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303: Neurology > Neuropathology > Flashcards

Neuropathology Flashcards

0
Q

What cells of the nervous system are most sensitive to hypoxia?

A

Neurons
Neuroglia
Microglia cells

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1
Q

What are two responses neurones have to injury?

A

Hypoxia

Neuronophagia

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2
Q

Describe the neuronal response to hypoxia

A

Shrinking of the cell body, becoming eosinophilic and angular with loss of Nissl substance
Changes occur within 12 hours
Affected neuron surrounded by clear space (swelling of astrocyte processes)
Nucleus becomes dark and pyknotic (triangular) and loss of nucleolus

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3
Q

Describe the neuronal response of neuronophagia.

A

Irreversible damage

Phagocytosis of affected cell

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4
Q

When does neuronophagia often occur?

A

Rapid neuronal death in hypoxia or viral infection

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5
Q 
Terminology:
Polio-
Leuko-
Encephalo-
Myelo-
Malacia-
A 
Polio = grey matter
Leuko = white matters
Encephalo = brain
Myelo = spinal cord
Malacia = necrosis
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6
Q

What is the term used to describe the reaction if the neuron cell body to axonal damage?

A

Central chromatolysis

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7
Q

Does central chromatolysis occur in the CNS, PNS or both?

A

Both

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8
Q

What occurs in the axonal reaction to damage?

A

central chromatolysis
Swelling, nucleus becomes peripheral, Nissl substance (rough endoplasmic reticulum) disperses
Pallor (pale colour to cell body)

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9
Q

What is the duration of the axonal reaction (central chromatolysis)?

A

Within a day, may persist for months

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10
Q

What is known as secondary demyelination?

A

Axonal (Wallerian) degeneration

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11
Q

What is the term used to describe the reaction that follows axon disruption?

A

Axonal (Wallerian) degeneration/secondary demyelination

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12
Q

Describe the axonal (Wallerian) degeneration process

A

24hr after injury: proximal and distal axonal stumps swell
Distal axon degenerates and fragments
1 month: axonal debris removed by phagocytosis
Myelin breaks down
Week(s): removal of myelin debris in PNS by macrophages (months/years in CNS)
PNS axon regrows (Schwann cell proliferation) 5-10mm/day - only occurs if connective tissue support remains suitably intact

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13
Q

What happens to the regeneration of axon sprouts in the PNS during axonal (Wallerian) degeneration process if there is loss of connective tissue integrity?

A

Fibres are unable to regenerate

Functional loss

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14
Q

When are viral inclusion bodies produced?

A

In viral infections e.g. Herpes simplex encephalitis and rabies

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15
Q

Where are viral inclusion bodies most likely found?

A

Neurons in specific locations: pyramidal cells of hippocampus/adjacent temporal cortex, Purkinje cells of cerebellum

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16
Q

What are interneuronal deposits?

A

Substances that accumulate within neurons

Permanent nature of cells make them prone to accumulating particular substances

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17
Q

Give an example of an intraneuronal deposit

A

Lewy bodies (Parkinson’s disease)

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18
Q

What disease are levy bodies present in?

A

Parkinson’s disease

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19
Q

What are Lewy bodies?

A

Abnormally phosphorylated neurofilaments in the substantia nigra/locus coerulus

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20
Q

What is a typical feature of spongiform encephalopathy?

A

Neuronal vacuolation

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21
Q

What is a vacuolated neuron?

A

Affected neuron with specific anatomic disruptions and vacuoles in the surrounding neuropil (due to swelling of astrocyte processes)

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22
Q

What causes vacuoles in the neuropil?

A

Swelling of astrocyte processes

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23
Q

What are the glial cells (neuroectodermal derivatives) of the nervous system?

A

Astrocytes
Oligodendrocytes
Ependyma

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24
Q

What are the functions of Astrocytes?

A 
Formation of blood brain barrier
Secretion of growth factors and chemokines (modulation of inflammation in CNS)
Metabolic buffering
Detoxification
Nutrient supply 
Glucose transport
Uptake of neurotransmitters
Electrical insulation
Antioxidant roles
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25
Q

What is the function of oligodendrocytes?

A

Formation of myelin sheaths in CNS

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26
Q

What is the function of expendyma cells?

A

Lines ventricles

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27
Q

What is gliosis?

A

Astrocytes response to injury (aka astrogliosis/astrocytosis)
Increased glial cell number and size
Fill small cavities/scars, wall off tumor/abscess

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28
Q

What is the result of oligodendrocyte damage?

A

Demylination - pale area

Poor proliferation/regeneration

29
Q

What are the bone marrow derivatives of the nervous system?

A

Microglia

30
Q

What are the functions of microglia?

A

Fixed macrophages in CNS (dead cells and lipids)

31
Q

What are the main causes for increased intracranial pressure?

A

Focal space-occupying lesions (tumour, abscess, haematoma, encephalitis
Increase CSF volume (hydrocephalus)
Compression in spinal cord (disc herniation, unstable vertebral articulations)

32
Q

What is a common response to increased intracranial pressure?

A

Herniation: movement of parts of the brain through natural openings into a different anatomical compartment

33
Q

What are the various types of herniations of the brain that can occur due to increased ICP?

A

Subfalcine: medial portion of cerebral hemisphere (cingulate gyrus) moves laterally under falx cerebri
Transtentorial: medial temporal lobe moves under the tentorium cerebelli
Tonsillar/coning: protrusion of cerebellar tonsils causally through foramen magnum

34
Q

What is the consequence of increased ICP in infants (neonates)?

A

Sutures and frontanelles allow expansion

35
Q

What are the clinical presentations of increased intracranial pressure?

A

Headache, dullness, nausea, vomiting (papilledema)

36
Q

Describe what a subfalcine herniation is.

A

Movement of the cingulate gurus (medial part of cerebral hemisphere) underneath falx cerebri - can compress on anterior cerebral artery

37
Q

Describe what a transrentorial herniation is.

A

Movement of the incus of the hippocampus and medial parts of temporal lobe beneath the tentorium

Can produce a grossly visible groove

38
Q

What are the possible consequences of a transrentorial herniation?

A

Movement mid brain compression - coma
Oculomotor nerve compression - ipsilateral pupil dilation
Aqueduct compression - further ICP increase
Posterior cerebral artery compression - occipital infarction - blindness
Arterial and venous tears in brain stem - haemorrhage

(Mass effect in one or both cerebral hemispheres)

39
Q

What are the consequences of cerebral oedema?

A

Herniation due to raised CSF, fixed volume of CNS compartment and lack of effective lymphatic drainage

40
Q

What are the possible causes of cerebral oedema?

A

Vascogenic
Cytoxic
Interstitial hypo-osmotic

41
Q

What is the most common form of oedema?

A

Vascogenic oedema

42
Q

What causes Vascogenic oedema?

A

Increased vascular permeability from trauma/vascular necrosis within infarcts/tumours
Second impact syndrome

43
Q

What causes cytoxic oedema?

A

Intracellular fluid accumulation due to toxins or ischemia and water overload

44
Q

What causes interstitial oedema?

A

Build up of fluid due to obstructive hydrocephalus (peri ventricular regions)

45
Q

What is hypo-osmotic oedema?

A

Oedema caused by water intoxication

46
Q

Which form of oedema can be treated by reducing brain swelling using diuretic agents?

A

Vascogenic

47
Q

What is hydrocephalus?

A

Increased CSF volume within cranial cavity

48
Q

How often is CSF renewed?

A

3-5 times per day

49
Q

What are the various types of hydrocephalus?

A

Internal (ventricular)
External (subarachnoid)
Communicating (ventricles and subarachnoid space)
Active
Arrested
Compensatory (increased CSF secondary it reduced volume of brain substance)

50
Q

What is the cause of hydrocephalus?

A

Obstruction of CSF flow

51
Q

What is the result of an obstruction at the foramen of Munro?

A

Unilateral ventricular hydrocephalus

52
Q

What is the result of an obstruction at the third ventricle or mesencephalic aqueduct?

A

Hydrocephalus of lateral ventricles

53
Q

What is the result of an obstruction at the foramina of Luschka (lateral apertures of fourth ventricle)?

A

Affects whole ventricular system

54
Q

What is the result of an obstruction of the subarachnoid?

A

While ventricular system and communicating

55
Q

Where do the obstructive materail causing hydrocephalus arise from?

A

Masses: neoplasms
Congenital malformations: non-patent mesencephalic aqueduct
Iflammation
Hernias

56
Q

What are causes of hydrocephalus by destroying arachnoid villi?

A

Vitamin A deficiency

Severe meningitis

57
Q

What are some of the ceerebral signs of hydrocephalus?

A 
Headache
Nausea
Blurred vision
Dullness
Confusion
Memory loss
Irritability
Poor intellectual performance
Urinary incontinence
58
Q

Are neurons more tolerable of hypoxia or ischemia?

A

Hypoxia

59
Q

Define the term malacia.

A

Necrosis in CNS (breakdown of Blood Brain Barrier)

Due to cardiac arrest, anesthetic accidents, atherosclerosis

60
Q

What is a “stroke”

A

Clinical term used for the syndrome resulting from infarction and haemorrhage in the CNS

60
Q

What are some of the causes of stroke

A

Aphasia, hemiplegia, blindness

Dependant on site affected

60
Q

What are some of the causes of arterial obstruction in CNS?

A 
In situ thrombosis (atherosclerosis)
Embolism of cardiac thrombi
Tumor
Air/fat
Arterial compression from herniation/masses
60
Q

What is excitocity?

A

Imbalance in stimulatory neurotransmitters seen in CNS disease, hypoxia/ischemia (glucose deprivation) resulting in penumbral death

Increased release of glutamate and aspartate
Reversible acute swelling of depolarised neuron (influx of sodium ions, chloride ions and water)
NDMAR opened by glutamate - Ca influx - generation of reactive oxygen and nitrogen species

60
Q

How can Astrocytes moderate the damage of exocitoxicity?

A

Convert glutamate to glutamine (neutralising free radicals)

61
Q

What aids in protecting the CNS from infections.

A

Bone, dura, blood brain barrier, microglia

62
Q

What are the possible routes for infectious agents to reach the CNS?

A

Haematogenous (bacteria)
Local extension (osteitis, sinusitis, tooth roots, vertebral abscesses, middle ear infections)
Direct implantation (skull fracture, penetrating injuries, grafts, surgical exposure)
Neural (rabies, tetanus toxin, prions)

63
Q

What happens if an infectious agent does gain access to the CNS?

A

Rapid dissemination via the ventricular system (CSF), aided by poor fibrous response and low degree of immuno-surveillance

64
Q

What are the two key bacterial infections?

A

Meningitis

Abscessation

65
Q

What are the key features of meningitis?

A

Subarachnoid purulent exudate (neutrophils)
More apparent in basal cisterns and sulci
CSF obstruction and hydrocephalus (oedema)
Superficial cortical necrosis and encephalitis
Some diffuse brain swelling

66
Q

What are the key features of abscessation?

A

Clinically appears to be SOL - surrounding oedema

Only thin capsule (collagen and astrocytosis

303: Neurology (7 decks)

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