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SA Clinical Neuroscience > S8) Neuropathology > Flashcards

S8) Neuropathology Flashcards

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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?

Study These Flashcards
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?

Study These Flashcards
A

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

25
CNS tumours are very rare. Regardless, identify some
- **Benign** – meningioma - **Malignant** – astrocytoma - **Others** – neurofibroma, ependymoma, neuronal *e.g. medulloblastoma*
26
What is a stroke?
A **stroke** is a sudden event producing a disturbance of CNS function due to vascular disease
27
What are the two broad categories of strokes?
- Cerebral infarction (85%) Ischaemic (thrombotic or embolitic) - Cerebral haemorrhage (15%)
28
Identify three risk factors for stroke
- Hyperlipidaemia - Hypertension ( due to **arterio**sclerosis → walls thicken) - Diabetes mellitus
29
Describe the pathogenesis of a stroke from an embolism (most common)
CAN COME FROM: - Heart – atrial fibrillation, mural thrombus - Atheromatous debris (carotid atheroma) - Thrombus over ruptured atheromatous plaque - DVT from patent foramen ovale - Aneurysm
30
Describe the pathogenesis of a stroke from a thrombosis
Thrombosis – over atheromatous plaque **inside the brain** **→** carotid bifurcation, Middel cerebral artery, basil artery → fragments can break off and spread to distal sites
31
Identify and describe two types of infarct in the brain
- **Regional** – named cerebral artery or carotid - **Lacuna** – Associated with hypertension (commonly affect the basal ganglia)
32
What are the two types of intracerebral haemorrhages?
- Intracerebral haemorrhage (10% of all strokes) - Subarachnoid haemorrhage (5% of all strokes)
33
Describe the occurrence of intracerebral haemorrhages
- Associated with **hypertensive vessel damage** - Deposition of **amyloid** around cerebral vessels in the elderly - Produces **space occupying lesion**
34
Describe how a subarachnoid haemorrhage usually presents
- Sudden severe headache - Loss of consciousness - Often **instantly** fatal → sudden raise in ICP
35
Describe the pathogenesis of subarachnoid haemorrhages
Pathogenesis poorly understood: - Male sex - Hypertension - Atheroma * loose tissue - Links to other diseases
36
What causes a subarachnoid haemorrhage?
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
what are the causes of raised ICP
→ heamatoma → tumours → space occupying lesions → cerebral oedema → infections
38
what do you observe with raised ICP
→ destruction of brain tissue around lesions → displacement of midline structures → brain shifts swelling, loss of sulcus and gyri are expanded
39
what is a duret haemmorage
lots of small bleeds accumulating together in the midbrain and pons =\> rapidly developing brain herniation
40
what is an extradural/epidural haematoma
→ 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
subdural haematoma
→ 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
ischemic stroke / cerebral infraction
→ damage is limited if there is collateral blood supply → watershed areas: areas that lie most distal to portion of the artery territory
43
which artery is most effected by emboli in the brain
→ middle cerebral as its a direct extension from the internal carotid artery
44
histology of cerebral ischaemia
45
spontaneous intracerebral haemmorage common sites
→ basal ganglia → thalamus → pons and cerebellum in diagram there is extension into the ventricular system
46
what is cerebral amyloid angiopathy
→ advancing age → lobar haemmorages involving cerebral cortices and tiny microharmmorages → Amyloid deposition in walls of meningeal vessels
47
what are amyloids
→ build up of abnormal protein → can cause blockage of vessels → can be strained with Congo red dyes
48
what are arteriovenous and cavernous malformations likely to cause
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
what are some examples of CNS tumours
1. primary → arises from the brain 2. secondary → arises from elsewhere, breast or lungs
50
Gliomas
51
what are three complications of infections in the CNS
1. meninges damaged 2. aggregates of acute inflammation 3. brain parenchyma
52
how can you test for meningitis
→ take a lumbar puncture and test the CSF * see raised proteins (neutrophils), increased pressure, reduced glucose * CT scans
53
histology of prions disease
shouldn't see any of these white spaces
54
features of neurodegenerative disease
55
Alzheimer's disease
→ caused from abnormal deposits of amyloid plaques and tau tangles in brain → altered mood, forget, can't communicate (severe)
56
Parkinson's disease
→ loss of dopaminergic neurones in the substantia nigra pars compacts → due to lewys bodies → hypokinesia picture shows a lewys body
57
Huntingdon's disease
→ 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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