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Clinical Neuroscience > Session 8: Neuropathology > Flashcards

Session 8: Neuropathology Flashcards

1
Q

Possible routes of entry for microorganisms into the CNS

A

Direct spread

Blood-borne spread

Iatrogenic

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2
Q

Give examples of direct spread.

A

Middle ear infection such as a cholesteatoma, base of skull fracture involving e.g. ethmoid bone.

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3
Q

Give examples of blood borne spread.

A

Sepsis

Into dural venous sinuses

Infective endocarditis where a part of the vegetation from one of the heart valves dislodge and end up in the brain.

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4
Q

Give examples of iatrogenic causes of CNS infection.

A

Ventriculo-peritoneal shunt

Surgery

Lumbar puncture

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5
Q

What is meningitis?

A

Inflammation of the leptomeninges

Can be with or without septicaemia and will cause a raise in ICP

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6
Q

Causative organism of meningitis in neonates.

A

E. coli

L. monocytogenes

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7
Q

Causative organism of meningitis in 2-5 yo

A

Haemophilus influenzae type B (HiB)

(Same as in epiglottitis)

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8
Q

How can you prevent meningitis from HiB?

A

Vaccination

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9
Q

Causative organism of meningitis in 5-30 yo

A

N. meningitidis

Several types but can immunise against some

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10
Q

Causative organism of meningitis in over 30 yo

A

S. pneumoniae

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11
Q

Causative organism of meningitis in immunocompromised individuals.

A

Parasites

Flukes

Various others

and of course the normal ones as well.

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12
Q

What is chronic meningitis caused by?

A

M. tuberculosis

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13
Q

Consequences of chronic meningitis

A

Granulomas

Meningeal fibrosis

Cranial nerve entrapment (facial nerve palsy e.g.)

Bilateral adrenal haemorrhage (Waterhouse-Friederichsen syndrome)

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14
Q

Complications of meningitis.

A

Death (Swelling -> ICP)

Cerebral infarction

Cerebral abscesss

Subdural empyema

Epilepsy

Systemic complications such as septicaemia.

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15
Q

Cause of encephalitis. (pathogen)

A

Usually viral and not bacterial

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16
Q

Encephalitis is inflammation of…

A

Parenchyma not meninges

However it can arise as a complication of meningitis.

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17
Q

Pathophysiology of encephalitis.

A

Neuronal cell death by the cirus and formation of inclusion bodies.

It is a lymphocytic inflammatory reaction.

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18
Q

Causative organism of encephalitis of the temporal lobe.

A

Herpes virus

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19
Q

Causative organism of encephalitis of the spinal cord motor neurones.

A

Polio

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20
Q

Causative organism of encephalitis of the brain steam.

A

Rabies

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21
Q

What are prions?

A

A prion protein called PrP which normal function is unclear but can be found in the synapse.

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22
Q

How can you get mutated PrPs?

A

Sporadic

Familial

Ingested

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23
Q

Explain the problem with mutated PrPs.

A

Interacts with normal PrP to undergo a post translational conformational change. This means that mutated PrPs can mutate normal PrPs and cause them to mutate.

The mutated PrP is extremely stable. They will aggregate and cause damage. Also they are resistant to disinfectants and radiation.

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24
Q

Explain the pathophysiology of prion disease.

A

PrP(sc) a mutated prion causes neuronal death and holes in grey matter due to their aggregation.

This will lead to spongiform encephalopathies

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25
Q

Give examples of spongiform encephalopathies.

A

Scrapie in sheep

Bovine spongiform encephalopathy in cows (aka Mad-Cow disease)

Kuru in tribes of New Guinea due to cannibalism

Variant Creutzfeldt-Jacob disease (vCJD)

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26
Q

Explain vCJD.

A

Different from classical CJD where each case has unique genetic prion sequence.

There is evidence of causal association of vCJD with BSE.

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27
Q

Classic CJD vs variant CJD.

A

Classic CJD is an intrinsic misfolded prion leading to mutated PrP.

In variant CJD it comes from mad cow disease, other people with vCJD etc… meaning it is already misfolded.

28
Q

Incubation period of vCJD.

A

15+ years.

29
Q

Define dementia.

A

Acquired global impairment of intellect, reason and personality without impairment of consciousness.

30
Q

Types of dementia

A

Alzheimer’s (50%) Sporadic/Familial, Early/Late

Vascular dementia (20%)

Lewy body

Picks disease

31
Q

What type of alzheimer’s is most common?

A

Sporadic-Late

32
Q

Pathophysiology of Alzheimer’s disease.

A

An exaggerated aging process where there is a loss of cortical neurones.

This leads to reduced brain weight and cortical atrophy.

Since there is neuronal damage neurofibrillary tangles will arise as well as senile plaques.

33
Q

Explain the process of neurofibrillary tangles in Alzheimer’s disease.

A

Intracellular twisted filaments of Tau protein.

Tau proteins normally binds and stabilises microtubules.

However when the Tau proteins become hyperphosphorylated this is no longer possible. This leads to a tangle formation.

34
Q

Explain the process of senile plaques in Alzheimer’s Disease.

A

The plaques are foci of enlarged axons, synaptic terminals and dendrites.

Amyloid depositions in vessels in the centre of plaques. This leads to reduced blood flow.

35
Q

Why is trisomy 21 associated with AD?

A

Because they commonly have an amyloid precursor protein gene mutation leading to incomplete breakdown of APP.

This leads to deposition of amyloid.

36
Q

Normal intracranial pressure.

A

0-10 mmHg

Can go up to 20 mmHg if coughing and straining.

37
Q

Compensation mechanisms to maintain normal pressure.

A

Reduced blood volume

Reduced CSF volume

Spatial change like brain atrophy.

Vascular mechanism maintain cerebral blood flow as long as ICP <60 mmHg. (Cushing’s reflex)

38
Q

Pathophysiology of space occupying lesions.

A

Deformation and destruction of the brain around the lesion.

Displacement of midline structures leading to loss of symmetry.

The brain can also shift within its cavity leading to an internal herniation or even external via foramen of magnum.

39
Q

Explain subfalcine herniation.

A

Same side as the mass where the cingulate gyrus is pushed un the free edge of the falx cerebri.

40
Q

Complications of subfalcine herniation.

A

Ischaemia of medial parts of the frontal and parietal lobe and also corpus callosum.

41
Q

Why is there ischaemia to the medial parts of the frontal and parietal lobe as well as the corpus callosum?

A

Due to compression of the anterior cerebral artery.

42
Q

Explain tentorial herniation.

A

The uncus/medial part of the parahippocampal gyrus herniates through the tentoral notch.

43
Q

Complications of tentorial herniation.

A

Damage to CN III on the same side.

Occlusion of blood flow in th eposterior cerebral and superiro cerebellar arteries.

44
Q

Why are tentorial haemorrhages frequently fatal?

A

Secondary haemorrhage into the brainstem (Duret haemorrhage)

45
Q

Explain tonsilar herniation.

A

Cerebellar tonsils pushed into the foramen magnum compressing the brainstem.

46
Q

Benign brain tumours.

A

Meningeal origin such as a meningioma

47
Q

Malignant brain tumours.

A

Astrocyte origins such as an astrocytoma (low grade)

A high grade such as grade 4 is very aggressive and an example is glioblastoma multiforme.

48
Q

How do astrocytomas spread?

A

Along the nerve tracts and through the subarachnoid space.

Often present with a secondary spinal tumour

49
Q

Give examples of other brain tumours.

A

Neurofibroma

Ependymoma

Neuronal like medulloblastoma

50
Q

Brain tumours from non-CNS tissues.

A

Lymphoma

Metastasis

51
Q

What is a stroke?

A

A sudden even producing a disturbance of CNS function due to vascular disease.

52
Q

Two broad categories of stroke.

A

Cerebral infarction (85%)

Cerebral haemorrhage (15%)

53
Q

Common risk factors of stroke

A

Hyperlipidaemia

Hypertension

Diabetes mellitus

Vascular disease

54
Q

Pathogenesis of cerebral infarct.

A

Embolism (most common)

Thrombosis over a atheromatous plaque

55
Q

Common origins of embolism.

A

From the heart - atrial fibrillatino or mural thrombus.

From atheromatous debris usually from a carotid atheroma.

Thrombus over ruptured atheromatous plaque.

Aneurysm.

56
Q

Types of infarct.

A

Regional (usually named after the cerebral artery or carotid)

Lacunar

57
Q

Explain lacunar infarcts and where to find them.

A

Less than 1cm and associated with hypertension

They commonly affect basal ganglia and internal capsule.

58
Q

What is special about cerebral haemorrhages?

A

They are spontaneous i.e. non-traumatic.

59
Q

Types of cerebral haemorrhage

A

Intracerebral haemorrhage

Subarachnoid haemorrhage

60
Q

Give causes of intracerebral haemorrhage.

A

Hypertensive vessel damage

Charcot-Bouchard aneurysm

Deposition of amyloid around cerebral vessels in the elderly

Inherited

61
Q

Consequence of intracerebral haemorrhage.

A

Produces large space occupying lesions leading to raised ICP.

62
Q

What is subarachnoid haemorrhage?

A

Rupture of berry aneurysm

63
Q

Pathogenesis of SAH is poorly understood but linked to what?

A

Male sex

Hypertension

Atheroma

Other disease

64
Q

Where are SAHs sited?

A

At branching points in the circle of willis

65
Q

Clinical presentation of SAHs.

A

Sudden severe headache also known as a thunderclap headache.

Sentinel headache

Loss of consciousness

Often instantly fatal

Clinical Neuroscience (22 decks)

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