Pathology - CNS & Eye Flashcards
(38 cards)
Common locations of saccular aneurysms in the cerebral circulation
90% near major arterial branch points, more common at anterior circulation around the Circle of Willis
- ACA & ACoA 40%
- MCA & AChoroidalA 34%
- ICA & PCoA 20%
- Basilar & PCoA
Multiple in 20-30% cases at autopsy
Risk factors for saccular aneurysm rupture
- Size: > 10 mm with 50% risk of rupture per year
- Acute increase in ICP (straining at stool, orgasm)
Pathological sequelae of SAH
Acute - ischaemic injury (stroke) from vasospasm
Late - meningeal fibrosis and scarring, obstruction of CSF flow and absorption
Death
Morphology of berry aneurysm
Medial muscular layer thins as approaching the aneurysm’s neck and gets thickened hyalinised intima, covered with normal adventitia
Natural history of a ruptured berry aneurysm
- Acute onset of headache, ALOC
- Initial mortality 25-50%
- Rebleeding is common
- Vasospasm in vessels other than the bleeding site -> secondary ischaemic injury
- During healing, meningeal fibrosis and scarring -> secondary hydrocephalus
Causes of ischaemic cerebral infarction
Arterial thrombosis
Cerebral emboli
Lacunar infarcts from small vessels
Cerebral arteritis
Arterial dissection
Venous infarction
Sources of cerebral thromboemboli
Left atrium/ventricle thrombus Valvular vegetations Carotid plaque PFO with paradoxical emboli
Main pathological processes causing ischaemic stroke
Thrombus - atherosclerosis
Embolism - AMI with mural thrombus, valvular heart disease, AF, vascular surgery/shower embolism, fat embolism, endocarditis
Vasculitis - infective vasculitis, autoimmune vasculitis, primary angiitis of CNS
Arterial dissection
Venous infarction - venous sinus thrombosis
Drugs - amphetamines, cocaine, heroin
Hypercoagulable state
Distinguishing pathological features of haemorrhagic and non-haemorrhagic stroke?
Haemorrhagic (red) - multiple, confluent, petechial haemorrhages associated with emboli, secondary to reperfusion via collaterals or dissolution of materials, greater risk if anticoagulated
Non-haemorrhagic (pale/bland anaemic) - usually associated with thrombosis
Importance of stroke pathology in relation to stroke thrombosys
- Complications higher with embolic/haemorrhagic CVAs
- In non-haemorrhagic CVA, little macroscopic change can be seen within the first 6 hours
- Reversible ischaemic penumbra
- Early treatment leads to better outcome and less haemorrhagic risk
Types of cerebral ischaemic injury
Global (e.g. hypoxic encephalopathy) - generalised reduction of cerebral perfusion
Focal - reduction of blood flow to a localised area of the brain
Pathological effects of HTN on brain
Lacunar infarcts (lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, pons)
Massive ICH
Hypertensive encephalopathy
Slit haemorrhages
Pathological mechanisms of cerebral oedema
Vasogenic - BBB disruption, incr vasc perm, fluid shift from intravascular to intercellular space
Cytotoxic - neuronal/glial/endothelial injury, from hypoxic or ischaemic insults or metabolic damage, leads to cellular swelling and intracellular oedema
Interstitial or ependymal oedema from high pressure hydrocephalus
Morphological findings of generalised cerebral oedema
- Flattened gyri
- Narrowing of sulci
- Compression of ventricles and basal cisterns
- Herniation
Major brain herniation locations
Subfalcine - cingulate gyrus under the falx cerebri
Transtentorial - medial aspect of the temporal lobe against the free margin of the tentorium
Tonsillar - cerebellar tonsils through the foramen magnum
Causes of dementia
- Alzheimer
- FTD
- Vascular
- Parkinson
- Creutzfeld-Jakob
- Neurosyphilis
- Toxins (heavy metals, alcohol)
Pathogenesis of Alzheimer
- Lysis of transmembrane protein Amyloid Precursor Protein (APP) by beta and gamma secretases produce Aβ and C-terminal portion of APP
- Aβ peptides aggregate into amyloid fibrils and can be directly neurotoxic
- C-terminal portion of APP is involved in cell signalling and transcription regulation
- Severity of AD is related to the loss of synapses
Main pathophysiological causes of spontaneous intracerebral haemorrhage
- Hypertension
- Cerebral amyloid
- Other: coagulopathy, neoplasm, vasculitis, aneurysm, vascular malformation
Areas of brain where hypertensive intracerebral haemorrhages most commonly occur
- Putamen 50-60%
- Thalamus
- Pons
- Cerebellum
Pathophysiology of cerebral amyloid angiopathy
- Deposition of amyloidogenic peptides in the walls of medium and small calibre meningeal and cortical vessels
- Results in weakening of the vessel wall and risk of haemorrhage
Types of intracranial bleeding in head injury
Extradural
Subdural
Subarachnoid and intraventricular
Intra-parenchymal
Sequence of events in extradural haemorrhage
- Dural artery tear (middle meningeal), usually associated with skull fracture
- Strips off the dura from the skull
- May be a lucid period before ALOC
Define concussion and clinical features
Altered consciousness secondary to a head injury, with
- transient neurological dysfunction
- transient respiratory arrest
- transient loss of reflexes
Features: headache, amnesia, n & v, concentration and memory impairment, perseveration, irritability, behaviour/personality change, dexterity loss, neuropsychiatric syndromes
Types of meningitis. Common organisms of bacterial meningitis in different age groups.
bacterial, viral, fungal, chemical/drug induced, chronic (TB, carcinomatous)
Neonate: E coli, GBS
Children: S pneumoniae, H influenzae
Adolescent/young adult: Neisseria meningiditis, S pneumoniae
Older adults: S pneumoniae,, Listeria
By organisms:
E coli & GBS: neonates
Pneumococci and Meningococci: all age groups beyond neonates
Haemophilus: children but decreased incidence with immunisation
Listeria: extremes of age
Unusual organisms: staph post neurosurgery, G neg in immunocompromised
