral amyloid angiopathy occur with?

A

Alzheimer’s disease

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83
Q

Which lobes are most affected by cerebral amyloid angiopathy?

A

Occipital lobes

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84
Q

What stain is used in cerebral amyloid angiopathy?

A

Congo Red

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85
Q

What is a Congo Red stain used to identify?

A

Amyloid

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86
Q

How do neurodegenerative diseases manifest macroscopically and microscopically?

A

Macroscopically - atrophy

Microscopically - neuronal loss and accumulation of abnormal proteins

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87
Q

Other names for Motor Neuron Disease?

A

Amyotrophic lateral sclerosis

Lou Gehrig’s Disease

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88
Q

Macroscopic pathology of ALS?

A

atrophy of motor cortex

atrophy of motor nerves

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89
Q

MND prognosis?

A

Death within 5 years due to respiratory failure or aspiration

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90
Q

Histology of MND?

A 
loss of motor neurons
loss of myelinated axons
gliosis
Bunina bodies
spherical inclusions
variety of proteins (most contain TDP43)
91
Q

What are akinetic-rigid disorders?

A

extrapyramidal

characterised by rigidity, bradykinesia and resting tremor (Parkinsonism)

92
Q

Examples of akinetic-rigid disorders?

A 
Parkinson's
Multiple System Atrophy
Progressive Supranuclear Palsy
Corticobasal degeneration
Wilson's disease, drug-induced parkinsonism, vascular parkinsonism
93
Q

What causes Parkinson’s Disease?

A

loss of dopaminergic neurons of the nigrostriatal system

loss of melanised neurons from the substantia niagra

94
Q

What protein is accumulated in Parkinson’s disease?

A

alpha-synuclein

95
Q

Familial forms of Parkinson’s?

A

SNCA, PARK2, PINK1, UCHL1, DJ1, LRRK2

96
Q

Hyperkinetic movement disorders are characterised by?

A

Chorea
Ballismus
Myoclonus
Dystonia

97
Q

What is ballismus caused by?

A

Damage to the subthalamic nucleus

98
Q

Huntington’s Disease features?

A

involuntary movements
psychiatric symptoms
dementia

99
Q

Gross appearance of Huntington’s Disease?

A

cerebral atrophy

atrophy of caudate, putamen and globus pallidus

100
Q

Microscopic appearance of HD?

A

neuronal loss and gliosis in basal ganglia

ubiquitin and huntingtin

101
Q

Inheritance pattern of HD?

A

AD
‘CAG’ expansion- longer expansion = earlier onset
huntingtin gene on chromosome 4

102
Q

Examples of degenerative ataxias?

A

Spinocerebellar ataxia
Friedrich ataxia
Ataxia-telangiectasia

103
Q

When does Friedrich’s ataxia present?

A

pre-adolescence

104
Q

What other diseases are associated with Friedrich’s ataxia?

A 
Hypertrophic Cardiomyopathy (60%)
Diabetes Mellitus (10%)
105
Q

Friedrich’s ataxia inheritance pattern?

A

Autosomal recessive

chromosome 9, frataxin, GAA expansion

106
Q

Features of temporoparietal, frontotemporal and subcortical dementias?

A

Temporoparietal - impairment of memory, later dysphasia and dyspraxia
Frontotemporal- behavioural disturbances, later memory loss
Subcortical- slowing of thought process, basal ganglia related

107
Q

What is the most common form of dementia?

A

Alzheimer’s Disease

108
Q

Where does Alzheimer’s disease occur?

A

Frontotemporal

Temporoparietal

109
Q

What percentage of Alzheimer’s has a positive family history?

A

10%

110
Q

Which proteins accumulate in Alzheimer’s?

A

Tau (tangles)

Beta-amyloid (plaques)

111
Q

Macroscopic pathology of AD?

A

atrophy
shrinkage of gyri, widening of sulci
hydrocephalus ex vacuo

112
Q

Early-onset AD forms of AD?

A

APP, PSEN1, PSEN2

113
Q

Connection between APOE gene and Alzheimer’s?

A

e2 isoform is protective

e4 isoform increases risk

114
Q

Classifications of human prion diseases?

A

Idiopathic/sporadic
Genetic
Acquired

115
Q

Idiopathic prion diseases?

A

Creutzfeldt-Jacob disease
Fatal insomnia
protease-sensitive prionopathy

116
Q

Genetic prion diseases?

A

Creutzfeldt-Jacob disease
Fatal insomnia
Gerstmann-Straussler-Scheinker

117
Q

Acquired prion disease?

A

From cows- BSE, mad cow disease
iatrogenic CJD
from humans- Kuru

118
Q

Causes of secondary CNS malformations?

A 
ischaemia/infarction
congenital/intrauterine infections
maternal factors (folic acid deficiency, toxins, diabetes)
119
Q

Early malformations are more likely _______ than later in gestation?

A

Genetic

Fatal

120
Q

Malformations related to early in gestation?

A 
neural tube defects
disorders of cerebral development
disorders of cerebellar, hindbrain and spinal cord development 
vascular disorders
hydrocephalus
121
Q

Range of neural tube defects?

A

Open NTDs- craniorachischisis, anencephaly, spina bifida cystica
Closed NTDs- encephalocele, spina bifida occulta

122
Q

What is raised in open NTDs?

A

maternal serum alpha-fetoprotein

123
Q

What is folic acid important in preventing?

A

Neural tube defects

124
Q

What is holoprosencephaly?

A

failure of the forebrain to develop properly

125
Q

What can cause holoprosencephaly?

A

maternal infection, diabetes, foetal alcohol syndrome

126
Q

What forms CNS and PNS myelin?

A

CNS - oligodendrocytes

PNS- Schwann Cells

127
Q

What is demyelination?

A

destruction of normally formed myelin with relative preservation of axons

128
Q

What is dysmyelination?

A

failure to form myelin normally

129
Q

Primary vs. secondary demyelination?

A

Primary- myelin exhibits the initial and most marked damage and axons are relatively preserved
Secondary- degeneration of myelin as a result of axonal or neuronal injury

130
Q

Effects of demyelination?

A

slowing of conduction velocity
conduction block
‘cross talk’ due to unstable demyelinated nerves

131
Q

What is ‘cross talk’?

A

miscommunication between unstable demyelinated nerves

i.e., sensory events result in motor phenomenon (unable to move after a hot bath, positional change causes pain)

132
Q

General aetiologies of demyelination?

A

Infective
Immune/inflammatory
Metabolic/toxic
Neoplastic

133
Q

General aetiologies of dysmyelination?

A

Genetics

134
Q

What HLA types are susceptible to MS?

A

A3, B7, DR2, DQ1

135
Q

When does MS have its onset?

A

usually in twenties

136
Q

Progression of MS?

A

exacerbations and remissions
visual or motor signs
slow progressive disability over decades

137
Q

Diagnosis of MS?

A

history
MRI (multiple lesions in space and time)
CSF
Visual Evoked Responses

138
Q

What causes death in patients with MS?

A

secondary complications

infection

139
Q

What is the key pathology behind MS?

A

Demyelinating plaques (Active, Inactive, Shadow)

140
Q

Where do demyelinating plaques occur?

A

Mostly in white matter

optic nerve, periventricular regions and spinal cord most common sites

141
Q

What is found in acute and chronic demyelinating plaques?

A

Acute- macrophages

Chronic- astrocytic gliosis

142
Q

What inflammation is seen around demyelinating plaques?

A

T lymphocytic perivenous inflammation

143
Q

What causes neuromyelitis Optica? (Devic’s disease)

A

inflammation and demyelination of the optic nerve and the spinal cord
distinct from MS

144
Q

2 types of NMO/Devic’s Disease?

A

Autoimmune (AQP4 positive)

Idiopathic (AQP4 negative)

145
Q

Symptoms of NMO/Devic’s Disease?

A

limb weakness, paralysis, bladder dysfunction

visual blurring, blindness

146
Q

Who is NMO/ Devic’s most common in?

A

women

African origin

147
Q

What is the likelihood of recurrence in NMO?

A

> 90%

148
Q

Outcome of NMO if left untreated?

A

50% are blind and wheelchair bound by 5 years

149
Q

Treatment for NMO?

A

mycophenolate mofetil
rituximab
azathioprine

150
Q

What is acute disseminated encephalomyelitis preceded by?

A

systemic viral illness or vaccination (few days- few weeks)

151
Q

Symptoms of acute disseminated encephalomyelitis?

A

acute onset
headache, vomiting, weakness, stupor, seizures, pyrexia
5-20% mortality

152
Q

Who does acute disseminated encephalomyelitis usually occur in?

A

young people

153
Q

What type of reaction is involved in acute disseminated encephalomyelitis?

A

T-cell mediated hypersensitivity reaction

154
Q

What is the name given to the more severe, hyperacute Acute disseminated encephalomyelitis?

A

Acute haemorrhagic leukoencephalopathy

155
Q

Main infective cause of demyelination?

A

Progressive Multifocal Leukoencephalopathy (PML)

156
Q

What is involved in progressive multifocal leukoencephalopathy?

A

subacute viral infection of oligodendrocytes

latent in host- reactivated in T-cell deficiency

157
Q

Treatment and outcome of Progressive Multifocal Leukoencephalopathy?

A

resistant to therapy
treatment aims to reduce immune suppression
usually fatal within 6 months

158
Q

Histology of Progressive Multifocal Leukoencephalopathy?

A

multiple demyelinated foci
inclusions in oligodendrocytes nuclei
enlarged ‘giant’ astrocytes

159
Q

What causes central pontine myelinolysis?

A

rapid correction of hyponatremia due to metabolic disorders

alcoholism, malnutrition, hyperemesis

160
Q

Symptoms of central pontine myelinolysis?

A 
rapid onset confusion
limb weakness
conjugate gaze palsies
hypotension
most cases fatal within weeks
161
Q

What are leukodystrophies?

A

genetic disorders of myelin formation

162
Q

How does X linked leukodystrophy present?

A

seizures
abnormal behaviour
muscle spasms

163
Q

What is involved is adrenoleukodystrophy?

A

adrenal insufficiency and dysmyelination

164
Q

Name 3 myelin proteins and state whether involved in CNS or PNS?

A

Proteolipid Protein (PLP)- >50% in CNS, minimal in PNS
Peripheral myelin protein 22 (PMP22)- 5% of PNS, not in CNS
Myelin Basic Protein (MBP)- in both CNS and PNS

165
Q

What is Guillain-Barre syndrome?

A

acute inflammatory demyelinating polyneuropathy (AIDP)

166
Q

Symptoms of Guillain-Barre syndrome?

A

acute onset
ascending flaccid paralysis
usually 2 weeks after viral or infective illness

167
Q

What antibodies are circulating in Guillain-Barre syndrome?

A

anti-myelin

antiganglioside

168
Q

What classifies chronic inflammatory demyelinating polyneuropathy?

A

> 2 months

recurring episodes of demyelination with remyelination and inflammation

169
Q

What percentage of patients with vasculitis also have peripheral neuropathy?

A

33%

170
Q

What is neurogenic muscle disease and what causes it?

A

denervation of muscle leads to muscle atrophy

caused by any process that affects the anterior horn cell or its axon (MND, spinal muscular atrophy)

171
Q

Causes of myopathies?

A

Acquired (inflammatory, toxins/drugs, paraneoplastic)

Genetic (dystrophies, congenital myopathies, protein inclusion myopathies)

172
Q

Types of inflammatory myopathies (myositis)?

A

inclusion body myositis
polymyositis
dermatomyositis

173
Q

Features of inflammatory myopathies?

A 
myalgia
muscle weakness
muscle tenderness
elevated inflammatory markers
muscle biopsy useful
174
Q

Two types of skeletal muscle dystrophinopathy?

A

Duchenne muscular dystrophy

Becker muscular dystrophy

175
Q

What cardiac disease is related to dystrophinopathy?

A

X-linked dilated cardiomyopathy

176
Q

What will be raised in muscle dystrophy?

A

muscle creatinine kinase (CK) due to muscle necrosis

177
Q

Structural abnormalities associated with congenital myopathies?

A

central nuclei
defects of the sarcomere network
nemaline rods

178
Q

When do symptoms of congenital myopathies usually present?

A

At birth or in early childhood

179
Q

Metabolic myopathies include defects in?

A

Glycogen storage/ glucose metabolism
Lipid metabolism
mitochondrial myopathies/cytopathies

180
Q

Glycogen storage disorders symptoms are induced by?

A

Exercise

181
Q

Most common enzymes involved in glycogen storage disorders are?

A

myophosphorylase (mcArdles)

phosphofructokinase

182
Q

What do 90% of Myasthenia Gravis patients have and what do the remaining 10% have?

A

anti-ACh receptor antibodies

remaining 10% have anti-tyrosine kinase receptor antibodies

183
Q

Symptoms of myasthenia gravis?

A

fatigable muscles
ptosis
painless muscle weakness
thymic hyperplasia

184
Q

Which HLAs are associated with myasthenia gravis?

A

A1, B7, DRW3

185
Q

What is acted on in Lambert-Eaton myasthenic syndrome?

A

Voltage-gated Calcium channels

186
Q

What is the major cause of Lambert-Eaton myasthenic syndrome?

A

Underlying malignancy

particularly Small Cell Lung Cancer

187
Q

Which is the most common form of meningitis?

A

Viral > bacteria

but viral is less severe also

188
Q

Most common bacterial cause of meningitis?

A

Neisseria meningitides

189
Q

Three ages of meningitis?

A

Infant (most common)
Toddler (second most common)
Over 4s- adult

190
Q

Causes of meningitis in an infant?

A

Group B strep
E coli
Listeria

191
Q

Causes of meningitis in a toddler and adult?

A

N. meningitidis

S. pneumoniae

192
Q

3 ‘NHS bacteria’ for meningitis?

A

Neisseria meningitidis
Haemophilus influenza B
Streptococcus pneumoniae

193
Q

What is the bacterial meningitis paradox?

A

mucosal pathogens commonly colonise the oropharynx but rarely go on to cause bacterial meningitis

194
Q

How much of the population’s nasopharynx is colonised by N. meningitidis?

A

5-30%

195
Q

What is the most major risk for bacterial meningitis?

A

Close contact (household contact) inc. 400x

196
Q

Clinical features of meningococcal sepsis?

A

headache, fever, vomiting, drowsiness
haemorrhagic rash, neck stiffness
infants- poor feeding, bulging fontanelle
neonates- respiratory distress

197
Q

Meningococcal septicaemia vs meningitis?

A

Sepsis- rash, bleeding, hypotension, 20% fatal, +/- meningism
Meningitis- no/mild rash, no bleeding, normotensive, 5% fatal, meningism and raised ICP

198
Q

How do people present with meningococcal syndromes?

A

55% present with septicaemia and meningitis
20% present with meningitis alone
25% present with septicaemia alone

199
Q

Contraindications of lumbar puncture in suspected meningitis?

A

Raised ICP
Shock
Respiratory distress

200
Q

Treatment of bacterial meningitis?

A

Early antibiotics
fluid resuscitation
10mg dexamethasone

201
Q

Is there evidence of increased risk in close contacts in NHS meningitis?

A

N- yes, 400x

S- no, no need for prophylaxis

202
Q

Types of CNS infection?

A 
bacterial (brain abscess)
viral (herpes, polio, measles)
fungal
parasitic
prion (CJD)
203
Q

Bacteria behind brain abscesses?

A

60% aerobic- staph, strep, gram neg bacilli

32% anaerobic- Bacteroides, fusarium

204
Q

Routes of infection for brain abscesses?

A

Direct (N.B., head injury, skull fracture)
Blood spread
Iatrogenic
site of abscess reflects route of entry

205
Q

Mortality from brain abscesses?

A

10%

206
Q

Who are at risk for a CNS Tuberculous infection?

A

children and immunosuppressed

207
Q

Features of CNS Tuberculous infection?

A 
caseous necrosis with granulomas
subacute onset
meningitic signs
drowsiness
cranial nerve palsies
increased ICP
208
Q

Where are tuberculomas endemic?

A

Indian subcontinent

209
Q

What bacteria causes syphilis?

A

Treponema pallidum

210
Q

What causes Lyme disease?

A

Borrelia burgdorferi spirochete

transmitted by ticks

211
Q

3 stages of Lyme disease?

A

1st - skin, erythema marginatum
2nd- weeks or months later- neurological or cardiac signs
3rd- years later, CNS and arthritis

212
Q

What can Lyme disease be confirmed by?

A

Western blot

213
Q

What accounts for over 80% of aseptic meningitis?

A

Enteroviruses

214
Q

What can cause viral encephalitis?

A 
Herpes simplex
Herpes zoster
Enteroviruses
Rabies
Measles
Cytomegaloviruses
Polyoma viruses
HIV
215
Q

What are poliomyelitis and polio-encephalitis?

A

Poliomyelitis- inflammation of the grey matter of the spinal cord
Polio-encephalitis- inflammation of the grey matter of the brain

216
Q

2 types of cytomegalovirus?

A

Congenital (maternal infection usually asymptomatic)

Acquired (usually complicates immunosuppression)

217
Q

Main complications of congenital cytomegalovirus?

A

deafness, convulsions, mental retardation, seizures, chorioretinitis

218
Q

What percentage of AIDs patients have CNS involvement?

A

80%

219
Q

3 causes of brain disease in AIDs patients?

A

direct HIV infection
opportunistic infections
tumours (cerebral non-Hodgkin lymphoma)

220
Q

Toxoplasmosis is carried by?

A

Cats

221
Q

When does transplacental spread of toxoplasmosis occur?

A

when the infection occurs during pregnancy, greatest risk between 10-24 weeks

222
Q

Commonest site involved in toxoplasmosis?

A

Basal ganglia

223
Q

What causes cerebral malaria?

A

Plasmodium falciparum

Pathology (13 decks)

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