Neuropathology

Question 1

Glial Cells

Answer 1

Astrocytes
Oligodendrocytes
Ependyma

Question 2

Glial cell importance

Answer 2

Reactive changes following stroke, in dementia and tumours

Question 3

Role of Microglia

Answer 3

Macrophage type population - phagocytically active

Question 4

Cellular composition of CNS

Answer 4

Neurons
Glial Cells (Astrocytes, Oligodendrocytes, Ependyma)
Blood vessels
Microglia
Connective tissue - meninges

Question 5

Schwann cells

Answer 5

Produces myelin in the PNS

Question 6

Oligodendrocytes

Answer 6

Produces myelin in the CNS

Question 7

Neuronal Degeneration

Answer 7

A reaction within the cell body that is assoc with axonal injury

Question 8

Responses to axonal injury

Answer 8

Increased RNA and protein synthesis
Swelling of cell body
Enlargement of cell nucleosus
Central chromatolysis (nissal granules)
Anterograde degeneration of axon occurs distal to site of injury (nearest node of Ranvier)
Myelin sheath breakdown

Question 9

Glial Reaction (Gliosis)

Answer 9

Most important histopathological indicator of CNS injury, regardless of cause.
Astrocytes: hyperlasia and hypertrophy
Nucleus enlarges
Cytoplasmic expansion

Question 10

Oligodendrocytes injury

Answer 10

Feature of demyelinating disorders

Question 11

Vascular Supply to the Brain

Answer 11

Branches of:
Internal carotid (anterior)
Vertebral arteries (posterior)

Question 12

Anterior Cerebral Artery (ischaemia/thrombus)

Answer 12

Frontal lobe dysfunction
Contralateral sensory loss in foot and leg
Paresis of arm & foot (relating sparing of thigh and face)

Question 13

Middle Cerebral Artery (ischaemia/thrombus)

Answer 13

Depends if dominant or non dominant hemispheres
Contralateral Hemiparesis
Contralateral Hemisensory loss
Aphasia / dysphasia (Dominant)
Apraxia

Question 14

Occipital Lobe

Answer 14

Homonymous hemianopia (with macular sparing)

Question 15

Cerebellum

Answer 15

Ataxia
Nystagmus
Intention tremor
Pendular reflexes

Question 16

MS plaques acute

Answer 16

Demyelinating plaques are yellow/brown, ill-defined edge that blends into surrounding white matter.

Question 17

MS plaques chronic

Answer 17

Well-demarcated grey/brown lesions in white matter

Classically situated around lateral ventricles

Question 18

Alzheimers Disease microscopic/histological appearance

Answer 18

Intracytoplasmic neurofibrillary tangles (tau protein)
Beta amyloid plaques (APP)
Amyloid angiopathy

Question 19

Dementia with Lewy Bodies

Answer 19

Visual hallucinations
Fluctuating levels of attention
Degeneration of the substantia nigra - remaining nerve cells contain Lewy bodies (immunochemical staining for protein ‘ubiquitin’
Development of features of PD

Question 20

Huntingtons Disease (HD)

Answer 20

Autosomal Dominant
Onset: age 35-50
Triad: emotional, cognitive & motor disturbance
Chorea
Myoclonus
Depression
Develop dementia later on in disease process

Question 21

HD Histological appearance

Answer 21

Loss of neurones in caudate nucleus and cerebral cortex

Question 22

Pick’s Disease

Answer 22

Progressive dementia in middle life (50-60)
Atrophy of cerebral cortex in frontal and temporal lobe
Histological landmarks are Pick’s cells (swollen neurones) and Pick’s bodies (intracytoplasmic filamentous inclusions)

Question 23

Pick’s Disease Symptoms

Answer 23

Related to damage to frontal and temporal lobes:
Personality and behavioural change
Speech and communication problems
Changes in eating habits
Reduced attention span

Question 24

Extradural Haematoma

Answer 24

Temparoparietal region fracture involving middle meningeal artery

Question 25

Shifts and Herniations (Raised ICP)

Answer 25

1. Falcine (subfalcine)
2. Uncal
3. Cerebellar
4. Transcalvarium

Question 26

Subfalcine (cingulate gyrus) herniation

Answer 26

Unilateral or asymmetric expansion of cerebral hemisphere displaces cingulate gyrus under the falx cerebri.
Often associated with compression of anterior cerebral artery - weakness and/or sensory loss in leg (ischaemic injury of portions of primary motor and/or sensory cortex).

Question 27

Tentorial herniation (uncal)

Answer 27

Medial aspect of temporal lobe (hippocampal uncus and parahippocampal gyrus) herniates over the tentorium cerebellii.
Compression of ipsilateral CN III and its parasympathetic fibres, pupillary dilatation and impairment of ocular movments.

Question 28

Tonsillar herniation (cerebellar)

Answer 28

Displacement of cerebellar tonsils through the foramen magnum.
Life-threatening - brainstem compression and compromises respiratory centres in medulla

Question 29

Transcalvarium herniation

Answer 29

A swollen brain will herniate through any defect in the dura and skull.
Reduction in level of consciousness, dilatation of pupil on ipsilateral side.
Bradycardia, increase in pulse pressure and increase in MAP.
Cheyne stokes respirations

Question 30

Clinical Signs of Raised ICP

Answer 30

Papilloedema
Nausea + Vomiting (pressure on vomiting centres in Pons and Medulla)
Headache (compression and distortion of dura)
Neck stiffness (pressure on dura around cerebellum and brainstem)

Question 31

Extradural Haemorrhage

Answer 31

Rupture of middle meningeal artery at pterion.

Uncal gyral/cerebellar herniation

Question 32

Subdural Haemorrhage

Answer 32

Blood between internal surface of dura mater and arachnoid mater.
Rapid change in velocity may cause tears of bridging veins.
Venous blood - onset of symptoms slower.