Neuro I(a) Flashcards
———–: Accumulation of excess fluid within the brain parenchyma
Cerebral odema
what are the 2 types of cerebral odema
1) Vasogenic oedema
2) Cytotoxic oedema
Patho of Cytotoxic Oedema
Intracelluar fluid accumulation due to Neuronal and glial cell membrane injury caused by hypoxic-ischaemia
Patho of Vasogenic Oedema
Extracellular fluid accumulation due to disruption of BBB (caused by isheamia, heamorrahge)
*() extra info
Macroscopic Features:
- Flattening of the gyri and narrowing of the intervening sulci
- Compression of the ventricular cavities
features of?
Cerebral Oedema
———- : Accumulation of excessive CSF within the ventricular system
Hydrocephalus
Causes/patho of Hydrocephalus
Choroid plexus tumours –> Overproduction of CSF –> Hydrocephalus (rarely)
Causes of Non-communicating Hydrocephalus
* Obstruction
Masses localised to the foramen of Monro or cerebral aqueduct –> Non-communicating Hydrocephalus
(patrial enlargement of the ventricular system)
Causes of Communicating Hydrocephalus
* No obstruction
Reduced CSF resorption (by arachnoid granulations) –> Communicating Hydrocephalus
(enlargement of the entire ventricular system)
CM of Hydrocephalus
1) Head enlargement, before suture closure
2) Ventricular dilatation and ↑ ICP, after suture fusion
What are the 3 types of Herniation syndromes
1) Subfalcine (Cingulate) herniation under Falx cerebri
2) Uncal Transtentorial herniation <>Tentorium cerebelli
3) Cerbellar tonsillar herniation into the Foramen magnum
Compliactions of Herniation in the brain
Vascular compromise of the compressed tissue –> Infarction -> Additional swelling –> Further Herniation
————-: Increase of the volume of tissue and fluid inside the skull beyond the limit –> Rise of intracranial pressure
Herniation
What are the 3 sites of brain herniation?
1) Falx cerebri –> (Subfalcine (Cingulate) herniation)
2) tentorium cerebelli -> (transtentorial [Uncinate] hernia)
3) Foramen magnum –> Tonsillar hernia)
Compression of which artery is caused by Subfalcine (Cingulate) Herniation ?
anterior cerebral artery
microscopic features:
- Cortical spongious alteration
- Peri-neuronal/ Peri-vascualar swelling of astrocytic processes
features of?
Cytotoxic Cerebal Oedema
Compression ————- nerve in a Transitional (Ucinate) Hernitation –> Pupilary dilatation
Third cranial nerve
In a Transtenotorial (Uncinate) Herniation , the compression of ———– –> Kernohan’s notch
Contralateral cerebral peduncle against the tentorium
In a Transtentorial (Uncinate) Herniation, the compression of ———– -> Ischaemic injury of the primary visual cortex
Posterior cerebral artery
What part of the brain is affected during a transtentorial herniation
medial temporal lobe , against the free margin of the tentorium
In a Transtentorial (Uncinate) Herniation , Tearing of penetrating veins and arteries will result in the Development of ————– (in the midbrain and pons)
Duret haemorrhages
Patho/ Complications of A Tonsillar Herniation
Displacement of the cerebellar tonsils through the foramen magnum –> Brain stem compression –> Life threatening condition, (due to serious damage of vital respiratory and cardiac centers in the medulla oblongata)
The 2 mechanisms that deprive O2 from the brain
1) Functional Hypoxia
2) Ischaemia due to tissue Hypoperfusion
Causes of Functional Hypoxia
- Partial pressure of oxygen (e.g. high altitude)
- Impaired oxygen-carrying capacity (e.g. Sever anaemia)
- Inhibition of oxygen use by tissue (e.g. Cyanide poisonig
causes of Ischaemia due to tissue hypoperfusion
i. Hypotension, ii. Vascular obstruction iii. Both
the 2 froms of Ischaemia due to tissue hypoperfusion
1) Transient
2) Permanent
cause of Global Cerebral Ischaemia
Severe systemic hypotension (as in cardiac arrest or shock)
Macroscopic Features of Global Cerebral Ischaemia:
* ————-, with ————— and narrowed sulci
* Poor demarcation between gray and white matter
Swollen brain, with widened gyri and narrowed sulci
What neuronal cells are affected by Global cerebral Ischaemia
- Pyramidal cells of hippocampus and neocortex
- Purkinje cells of the cerebellum
Which type of Global Cerberal Ischaemia is this?
Macroscopic features:
i. swollen brain and widened Gyri w/ narrowed sulci
Microscopic features:
i. Cytoplasmic eosinophilia,
ii. Nuclear pyknosis and karyorrhexis,
iii. Neutrophil infiltrates
* Pyknosis –> Karyorrehxis are death steps of the cell nucleus
Cerebral infarction (Early changes 12-24 hrs)
Which type of Global Cerberal Ischaemia is this?
Macroscopic features:
i. swollen brain and widened Gyri w/ narrowed sulci
Microscopic features:
i. Tissue necrosis,
ii. Macrophages,
ii. vascular proliferation,
iv. Reactive gliosis
v.Reactive astrocytes
Cerebral infarction (Subacute changes 24 hrs-2 wks)
Which type of Global Cerberal Ischaemia is this?
Macroscopic features:
i. swollen brain and widened Gyri w/ narrowed sulci
Microscopic features:
i. Removal of necrotic tissue,
ii. Gliosis
Cereral changes (Repair >2wks)
Immunohistochemistry used to stain Astrocytes
GFAP
Marker used for microglia staining
* microglia –> macrophages of the brain
CD68
* stains macropahges
cause of “Watershed infarcts”
Hypotensive episodes
(Anaphylactic shock, sudden blood loss, sever infections)
location of “Watershed infarcts”
The border-zone between the anterior and middle cerebral artery distributions
CF of “watershed” infarcts
1) Transient post-ischaemic confusional state –> Complete recovery (mild insult)
2) Sever global cerebral ischaemia–> Widespread neuronal death; Severely neurologically impaired and in a persistent vegetetative state
Which is more common an Embolic infarction or thrombotic infarction?
Embolic Infarction
Most common site of embolic infarction
Middle Cerebral Artery (MCA)
Sources of emboli in an Embolic Infarction
- Cardiac mural thrombi (Predisposing factor: Atrial fibrillation)
- Thrombo-emboli from atheromatous plaques
- Emboli of venous origin + Cardiac defect -> Paradoxical embolism
Thrombotic occlusion result to –>
Cerberal infactions
Patho of Thrombotic occlusions
Development of thrombosis on pre-existing atheromatous plaques
locations of thrombotic occlusions
Carotid bifurcation (,origin of middle cerebral artery)
*carotid bifurcation is the point where the common carotid artery divides into internal and external carotid arteries
The 2 types of infarcts
1) Non-haemorrhagic (Result of acute vascular occlusions)
2) Haemorrhagic (Result of reperfusion of ischaemic tissue, either through collaterals or dissolution of emboli)
*reperfusion->restortion of blood flow to a tissue that has been blocked
Micro features of ?
Haemorrhaging infarct
Causes of an Intracranial Haemorrhage
1) Hypertension
2) Structural lesions (e.g. arteriovenous and cavernous malformations)
3) Traumas
4) Tumours
Epi of primary brain parenchymal haemorrhage
Peak incidence: ~60 years of age
cause of Primary brain parenchymal Haemorrhage
Rupture of a small intra-parenchymal vessel, due to chronic hypertension
locations of Primary brain parenchymal Haemorrhage
- Basal ganglia
- Thalamus
- Pons
- Cerebellum
Clinical manifestions of
Primary brain parenchymal Haemorrhage
Depending on the location and size of the haemorrhage
Macroscopic Features:
Blood extravasation -> Compression of the neighbouring brain parenchyma –> Cavity formation with brown discoloured rim
Microscopic Findings -Early findings:
* Extra-vasated, clotted blood
* Anoxic neural changes of the adjacent neuropil
* Oedema of the brain parenchyma, around the haemorrhagic focus
features of?
* Anoxic: complete loss of O2 supply
Primary brain Parenchymal Haemorrhage (Early findings)
Late Microscopic findings of Primary brain parenchymal haemorrhage:
* Pigment and ——————–
* ——————— at the periphery of the lesion
- Pigment and lipid-laden macrophages
- Reactive astrogliosis at the periphery of the lesion
cause/ patho of Cerebral Amyloid Angiopathy
Deposition of amyloidogenic peptides in the walls of small- and medium-sized meningeal and cortical vessels
location of Cerebral Amyloid Angiopathy
Lobes of the cerebral cortex
Histochemical stain for Beta Amyloid (in Cerebral Amyloid Angiopathy)
Apple-green birefringence on Congo-red
stain used for Haemosiderin (in Cerebral Amyloid Angiopathy)
Pearl’s/Prassin blue iron staining
Pathologocial identifcation of cerebral Amyloid Angiopathy
1) Aβ immuno stain/ Congo red stain for Beta Amyloid
2) Pearl’s blue iron stain for Haemosiderin
causes of Subarrachnoid haemorrahge & Saccular aneurysms
- Rupture of a berry aneurysm (most common)
- Vascular malformation
- Trauma
- Rupture of an intra-cerebral haemorrhage into the ventricular system
- Tumours
patho of subarachnoid haemorrhage & Saccular Aneurysms
Acute increase in intracranial pressure (1/3 of cases) –> Rupture of a saccular aneurysm –> Accumulation of blood in the sub-arachnoidal space
loactions of Subarachnoid haemorrhage & Saccular Aneurysms
~90% of Berry aneurysms in the anterior circulation
Microscopic Findings:
* Absent muscle wall and intimal elastic lamina (thinning of vessels)
* Presence of a thickened hyalinised intima, and the adventitia
features of?
Subarachnoid haemorrhage & saccular aneurysms
CF of Subarachnoid haemorrhage & saccular aneurysms
- Sudden, severe headache
- Rapid loss of consciousness
- Death (from the first bleed in 25-50% of cases)
- blood in CSF
- Postive Kernig & Burdzinski sign
Complications of Subarachnoid haemorrhage & Saccular aneurysms
Ischaemic injury d/t vasospasm (early period after rupture of an aneurysm)
the 4 types of Vascular Malformations
1) Arterio-Venous Malformations (AVMs)
2) Cavernous Malformations
3) Capillary Telangiectasias
4) Venous Angiomas
Epi of AVMs (Anter-venous mal.)
Most common vascular malformation
* M:F = 2:1; Age: 10-30 years
CM of AVMs
- Seizures
- Intracerebral or subarachnoid haemorrhage
Macroscopic Features:
* Tangled network of worm-like vascular channels
Microscopic Findings:
* Enlarged blood vessels, separated by gliotic tissue (shown w/ GFAP)
* Presence of haemo-siderophages
features of?
AVMs (Arterio-venous malformations)
loc of Cavernous Malformations
Cerebellum, Pons
Microscopic Findings:
* Distended, loosely organised vascular channels (Back to back dilated vesseles- Trichome stain)
* Collagenised walls
* No intervening nervous tissue
* Foci of old haemorrhage, infarction and calcification
features of?
Cavernous (Vascular) Malformation
Micro:
* Dilated thin-walled vascular channels
* Intervening normal brain parenchyma
* several large, thin-walled vascualr spaces
* “Pencil fibers” = white matter tracts of the basal ganglia
features of?
Capillary Telangicetasias
Micro:
* Aggregates of ectatic venous channels
* Capillary Hindus resembles the head of medusa
features of?
Venous Angiomas (Varcies)
