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M2 NENTE Anatomy > 5.5 CNS pathology > Flashcards

5.5 CNS pathology Flashcards

1
Q

What is this neural tube malformation describing?

failure of one or more vertebrae to close properly, from asymptomatic (occulta) to meningoceles or myelomeningoceles

A

spinal bifida

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2
Q

what is this neural tube malformation called?

protrusion of meninges through parietal foramina or abnormal bony openings of the skull

A

cranial defects- from absent skill bones (acrania) to cranial meningoceles

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3
Q

[Malformation of brain: Chiari malformation]

  • structural defect in the cerebellum, characterized by a ______________ through the foramen magnum
  • Can sometimes lead to non-communicating hydrocephalus as a result of obstruction of cerebrospinal fluid (CSF) outflow
A

downward displacement of one or both cerebellar tonsils

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4
Q

[Malformation of neuroaxis]

What is this condition describing?

  • group of neuro-oculo-cutaneous syndromes or neurocutaneous disorders involving structures arising from the embryonic ectoderm
A

Phakomatoses

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5
Q

[Malformation of neuroaxis]

What is this condition describing?

  • formation of various small tumours from neuroectoderm in the eye, skin or internal organs
A

Neurofibromatosis type I (NF-1)

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6
Q

how is the brain injured from secondary trauma related injury?

A
  • Brain may be damaged from secondary injury – due to acceleration and deceleration causing brain to hit the skull
  • Shearing forces may lead to diffuse axonal injury, leading to neuronal death, disability or haemorrhage
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7
Q

What is inflammation of the meninges called?

A

meningitis

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8
Q

what is inflammation of the brain parenchyma, most often of viral origin called?

A

encephalitis

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9
Q

what is inflammation of the spinal cord called?

A

myelitis

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10
Q

what is simultaneous inflammation of the brain parenchyma (encephalitis) and the meningitis (meningitis) called?

A

Meningoencephalitis

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11
Q

What are abnormally folded proteins, specific causative agent in the brain, leading to spongiform encephalopathy (CJD called?

A

Prions

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12
Q

What is this autoimmune disease that leads to destruction of myelin?

A

Multiple sclerosis

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13
Q

What is the condition where there is specific gene abnormality that leads to abnormal development or destruction of the white matter (myelin sheath) of the brain?

A

Leukodystrophy

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14
Q

Tay-Sachs disease (progressive neurodegeneration due to _____________)

A

intracellular accumulation of GM2 gangliosides

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15
Q

In descending order, ranked the sensitivity to nervous system cells to decreased oxygen

A

Neurones > oligodendrocytes > astrocytes > endothelial cells

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16
Q

What is the neuronal response in within 12 hours of an irreversible hypoxic-ischemic insult in an acute injury?

A

shrinkage of the cell body, pyknosis of nucleus, disappearance of nucleolus, loss of Nissl substance and intense eosinophilia of the cytoplasm (“red neurons”)

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17
Q

What is the neuronal response in within 12 hours of an irreversible hypoxic-ischemic insult in an axonal injury?

A

cell body enlargement and rounding, peripheral displacement of the nucleus, enlargement of the nucleolus, and peripheral dispersion of Nissl substance (central chromatolysis

o Wallerian degeneration – degeneration of myelin and axons distal to injury

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18
Q

What are the intracellular inclusions seen in Herpes?

A

Cowdry bodies

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19
Q

What are the intracellular inclusions seen in Rabies infection?

A

Negri bodies

20
Q

What is accumulated in neurones during normal aging, thought to play a role in development of neurodegenerative disorders?

A

Lipofuscin

21
Q

What is the abnormal protein seen in Alzheimer’s disease?

A

Neurofibrillary tangles

22
Q

What is the abnormal protein see in Parkinson’s?

A

lewy bodies

23
Q

What is the response to astrocytes in response to injury?

A
  • astrocytes are the principal cells responsible for repair and scar formation on the brain during gliosis
  • In response to injury, astrocytes undergo both hypertrophy and hyperplasia
  • Cytoplasm expands and takes on a bright pink hue, and the cell extends multiple stout, ramifying processes (gemistocytic astrocytes)
  • Astrocytes proliferate and fill up the defect, leading to a glial scar
24
Q

What is the response to microglial cells in response to injury?

A

resident macrophages of the CNS, phagocytic function
o After an injury, they become activated and elongated (rod cells), aggregating around the injured area, forming microglial nodules
o Neurophagia – microglial cells surround and phagocytose dead or dying neurones

25
Q

what is the mechanism behind cytotoxic oedema seen in tumours and infections?
- May follow generalised hypoxic, ischaemic or exposure to certain toxins

A
  • Increased in intracellular fluid secretion secondary to neuronal and glial cell injury
26
Q

What is the mechanism seen in vasogenic oedema?

- May proliferate around infarcts, tumours or part of an inflammatory response

A
  • Defect in blood brain barrier, allowing fluid to shift from the vascular component to the extracellular spaces of the brain
27
Q

What is global cerebral ischaemia caused by?

A

Widespread cerebral ischemia not due to vascular occlusion

  • Severe hypotension with global hypoperfusion – usually in the setting when systolic blood pressure falls below 50 mmHg e.g. cardiac arrest or shock
  • This leads to Diffuse brain swelling and injury – when the insult is mild, there may be only a transient post-ischaemic confusional state, with eventual complete recovery
28
Q

Which part of the brain is most sensitive to a drop in blood pressure?

A

o Watershed infarction – border areas of arterial territory (e.g. between ACA and MCA)
- Purkinje cells of cerebellum and laminar cortical necrosis

29
Q

Ischaemic stroke
- Considerations – reduction of blood flow in a specific artery will affect the area that it supplies, presenting with characteristic neural deficits
-Collateral flow through ____________ may limit the damage in an ischaemic stroke – linkage of carotid and vertebral-basilar systems
o However, there are anatomical variants of the circle of Willis – communication arteries may vary in diameter and position
o Marked atherosclerosis may result in luminal narrowing, reducing blood flow
- Some parts of the brain are supplied by perforating arteries – end arteries with no collateral flow
o Some areas such as the ________________ supplied by such arteries – poorer outcome

A

circle of Willis;

basal ganglia and internal capsule are

30
Q
  • ____________area – may remain viable for several hours after an ischemic event due to the collateral arteries
    o Such areas are often closer to collateral vessels between the anterior, middle and posterior cranial arteries
    o Goal of stroke therapy is to revive this area – a higher volume of penumbra around a cerebral infarction means a greater volume of potentially salvageable brain matter by thrombolysis and thrombectomy
A

Penumbra

31
Q

What are the common extra cranial sites for formation of thrombi thrombi?

A

– common carotid artery bifurcation, vertebral artery origin (near branching sites

32
Q

what are common intra cranial sites for formation of arterial thrombi?

A

circle of Willis, middle cerebral artery origin, basilar artery

33
Q

what are common intra cranial sites for formation of venous thrombi?

A

superior sagittal sinus

34
Q

which artery is most affected by emboli?

A

middle cerebral artery?

35
Q

what is the timescale of infarction when there is: No changes on gross or light microscopy

A

< 12 hours

36
Q

what is the timescale of infarction when there is: Earliest light microscopy changes in the form of ischemic cells (red dead neurons)

A

12 to 24 hours

37
Q

what is the timescale of infarction when there is: Neutrophil with vascular response

A

24 to 48 hours

38
Q

what is the timescale of infarction when there is: Soft swollen (vasogenic and cytotoxic edema) surrounding oedema and midline shift – increased intracranial pressure and risk of herniation

A

48 hours

39
Q

what is the timescale of infarction when there is: Macrophages start replacing neutrophils, clearing debris (phagocytosis)
Infarct becomes gelatinous and friable and more defined as oedema subsides in the first week
- Tissue liquefies – fluid filled cavity which expands till all of the dead tissue is removed

A

48 hours to 2/3 weeks

40
Q

what is the timescale of infarction when there is:Astrocytic glial reaction starts and continues for weeks to months, forming a gliotic scar – parts of infarct are cystic if it is large (cystic cavity with surrounding gliosis)

A

From 1st week

41
Q

Lacunar infarct – small vessel pathology

  • On the background of __________- underlying arteriolosclerosis, lipohyalinosis, involving _____________
  • Small infarcts in deep cortex and deep nuclei – if multiple, may lead to cognitive deficits (multi-infarct dementia
A

hypertension;

smaller penetrating arteries

42
Q

Venous infarcts – superior sagittal sinus thrombosis, a difficult clinical diagnosis

  • Risk factors – hypercoagulable states (dehydration, phlebitis, pregnancy, birth control pill)
  • Typically, ______________
A

frontal lobe haemorrhagic infarctions

43
Q

Intraparenchymal haemorrhage

  • Stroke secondary to vessel rupture – risk factors include ______________, cerebral amyloid angiopathy, arteriovenous malformations and tumours
    o Most common in mid to late adult life, with a peak incidence at about 60 years of age
  • Spontaneous haemorrhages (non-traumatic bleed)
  • Hypertension-related haemorrhage – massive deep brain parenchymal haemorrhage (>50% of all significant bleeds and 15% of hypertensive deaths)
    o Involvement of the ______________
    o Putamen is involved in 50% of cases, may also involve thalamus, pons, cerebellum
    o Small arteries and arterioles – arteriolosclerosis of penetrating arteries can lead to slit haemorrhages
    o _____________ – weakening of blood vessels in accelerated atherosclerosis
    o Microaneurysms of Charcot Bouchard – involves vessels < 300 µm
    o Petechiae haemorrhages and fibrinoid necrosis in malignant hypertension
  • Cerebral amyloid angiopathy – another cause of parenchymal haemorrhages, more common in peripheral lobes
    o Massive lobar haemorrhages or small cortical haemorrhage (< 1mm), more common in the elderly (~15% of bleeds)
    o Due to ß-amyloid peptide deposition in __________________
    o May co-exist with Alzheimer disease
A

hypertension (most common);

deep white matter or deep grey matter, brainstem and cerebellum;

Lipohyalinosis;

cortical and leptomeningeal arteries

44
Q

Arteriovenous malformation
- Vascular malformation – tangled mass of abnormal thick-walled arteries and veins, accounts for 1.5 to 4% of all brain masses, with a 2 to 4% yearly risk of bleeding
o Location – _____________
o Commonly manifests in young adults of 10 to 30 years, manifests with seizures, an intracerebral haemorrhage or a subarachnoid haemorrhage
o In the newborn period, large arteriovenous malformations may lead to ________________ due to blood shunting from arteries to veins
- May involve subarachnoid vessels extending into brain parenchyma or occur exclusively within the brain
o On gross inspection, they resemble a __________________
o Large calibre, thick-walled vessels within brain parenchyma

A

MCA > ACA > PCA;

high output congestive heart failure;

tangled network of wormlike vascular channels

45
Q

Saccular (Berry) aneurysms – results in subarachnoid haemorrhages
- ______________ in cerebral artery – rupture accounts for 25% of cerebrovascular deaths
o Annual risk of rupture – 0.05 to 2% (increases with size, 50% if >10mm), multiple aneurysms are also possible (20%)
o Male to female ratio of 1:2, incidence in adults peak in the 6th decade

  • Occurs at ________________ – some connective tissue diseases predispose to aneurysm formation presumably involves an inherent weakness of the arterial wall exposed to the non-laminar flow pattern of blood, which is then exposed to shear stresses
A

Sac-like dilatation;

branch points in circle of Willis

M2 NENTE Anatomy (24 decks)

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