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Flashcards in Neuropathology Deck (28):

What are the causative organisms for (lepto)meningitis in different age groups?

Neonates: E. coli, L. monocytogenes,

2-5yrs: H. influenzae B

5-30yrs: N. meningitidis types

30yrs+ S. pneumoniae


What are the causative organisms in "chronic meningitis"?

M. tuberculosis = granulomatous inflammation fibroses meninges and entraps nerves


Give some possible complications from (lepto)meningitis.

Swelling ---> raised ICP ---> death

Cerebral infarct ---> neurological deficit

Cerebral abscess (reduced immune function, do not seek help e.g. elderly, alcoholics)

Subdural empyema


Systemic (septicaemia


Differentiate meningitis and encephalitis.

Encephalitis is classically viral, not bacterial
e.g. in CMV can have owl's eye inclusions (replicating virions) on histology

Encephalitis affects brain parenchyma, not meningitis


What is the pathophysiology of prion disorders?

Mutated prion proteins (sporadic, familial, or ingested) interact with normal prion proteins to cause a post-translational conformational change

Aggregate forms which is extremely stable and causes neuronal death

Neuronal death forms "holes" in grey matter (spongiform encephalopathy) which causes a rapid onset of dementia-like presentation

note: prions are not infections (cannot be cultured)


What is the pathophysiology of Alzheimer's disease?

Sporadic/familial, early/late

Exaggerated ageing process

Loss of cortical neurones causing a reduction in brain weight and cortical atrophy

Neuronal damage is caused by neurofibrillary tangles (intracellular twisted filaments of tau protein - tau normally stabilises microtubules but becomes hyperphosphorylated in Alzheimer's)

Senile plaques form = "cotton wool" appearance with foci of enlarged axons, synaptic terminals, and dendrites with amyloid deposition in the centre of the plaque (forms "halo")

note: amyloid deposition also occurs in Down's syndrome (which causes early onset Alzheimer's disease) and hereditary disorders (mutations causing incomplete breakdown of myeloid precursor protein)


What is the normal intracranial pressure? How does the brain attempt to compensate for raised intracranial pressure?

Normal ICP = 0-10mmHg (coughing and straining = 20mmHg)

Compensation mechanisms:
- brain atrophy
- reduced blood volume
- reduced CSF volume

Vascular mechanisms maintain cerebral blood flow as long as ICP


What damage is caused by expanding focal lesions in the brain?

Deformation/destruction of brain around the lesion

Sulci flattened against the skull

Displacement of midline structures causing loss of symmetry

Internal herniation)


Give some examples of causes of raised intracranial pressure.

Expanding focal lesions e.g.
- tumour
- haematoma
- abscess
- infarction ---> oedema

Global increase in brain mass e.g.
- oedema
- inflammation (meningitis or encephalitis)
- trauma


Describe the events of subfalcine herniation.

Occurs the same side as the lesion

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

Ischaemia of the medial frontal and parietal lobes and the corpus callosum (compression of the anterior cerebral artery)


Describe the events in tentorial herniation.

Uncus/medial part of parahippocampal gyrus (temporal lobe) herniates through tentorial notch

Damages occulomotor nerve, cerebral peduncles

Occludes posterior cerebral and superior cerebellar arteries

Causes Duret haemorrhages in midbrain/pons ---> Cushing's reflex (common mode of death in people with large brain tumours and intracranial haemorrhages)


Describe the events in tonsillar herniation.

Cerebellar tonsils (+/- medulla) pushed into foramen magnum ---> compresses brainstem


Describe the progression of the presentation of raised intracranial pressure.

Prodromal phase:
- headache
- vomiting
- papilloedema

Acute phase:
- oculomotor nerve compression ---> pupil dilatation
- brainstem compression ---> coma

Compression of cerebral peduncles ---> hemiparesis on same/opposite/both sides, decerebrate rigidity

Further herniation ---> apnoea and cardiac arrest


Give some examples of benign and malignant brain tumours.

Benign tumours e.g. meningioma

Malignant tumours e.g. astrocytoma
- spread along the nerve tracts, through the subarachnoid space, spinal secondaries
- grade 1 = common in children, space-occupying lesion ---> epilepsy
- grade 4 = adults, 3-6 month prognosis


Contrast primary and secondary mechanisms of head injury.

PRIMARY (due to force causing the injury) =

---> DIFFUSE = direct tearing to axons at sites of differing density (e.g. junction between white and grey matter), heals by gliotic scarring, rotational force is esp. severe

---> FOCAL DAMAGE (coup and contrecoup) = bruising/laceration of brain as it hits the inner surface of the skull + tearing of blood vessels ---> haemorrhage

SECONDARY (reaction to primary damage itself, worsening the injury) e.g. bleeding into brain ---> vasoconstriction ---> secondary ischaemia


What is the mechanism of the primary head injuries?

Sustained at time of impact

Movement of brain greatest when head is moving and hits an object (not being stationary and then being hit by an object)

Greatest damage is at front and back of the brain

Coup = at site of impact
Contrecoup = opposite to the site of impact


What are some of the potential long-term effects of head injury?

Diffuse axonal injury:
- vegetative state
- dementia
- gliotic scarring ---> epilepsy

Haemorrhage ---> hydrocephalus

Infection: scarring, abscess

Raised intracranial pressure

Focal neurological deficit


What are the different mechanisms of stroke?

- aneurysm
- thrombus over ruptured atheromatous plaque
- atheromatous debris (carotid atheroma)
- thrombus originating in heart in AF
- mural thrombus originating from heart

Thrombosis over an atheromatous plaque

Haemorrhage into plaque
- spasm
- occlusion


Describe the pathophysiology of intracerebral haemorrhage.

Associated with hypertensive vessel damage

Common cause is Charcot-Bouchard aneurysms (microaneurysms in vessels of basal ganglia)

Deposition of amyloid around cerebral vessels in the elderly

Can be inherited

Produces space-occupying lesion ---> raised ICP


Describe the pathophysiology of subarachnoid haemorrhages.

Rupture of "berry" aneurysms at branching points in circle of Willis

Associated factors:
- male
- hypertension
- atheroma
- polycystic kidney disease

Can present with thunderclap headaches or sentinel headaches (little headaches worsening over time)


What are the different modes of transmission of neurological infections?

Direct spread
e.g. otitis media, base of skull fracture

e.g. sepsis, infective endocarditis

e.g. V-P shunt, surgery, LP


What type of blood characterises the different types of cranial haemorrhages?

Extradural = arterial (middle meningeal artery)

Subdural = venous (bridging cortical veins)

Subarachnoid = arterial (rupture of berry aneurysm)


What are the different types of hydrocephalus?

Communicating (external) = non-obstructive; flow of CSF blocked after it exits ventricles
- most commonly due to scarring of the meninges where arachnoid granulations are along the superior sagittal sinus

Non-communicating (internal) = obstructive; flow of CSF blocked in passages connecting the ventricles
- e.g. aqueductal stenosis


Contrast CT and MRI scans.

CT scan = rotating X-rays
- good for imaging bone structures
- usable when metal present
- faster than MRI scan
- less claustrophobic

MRI scan = magnets and pulsing radio waves (body tissues containing H+ emit radio signals)
- no iodine contrast used
- no radiation exposure
- higher detail in soft tissue structures
- adjust radio waves/magnetic fields to highlight types of tissue
- change imaging plane without moving patient


Why is it advisable to use CT instead of X-ray to image a fracture of the petrous temporal bone?

Petrous temporal bone is very dense and cannot be positioned to be free of overlying structures, therefore is difficult to image using X-rays

CT scan allows thin slices of images - study sequence of slices to determine the extent and direction of the fracture


What structures are dark and bright on T1 MRI scans?

- air
- bone
- stones
- fast-flowing blood

- ligaments
- tendons
- scars
- kidneys
- gonads
- oedema
- urine
- bile
- simple cysts
- spleen

- abscesses
- complex cysts
- synovial fluid

- fat
- fatty bone marrow
- blood products
- slow flowing blood
- contrast agents


What structures are dark and bright on T2 MRI scans?

- air
- bone
- stones
- fast-flowing blood

- ligaments
- tendons
- scars
- bone islands
- liver
- pancreas
- adrenals
- hyaline cartilage
- muscle

- liver
- pancreas
- adrenals
- hyaline cartilage
- muscle
- fat
- fatty bone marrow

- fat
- fatty bone marrow
- kidneys
- gonads
- oedema
- urine
- bile
- simple cysts
- bladder
- spleen


What are Le Fort fractures?

1 = fracture of maxilla just above the teeth which remain in detached portion of bone

2 = body of maxilla separated from facial skeleton, with fracture through nose and vertical fractures from the floor of the orbit

3 = horizontal fracture through nose, sphenoid bone, the fronto-zygomatic structures, zygomatic arches; maxilla and other bones of the face are entirely separated from the cranium