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Nervous System > Pathology > Flashcards

Pathology Flashcards

1
Q

What are 3 clinical presentations associated with ↑ICP?

A

1) Nausea
2) Headache
3) Altered conscious level
4) Papilloedema

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2
Q

What is the clinical definition of raised ICP?

A

Increase in mean CSF pressure
- normal 7-15mmHg in supine adult

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3
Q

What are 3 causes of ↑ICP?

A

Diffuse conditions:
1) Cerebral oedema
- infection
- infarction
- trauma
2) Hydrocephalus

Localised conditions:
3) Space-occupying lesions
- tumours
- haemorrhage/infarct
- abscess

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4
Q

What is hydrocephalus?

A

Increase in CSF in CNS due to disturbance of formation, flow or absorption

  • Normal 120-150ml
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5
Q

What are the 2 types of hydrocephalus and how are they different?

A

1) Communicating
- between ventricles and subarachnoid space
- causes:
(i) venous drainage insufficiency (eg. thrombosis)
(ii) defective absorption (eg. SAH)
(iii) Overproduction (eg. meningitis)

2) Non-communicating
- obstruction between ventricular and subarachnoid space
- causes (eg.)
(i) congenital (eg. Arnold Chiari malformation)
(ii) mass lesions (eg. tumour, cysts, haematoma)
(iii) meningitis (via scarring, ventricular outflow obstuction)

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6
Q

What are 3 complications of raised ICP?

A

1) Cerebral herniation
2) Loss of consciousness
3) Bradycardia
4) Hypertension
5) Neurogenic pulmonary oedema

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7
Q

What is cerebral herniation?

A

The displacement of parts of the brain past rigid dural folds or through and opening into another compartment due to raised ICP

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8
Q

What are 3 forms of cerebral herniation?

A

1) Subfalcine
2) Uncal(Transtentorial)
3) Tonsilar (“coning”)

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9
Q

What is the (i) location (ii) cause and (iii) sequelae of subfalcine herniation?

A

i) Cingulate gyrus below falx cerebri
ii) cerebral hemisphere lesion
iii) usually clinically silent BUT
- can cause infarct (compression of anterior cerebral artery)

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10
Q

What is the (i) location (ii) signs/sequelae of uncal (transtentorial) herniation

A

i) medial temporal lobe through tentorium cerebelli
ii)
a) Loss of consciousness
b) CNIII compression → ipsilateral fixed & dilated pupil
c) Posterior cerebral artery compression → cortical blindness

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11
Q

What is the (i) location (ii) cause and (iii) sequelae of tonsillar herniation “coning”?

A

i) Cerebellar tonsils through foramen magnum
ii) posterior fossa SOLs
iii) neck stiffness, “coning”
- compression of cardiac and respiration centers in medulla and pons → cardiorespiratory arrest

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12
Q

What is “coning” in cerebral haemorrhage?

A

Tonsillar herniation → compression of cardiac and respiration centers in medulla and pons → cardiorespiratory arrestc

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13
Q

What are the 2 main pathogeneses of cerebrovascular disease?

A

1) Ischaemia and infarction
a) global hypoperfusion (eg. shock)
b) focal cerebral ischaemia (eg. thromboemboli)

2) Haemorrhage
a) Hypertension
b) Vascular malformations
c) Aneurysms

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14
Q

What is the clinical definition of a stroke?

A

Neurologic signs and symptoms that can be explained by a vascular mechanism, have an acute onset, and persist beyond 24hrs

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15
Q

What are 3 clinical manifestations of a stroke?

A

1) Localising signs (eg. hemiparesis)
2) Raised ICP (eg. haemorrhage, cerebral oedema)
3) Sudden severe headache (eg. ruptured vascular malformation)

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16
Q

What are 6 risk factors for cerebrovascular accidents?

A

1) HTN
2) DM
3) Atherosclerosis
4) Transient Ischaemic Attacks (TIA)
5) Afib
6) Vascular malformations/abnormalities
7) Coagulopathies

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17
Q

What is a transient ischaemic attack?

A

Temporary cerebrovascular insufficiency:
- transient episode of neurologic dysfunction caused by: focal brain, spinal cord or retinal ischemia
- NO acute infarction

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18
Q

Where do watershed infarcts of the brain most commonly occur?

A

Areas between those supplied by middle and anterior cerebral arteries

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19
Q

What does an intracranial watershed infarct result in?

A

Cortical pseudolaminar necrosis

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20
Q

What are 3 causes of global hypoperfusion?

A

1) Cardiac arrest
2) Shock
3) Severe hypotension

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21
Q

What is the pathogenesis of focal cerebral ischaemia?

A

Arterial occlusion due to thromboemboli resulting in reduced flow in a localised area of the brain

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22
Q

What are 3 underlying causes of thromboemboli in focal cerebral ischaemia?

A

1) Atherosclerosis
2) Arteriosclerosis
3) Vasculitis

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23
Q

What are 2 types of brain infarcts?

A

1) Pale/bland/non-haemorrhagic

2) Red/Haemorrhagic

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24
Q

What is the clinical significance of differentiating pale and red infarcts?

A

Pale can be treated with thrombolytics unlike red (contraindicated)

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25
Q

How do the pathogenesis of pale and red infarcts in focal cerebral ischaemia?

A

Pale:
1) Thrombosis eg.
- atherosclerosis
- arteriolosclerosis

Red:
1) Venous Thrombosis
Emboli:
2) Carotid artery atheroma
3) Cardiac thrombi (post AMI, Afib, valvular disease)
4) Fat emboli (post bone trauma)

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26
Q

What form of necrosis is secondary to a cerebral infarction?

A

Liquefactive

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27
Q

How does the gross morphology of a pale infarct of the brain change over time?

A

48hrs:
- soft, swollen
- pale, indistinct grey-white matter junction

2-10D:
- gelatinous, friable

10D-3wks:
- liquid filled cavity

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28
Q

How does the gross morphology of a pale cerebral infarct change over time?

A

12hr:
- ischaemic neuronal change (red neurons, oedema)

<48hrs
- Neutrophils

2D:
- foamy macrophages

1-3wks:
- ↑↑macrophages
- reactive gliosis (astrocytes)

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29
Q

What are the 4 causes of intracerebral haemorrhage?

A

1) Hypertension (smaller vessels)
- hyaline arteriolosclerosis
- fibrinoid necrosis
- charcot bouchard microaneurysms → rupture

2) Cerebral amyloid angiopathy
- amyloid deposition → weakened wall (leptomeningeal, cortical arterioles)

3) Structural vascular abnormalities
- Arteriovenous malformation
- Berry/saccular aneurysms (in circle of willis)

4) Coagulopathies

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30
Q

Which part of the brain do Charcot Bouchard microaneurysms most commonly occur?

A

Smaller vessels of the (i) Basal Ganglia and (ii) Thalamus

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31
Q

In which demographic are intracerebral haemorrhages due to structural vascular abnormalities seen?

A

Younger px
- sudden presentation

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32
Q

What are three effects of hypertension in the brain?

A

1) Lacunar infarcts
2) Hypertensive encephalopathy
3) Hypertensive intracerebral haemorrhage

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33
Q

What are lacunar infarcts and where do they most commonly occur?

A

Arteriolar sclerosis → occlusion → multiple small infarcts (lacunar infarcts <15mm)

Occur in:
deep penetrating vessels of basal ganglia, cerebral white matter, brainstem (eg. lenticular nucleus, thalamus, internal capsule, caudate nucleus, pons)

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34
Q

True or false: Lacunar infarcts are always a medical emergency.

A

False.
Site dependent
- may be clinically silent

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35
Q

What are the 2 main clinicopathologic entities in hypertensive encephalopathy?

A

1) Acute hypertensive encephalopathy (malignant hypertension)

2) Multi-infarct dementia

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36
Q

How are acute hypertensive encephalopathy/malignant hypertension and multi-infarct dementia different?

A

1) Clinical S/S:
MH: non-specific (headache, confusion, convulsion → coma)

MID: progressive dementia, gait abnormalities, focal neurological deficits

2) Pathogenesis:
MH: cerebral edema/herniation + petechial haemorrhages + fibrinoid necrosis of arterioles

MID: multifocal vascular disease (eg. thromboemboli)

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37
Q

Multi-infarct dementia is usually an (acute/progressive) condition affecting _______ age group.

A

Progressive
Middle aged to elderly (55-75y/o)

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38
Q

What is the most common cause of primary brain parenchymal haemorrhage?

A

Hypertensive intracerebral haemorrhage

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39
Q

What are the 3 forms of extra-axial intracranial haemorrhage?

A

1) Subarachnoid
- non-traumatic
- ruptured saccular aneurysms or arteriovenous malformations

2) Subdural
- traumatic

3) Epidural/extradural
- trauma

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40
Q

Which of the extra-axial intracranial haemorrhages are non-traumatic in aetiology?

A

Subarachnoid

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41
Q

What are 2 causes of subarachnoid haemorrhage?

A

1) Ruptured saccular (berry) aneurysms

2) Ruptured arteriovenous malformations

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42
Q

What is a “thunderclap headache” most commonly associated with?

A

Subarachnoid haemorrhage

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43
Q

What structure are berry aneurysms found on in an intracranial aneurysms?

A

Circle of Willis
- esp at junctions of communicating arteries

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44
Q

True or false: A “thunderclap” headache is a medical emergency.

A

True
a/w saccular “berry” aneurysm causing subarachnoid haemorrhage
- requires urgent surgical intervention (50% die w 1st bleed)

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45
Q

What genetic condition is associated with saccular aneurysms?

A

AD polycystic kidney disease

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46
Q

What are 4 forms of vascular malformations that increase a px risk of intracranial haemorrhage?

A

1) Arteriovenous malformation
2) Cavernous angioma
3) Capillary telangiectasis
4) Venous angioma

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47
Q

What are 2 intracranial complications of vascular malformations eg. arteriovenous malformations?

A

1) Intracerebral haemorrhage (CVA)
2) Subarachnoid haemorrhage

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48
Q

What does a laceration of the middle meningeal artery most likely lead to?

A

Epidural hematoma

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49
Q

What does a tear in the bridging veins in the subdural space most commonly lead to?

A

Subdural haemorrhage

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50
Q

What is the difference between the aetiology of a subdural and epidural haemorrhage?

A

Epidural
- laceration of artery (eg. middle meningeal)

Subdural
- venous bleed (eg. tear in subdural bridging veins)

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51
Q

What are 2 differences between acute and chronic subdural haematomas?

A

1) Cause
A: Acceleration-decelearion injuries → cerebral contusion (need rapid surgical decompression)
C: minor head trauma

2) Prognosis
A: high mortality rate
C: good prognosis

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52
Q

How would chronic subdural haemorrhage differ from an acute one on gross morphology?

A

Chronic: signs of organisation (fibrosis)

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53
Q

Which form of intracranial bleed is most likely in a temporal bone fracture?

A

Epidural haematoma (laceration of middle meningeal artery)

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54
Q

What is the classical clinical Hx of an epidural haematoma?

A

Head trauma
→ lucid interval
→ Sudden deterioration (eg. vomiting, restlessness, loss of consciousness)

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55
Q

What is a “lenticular (convex)” appearance on a head CT indicative of?

A

Epidural haemorrhage

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56
Q

What are 4 causes of intracerebral petechial haemorrhages?

A

1) Fat embolism (eg. after surgery)
2) Malaria
3) Vasculitis
4) Acute hypertensive encephalopathy

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57
Q

What are 2 conditions that are commonly associated with a ruptured berry aneurysm?

A

1) Polycystic kidney disease
2) Aortic coarctation

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58
Q

(Primary/secondary) tumours are more common in children.

A

Primary

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59
Q

What type of cells are arachnoid cells?

A

Meningothelial cells

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60
Q

What is the cellular origin of the meningiomas?

A

Menigothelial cells

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61
Q

What is the cellular origin of gliomas?

A

Glial tissue

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62
Q

What is the cellular origin of central neurocytoma?

A

Neurons

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63
Q

What is the cellular origin of medulloblastoma?

A

Embryonal

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64
Q

What are 2 cancers of the brain ventricles?

A

1) Choroid plexus tumours
2) Ependymomas (periventricular)

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65
Q

What are 3 cancers of brain parenchyma?

A

1) Medulloblastoma (embryonal)
2) Central neurocytoma
3) Gliomas

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66
Q

What are 3 brain tumours of midline structures?

A

1) Pituitary tumour
2) Germ cell tumours (children)
3) Pineal gland tumours

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67
Q

Meningiomas originate from _______________ cells usually occurring in the ________________ of the brain.

A

Arachnoid/Meningiothelial cells

Falx, cerebral convexities

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68
Q

Meningiomas are (common/rare), (fast/slow-growing) and may invade ___________.

A

Common and slow-growing
May invade skull bone

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69
Q

What syndrome is most common associated with meningiomas?

A

NF-2

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70
Q

Meningiomas are more common in (male/female) and the most common subtype is ___________________.

A

F > M

Commonest: Meningothelial type

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71
Q

What are 3 histological features of meningiomas?

A

1) Meningothelial whorls
2) Uniformed ovoid cells
3) Psammoma bodies
4) Nuclear inclusions

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72
Q

What are 3 forms of gliomas?

A

1) Astrocytoma
- WHO grade I-IV

2) Oligodendrogliomas
- WHO grade II-III

3) Ependymomas
- WHO grade II-III

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73
Q

What are the different types of astrocytomas?

A

1) Pilocytic (Grade I)
- children
- supra/infra-tentorial

2) Astrocytoma (Grade II-IV)
- IDH mutant

3) Glioblastoma (Grade IV)
- IDH wild-type

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74
Q

True or false:
IDH1 mutant gliomas are more favorable to wild type.

A

True.
Astrocytoma better prognosis than Glioblastoma

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75
Q

What is the histological appearance of pilocytic astrocytoma?

A

Astrocytes with long fibrillary cytoplasmic processes

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76
Q

Which demographic is most commonly afflicted with pilocytic astrocytoma?

A

Children

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77
Q

What are 2 histological characteristics of glioblastoma?

A

1) Palisading necrosis
2) Nuclear pleomorphism

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78
Q

What is the specific genetic profile of oligodendrogliomas?

A

IDH1 mutation and whole arm deletion of 1p and 19q

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79
Q

Which part of the brain is most commonly affected by oligodendrogliomas?

A

Cerebral cortex

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80
Q

True or false: Oligodendrogliomas are chemosensitive.

A

True

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81
Q

What is the histological appearance of oligodendrogliomas?

A

Uniformed round cells with “fried egg” appearance

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82
Q

Why does central neurocytoma cause raised ICP?

A

Near 3rd ventricle → compressive

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83
Q

Central neurocytomas usually affect ______ and have (good/poor) prognosis.

A

Adults
relative good prognosis

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84
Q

What is the difference between a CNS neuroblastoma and medulloblastoma?

A

Both aggressive embryonal brain parenchymal tumours in children

CNS neuroblastoma
- supratentorial
- poor prognosis

Medulloblastoma
- Medulloblastoma
- commoner

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85
Q

How are medulloblastomas classified?

A

According to molecular profile
- WNT and SHH activation status
- TP53 mutant/WT

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86
Q

What are the 2 treatment options for medulloblastoma?

A

Surgery and radiotherapy

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87
Q

Where do medulloblastomas commonly occur?

A

Cerebellum:
- Vermis (children)
- Hemispheres (adults)

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88
Q

Medulloblastomas are (aggressive/indolent) and spread via _______ causing ______________.

A

Aggressive
Spread via CSF → hydrocephalus

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89
Q

What are 3 histological features of medulloblastoma?

A

1) Sheets of small cells, high N/C ratio, mitoses
2) “Carrot shaped” nuclei
3) Rosettes

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90
Q

What are 2 histological features of ependymomas?

A

1) Perivascular pseudorosettes
2) True rosettes (canals)

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91
Q

What are ependymomas and where are they most commonly located (3)?

A

Gliomas of the ventricles
1) Periventricular
2) Intraparenchymal (supertentorial or infratentorial esp posterior fossa)
3) Spinal cord

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92
Q

What are 3 demographics that are most commonly seen with ependymomas?

A

1) Children (esp posterior fossa)
2) Young adults
3) NF-2 px

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93
Q

True or false:
Unlike medulloblastomas and choroid plexus tumours, ependymomas cannot cause hydrocephalus.

A

False.
All 3 can lead to hydrocephalus

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94
Q

What are the 2 forms of choroid plexus tumours?

A

1) Papilloma
2) Carcinoma (greater N/C ratio, cellularity)

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95
Q

What are 2 forms of sellar tumours?

A

1) Pituitary adenomas
2) Craniopharyngiomas

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96
Q

What are 2 forms of pituitary tumours?

A

1) Endocrine
- adenoma (commonest)
- carcinoma

2) Embryonal remnant tumours
- Craniopharyngiomas

97
Q

What are 2 clinical effects of pituitary tumours?

A

1) Visual field defects
- optic chiasma compression → bitemporal hemianopia

2) Endocrine effects
- functional hypersecretion

98
Q

Where do craniopharyngiomas arise from?

A

Tooth-forming epithelium within suprasellar region

99
Q

Which 2 demographics are most commonly affected by craniopharyngioma?

A

1) Children
2) Adults (50s-60s)

100
Q

What are the 2 types of craniopharyngiomas?

A

1) Adamantinomatous
2) Papillary

101
Q

What is the gross appearance of an adamantinomatous craniopharyngioma?

A

Cystic, containing yellow viscous fluid (“engine oil” appearance)

102
Q

What is the histological appearance of adamantinomatous craniopharyngioma (3)?

A

1) Cysts lined by stratified squamous epithelium

2) “Wet keratin”

3) Calcifications

103
Q

What are 2 germ cell tumours of the CNS?

A

1) Teratoma
2) Germinoma

Less common:
3) Embryonal carcinoma
4) Yolk sac tumour
5) Choriocarcinoma

104
Q

CNS germ cell tumours EPC:
Children (</>) Adults
Males (</>) Females
Pineal gland (</>) Suprasellar region

A

Children > Adults
M > F
Pineal gland > Suprasellar region

105
Q

What are 2 forms of pineal tumours?

A

1) Pineocytoma
2) Pineoblastoma
- high grade, primitive

106
Q

Primary CNS lymphomas are mostly ________ in origin and are seen in ___________ px.

A

B cell, non-Hodgkin’s

Immunosuppressed px (eg. AIDS → EBV lymphomas)

107
Q

What are 3 histological features of schwannomas?

A

1) Spindled cells
2) Nuclear palisading
3) Hyalinised vessels

108
Q

What are 3 examples of peripheral nerve sheath tumours?

A

1) Malignant

Benign:
2) Schwannoma
3) Neurofibroma

109
Q

How are schwannomas different from neurofibromas?

A

Schwannoma
- well circumscribed/encapsulated
- attached to nerve

Neurofibroma
- non-encapsulated
- cutaneous/deep nerves

110
Q

What is the histological appearance of neurofibroma?

A

1) Spindle cells within loose stroma

2) Collagen fibres within stroma

111
Q

What are 4 examples of neurocutaneous syndromes?

A

1) Neurofibromatosis 1
2) Neurofibromatosis 2
3) Tuberous sclerosis
4) Von Hippel-Lindau Disease

112
Q

Neurocutaneous syndromes often show a __________ inheritance pattern and present in _______________.

A

AD

Present:
- tumours
- Skin hamartomas
- nervous system

113
Q

In NF1, the ____________ gene, which functions as a ______________, is mutated.

A

NF-1 gene for neurofibromin (17q)
- TS gene for signal transduction

114
Q

What is the inheritance pattern of NF-1?

A

AD

115
Q

What are 4 manifestations of NF-1 syndrome?

A

Neural tumours:
1) Neurofibromas (skin, CNVIII, radiculopathy, plexiform)

2) Optic nerve glioma
3) Hamartomas (Lisch nodules)

Other abnormalities:
4) Cutaneous
5) MSK
6) Renal

116
Q

How does NF- progress to malignancy?

A

Sarcomatous transformation of neurofibromas → malignant nerve sheath tumours

117
Q

NF2 is a result of a mutation in the _________ gene.

A

NF2 (Merlin) gene

118
Q

What is the inheritance pattern of NF-2?

A

AD
- or de-novo mutation

119
Q

How is NF-2 diagnosed?

A

At least 1 of:
1) Bilateral vestibular schwannomas
2) 1° wNF2 and
i) Unilateral vestibular schwannoma OR
ii) Any two of: meningioma, schwannoma, glioma, neurofibroma, posterior subcapsular lenticular opacities

3) Unilateral vestibular schwannoma and
i) Any two of: Meningioma, schwannoma, glioma, neurofibroma, posterior subcapsular lenticular opacities

4) Multiple meningiomas and
i) Unilateral vestibular schwannoma OR
ii) Any two of: schwannoma, glioma, neurofibroma, cataract

120
Q

In tuberous sclerosis, the __________ genes are mutated.

A

TSC1 and 2
- participate in cell proliferation

121
Q

What are 4 manifestations of tuberous sclerosis?

A

1) Brain: cortical tubers, hamartomas
2) Skin: adenoma sebaceum, shagreen patch, ungual fibroma
3) Lung lesions
4) Renal angiomyolipomas

122
Q

What is the inheritance pattern of tuberous sclerosis?

A

AD

123
Q

What is the inheritance pattern of Von-Hippel Lindau syndrome?

A

AD
- variable penetrance

124
Q

In Von-Hippel Lindau syndrome the __________ gene is affected.

A

VHL TS gene (3p25-26)
- angiogenesis + cell cycle

125
Q

What are 5 manifestations of Von-Hippel Lindau Syndrome?

A

1) Hemangioblastomas
- retinal, cerebellar, supratentorial

2) Cysts
- renal, pancreatic, adrenal

3) RCC

4) Paraganglioma

5) Phaeochromocytomas

6) Endolymphatic sac tumour (inner ear)

126
Q

What are 2 examples of paraneoplastic syndromes of the CNS?

A

1) Paraneoplastic cerebellar degeneration
2) Limbic encephalitis

127
Q

What are 4 components of the Brain’s natural barrier against infection?

A

Physical:
1) Skull
2) Dura mater
3) BBB

Cell:
4) Microglia
5) WBCs

128
Q

What are 3 routes of CNS infection?

A

1) Local
- disruption of coverings (eg. trauma, spina bifida)

2) Regional
- sinusitis, otitis media, dental carries, facial infections

3) Blood borne
- septicemia
- septic emboli

4) Peripheral nerves
- rabies, HSV

129
Q

What are 4 patterns of CNS infection involvement?

A

1) Meningitis
2) Subdural empyema, extradural abscess
3) Localised infection
4) Encephalitis

130
Q

What are 3 clinical presentations of meningitis?

A

1) Headache
2) Fever
3) Neck Stiffness
4) Photophobia

131
Q

What is the most common clinical presentation of encephalitis?

A

Altered mental state

132
Q

What are 3 clinical presentation of an intracranial abscess?

A

1) Swinging fever
2) Localising signs of CNS disease
3) Raised ICP
- vomiting, LOC

133
Q

What are 3 investigations for a CNS infection?

A

1) Imaging
- localise

Sterile samples:
2) CSF microscopy/culture/labs
3) Blood culture

134
Q

What are 5 infective causes of meningitis?

A

Bacterial:
1) E. coli
2) Listeria cytomonogenes
3) H. influenzae
4) Neisseria meningitides
5) Strep pneumo
6) TB

Aseptic:
7) Echovirus
8) Coxsackie

Fungal:
9) Cryptococcus neoformans
10) Candida albicans

135
Q

What are 2 bacterial causes of meningitis in neonates?

A

1) E. coli
2) Listeria monocytogenes

136
Q

What is the main bacterial cause of meningitis in infants?

A

Haemophilus influenzae

137
Q

What is the main cause of meningitis in adolescents?

A

Neisseria meningitides

138
Q

What are 2 bacterial causes of meningitis?

A

1) Neisseria meningitides
2) Strep pneumoniae

139
Q

Which part of the brain does TB usual infect?

A

Base of brain

140
Q

What are 2 aseptic causes of meningitis?

A

1) Echovirus
2) Coxsackie

141
Q

What are 2 fungal causes of meningitis?

A

1) Cryptococcus neoformans
2) Candida albicans

142
Q

Which Ix is most important in the management of meningitis?

A

CSF exam (spinal tap)

143
Q

What would the CSF of a px with meningitis show?

A

1) Cloudy
2) Cytology
- bacterial: ++polymorphs
- viral: lymphocytes++
- TB: either

144
Q

What are 4 complications of meningitis?

A

1) Brain infarct
2) Meningeal fibrosis → hydrocephalus
3) Damage to cranial nerves
4) Raised ICP
5) Mental retardation (in children)

145
Q

What are 2 gross features of tuberculous meningitis?

A

1) Gelatinous exudate on base of brain
2) White granules on tubercles (granulomas)

146
Q

What are 3 complications of tuberculous meningitis?

A

1) Obliterative endarteritis
- cerebral ischemia, infarct

2) Fibrous adhesions in arachnoid mater
- cranial nerve deficits
- hydrocephalus

3) Tuberculoma of brain

147
Q

Where do subdural empyemas usually originate from?

A

1) Skull infection
2) Paranasal sinus infection

148
Q

What are 2 clinical manifestations of subdural empyema?

A

1) Local symptoms
- thrombophlebitis of bridging veins → localised infarct

2) Meningitis symptoms
- Headache, Fever, Neck Stiffness, Photophobia

149
Q

How are subdural empyemas treated?

A

Surgical drainage

150
Q

Where do extradural abscesses originate from?

A

1) Sinusitis
2) Iatrogenic

151
Q

What is a condition that is commonly a/w extradural abscesses and what is the main concern with this condition?

A

Osteomyelitis
→ spinal cord epidural infection → cord compression

152
Q

How do the aetiologies of single vs multiple cerebral abscesses differ?

A

Single:
- local source (otitis media, sinusitis, skull trauma, iatrogenic, facial infections, etc.)

Multiple:
- septicaemia, septic emboli (eg. infective endocarditis)

153
Q

What are 4 common infective causes of cerebral abscesses?

A

Usually bacterial:
1) Strep
2) Staph aureus
3) Bacteroides
4) E. coli

154
Q

What is the causative organism of neurosyphilis?

A

Treponema pallidum

155
Q

What are 7 causes of localised infections in the CNS?

A

Bacterial:
1) Strep
2) Staph aureus
3) Bacteroides
4) E. coli

Spirochaetes:
5) Treponema pallidum

Fungal:
6) Candida spp.
7) Cryptococcus
8) Aspergillosis

Parasitic:
9) Toxoplasma gondii
10) Taenia solium
11) Amoeba (eg. Naegleria, acanthamoeba)

156
Q

What is the typical imaging presentation of CNS toxoplasmosis?

A

Multiple ring-enhancing lesions on CT/MRI

157
Q

In which demographic does CNS toxoplasmosis most commonly occur?

A

HIV+ px

158
Q

Encephalitides are usually (bacterial/viral/parasitic/fungal/idiopathic)

A

Viral

159
Q

How do the causes of encephalitides differ?

A

Acute: Acute meningoencephalitis
i) HSV, measles, CMV, HIV
ii) Fetal nervous system: rubella, CMV

Delayed / subacute:
a) Subacute sclerosing panencephalitis → Measles
b) Reactivation → VZV

Prion disease

160
Q

Which virus(es) tend to target neurons and glial tissue?

A

1) HSV (esp temporal lobe)
2) Rabies

161
Q

Which virus(es) tend to target motor neurons?

A

1) Poliovirus
2) Enteroviruses

161
Q

Which virus(es) tend to target microglia?

A

HIV

161
Q

Which virus(es) tend to target dorsal root ganglia?

A

VZV

162
Q

What are 3 histological features of HSV1 encephalitis?

A

1) Cowdry type A nuclear inclusion
2) Tissue necrosis and haemorrhage
3) Perivascular lymphocytic infiltrates

163
Q

Which demographics are most commonly afflicted with HSV1 encephalitis?

A

1) Children
2) Young adults (10% Hx of labial HSV)

164
Q

What is common clinical presentation of HSV1 encephalitis?

A

Alteration in mood, memory, behaviour

165
Q

Describe the pathogenesis of rabies.

A

Virus ascends from wound site → spinal ganglion → CNS → severe encephalitis (1-3mths depending on site)

166
Q

How does rabies typically present?

A

Early: nonspecific
- malaise, fever, headache
- focal paraesthesia around wounds

Advanced:
i) marked CNS excitability
- painful touch, violent motor responses, convulsions
ii) pharyngeal muscle contraction when swallowing
- foaming, hydrophobia
iii) mania and stupor → coma and death

167
Q

What is the characteristic histological finding in rabies?

A

Negri bodies
- cytoplasmic round/oval eosinophilic inclusions i
- in (i) pyramidal/hippocampal neurons (ii) purkinje cells (cerebellum)

168
Q

Describe the pathogenesis of poliomyelitis.

A

Fecal-oral route → multiplies in lymphoid tissues (tonsils, peyer’s patches, lymph nodes, etc.)
→ Viraemia
→ invade CNS

169
Q

True or false: poliomyelitis is rarely self-limiting as it frequently penetrates CNS in viraemia.

A

False.
Most self-limiting inflammation of meninges, rarely penetrate CNS

170
Q

What is the main complication/sequelae from poliomyelitis penetrating the CNS?

A

Damage motor neurons → flaccid paralysis + hyporeflexia

171
Q

What are 2 types of CNS infections by HIV?

A

1) Aseptic meningitis
2) Encephalitis

172
Q

How does HIV present in the spinal cord?

A

Vacuolar myelopathy
- holes in myelin sheath
- posterior columns
- corticospinal tract

173
Q

How does CNS involvement of HIV present?

A

1) Imbalance
2) Sensory loss
3) Slowly progessive painless leg weakness, stiffness

174
Q

What are 2 pathologies a/w HIV encephalitis?

A

1) Opportunistic infections in CNS (eg. toxoplasmosis, CMV, fungi, PML)

2) CNS lymphomas

175
Q

What are 3 histological features of HIV encephalitis?

A

1) Multinucleated giant cells
2) Microglial nodules
3) Perivascular lymphocyte cuffing

176
Q

What are 4 pathologies of neurosyphilis?

A

1) Tertiary syphillis
2) Meningovascular syphilis
3) Brain: general paresis of the insane
4) Spinal cord: tabes dorsalis

177
Q

What are 2 histological features of meningovascular syphilis?

A

1) Granulomatous meningitis
2) Subintimal vessel thickening

178
Q

How does neurosyphilis of the brain usually present?

A

Dementia
- neuronal loss

179
Q

How does neurosyphilis of the spinal cord present?

A

Tabes dorsalis
- posterior column demyelination → charcot joints, skin damage

180
Q

What are 3 CNS pathologies caused by fungi?

A

1) Vasculitis and thrombosis → infarction, hemorrhage

2) Meningitis (Cryptococcus)

3) Parenchymal invasion → abscess granulomas (Candia, Cryptococcus)

181
Q

What are the modes of prion transmission?

A

1) Genetic
2) Sporadic
3) Transmissible
- contaminated transplantation tissue, food ingestion

182
Q

What is the pathogenesis of prion diseases?

A

“Spreading”/accumulation of misfolded prion protein (PrP)
→ “Spongiform encephalopathy”
→ neuronal death

183
Q

What are 2 histological features of prion disease?

A

1) Spongiform transformation
- cerebral cortex, deep grey matter

2) Amyloid deposits and plaques

184
Q

What are 2 aetiologies for CNS malformations?

A

1) Prenatal/perinatal insult
a) Nutritional deficiency
- folate → neural tube defects
b) radiation → neural tube defects, anencephaly
c) infections, drugs, toxins, etc.

2) Genetics

185
Q

What are neural tube defects and why are they pathogenic?

A

Failure of part of tube to close/re-opening of tube
→ abnormalities of neural tissue and overlying bone/soft tissue

186
Q

Neural tube defects occur during ____________ of embryogenesis and can be detected in utero via ________.

A

3-4 week

Detected via:
- amniotic fluid and maternal blood

187
Q

What is the main cause of spina bifida?

A

Folate deficiency

188
Q

How can spina bifida be treated?

A

Folic acid (0.4mg) in periconceptional period

189
Q

What are 3 neural tube defects?

A

Brain:
- anencephaly
- encephalocele

Spinal cord:
- spina bifida/spinal dysraphism

190
Q

Anencephaly occurs in a ______ neural tube defect, (F </> M) and results in disrupted _________________________, sparing the ______________.

A

Anterior neural tube defect (F>M)
- disrupted forebrain development → absent brain and calvarium in the cerebrovasculosa

  • spares posterior fossa
191
Q

How does spina bifida present?

A

Occulta → hairy patch

Myelomeningocele/meningocele
- LL weakness/paralysis
- Skeletal abnormalities (club feet, hip dislocation)
- Bladder and bowels dysfunction, UTIs
- Pressure ulcers

192
Q

What are 3 examples of forebrain abnormalities?

A

1) Polymicrogyria
2) Lissencephaly
3) Holoprosencephaly

193
Q

How does polymicrogyria present?

A

1) Seizures
2) Mental retardation
3) Hemi/Quadriparesis

194
Q

How does Lissencephaly present?

A

1) Dysphagia, aspiration
2) Seizures
3) Severe psychomotor retardation

195
Q

How does holoprosencephaly present?

A

1) Facial midline abnormalities (eg. cyclopia)
2) Early mortality
3) Movement disorders
4) Feeding problems

196
Q

What is the pathogenesis of holoprosencephaly?

A

Trisomy 13, maternal DM
→ incomplete separation of the cerebral hemispheres across midline

197
Q

What are 2 examples of posterior fossa anomalies?

A

1) Arnold Chiari Malformation
2) Dandy Walker Syndrome

198
Q

What is a Arnold Chiari Malformation?

A

Chiari type II malformation
- small posterior fossa
- cerebellar tonsils displaced through foramen magnum

199
Q

What are 2 associations of Arnold Chiari Malformation?

A

1) Hydrocephalus
2) Spina bifida myelomeningocele

200
Q

What are 3 clinical features of Arnold Chiari Malformation?

A

1) Headache especially on Valsalva maneouvre
2) Muscle weakness, fatigue
3) Brainstem damage/death

201
Q

What is Dandy Walker Syndrome?

A

Enlarged posterior fossa
- cerebellar vermis absent/shrunken
- central open cyst

202
Q

What are 4 clinical presentations of Dandy Walker Syndrome?

A

1) Slow motor development (infants)
2) Gradual skull enlargement
3) Raised ICP → vomiting, irritability, convulsion
4) Poor coordination, eye and face muscles

203
Q

What are 4 neurodegenerative diseases?

A

1) Dementia
- eg. Alzheimer disease

2) Movement disorder
- eg. Parkinson disease (substantia nigra)
- Huntington Chorea (basal ganglia)

3) Motor weakness
- eg. Motor neurone disease

4) Others
- eg. spinocerebellar degenerations, Friedreich’s ataxia, etc.

204
Q

Describe 2 genetic predispositions in early onset Alzheimer disease?

A

1) Chromosome 21
- Amyloid Precursor Protein → Aß (ß amyloid peptides) deposition

2) Chromosome 19
- ApoE4 subtype → tau hyperphosphorylation

205
Q

What are 3 clinical features of Alzheimer disease?

A

1) Progressive cognitive decline
2) Immobility
3) Pneumonia

206
Q

What are 2 demographics that are most commonly afflicted by Alzheimer disease?

A

1) >80y/o (20%)
2) younger with Chromosome 21 APP or Chromosome 19 Apo E4 mutation

207
Q

What is the the pathogenesis of Alzheimer’s disease?

A

Abnormal protein deposition
i) amyloid (neuritic/senile) plaque
ii) Neurofibrillary tangles
→ neuronal damage and loss

208
Q

What is the main gross feature of Alzheimer’s disease?

A

Small, atrophied brain
- temporal lobe most affected

209
Q

What are 2 histological features of Alzheimer’s disease?

A

1) Amyloid/Neuritic/Senile plaques
- collections of dilated, tortuous neuritic process surrounding a core of ß amyloid

2) Neurofibrillary tangles
- hyperphosphorylated tau protein within neurons

210
Q

What are 3 clinical features of Parkinson disease?

A

1) Rigidity
2) Slowing of voluntary movements
3) Rest tremor

211
Q

Describe the genetic pathogenesis of Parkinson disease.

A

Disorder of α-synuclein gene → accumulation of α-synuclein protein → lewy bodies

212
Q

What are 2 pathologies of Parkinson disease?

A

1) Loss of nerve cells from substantia nigra (midbrain)
- ↓ dopamine to basal ganglia
- pallor in substantia nigra

2) Lewy bodies in neuron

213
Q

What is the gross appearance of Parkinson’s disease?

A

Pallor in substantia nigra

214
Q

What is the histological feature of parkinson’s disease?

A

Lewy bodies in neurons

215
Q

What are 4 clinical presentations of Huntington’s Chorea?

A

1) Personality alterations
2) Cognitive decline
3) Abnormal movements
4) Death from aspiration, heart disease

216
Q

What are 3 gross features of Huntington’s Chorea?

A

1) Small brain with atrophy of caudate nucleus and frontal lobe

2) Atrophied putamen and globus pallidus (later)

3) Dilated ventricles

217
Q

What is the inheritance pattern of Huntington Chorea?

A

AD

218
Q

Describe the pathogenesis of Huntington’s disease?

A

Mutattion in Huntingtin gene
→ ↑TNR → accumulation of Huntingtin protein in neurons of stratium (caudate nucleus, putamen) & cortex
→ atrophy + neuronal inclusions →
i) loss of striatal neurons → motor dysfunction
ii) loss of cortical neurons → cognitive decline

219
Q

Why is Huntington’s chorea associated with anticipation?

A

↑TNR → earlier age of onset
- Spermatogenesis → ↑TNR → paternal transmission a/w anticipation (early onset in next generation)

220
Q

What are 7 metabolic/toxic causes of CNS disease?

A

Deficiencies
1) Vit. B1 (Thiamine)
2) Vit. B12

Storage Diseases:
3) Niemann Pick disease
4) Tay-Sachs disease

Hepatic encephalopathy (5)
CO poisoning (6)
Alcohol-related (7)

221
Q

What CNS disease is caused by Vit. B1 defiency?

A

Wernicke encephalopathy

222
Q

What disease is caused by Vit. B12 deficiency?

A

Subacute combined degeneration spinal cord

223
Q

What are 2 CNS pathologies caused by CO poisoning?

A

1) Necrosis of globus pallidus
2) Diffuse cortical necrosis

224
Q

What are 3 CNS pathologies caused by alcohol?

A

1) Fetal alcohol syndrome
- growth retardation, cerebral malformations

2) Acute intoxication
- respiratory depression → death

3) Chronic alcoholism
- cerebral cortical atrophy
- cerebellar atrophy
- Wernicke encephalopathy
- Korsakoff’s psychosis

225
Q

What is the pathogenesis of Thiamine deficiency CNS pathology?

A

Thiamine deficiency → damage to medial thalamus and mammillary bodies + generalised atrophy

226
Q

What is Wernicke encephalopathy?

A

Acute development of psychotic symptoms of ophthalmoplegia

227
Q

What is the gross appearance of Wernicke encephalopathy?

A

Hemorrhage and necrosis in mamillary bodies, walls of 3rd adn 4th ventricles

228
Q

What is Korsakoff’s syndrome?

A

Chronic alcohol abuse characterised by:
1) Anterograde amnesia
2) Retrograde amnesia
3) Confabulation
4) Meager content in conversation
5) Lack of insight
6) Apathy

229
Q

What is the gross appearance of Korsakoff’s syndrome?

A

Cystic spaces with haemosiderin-laden macrophages

230
Q

What are 3 presentations of Horner’s syndrome?

A

Sympathetic system failure:
1) Ptosis
2) Miosis
3) ±Ptosis

231
Q

What is Harlequin’s syndrome?

A

Unilateral blockade of the T2-T3 fibers carrying sudomotor and vasomotor supply

  • asymmetric sweating and flushing on the upper thoracic region of the chest, neck and face
232
Q

What are the neurological effects of a Pancoast tumour?

A

Apical lung tumour:
1) T1/lower brachial plexus lesions
2) Sympathetic outflow → anhydrosis
3) Phrenic nerve → hemidiaphragm paralysis
4) Recurrent laryngeal nerve → dysphonia

233
Q

What are 3 conditions in which dorsal column involvement is seen?

A

1) B12 deficiency
2) Syphilis
3) Copper deficiency

234
Q

What are 2 ways that Guillian-Barre may be life-threatening?

A

1) Type 2 Respi failure
2) Cardiac arrythmias

235
Q

How is Guillain-Barre syndrome treated?

A

1) IVIG
2) Supportive

236
Q

Why does Guillain Barre syndrome not cause wasting despite being a LMN disease?

A

Wasting takes too long, GBS is a one-off attack

237
Q

How does hydrocephalus present in babies?

A

Enlarged/protruding fontanelles

Nervous System (14 decks)

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