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Nervous System And Neuropsychiatry > Session 8 L3: Neuropathology > Flashcards

Session 8 L3: Neuropathology Flashcards

1
Q

How do microorganism gain entry to the brain?

A
  • Direct spread e.g. middle ear infection (cerebral abscess), base of the skull fracture (predisposed to infection spread), cribriform plate
  • Blood borne e.g. sepsis, infective endocarditis
  • Iatrogenic e.g. V-P shunt, surgery, lumbar puncture
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2
Q

What is meningitis?

A
  • Inflammation of the leptomeninges (PIA+ARACHNOID)

- Can happen with or without septicaemia

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3
Q

What are causative organism in meningitis?

A 
Neonates – E.coli, L.monocytogenes
2-5 years – H.Influenzae type B
5-30 years – N.Meningitidis
Over 30 years – S.pneumoniae
Various in immunocompromised individuals
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4
Q

What is a common cause of chronic meningitis?

A
  • Caused by M tuberculosis commonly.

- Results in granulomatous inflammation, fibrosis of meninges and nerve entrapment

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5
Q

What are the complications of meningitis?

A

Local

  • Death (swelling leading to RICP)
  • Cerebral Infarction leading to neurological deficit
  • Cerebral abscess
  • Subdural empyema
  • Epilepsy

Systemic

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6
Q

What is classically the cuase of encephalitis?

A
  • Classically viral and not bacterial

- Affects the parenchyma not meninges

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7
Q

What are lobes affected by viruses?

A

Temporal lobe - Herpes virus

Spinal cord motor neurons - Polio

Brain stem - Rabies

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8
Q

What are prions?

A
  • Key is prion protein (PrP)

- Normal constituent of synapse

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9
Q

How are prions transmitted?

A
  • Sporadic mutation
  • Familial
  • Ingested
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10
Q

How do mutated PrP affect normal PrP?

A
  • Mutated PrP interacts with normal PrP to undergo a post translational conformational change
  • Extremely stable structure
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11
Q

How do prions cause disease?

A

PRPsc aggregates lead to neuronal death and holes in grey matter

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12
Q

What are examples of Prion disease?

A
  • Spongiform encephalopathies
  • Scrapie in sheep
  • BSE in cows
  • Kuru in tribes of New Guinea
  • Variant Creutzfeld-Jacob disease
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13
Q

What is vCJD?

A
  • Different from classical CJD
  • Each case has unique genetic prion sequence
  • Strong laboratory and epidemiological evidence of causal association of vCJD with BSE
  • Prolonged incubation period 15+ years
  • Link to tradition butchery in area in 1980s
  • Prions not eradicated by traditional sterilization
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14
Q

What are the characteristic features of classical CJD?

A
  • Median age of death is 68 years
  • Median duration of illness is 4-5 months
  • Periodic sharp waves on EEG often present
  • Presence of florid plaques on neuropathology is rare or absent
  • Immunohistochemical analysis of brain tissue shows variable accumulation
  • Agent isn’t detected readily in lymphoid tissue
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15
Q

What are the characteristic features of classical CJD?

A
  • Median age at death is 28 years
  • Median duration of illness is 13-14 months
  • Periodic sharp waves on EEG is often absent
  • Presence of florid plaques on neuropathology is present in large number
  • Immunohistochemical analysis of brain tissue shows marked accumulation of protease resistance prion protein
  • Agent is detected readily in lymphoid tissue
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16
Q

What are the signs and symptoms of classic CJD?

A
  • Dementia

- Early neurological signs

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17
Q

What are the signs and symptoms of vCJD?

A
  • Prominent psychiatric/behavioural symptoms
  • Painful dyesthesiasis
  • Delayed neurological signs
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18
Q

What are some cause of dementia?

A

Alzheimer’s – sporadic/familial, early/late

Vascular dementia – gradual ischaemic damage so gradual degeneration of neurones

Lewy body

Picks disease

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19
Q

What is dementia?

A

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

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20
Q

What are the features of brain in Alzheimer’s disease?

A
  • Loss of cortical neurones so decrease in brain weight and cortical atrophy
  • Exaggerated agin process
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21
Q

What are the microscopic features of Alzheimer’s disease?

A
  • Neurofibrillary tangles

- Senile plaques

22
Q

What are neurofibrillary tangles?

A
  • Intracellular twisted filaments of Tau protein
  • Tau normally binds and stabilises microtubules
  • Tau becomes hyperpolarised in AD causing Tauopathy
23
Q

What are senile plaques?

A
  • Foci of enlarged axons, synaptic terminals and dendrites
  • Amyloid deposition in vessels in centre of plaque
  • Amyloid deposit is central to pethogenesis
24
Q

Which condition is Alzheimer’s disease more early onset?

A
  • Down’s Syndromes
  • Trisomy 21
  • Familial Alzheimer’s is more common
  • Mutation of 3 genes on chromosome 21 is the cause
25
Q

What are are the 3 genes on chromosome 21 that are implicated to cause Alzheimer’s?

A
  • Amyloid precursor protein gene
  • Presenilin (PS) genes 1 and 2 code for components of secretase enzyme
  • Leads to incomplete breakdown of APP and amyloid is deposited
26
Q

Which processes increase the intracranial pressure?

A
  • Coughing and straining increase to 20 mmHg

- Only significant if the increased main for several minutes

27
Q

How can increased in ICP be compensated?

A

Compensation mechanism maintain normal pressure by:

  • Reducing blood volume
  • Reduced CSF volume
  • Spatial such as brain atrophy
28
Q

What is the effect of expanding lesions?

A
  • Deformation or destruction of the brain around the lesion
  • Displacement of midline structures – loss of symmetry
  • Brain shift result in internal herniation. Brains squished against bony structures and extrudes through foramina
29
Q

What is a hernia

A

Protrusion of an organ or part of an organ through wall that normally contains it

30
Q

What are the different types of herniation?

A
  • Subfalcine
  • Tentorial
  • Tonsilar
31
Q

What is a subfalcine herniation?

A
  • Same side as mass
  • Cingulate gyrus pushed under the free edge of the falx cerebri
  • Ischaemia of medial parts of the frontal and parietal lobe and corpus callosum due to compression of anterior cerebral artery leading to infarction
32
Q

What is a tentorial herniation?

A
  • Uncus/medial part of the parahippocampal gyrus through the tentorial notch
  • Damage to the oculomotor nerve on the same side (clinical sign)
  • Occlusion of blood flow in posterior cerebral and superior cerebellar arteries
33
Q

Why is a tectorial herniation often fatal?

A
  • Frequently fatal because of secondary haemorrhage into the brainstem leading to duret haemorrhage
  • Common mode of death in those with large brain tumours and intracranial haemorrhage
34
Q

What is a tonsillar herniation?

A

-Cerebellar tonsils pushed through into the foramen magnum compressing the brainstem

35
Q

What are cancers of the brain?

A
  • Meningioma (benign)
  • Astrocytoma (malignant)
  • Neurofirbroma
  • Ependymoma
  • Neuronal e.g medulloblastoma
  • Tumors from non CNS
36
Q

What is a meningioma?

A

Tumour from a meningeal origin

37
Q

What is an astrocytoma?

A
  • Astrocyte origin to astrocytoma (grade 1 to grade 4)
  • Spread along nerve tracts and through sub arachnoid space often presents with a spinal secondary
  • Grade 1 is more common in children
  • Grade 4 is very aggressive and spreads through CNS very well. Interrupt the somatic systems
38
Q

What are tumours from non-CNS origin?

A
  • Lymphoma

- Metastasis – the most common

39
Q

What is a stroke?

A

Sudden event producing a disturbance of CNS function due to vascular disease.

40
Q

What are the 2 broad categories of stroke?

A

Cerebral infarction – 85 % of strokes

Cerebral haemorrhage – 15% of strokes

41
Q

What are risk factors for stroke?

A
  • Hyperlipidaemia
  • Hypertension
  • Diabetes mellitus
  • Vascular disease
42
Q

What is the pathogenesis of a stroke?

A
  • Embolism

- Thrombosis

43
Q

What are common causes of an embolism to the brain?

A
  • Heart – atrial fibrillation, mural thrombus
  • Atheromatous debris (carotid atheroma)
  • Thrombus over ruptured atheromatous plaque
  • Aneurysm
44
Q

What are the types of infarct?

A
  • Regional

- Lacuna

45
Q

What can cause regional infarct?

A

Occlusion to Named cerebral artery or carotid

46
Q

What can cause lacuna infarcts?

A
  • Less than 1cm
  • Associated with hypertension
  • Commonly affect the basal ganglia
47
Q

What are the features of intracerebral aneurysms?

A
  • Associated with hypertensive vessel damage
  • Charcot-Bouchard aneurysms
  • Deposition of amyloid around cerebral vessels in the elderly
  • May be inherited
  • Produces space occupying lesion – RICP
48
Q

What are the common causes of sub arachnoid haemorrhages?

A

Rupture of Berry Aneurysms

49
Q

What are risk factors involved in the pathogenesis of sub arachnoid haemorrhages?

A
  • Male sex
  • Hypertension
  • Atheroma
  • Links to other diseases
50
Q

What are the symptoms of a subarachnoid haemorrhage?

A
  • Sudden severe headache – thunderclap
  • Sentinel headache
  • Loss of consciousness
  • Often instantly fatal
51
Q

Where does a berry aneurysm commonly occur?

A

Sited at branching points in the Circle of Willis

Nervous System And Neuropsychiatry (20 decks)

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