Neuro I(a) Flashcards by Elyaa Saleh

———–: Accumulation of excess fluid within the brain parenchyma

Cerebral odema

How well did you know this?

Not at all

Perfectly

what are the 2 types of cerebral odema

1) Vasogenic oedema
2) Cytotoxic oedema

How well did you know this?

Not at all

Perfectly

Patho of Cytotoxic Oedema

Intracelluar fluid accumulation due to Neuronal and glial cell membrane injury caused by hypoxic-ischaemia

How well did you know this?

Not at all

Perfectly

Patho of Vasogenic Oedema

Extracellular fluid accumulation due to disruption of BBB (caused by isheamia, heamorrahge)

*() extra info

How well did you know this?

Not at all

Perfectly

Macroscopic Features:

Flattening of the gyri and narrowing of the intervening sulci
Compression of the ventricular cavities

features of?

Cerebral Oedema

How well did you know this?

Not at all

Perfectly

———- : Accumulation of excessive CSF within the ventricular system

Hydrocephalus

How well did you know this?

Not at all

Perfectly

Causes/patho of Hydrocephalus

Choroid plexus tumours –> Overproduction of CSF –> Hydrocephalus (rarely)

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

Causes of Communicating Hydrocephalus

* No obstruction

Reduced CSF resorption (by arachnoid granulations) –> Communicating Hydrocephalus
(enlargement of the entire ventricular system)

How well did you know this?

Not at all

Perfectly

CM of Hydrocephalus

1) Head enlargement, before suture closure
2) Ventricular dilatation and ↑ ICP, after suture fusion

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Compliactions of Herniation in the brain

Vascular compromise of the compressed tissue –> Infarction -> Additional swelling –> Further Herniation

How well did you know this?

Not at all

Perfectly

————-: Increase of the volume of tissue and fluid inside the skull beyond the limit –> Rise of intracranial pressure

Herniation

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

Compression of which artery is caused by Subfalcine (Cingulate) Herniation ?

anterior cerebral artery

How well did you know this?

Not at all

Perfectly

microscopic features:
- Cortical spongious alteration
- Peri-neuronal/ Peri-vascualar swelling of astrocytic processes

features of?

Cytotoxic Cerebal Oedema

How well did you know this?

Not at all

Perfectly

Compression ————- nerve in a Transitional (Ucinate) Hernitation –> Pupilary dilatation

Third cranial nerve

How well did you know this?

Not at all

Perfectly

In a Transtenotorial (Uncinate) Herniation , the compression of ———– –> Kernohan’s notch

Contralateral cerebral peduncle against the tentorium

How well did you know this?

Not at all

Perfectly

In a Transtentorial (Uncinate) Herniation, the compression of ———– -> Ischaemic injury of the primary visual cortex

Posterior cerebral artery

How well did you know this?

Not at all

Perfectly

What part of the brain is affected during a transtentorial herniation

medial temporal lobe , against the free margin of the tentorium

How well did you know this?

Not at all

Perfectly

In a Transtentorial (Uncinate) Herniation , Tearing of penetrating veins and arteries will result in the Development of ————– (in the midbrain and pons)

Duret haemorrhages

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

The 2 mechanisms that deprive O2 from the brain

1) Functional Hypoxia
2) Ischaemia due to tissue Hypoperfusion

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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)

Neuro I(a) Flashcards

(71 cards)