28. CNS Pathology Flashcards
1
Q
A
2
Q
Most common cerebrovascular diseases
A
- 1. Hypertensive intraparenchymal hemorrhage (MC)
- Global ischemia
- Embolism
- 4. Ruptured aneurism
3
Q
When BF is reduced to the brain, survival depends on:
A
- 1. Collateral flow
- 2. Duration of ischemia (less than 24 hours = TIA; more than 24 hours = stroke)
- 3. Magnitude and rapidity of flow reduction
4
Q
Watershed areas 1st to be damaged to ischemia and infarction in global ischemia, because they are the most distal branches of major arteries.
In global cerebral ischemia or hypoxic encephalopathy, what type of damage do we see when watershed areas are affected?
A
Sickle-shaped band of necrosis
5
Q
- Watershed areas 1st to be damaged to ischemia and infarction in global ischemia, because they are the most distal branches of major arteries. The border zone between which arteries in the cerebral hemispheres are most at risk for an infarct following global ischemia?
- What can cause this?
A
ACA/MCA
- Occlusion of the internal carotid artery
- Hypotension in patients with carotid stenosis
6
Q
Symptoms if ischemia and infarction of ACA/MCA?
A
- Proximal arm and leg weakness.
- Transcortical aphasia: language problems
7
Q
Symptoms if ischemia and infarction of MCA/PCA?
A
- Higher-order visual processing
8
Q
Which pattern of injury is seen in the cerebral neocortex following global ischemia?
A
Pseudolaminar necrosis
9
Q
Carotid Stenosis
- What is it?
- What is it most commonly due to?
A
-
Carotid stenosis is MC due to atherosclerosis. Thrombi can form and embolize, leading to stenosis of the internal carotid artery. This can ⬇︎ blood and O2 to the following arteries:
- 1. MCA
- 2. ACA
- 3. Opthalamic artery
10
Q
What are symptoms of carotid stenosis?
A
Bc can ⬇︎ blood and O2 to the MCA, ACA and opthalamic artery =>
- Contralateral face-arm or face-arm leg motor/sensory weakness
- Contralteral changes in visual field
- Aphasia or neglect
- Carotid bruit in diastole
11
Q
Carotid bruit heard in diastole is indicative of what?
A
- stenosis of internal carotid artery
12
Q
How to correct carotid stensois?
A
- Angioplasty/stenting
- Endarterectomy
13
Q
Focal cerebral ischemia, focal neurological deficits is most often due to what?
A
- Embolism
- Thrombus
- Atherosclerosis in HTN
14
Q
Symptoms of Focal Cerebral Ischemia
A
- Less than 24 hours: TIA
- More than 24 hours: stroke (regional ischemia that causes focal neurological deficits)
15
Q
Thrombosis
- MC due to: ______
- MC sites of primary thrombosis: ________
A
- Atherosclerosis
- MC sites of primary thrombosis:
- Carotid bifurcation
- origin of Middle Cerebral Artery (MC)
- Either end of the basialr artery
16
Q
How does a thrombus form?
A
- Rupture, ulceration or erosion of plaque exposes blood to thrombogenic substances => blood is exposed to subendothelial collagen/necrotic debris in plaque => thrombus => pale wedge-shaped infarction at periphery of CTX
17
Q
what is this?
A
subarachnoid hemorrhage: only thing that will cause bleeding at BOTTOM of brain
18
Q
What is the risk factor most commonly associated with deep brain parenchymal hemorrhages?
A
HTN
19
Q
What causes Charcot-Bouchard microaneurysms?
A
Chronic HTN
20
Q
What is a Charcot-Bouchard microaneurysm vs. Saccular (berry) aneurysm?
Where is each most commonly seen?
A
- Charcot-Bouchard occur in vessels less than 300 um in diameter; most often within basal ganglia
- Saccular (berry) aneurysms occur in larger intracranial vessesl in the subarachnoid space
21
Q
Intracerebral/ intraparenchymal hemorrhage vs subarachnoid hemorrage.
- MC due to what?
- MC seen in who?
- Sx?
A
Intracerebral/intraparenchymal hemorrhage
- MC due to: Rupture of Charcot Brousad microaneurysms (in pts who have HTN)
- MC in: HTN patients
- Sx: HA, N/V => coma
Subarachnoid hemorrhage
- MC due to: R_upture of Berry/Saccular aneurysms_ in the Anterior Circle of Willis at the branch points of Anterior Communicating Artery; rupture easily bc no media
- MC in: Marfans and APKD (bc they’re more likely to have berry aneuryms)
- Sx: Worse HA of life with nuchal rigidity
22
Q
What is most commonly affected by a embolic infarction?
Where do emboli most often lodge?
A
- L side of heart => Middle cerebral artery (MCA)
- Where BV branch of pre-existing areas of stenosis
23
Q
What is characteristic of bone marrow embolization?
A
- Shower hemorrhages = widespread white matter hemorrhages
24
Q
What are heritable coagulation factor disorders that cause hypercoagulability?
A
- Protein S and C defiency
- Antithrombin III deficiency
25
What are **hypercoagulable states?**
1. **Dehydration**
2. **Adenocarcinomas/malignancies**
3. **Surgery, trauma, childbirth**
4. **DIC**
5. **Hematologic disorders (sickle cell, leukemia, polycythemia)**
26
Symptoms in **ischemic strokes** vs **hemorrhagic strokes** take how long to come about?
Ischemic stroke = **over 2 hours**
Hemorrhagic = **immediately**
27
MCC of **TIA**
**1. Thrombi**
**2. Embolism**
**3. Vasospasm**
or anything causing a blockage
28
How should a patient with a **TIA** be treated?
Evaluate immediately for **treatable causes of ischemic cerebrovascular disease: emboli, thrombus or vasospasm**
29
Hemorrhagic strokes are red because we usually get reperfusion. Ischemic event damages vessel =\> blood comes back in after it opens up =\> leaks inside the brain
Ischemic stokes can lead to hemorrhagic conversion: fragile vessels rupture =\> secondary hemorrhage.
30
What are the four main injuries due to effects of **hypertension** on the brain?
1. **Lacunar infarcts (lacunar means small)**
2. **Slit hemorrhages**
3. **Acute hypertensive encephalopathy**
4. **Hypertensive intracerebral hemorrhage**
31
**_Lacunar Infarcts/Lacunar Strokes_**
* What are they caused by?
* What are they?
* Where do they occur?
* SX?
* **Lacunar infarcts** occur in people with **HTN**
* **_HTN_ =\> Arteriolosclerosis** of **lenticulostriate arteries**, which are branches of the Middle Cerebral Artery that provide blood to the deep parenchyma of the brain (thalmus, BG, internal capsule, deep white matter) =\> multiple small (\<15mm) cavitary infarcts called lacunes in the (thalmus, BG, internal capsule, deep white matter)
* **Sx**
* Thalamus =\> contalateral somatosensory deficits
* BG: hemiballismus
32
**Other HTN Cerebrovascular Disease?**
**1. Vascular multi-infarct dementia**
**2. Binswanger Disease**
**3. Charcot Brousard Microaneuryms**
4. **CAA** (Cerebral Amyloid Angiopathy)
5. **CADASIL** (Cerebral AD Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
33
What are **slit hemorrhages?**
* HTN =\> small veins to repture, which resorb overtime and leave **slit-like cavities** surrounded by hemosidering MO and gliosis.
34
What is **acute HTN encephalopathy?**
Clinicopathologic syndrome caused by **malignant HTN.**
1. **Edema in brain** with or without transtenrotial or tonsillar herniation
2. **Petechaie and fibrinoid necrosis in arterioles** in the grey and white matter
35
Symptoms of vascular mulit-infarct dmentia?
1. Dementia
2. Gait abnormalities
3. Pseudobulbar signs
36
**Binswanger** Disease
**Vascular dementias** due to infarcts in **_only_** white matter (loss of myelin and axons)
37
**Charcot-Bouchard microaneurysms**
**Microaneurysms** that occur due to **chronic HTN** in the ***_BG_*** and are the MCC of **intraparenchymal hemorrhage**
38
**_CAA (Cerebral Amyloid Angiopathy)_**
**MC in?**
* **B-amyloid plaque**s that deposit in the walls of the artery after recurrent hemorrhagic strokes, making them weak and prone to rupture ==\> **microbleeds**
* **Older patients** and **Alz (same AB amyloid)**
39
**CADASIL (Cerebral AD Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)**
**First detected?**
1. **Rare cause of recurrent strokes** and **dementia** due to **mutations in NOTCH3 gen**e, expressed in **vascular smooth muscles** ==\> thickening of media and adventitia, **loss of smooth muscle cells** and **basophilic PAS+ deposits**
2. **First detectable at 35 YO,** however infarcts typically occur 10-15 year later in other cases
40
**RF** for a stroke
1. **HTN**
2. **DB**
3. **Hypercholesterolemia**
4. **Cigarrette smoking**
5. **Cardiac Disease (Valvular, a-fib, PFO)**
41
What histological findings are common with age and represent a DEGENERATION of astrocytes?
**Corpera amylcia:** PAS+, intracytoplasmic, lamellated polyglucasan bodies; also have HSP
42
markers of **microglia**
**CR3**
**CD86**
43
AVMs are MC where and in whom?
Subarachnoid space =\> deep parenchyma
M 10-30 YO
44
AVMs can cause what
intracerebral or SAH;
damage starts on surface of brain =\> deeper
45
Neural tube defects are MC assx with what?
1. T1DM/obesity
2. Folic acid def
46
Microcephaly is associated with
hiv
zika
FAS
47
neuronal heterotropias are due to?
assoociated with
mutations on genes on x chr: DCX and filamin A
epilepsy
48
when does holoproscencephly occur
ass w
5-6 weks due to SHH signaling
FAS, trisomy 13 and 18
49
small posterior fossa and hernitation of cerebellum into foramen magnum
Chiari
50
Chiari type 1
what herniates
MC in who
cerebellar tonsils
asx in childhood; sx in adulthood due to obstructive hydrocephalys and cerebellar sx (ataxia
51
chiari type 1 malf is assx with
syringomyelia: bilateral loss of pain and temp in UE
52
chiari type 2 is assx with
**lumbosacral myelomeningecele (=paralysis/sensory loss below level of lzn)**
53
what do you see in chiari type 2 malform
herniation of tonsils AND vermis
aqueductal stenosis
54
syringomyelia presents when
20-30s
55
dandy walker malformation
huge posterior fossa
no cerebellum vermis
enlarged roofless 4th ventricle =\> cyst in posterior fossa
-pushes up on tentorium =\> obstructive hydrocephalus
56
joubert syndrome
1. Hypoplasia of vermis
2. Lengthing of superior cerebral peduncles =\> molar tooth signs
3. altered brainstemp shape
