S8.2 - Neuropathology

Question 1

how may infectious microorganisms enter the CNS ?

Answer 1

– Direct spread – e.g. middle ear infection,
base of skull fracture
– Blood-borne – sepsis, infective endocarditis
– Iatrogenic – V-P shunt, surgery, lumbar
puncture

Question 2

meningitits is inflamation of the what ?

Answer 2

leptomeningies which is made up of arachna mater and pia mater

Question 3

what causes chronic meningitis ?
what is it ?
what can occur as a complication ?

Answer 3

M. tuberculosis
– Granulomatous inflammation
– Fibrosis of meninges
– Nerve Entrapment

Bilateral adrenal haemorrhage (Waterhouse-Friederichsen syndrome) can occur as a complication

Question 4

outline enchephalitis

where does herpes, polio and rabies specifically affect in the CNS ?

Answer 4

Classically viral not bacterial
• Parenchyma not meninges
– Neuronal cell death by virus
• Inclusion bodies
– Temporal lobe
• Herpes virus
– Spinal cord motor neurons
• Polio
– Brain stem
• Rabies
– Lymphocytic inflammatory reaction

Question 5

What is the psychopathology of prion disease

Answer 5

• Mutated PrP sporadic, familial or ingested
• Mutated PrP interacts with normal PrP to
undergo a post translational conformational change
• Extremely stable structure
this causes normal prion protiens to change confirmaiton causing aggregations

PrPSC aggregates
- Neuronal death and “holes” in grey matter - Spongiform encephalopathies

Question 6

CJD vs vCJD

Answer 6

Creutzfeld Jacob disease (CJD) and Variant CJD (vCJD)

• Strongly linked to BSE through ingestion of
prions
• Essential difference compared to classical
CJD is that there seems to be a much higher
prion load associated with earlier age at
death and more prominent pshychiatric symptoms

Question 7

Define dementia

what are the 4 types ?

Answer 7

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

– Alzheimer’s (50%) – Sporadic/Familial, Early/Late
– Vascular dementia (20%)
– Lewy body
– Picks disease

Question 8

pathophys of alzheimers

Answer 8

• Loss of cortical neurones
o Leading to cortical atrophy and decreased brain weight
o Damage caused by neurofibrillary tangles and amyloid
plaques

Tangles
• Intracellular twisted filaments of Tau protein
• Tau normally binds to microtubules
• Hyperphosphorylation of tau is thought to
lead to tangle formation

Plaques
• Amyloid deposition in centre of plaque associated with vessels - leads to the symptoms shown

Question 9

what is an SOL what will it do to a brain

Answer 9

it is a space occupying lesion
this destroys surrounding tissue
it will lead to a rise in ICP
this can push structures away from the midline and lead to internal herniations

Question 10

two types of herniation are

Answer 10

tentorial and subfalcine

Question 11

outline a subfalcine herniation

Answer 11

o Subfalcine herniation

Cingulate gyrus is pushed under the free edge of the
falx cerebri

Herniated brain can become ischaemic due to
compression of anterior cerebral artery (which
normally loops up around corpus callosum and can
get pinched)

Question 12

outline a tentorial herniation

Answer 12

o Tentorial herniation

Medial temporal lobe (classically the uncus) pushed
down through the tentorial notch (free edge of
tentorium cerebelli)

Can compress ipisilateral oculomotor nerve and
ipsilateral cerebral peduncle causing ipsilateral third
nerve palsy but contralateral UMN signs in limbs

Can be complicated by secondary brainstem
haemorrhage (Duret haemorrhage) – often fatal

Usual mode of death for those with large brain
tumours or severe intracranial haemorrhage

Question 13

Brain tumours are an SoL- name some of the key ones, not all

Answer 13

Benign
• Meningioma (from meninges)

Malignant
• Astrocytoma
o Low grade slow growing

o High grade aka glioblastoma multiforme
o Direct spread along white matter pathways
o Can also spread to distant parts of CNS via CSF

Others
• Neurofibroma (from Schwann cells of
peripheral or cranial nerve)

• Ependymoma (from ependymal cells lining
ventricular system)

• Neuronal tumours (from neurones, extremely rare)

• From non-CNS tissues
o Lymphomas
o Metastases (most common of all
brain tumours)

Question 14

risk factors for a stroke are…

Answer 14

Risk factors include hyperlipidaemia, hypertension, smoking, diabetes

Question 15

outline the pathogenisis of a stroke

Answer 15

Pathogenesis
• Embolism (most common)

Heart (due to AF, mural thrombus)
Atheromatous debris (carotids)
Thrombus over ruptured plaque
Aneurysms

• Thrombosis
o Over atheromatous plaque

you will then see
cerebral infarctions, intracerebral and subarachnoid haemorrhages

Question 16

outline the 2 types of cerebral infarction

Answer 16

Cerebral infarction (85% of all strokes)
• Regional
o In the territory of a named cerebral artery

• Lacunar
o Small (less than 1cm area affected)
o Associated with hypertension
o Commonly affect basal ganglia and internal capsule

Question 17

outline intracerebral hemmorage

Answer 17

o Intracerebral haemorrhage (10% of all strokes)
Charcot-Bouchard aneurysms are seen
Produces a space occupying lesion

Question 18

outline subarachnoid hemmorage

Answer 18

o Subarachnoid haemorrhage (5% of all strokes)
Rupture of berry aneurysms, usually found at
branch points in circle of Willis
Blood in subarachnoid space can cause secondary
spasm of cerebral arteries

Associations
• Male
• Hypertension
• Atherosclerosis

 Symptoms
• Thunderclap headache
• May be preceded by a ‘sentinel’ headache
• Loss of consciousness
• Often instantly fatal