HNS34 Pathology Of Raised Intracranial Pressure And Cerebrovascular Disease Flashcards
Intracranial pressure
Pressure of CSF within cranial cavity
Normal range: <10 mmHg (150 mmH2O)
Increased ICP: elevation of mean CSF pressure >15 mmHg (200 mmH2O) when measured with patient in lateral decubitus position (側臥) (i.e. perform during lumbar puncture)
Increased ICP consideration of causes
- Rigid cranium separated in compartments
- Space occupying lesions
- Haematoma
- Tumour
- Abscess - Secondary effects from space occupying lesions
- Brain edema (Swelling of brain ***itself due to destruction of BBB —> ↑ capillary permeability)
- Hydrocephalus
Increased ICP considerations of effect
- Age
- Elderly: atrophic brain allow more room for ICP to build up
- Infant: unfused suture allow more room for ICP to build up - Stage of spatial compensation
- Initial phase: achieved by **reduction in CSF volume + venous space (intracranial veins) —> buffers for potential space in brain
- If rate is of space-occupying lesion is slow —> compensatory **cerebral atrophy, ***erosion of skull bone
- when all available space used up —> critical point —> further ↑ in volume —> abrupt ↑ in ICP - Rate of ICP change
- Slow-growing tumour —> slowly compress brain
- Intracranial bleeding (quick) - Pressure gradient
- Determines which structure of brain will be compressed —> impinged on sharp edge of dura —> compressed / herniation of brain structure (e.g. foramen magnum) - Dural folds
- Falx cerebri (separate left/right hemisphere)
- Tentorium cerebelli (posterior cranial fossa, separate cerebellum from cerebrum)
***Signs and symptoms of Raised ICP
- Herniation
- Headache (stretching of meninges)
- Projectile vomiting (distortion of brainstem)
- Separation of sutures of the vault (infants)
- Erosion of skull bone (long sustained increased ICP)
***Herniation
Classified on the part that is herniated and structure which it has been pushed
Sites:
- ***Transtentorial / Uncal herniation (大腦唧落小腦)
- ***Cerebellar tonsil herniation / Tonsillar herniation / Coning (小腦唧落腦幹)
- Subfalcine / Supra callosal herniation (Corpus callosum) (左腦唧去右腦)
- Transcalvarial / Fungus herniation (during surgery when brain herniates through skull incision site)
- Reversed tentorial herniation (lesion in cerebellum —> push upward)
***Effects of Transtentorial herniation
- Ipsilateral ***CN3 compressed (impinged against edge of Tentorium cerebelli)
—> fixed dilated pupils (early signs), eye deviates laterally due to unopposed action of CN6
—> monitor patient’s pupillary reflex - ***PCA compressed (impinged against edge of Tentorium cerebelli)
—> infarction of ipsilateral occipital cortex
—> cortical blindness - Contralateral ***Cerebral peduncle compressed (brainstem pushed against free edge of tentorium to contralateral side)
—> “ipsilateral” hemiplegia
—> left herniation —> right cerebral peduncle compression —> left hemiplegia
—> false localising signs - ***Midbrain / Pons compressed
—> haemorrhage + infarction within
—> loss of consciousness, ↓ HR, changes in respiration, ↑ BP due to ↑ sympathetic activity
—> Lethal - ***Aqueduct compressed
—> CSF circulation blocked
—> hydrocephalus - Optic nerve + ***Retinal vein compressed
—> papilloedema (early signs)
Effect of Cerebellar tonsil herniation / Coning
Downward displacement of Cerebellar tonsils through Foramen magnum
—> Compress **Medulla (control respiration)
—> **Apnea
—> Lethal
***Hydrocephalus
↑ CSF volume in ventricles in:
- Ventricles
- Subarachnoid space
- Both
Primary hydrocephalus:
- Obstruction to flow of CSF
- Infection
- Tumour
- Blood clot
- Tuberculous meningitis —> blockage of subarachnoid space due to fibrosis - Increased production
- Impaired absorption
Secondary hydrocephalus:
1. Compensatory ↑ in CSF (due to brain atrophy)
Brain swelling (↑ volume of brain itself)
- Cerebral edema
- Vasogenic
- Cytotoxic
- Hydrocephalic / Interstitial
(2. Vasodilatation
- hypoxia
- hypercapnia
- loss of vasomotor tone —> complicate acute brain damage)
***Cerebral edema
- Vasogenic
- Pathogenesis: **↑ Capillary permeability / ↑ Filtration pressure (defective BBB)
- Location: **White matter
- Edema fluid composition: ***Plasma filtrate including plasma protein (Water, Na, Protein)
- Clinical disorder:
—> Brain tumour
—> Abscess
—> Infarction
—> Haemorrhage - Cellular / Cytotoxic
- Pathogenesis: **Cellular swelling - glial neuronal, endothelial
- Location: **White + Gray matter
- Edema fluid composition: ***↑ Intracellular Na + H2O
- Clinical disorder:
—> Hypoxia (disturbance of cellular osmoregulation)
—> Hypo-osmolality due to water intoxication
—> Purulent meningitis - Interstitial / Hydrocephlic
- Pathogenesis: ↑ Brain fluid due to ↑ **resistance of CSF absorption
- Location: **Periventricular white matter
- Edema fluid composition: ***CSF
- Clinical disorder:
—> Hydrocephalus
—> Purulent meningitis
Cerebrovascular accident (Stroke) vs Transient ischaemic attack (TIA)
Stroke:
- ***Rapid onset
- ***Focal cerebral dysfunction
- ***Associated structural brain damage
- Presumed vascular origin (due to quick onset nature)
- Last >24 hours
TIA:
- ***Fully reversible
- ***Neurological deficit
- ***NO structural brain damage
- NOT complete vascular blockage
- Last <24 hours
2 types of Stroke (CVA)
Infarction (70%)
- Atherosclerotic / Thrombotic
- Emboli (from heart / heart valves)
- others
Haemorrhage (30%)
- Hypertension
- Berry aneurysm
- others
***Cerebral infarction: Gross appearance + Morphological changes + Microscopic appearance
Gross appearance:
- Pale / Haemorrhagic (blood from recanalisation leaked out from necrotic vessels)
- Tissue necrosis
**Morphological changes:
Pale infarct
—> **Swollen + slightly softened initially (potentially Transtentorial herniation!!!)
—> Cracking + **Liquefaction (4-5 days)
—> Shrunken / **Resorption with replacement by fluid-filled cavities (as in old infarcts) (weeks - months)
Microscopic appearance:
Ischaemic necrosis (6-8 hours)
—> **Swelling of neurons
—> **Microglia / Macrophages (6-12 hours)
—> Heavy filtration of macrophage + ***Astrocytic proliferation around border (healing process by fibrosis) (1st week)
Time / age:
- Acute / Old infarct
Mechanism:
- Occlusive
- Boundary zone
***Cerebral infarction: Causes
- ***Atherosclerosis (Occlusive) - large / small vessels
- ***Emboli (Occlusive) - from mural thrombi of heart / bifurcation of common carotid artery
- Hypotension - watershed areas (boundary zone infarct)
- Vasculitis (prudent meningitis e.g. TB meningitis / Haemophilus influenzae)
- Vasospasm (subarachnoid haemorrhage)
- Vascular collapse of raised ICP
- Venous occlusion —> haemorrhagic infarcts
- others (sickle cell anaemia, polycythaemia rubra vera, migraine, hyperlipidaemia)
Blood supply of brain
- Internal carotid artery (Anterior)
—> Middle cerebral artery (commonly infarcted) —> Penetrating artery
—> Anterior cerebral artery - Vertebral artery (Posterior)
—> Basilar artery —> Posterior cerebral artery
Atherosclerotic arterial disease
Occlusion / Stenosis:
- Carotid artery
- Vertebral arteries
- Intracranial cerebral arteries
Bifurcation of common carotid artery / Origin of internal carotid artery —> Turbulence —> Haemodynamic stress —> Atherosclerosis —> Atheroma rupture —> Emboli —> TIA
Heart emboli causes
Example:
- Atrial fibrillation
- Chronic rheumatic heart disease
- Endocarditis —> thrombus
- MI —> thrombus
***Deep penetrating artery / Small vessel disease
Basal ganglia, Thalamus, Pons, Internal capsule
Large Middle cerebral artery
—> Small penetrating artery (Lenticulo-striate arteries)
—> Sharp angle
—> Huge haemodynamic stress
—> **Lipohyalinosis: **Hyalinization degeneration + **Fibrinoid degeneration (collagen deposition) of vessel wall with lipid deposition + **Accumulation of foamy macrophages (Severe in hypertension)
—> Progressive narrowing of lumen / Weakening with progressive dilatation of lumen
—> **Occlusion / **Microaneurysm
—> Small deep cerebral infarct (Lacunar infarct) / Hypertensive cerebral haemorrhage
—> affecting corresponding structures
Hypertensive management is important
Boundary zone infarcts
Most often seen in borders between Anterior + Middle cerebral arterial beds
Zone between 2 arterial beds
—> maximally deficient in blood supply
—> progressive and gradual ischaemia + necrosis
Cause:
Diffuse intracranial atherosclerosis + Drop in systemic BP / Congestive heart failure
Presentation:
Patients do NOT produce clear focal neurological signs
Cerebral infarct complications
Small brain infarct despite their small size can impinge on internal capsule
—> Hemiplegia (contralateral)
Intracranial haemorrhage 3 layers
- Intracerebral
- Microaneuryms —> Hypertension (haemorrhagic stroke) - Subarachnoid
- ***Saccular aneurysms (form a Sac-like aneurysm)
- Arteriovenous malformation (AVM) bleeding
- Blood disorders, other causes - Epidural / Subdural
- Trauma
Sites:
- Deep brain
- Cerebellum
- Pons
***Intracerebral haemorrhage causes
- Abnormalities of blood vessels
- **Microaneurysm in hypertension (located in **deep penetrating artery)
- **Saccular aneurysm (located in **big cerebral artery, in **subarachnoid space)
- mycotic aneurysm
- **Arteriovenous (vascular) malformation
- congophilic angiopathy (amyloid deposition in pial/intra-cortical arterioles, esp. in lobar sites)
- arteritis - Blood disorders
- thrombocytopenia (multifocal, lobar)
- coagulopathies (bleed into subdural space)
- anti-coagulants - Abnormalities of brain tissue
- infarct
- tumour (massive haemorrhage in primary and secondary intra-parenchymal tumours e.g. metastatic choriocarcinoma) - Traumatic
- Idiopathic
- Miscellaneous e.g. drugs (amphetamine), alcohol
Hypertensive cerebral and cerebellar haemorrhage
Spontaneous intracerebral haemorrhage
Basal ganglia, Pons, Cerebellum
—> Small vessel disease in deep penetrating artery
—> **Lipohyalinosis
—> Weakening with progressive dilatation of lumen
—> **Microaneurysm
—> Rupture due to hypertension
—> Massive intracerebral haemorrhage
—> **Dissect through brain tissue + extend into **ventricular system
—> **Secondary oedema of surrounding brain tissue + **Obstructive hydrocephalus + ***Herniation
Vascular malformation
- Aka Angiomas
- Unknown rupture cause
4 main types:
- AVM
- Venous angiomas
- Cavernous angiomas
- Capillary angiomas
- **Presentation:
1. Asymptomatic
2. Haemorrhage
3. Space occupying effect
4. Steal (drain blood away from other parts of brain —> epilepsy / neurological dysfunction)
Saccular aneurysms / Berry aneurysms
- Located in **big cerebral artery in **subarachnoid space
- Unknown cause (NOT degenerative cause)
- occurs at ALL ages past puberty, 25% multiple aneurysms —> bilateral as mirror image aneurysms
- 60% asymptomatic, 40% symptomatic of which 90% rupture + bleed, 10% compression
—> Rupture reason unknown - 90% ***Anterior circulation (Arterial bifurcation)
—> 30% Internal carotid (terminal bifurcation and angle with PCA)
—> 30% Origin of Anterior communicating from Anterior cerebral
—> 30% Middle cerebral (esp. at origin of first main branches within Sylvian fissure)
—> 10% Posterior: vertebrobasilar system - Co-existing lesions:
—> Adult polycystic kidneys
—> Coarctation of aorta
Size:
- 5-10mm —> rupture
- 30mm —> compression
Effect:
Bleeding into Subarachnoid space
—> **Meningeal irritation
—> Sudden really severe headache / **Neck rigidity
Complications:
- Rebleeding
- Cerebral ischaemia + infarction (due to Vascular spasm)
- Hydrocephalus
- Expanding haematoma
- Epilepsy
