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Semester 5 - CNS > Session 12 - Pathology of the Brain > Flashcards

Session 12 - Pathology of the Brain Flashcards

1
Q

Give three ways infections can enter the CNS

A

o Direct Spread
 E.g. middle ear infection, base of skull fracture
o Blood Borne
 Sepsis, infective endocarditis
o Iatrogenic
 Ventriculoperitoneal Shunt, lumbar puncture

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2
Q

What can cause a cerebral abscess?

A

Temporal lobe abscesses can result from an untreated middle ear infection.

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3
Q

What is meningitis?

A

Meningitis is inflammation of the Leptomeninges (Pia and Arachnoid Mater). It presents with a severe headache, neck stiffness, aversion to bright lights and a non-blanching rash.

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4
Q

Give two ways in which meningitis is classified?

A

Acute or Chronic and as Bacterial or Non-Bacterial.

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5
Q 
Give causes on meningitis at 
neonates
2-5 
5-30
>30 
Immunocompromised individuals
A 
o	Neonates
	E. Coli, L. Monocytogenes
o	2 – 5 years
	H. Influenzae type B (HiB)
o	5 – 30 years
	N. Meningitides (A, B and C types – B&C have vaccinations available) 
o	> 30 years
	S. Pneumoniae
o	Immunocompromised individuals
	Various
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6
Q

What is the course of chronic meningitis

A

patients presenting with sub-acute headaches, increasing confusion and neurological signs.

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7
Q

What is the classical causative organism of chronic meninigitis and what does it cause?

A

The classic causative organism is Mycobacterium Tuberculosis, leading to Granulomatous inflammation and fibrosis of the meninges, which leads to the entrapment of cranial nerves.

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8
Q

Give five complications of meninigitis

A

o Death
 Swelling and raised intracranial pressure
o Cerebral Infarction
o Cerebral Abscess
o Subdural Empyema
 Infection and pus in-between Dura and Arachnoid Mater
o Epilepsy – particularly in children if it has caused a focal brain lesion

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9
Q

What is encephaliis

A

. It is infection of the brain tissue itself (parenchuma), not the meninges. Consequently the brain cells and becomes very haemorrhagic.

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10
Q

What causes encephalitis

A

Herpes virus/poli/rabies

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11
Q

What can be damaged in encephalitis

A 
o	Neuronal cell death due to virus
o	Temporal Lobe
	Herpes Virus
	Children can present with this and become rapidly unwell
o	Spinal Cord Motor Neurones
	Polio
o	Brain Stem
	Rabies
o	Lymphocytic Inflammation Reaction
	Perivascular cuffing with lymphocytes in Virchow-Robin Space (the spaces around vessels in the brain)
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12
Q

Give one distinct histological cause of encephalitis (tyep of virus)

A

Cytomegalovirus (CMV)
o Owls eye inclusions
 Viral replication taking over the cell body machinery
o Eventual cell body destruction and neuronal death

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13
Q

What is toxoplasmosis caused by?

A

o Caused by the intracellular protozoan parasite Toxoplasm Gondii, which lives in the guts of cats. Humans are infected via contaminated cat faeces

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14
Q

What is the pathology of toxoplasmosis?

A

o Toxoplasms in cell bodies
o Destruction of cell body and death of neurone
o Particularly common cause of death in AIDs

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15
Q

What is a prion protein and how can it go awry?

A

o Prion protein (PrP) is a normal constituent of the synapse

o Mutated PrP can occur sporadically, familially or be ingested

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16
Q

How do mutated PrPs cause damage?>

A

o Mutated PrP interacts with normal PrP to undergo a post translational conformational change
 Mutated PrP creates more mutated PrP
o Acts like an infection, but isn’t an infection
Mutated PrP forms aggregates, which causes neuronal death and “holes” in grey matter – Spongiform Encephalopathies

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17
Q

Define dementia

A

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

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18
Q

Give four most common causes of dementia with % for first two

A 
o	Alzheimer’s – 50%
	Sporadic/Familial
	Early/Late
o	Vascular Dementia – 20% 
o	Lewy Body
o	Pick’s disease
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19
Q

What occurs in alzheimerers and what causes it?

A 
o	Increased loss of cortical neurones
	Decreased brain weight
	Cortical atrophy
o	Due to neuronal damage
	Neurofibrillary tangles – Intracellular twisted filaments of Tau Protein
	Senile plaques – Amyloid deposition
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20
Q

What two proteins cause alzheimers?

A

 Neurofibrillary tangles – Intracellular twisted filaments of Tau Protein
 Senile plaques – Amyloid deposition

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21
Q

What are the three contributors to ICP

A

Brain
Blood
Cerebrospinal fluid

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22
Q

What must happen for ICP to remain stable when onechanges?

A

Therefore, for intracranial pressure to remain stable a change in the volume of any one of them must be accompanied by an equal and opposite change in the other two.

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23
Q

What is normal ICP and when is it raised physiologically, and to what level?

A

Normal Intracranial Pressure is 0-10mmHg and rises to 20mmHg when coughing and straining.

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24
Q

What three compensation mechanisms maintain normal ICP

A

Compensation mechanisms maintain normal pressure
o Spatial – brain atrophy
o Reduced blood volume
o Reduced CSF volume

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25
Q

Up to what pressure of ICP can blood flow to brain be maintaind?

A

Compensation mechanisms maintain normal pressure
o Spatial – brain atrophy
o Reduced blood volume
o Reduced CSF volume

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26
Q

Give four causes of raised ICP

A

Haemorrhage
Tumours Meningitis
Cerebral infarction

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27
Q

What does massivwely raised ICP cause?

A

). Increasing pressure within the closed box of the skull results in compression and herniation of key parts of the brain. Three areas are involved:
o The Cingulate Gyrus
o The Uncus
o The Cerebellar Tonsils

28
Q

Give a main cause of raised ICP

A

Expanding lesion

29
Q

What does an expanding lesion do when causing raised ICP (4)

A

o Deformation or destruction of the brain around the lesion
o Sulci flattened against the skull
o Displacement of midline structures – loss of symmetry
o Brain shift resulting in internal herniation of parts of the brain

30
Q

Define herination

A

– A protrusion of an organ or part of an organ through wall that normally contains it.

31
Q

What two structures divide the brain up?

A

o Falx Cerebri – In the midline between the two cerebral hemispheres
o Tentorium Cerebelli – Lies on the superior face of the cerebellum

32
Q

Name four herniations

A

Subfalcine
Central (tentorial) herniation
uncal herniation
Tonsilar herniation

33
Q

What occurs in 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 -> Infarction

34
Q

What occurs in uncal herniation?

A

 Uncus/medial part of the parahi[ppocampal gyrus through the tentorial notch
 Damage to the oculomotor nerve on the same side
 Occlusion of blood flow in posterior cerebral and superior cerebellar arteries
 Frequently fatal because of secondary haemorrhage into brainstem -> Duret haemorrhage
 Common mode of death in those with large brain tumours and intracranial haemorrhage

35
Q

What happens in tonsillar herniation?

A

 Cerebellar tonsils pushed into the foramen magnum, compressing the brainstem

36
Q

What are three stages of raised ICp?

A

Prodromal phase
Acute phase
Compression of peduncles

37
Q

What occurs in prodromal phase of raised ICP 3

A

o Headache
o Vomiting
o Papilloedema

38
Q

What two thing soccur in acute phase of raised icp

A

o Occulomotor nerve compression – Dilation of pupil

o Compression of brain stem – Coma

39
Q

What occurs in compression of trhe cerrebral peduncles

A

Hemiparesis

40
Q

Name a benign tumour of the brain

A

o Meningioma

41
Q

Give four malignant tumours of brain

A

Astrocytoma
Neurofibroma
Ependymoma
Neuronal

42
Q

Outline course of astrocytoma

A

 Grade 1  Grade 4 (Grade 4 are extremely aggressive, life expectancy of a few months)
 Spread along nerve tracts and through sub-arachnoid space
 Often presents with a spinal secondary
 Never metastasise outside of the CNS

43
Q

What is a common cause of brain tumour/

A

Secondary metastases (lung, breast)

44
Q

What are two phases of head injury

A

Primary damage

Secondary damage

45
Q

What is focal primary damage?

A

 Bruising and laceration of the brain as it hits the inner surface of the skull
 Tearing of blood vessels and nerves as the brain moves, leading to haemorrhage
 Coup – Damage at site of impact
 Contracoup – Damage on opposite side of the brain, often of greater severity

46
Q

What is diffuse primary damage?

A

 Direct tearing to axons – Diffuse Axonal Injury (DAI)
 Micro-tears to axons at sites of differing densities of brain substance, e.g. junction of white and grey matter
 Tearing of nerves and small vessels
 Tearing of the pituitary stalk
 Heals by gliotic scarring

47
Q

What is secondary damage?

A

Reaction of the primary damage makes the injury worse

48
Q

What can occur as secondary damage

A

Extradural haemorrhage
Subdural haematoma
Stroke

49
Q

What is extradural haemorrhage

A

o Classically due to a Pterion Fracture
o Bleeding from the Middle Meningeal Artery
 Under Arterial Pressure
 Rapid increase in Intracranial Pressure

50
Q

What is the pterion?

A 
The Pterion is a ‘H-shaped’ junction of 4 bones, which lies on the lateral aspect of the skull and is the thinnest part of the Calveria. Bone fragments from fractures may rupture the Middle Meningeal Artery, leading to an Extradural Haemorrhage. The bones that make up the Pterion are:
o	Frontal
o	Parietal
o	Sphenoidal (greater wing)
o	Temporal
51
Q

What occurs in subdural haematoma?

A

o Bridging veins from surface of the cerebral hemispheres connect with vessels in the dura
o These bridging veins are susceptible to tearing as they pass through the subdural space
o Brain floats freely within the CSF, but the vessels are fixed
 Sudden brain movement will tear the bridging veins
 Venous Bleeds
 Blood accumulates much more slowly, therefore no sudden increase in intracranial pressure

52
Q

What two groups are susceptible to subdrual haematomas

A

o The elderly and alcoholics are particularly susceptible due to shrinking of the brain

53
Q

Give two broad categories of stroke and their relative incidence/

A
  • Two broad categories
    o Cerebral infarction – 85%
    o Cerebral haemorrhage – 15%
54
Q

Three main stroke risk factors

A

o Hyperlipidaemia
o Hypertension
o Diabetes mellitus

55
Q

Give two causes of stroke/

A 
-	Embolism 
o	Atrial fib, mural thrombus 
o	Atheromatous debris 
o	Thrombus over ruptured atheromatous plaque (often in basilar artery) 
o	Aneurysm 
-	Thrombosis 
o	Over plaque
56
Q

What is a tia

A

o Fibrin emboli from atheroma in carotids
o Lasts <24hrs and completely resolved
o Mary precede full stroke

57
Q

Give two types of haemorrhagic stroke

A

o Intracerebral Haemorrhage (directly into the brain) – 10% of all strokes
o Subarachnoid Haemorrhage (into the subarachnoid space) – 5% of all strokes

58
Q

What is intracerebral haemorrhage?

A

Bleeding directly into brain as a result of hypertensive vessel damage
 Blow out lesion – “blood blows straight out”
 Rapid death (“dead before you hit the floor

59
Q

How can subarachoid haemorrhage occur?

A

o Rupture of Berry Aneurysms
 Can be inherited – Congenital abnormalities of blood vessels
 Associated with polycystic kidney disease
 In non inherited patients linked to Atheroma
 Sited at branching points in the Circle of Willis

60
Q

How does subarachnoid haemorrhage occur?>

A

o Sudden, severe Thunderclap headache
o Sentinel headache (slowly worsening headache for a few days previously, aneurysm starting to rupture)
o Loss of consciousness
o Often instantly fatal

61
Q

What is MS?

A

MS is a chronic, autoimmune, T-cell mediated inflammatory disorder of the CNS. Multiple plaques of demyelination occur throughout the white matter of the brain and spinal cord, occurring sporadically over years.

62
Q

Give three main clinical patterns of MS

A

Relapsing remitting MS
Secondary progressive MS
Primary progressive MS

63
Q

What is remitting relapsing MSF and how common is it?

A

 85-95% of MS

 Symptoms occur in attacks, with onset over days and recovery over weeks

64
Q

What is secondary progressive MS?

A

 Late stage of MS consisting of gradually worsening disability, progressive slowly over years
 75% of patients with relapsing-remitting MS will eventually progress to secondary progressive MS

65
Q

What is primary progressive MS?

A

 The least common form of MS (10-15%)
 Characterised by gradually worsening disability without relapses or remission
 Typically presents later
 Associated with fewer inflammatory changes on MRI

66
Q

Give 7 symptoms of MS

A 
o	Visual changes
o	Sensory Symptoms
	Sensation of water trickling down the skin
	Reduced vibration sensation
o	Ataxia
o	Bladder hyper-reflexia causing urinary urgency and frequency
o	Neuropathic pain is common
o	Fatigue
o	Spasticity
o	Temperature Sensitivity
	Uhthoff’s Phenomenon
	Temporary worsening of pre-existing symptoms with increases in body temperature
	E.g. after exercise or a hot bath
67
Q

Give two consequences to the CNS of supressed immunity

A

o Meningitis
 Vulnerability to unusual organisms
o HIV
 May cause neuropathy and rarely encephalopathy

Semester 5 - CNS (25 decks)

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