Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HNNS > HNS34 Pathology Of Raised Intracranial Pressure And Cerebrovascular Disease > Flashcards

HNS34 Pathology Of Raised Intracranial Pressure And Cerebrovascular Disease Flashcards

1
Q

Intracranial pressure

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Increased ICP consideration of causes

A
  1. Rigid cranium separated in compartments
  2. Space occupying lesions
    - Haematoma
    - Tumour
    - Abscess
  3. Secondary effects from space occupying lesions
    - Brain edema (Swelling of brain ***itself due to destruction of BBB —> ↑ capillary permeability)
    - Hydrocephalus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Increased ICP considerations of effect

A
  1. Age
    - Elderly: atrophic brain allow more room for ICP to build up
    - Infant: unfused suture allow more room for ICP to build up
  2. 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
  3. Rate of ICP change
    - Slow-growing tumour —> slowly compress brain
    - Intracranial bleeding (quick)
  4. 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)
  5. Dural folds
    - Falx cerebri (separate left/right hemisphere)
    - Tentorium cerebelli (posterior cranial fossa, separate cerebellum from cerebrum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

***Signs and symptoms of Raised ICP

A
  1. Herniation
  2. Headache (stretching of meninges)
  3. Projectile vomiting (distortion of brainstem)
  4. Separation of sutures of the vault (infants)
  5. Erosion of skull bone (long sustained increased ICP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

***Herniation

A

Classified on the part that is herniated and structure which it has been pushed

Sites:

  1. ***Transtentorial / Uncal herniation (大腦唧落小腦)
  2. ***Cerebellar tonsil herniation / Tonsillar herniation / Coning (小腦唧落腦幹)
  3. Subfalcine / Supra callosal herniation (Corpus callosum) (左腦唧去右腦)
  4. Transcalvarial / Fungus herniation (during surgery when brain herniates through skull incision site)
  5. Reversed tentorial herniation (lesion in cerebellum —> push upward)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

***Effects of Transtentorial herniation

A
  1. 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
  2. ***PCA compressed (impinged against edge of Tentorium cerebelli)
    —> infarction of ipsilateral occipital cortex
    —> cortical blindness
  3. 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
  4. ***Midbrain / Pons compressed
    —> haemorrhage + infarction within
    —> loss of consciousness, ↓ HR, changes in respiration, ↑ BP due to ↑ sympathetic activity
    —> Lethal
  5. ***Aqueduct compressed
    —> CSF circulation blocked
    —> hydrocephalus
  6. Optic nerve + ***Retinal vein compressed
    —> papilloedema (early signs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effect of Cerebellar tonsil herniation / Coning

A

Downward displacement of Cerebellar tonsils through Foramen magnum
—> Compress **Medulla (control respiration)
—> **Apnea
—> Lethal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

***Hydrocephalus

A

↑ CSF volume in ventricles in:

  1. Ventricles
  2. Subarachnoid space
  3. Both

Primary hydrocephalus:

  1. Obstruction to flow of CSF
    - Infection
    - Tumour
    - Blood clot
    - Tuberculous meningitis —> blockage of subarachnoid space due to fibrosis
  2. Increased production
  3. Impaired absorption

Secondary hydrocephalus:
1. Compensatory ↑ in CSF (due to brain atrophy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Brain swelling (↑ volume of brain itself)

A
  1. Cerebral edema
    - Vasogenic
    - Cytotoxic
    - Hydrocephalic / Interstitial

(2. Vasodilatation
- hypoxia
- hypercapnia
- loss of vasomotor tone —> complicate acute brain damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

***Cerebral edema

A
  1. 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
  2. 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
  3. Interstitial / Hydrocephlic
    - Pathogenesis: ↑ Brain fluid due to ↑ **resistance of CSF absorption
    - Location: **    Periventricular white matter
    - Edema fluid composition: ***CSF
    - Clinical disorder:
    —> Hydrocephalus
    —> Purulent meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cerebrovascular accident (Stroke) vs Transient ischaemic attack (TIA)

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

2 types of Stroke (CVA)

A

Infarction (70%)

  1. Atherosclerotic / Thrombotic
  2. Emboli (from heart / heart valves)
  3. others

Haemorrhage (30%)

  1. Hypertension
  2. Berry aneurysm
  3. others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

***Cerebral infarction: Gross appearance + Morphological changes + Microscopic appearance

A

Gross appearance:

  1. Pale / Haemorrhagic (blood from recanalisation leaked out from necrotic vessels)
  2. 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

***Cerebral infarction: Causes

A
  1. ***Atherosclerosis (Occlusive) - large / small vessels
  2. ***Emboli (Occlusive) - from mural thrombi of heart / bifurcation of common carotid artery
  3. Hypotension - watershed areas (boundary zone infarct)
  4. Vasculitis (prudent meningitis e.g. TB meningitis / Haemophilus influenzae)
  5. Vasospasm (subarachnoid haemorrhage)
  6. Vascular collapse of raised ICP
  7. Venous occlusion —> haemorrhagic infarcts
  8. others (sickle cell anaemia, polycythaemia rubra vera, migraine, hyperlipidaemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Blood supply of brain

A
  1. Internal carotid artery (Anterior)
    —> Middle cerebral artery (commonly infarcted) —> Penetrating artery
    —> Anterior cerebral artery
  2. Vertebral artery (Posterior)
    —> Basilar artery —> Posterior cerebral artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Atherosclerotic arterial disease

A

Occlusion / Stenosis:

  1. Carotid artery
  2. Vertebral arteries
  3. Intracranial cerebral arteries
Bifurcation of common carotid artery / Origin of internal carotid artery
—> Turbulence
—> Haemodynamic stress
—> Atherosclerosis
—> Atheroma rupture
—> Emboli
—> TIA
17
Q

Heart emboli causes

A

Example:

  1. Atrial fibrillation
  2. Chronic rheumatic heart disease
  3. Endocarditis —> thrombus
  4. MI —> thrombus
18
Q

***Deep penetrating artery / Small vessel disease

A

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

19
Q

Boundary zone infarcts

A

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

20
Q

Cerebral infarct complications

A

Small brain infarct despite their small size can impinge on internal capsule
—> Hemiplegia (contralateral)

21
Q

Intracranial haemorrhage 3 layers

A
  1. Intracerebral
    - Microaneuryms —> Hypertension (haemorrhagic stroke)
  2. Subarachnoid
    - ***Saccular aneurysms (form a Sac-like aneurysm)
    - Arteriovenous malformation (AVM) bleeding
    - Blood disorders, other causes
  3. Epidural / Subdural
    - Trauma

Sites:

  1. Deep brain
  2. Cerebellum
  3. Pons
22
Q

***Intracerebral haemorrhage causes

A
  1. 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
  2. Blood disorders
    - thrombocytopenia (multifocal, lobar)
    - coagulopathies (bleed into subdural space)
    - anti-coagulants
  3. Abnormalities of brain tissue
    - infarct
    - tumour (massive haemorrhage in primary and secondary intra-parenchymal tumours e.g. metastatic choriocarcinoma)
  4. Traumatic
  5. Idiopathic
  6. Miscellaneous e.g. drugs (amphetamine), alcohol
23
Q

Hypertensive cerebral and cerebellar haemorrhage

A

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

24
Q

Vascular malformation

A
  • Aka Angiomas
  • Unknown rupture cause

4 main types:

  1. AVM
  2. Venous angiomas
  3. Cavernous angiomas
  4. Capillary angiomas
  • **Presentation:
    1. Asymptomatic
    2. Haemorrhage
    3. Space occupying effect
    4. Steal (drain blood away from other parts of brain —> epilepsy / neurological dysfunction)
25
Q

Saccular aneurysms / Berry aneurysms

A
  • 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:

  1. Rebleeding
  2. Cerebral ischaemia + infarction (due to Vascular spasm)
  3. Hydrocephalus
  4. Expanding haematoma
  5. Epilepsy

HNNS (58 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions