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SA Clinical Neuroscience > S8) Neuropathology > Flashcards

S8) Neuropathology Flashcards

1
Q

The CNS is normally sterile. However, microorganisms gain entry by 4 possible routes.

Identify them

A
  • Direct spread e.g. middle ear infection, base of skull fracture, air sinuses
  • Blood-borne e.g. sepsis, infective endocarditis
  • Iatrogenic e.g. ventricular-peritoneal shunt, surgery, lumbar puncture

- peripheral nerves eg HZV, viruses

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2
Q

What is meningitis?

A
  • Meningitis is the inflammation of the leptomeninges, with/without septicaemia
  • Prompt diagnosis and treatment is life saving
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3
Q

What are the causative organisms of meningitis in patients of various ages?

A
  • Neonates – E. Coli, L. monocytogenes
  • 2 - 5 years – H. influenzae type B (HiB)
  • 5 - 30 years – N. Meningitides (types)
  • Over 30 years – S. pneumoniae
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4
Q

Describe, in three steps, how chronic meningitis might occur

A

M. tuberculosis:

⇒ Granulomatous inflammation

⇒ Fibrosis of meninges

⇒ Nerve entrapment

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5
Q

Identify five complications of meningitis

A
  • Death (swelling → RICP)
  • Cerebral Infarction → neurological deficit
  • Cerebral abscess
  • Subdural empyema
  • Epilepsy
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6
Q

What is encephalitis?

A
  • Encephalitis is the classically viral inflammation of the brain parenchyma due to infection
  • Neuronal cell death by virus occurs, with the inclusion bodies
  • will see lots of lymphocytes
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7
Q

Identify the causative organisms for encephalitis in the following areas:

  • Temporal lobe
  • Spinal cord motor neurons
  • Brain stem
A
  • Temporal lobe e.g. herpes virus
  • Spinal cord motor neurons e.g. polio
  • Brain stem e.g. rabies
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8
Q

How might mutated prion proteins enter the body?

A
  • Sporadic mutation
  • Familial mutation
  • Ingested
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9
Q

What is the effect of the mutated PrP on the body?

A

Mutated PrP interacts with normal PrP to undergo a post translational conformational change

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10
Q

What occurs in prion disease?

A

PrPSC (protein) aggregates leading to neuronal death and holes in grey matter

→ lose synapses

→ lack if inflammation

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11
Q

What is dementia?

A

Dementia is the acquired global impairment of intellect, reason and personality without impairment of consciousnes

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12
Q

Identify four common forms of dementia

A
  • Alzheimer’s (50%)
  • Vascular dementia (20%)
  • Lewy body
  • Picks disease
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13
Q

Describe some defining features of Alzheimer’s Disease

A

Exaggerated aging process due to:

  • Loss of cortical neurones – ↓ brain weight, cortical atrophy
  • ↑ neuronal damage – neurofibrillary tangles, senile plaques
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14
Q

In three steps, describe how neuronal damage occurs in AD due to neurofibrillary tangles

A

⇒ Intracellular twisted filaments of Tau protein

⇒ Tau normally binds and stabilises microtubules

⇒ Tau becomes hyperphosphorylated in AD

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15
Q

In two steps, describe how neuronal damage occurs in AD due to senile plaques

A

⇒ Foci of enlarged axons, synaptic terminals and dendrites

⇒ Amyloid deposition in vessels in centre of plaque

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16
Q

In Down’s syndrome, there is early onset AD.

Explain why

A
  • Mutations of 3 genes on chromosome 21:

I. Amyloid precusor protein (APP) gene,

II. Presenilin (PS) genes 1 and 2 code for components of secretase enzyme

  • Leads to incomplete breakdown of APP and amyloid is deposited
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17
Q

What is the value for normal intracranial pressure?

A

0 - 10mmHg

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18
Q

Which physiological mechanisms increase ICP?

A

Coughing and straining increase ICP to 20 mmHG

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19
Q

Identify the three compensation mechanisms that maintain normal pressure

A
  • Reduced blood volume
  • Reduced CSF volume
  • Spatial – brain atrophy
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20
Q

How are vascular mechanisms affected by ICP?

A

Vascular mechanisms maintain cerebral blood flow as long as ICP < 60mmHg

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21
Q

State the three effects of an expanding lesion in the brain

A
  • Deformation/destruction of the brain around the lesion
  • Displacement of midline structures – loss of symmetry
  • Brain shift resulting in internal herniation
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22
Q

What occurs in a subfalcine herniation?

A
  • In a subfalcine herniation, the cingulate gyrus is pushed under the free edge of the falx cerebri
  • Infarction of medial parts of frontal lobe, parietal lobe and ischemia of corpus callosum due to compression of anterior cerebral artery → infarction

normla on left and abnormal on right

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23
Q

What occurs in a trans-tentorial herniation?

A
  • In a tentorial herniation, the uncus / medial part of the parahippocampal gyrus herniates through the tentorial notch
  • Ipsilateral occulomotor nerve damage and occlusion of posterior cerebral and superior cerebellar arteries = ischameia
  • Often fatal due to secondary haemorrhage into the brainstem (duret haemorrhage)
  • pushes onto the cerebellum
24
Q

What occurs in a tonsillar herniation?

A

In a tonsillar herniation, the cerebellar tonsils (at the bottom) are pushed into the foramen magnum compressing the brainstem

25
Q

CNS tumours are very rare.

Regardless, identify some

A
  • Benign – meningioma
  • Malignant – astrocytoma
  • Others – neurofibroma, ependymoma, neuronal e.g. medulloblastoma
26
Q

What is a stroke?

A

A stroke is a sudden event producing a disturbance of CNS function due to vascular disease

27
Q

What are the two broad categories of strokes?

A
  • Cerebral infarction (85%) Ischaemic (thrombotic or embolitic)
  • Cerebral haemorrhage (15%)
28
Q

Identify three risk factors for stroke

A
  • Hyperlipidaemia
  • Hypertension ( due to arteriosclerosis → walls thicken)
  • Diabetes mellitus
29
Q

Describe the pathogenesis of a stroke from an embolism (most common)

A

CAN COME FROM:

  • Heart – atrial fibrillation, mural thrombus
  • Atheromatous debris (carotid atheroma)
  • Thrombus over ruptured atheromatous plaque
  • DVT from patent foramen ovale
  • Aneurysm
30
Q

Describe the pathogenesis of a stroke from a thrombosis

A

Thrombosis – over atheromatous plaque inside the brain

→ carotid bifurcation, Middel cerebral artery, basil artery

→ fragments can break off and spread to distal sites

31
Q

Identify and describe two types of infarct in the brain

A
  • Regional – named cerebral artery or carotid
  • Lacuna – Associated with hypertension (commonly affect the basal ganglia)
32
Q

What are the two types of intracerebral haemorrhages?

A
  • Intracerebral haemorrhage (10% of all strokes)
  • Subarachnoid haemorrhage (5% of all strokes)
33
Q

Describe the occurrence of intracerebral haemorrhages

A
  • Associated with hypertensive vessel damage
  • Deposition of amyloid around cerebral vessels in the elderly
  • Produces space occupying lesion
34
Q

Describe how a subarachnoid haemorrhage usually presents

A
  • Sudden severe headache
  • Loss of consciousness
  • Often instantly fatal

→ sudden raise in ICP

35
Q

Describe the pathogenesis of subarachnoid haemorrhages

A

Pathogenesis poorly understood:

  • Male sex
  • Hypertension
  • Atheroma
  • loose tissue
  • Links to other diseases
36
Q

What causes a subarachnoid haemorrhage?

A

A subarachnoid haemorrhage is caused by the rupture of ‘berry’ aneurysms

→ shearing of meningeal blood vessels

TRAUMATIC: basal skull fractures

SPONTANEOUS: berry, amyloid angiopathy, vertebral artery dissection

normally in anterior circulating area

37
Q

what are the causes of raised ICP

A

→ heamatoma

→ tumours

→ space occupying lesions

→ cerebral oedema

→ infections

38
Q

what do you observe with raised ICP

A

→ destruction of brain tissue around lesions

→ displacement of midline structures

→ brain shifts

swelling, loss of sulcus and gyri are expanded

39
Q

what is a duret haemmorage

A

lots of small bleeds accumulating together in the midbrain and pons => rapidly developing brain herniation

40
Q

what is an extradural/epidural haematoma

A

→ damage to the middle meningeal artery

→ trauma to the side of the head and temporal bone

→ blood accumulates between the dura and the skull

→ lucid intervals (takes a while for the dura mater to break away from the skull and for the blood to peel away the dura)

41
Q

subdural haematoma

A

→ shearing of bridging veins

→ between the dura and the arachnoid

ACUTE: traumatic and rapid blood accumulation

CHRONIC: elderly and chronic alcoholics (brain atrophy so more space between the two layers)

→ check if the elderly are on warfarin or anticoagulants

→ a lot of blood can develop before clinical signs develop

42
Q

ischemic stroke / cerebral infraction

A

→ damage is limited if there is collateral blood supply

→ watershed areas: areas that lie most distal to portion of the artery territory

43
Q

which artery is most effected by emboli in the brain

A

→ middle cerebral as its a direct extension from the internal carotid artery

44
Q

histology of cerebral ischaemia

A
45
Q

spontaneous intracerebral haemmorage common sites

A

→ basal ganglia

→ thalamus

→ pons and cerebellum

in diagram there is extension into the ventricular system

46
Q

what is cerebral amyloid angiopathy

A

→ advancing age

→ lobar haemmorages involving cerebral cortices and tiny microharmmorages

→ Amyloid deposition in walls of meningeal vessels

47
Q

what are amyloids

A

→ build up of abnormal protein

→ can cause blockage of vessels

→ can be strained with Congo red dyes

48
Q

what are arteriovenous and cavernous malformations likely to cause

A

intracerebral haemorrhage

  • Arteriovenous malformations: very common, worm like and tangled subarachnoid vessels that can break
  • Cavernous malformations: losse vascular channels, distended and thin walled in the cerebellum and the pons
49
Q

what are some examples of CNS tumours

A
  1. primary → arises from the brain
  2. secondary → arises from elsewhere, breast or lungs
50
Q

Gliomas

A
51
Q

what are three complications of infections in the CNS

A
  1. meninges damaged
  2. aggregates of acute inflammation
  3. brain parenchyma
52
Q

how can you test for meningitis

A

→ take a lumbar puncture and test the CSF

  • see raised proteins (neutrophils), increased pressure, reduced glucose
  • CT scans
53
Q

histology of prions disease

A

shouldn’t see any of these white spaces

54
Q

features of neurodegenerative disease

A
55
Q

Alzheimer’s disease

A

→ caused from abnormal deposits of amyloid plaques and tau tangles in brain

→ altered mood, forget, can’t communicate (severe)

56
Q

Parkinson’s disease

A

→ loss of dopaminergic neurones in the substantia nigra pars compacts

→ due to lewys bodies

→ hypokinesia

picture shows a lewys body

57
Q

Huntingdon’s disease

A

→ effects the basal ganglia

→ hyperkinesia

→ autosomal dominant

→ mutant protein is broken down into aggregates of Huntingdon protein

  1. picture shows loss of white matter and the broadening of the sulcus

SA Clinical Neuroscience (23 decks)

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