Cerebrovascular Disease & CNS Trauma Flashcards
1
Q
- REGIONAL ischemia to the brain that results in FOCAL neurologic deficits lasting > 24 hours
- subtypes include thrombotic, embolic and lacunar
- 4th most common cause of death in the US (incidence & prevalence is declining)
A
Ischemic Stroke
2
Q
- REGIONAL ischemia to the brain that results in FOCAL neurologic deficits lasting < 24 hours
A
Transient Ischemic Attack (TIA)
3
Q
- Oxygen (supplied by cerebral blood flow), not glucose, is the limiting factor in cerebral metabolism
- cerebral blood flow is subject to autoregulation over wide range of arterial & intracranial pressures
Cerebral Perfusion Pressure = Systemic Arterial Blood Pressures - Intracranial Pressure
A
Cerebral Metabolism
4
Q
Hypoxia vs. Ischemia
A
H: blood flow normal, but blood O2 content reduced
I: Blood O2 content normal, but reduced blood flow, e.g., cardiac arrest, hypovolemic shock
I more damaging than H b/c toxic metabolic wastes accumulate
Irreversible brain damage after 10 min of O2 deprivation
5
Q
Vulnerable cells to Hypoxia/Ischemia
A
Vulnerability: Neurons»_space; Oligodendrocytes > astrocytes > blood vessels
Vulnerable Neurons:
- Hippocampal pyramidal neurons in Somner sector (CA 1)
- Pyramidal neurons of cerebral cortex (layers 3 & 5)
- Purkinje cells (GABAergic cells) of cerebellum
6
Q
Middle Cerebral Artery Supply, Lesion & Symptoms
A
- Supplies lateral surface, including Sylvian Fissure
- Contralateral Hemiparesis and Hemisensory loss (face, arm>leg)
- Eye deviation (toward lesion)
- Aphasia: inability to express or comprehend language
- Apraxia: inability to execute previously learned tasks or movements
- contralateral visual field defect
- Neglect
7
Q
Anterior Cerebral Artery Supply, Lesion & Symptoms
A
- Supplies anteromedial surface, including interhemispheric fissure
- Hemiparesis and hemisensory loss (leg>arm, face)
- lack of initiative (assoc w/ frontal lobe)
8
Q
- artery that branches into the Middle Cerebral Artery & Anterior Cerebral Artery
A
Internal Carotid Artery
9
Q
Posterior Cerebral Artery Supply, Lesion & Symptoms
A
- Supplies posterior and inferior surfaces
- Contralateral visual field defect
10
Q
- deep perforating central branches that supply deep regions of the cerebral hemispheres (basal ganglia)
A
Lenticulostriate arteries (central branches of the MCA)
Lacunar strokes: Mainly caused by Hypertension, DM, smoking
Lacunar syndromes:
- Pure motor syndrome
- Pure sensory syndrome
- Sensorimotor syndrome
- Ataxic Hemiparesis
- Clumsy Hand Dysarthria
11
Q
Global Cerebral Hypoxia/Ischemia Stroke
A
Etiology:
- low perfusion
- acute decrease in blood flow
- chronic hypoxia
- repeated episodes of hypoglycemia
- may damage neurons without damaging glia or blood vessels
- watershed zones are most vulnerable, and are more likely to experience full parenchymal injury
12
Q
Focal/Regional Ischemic Stroke
A
- due to occlusion of single artery or arterial branch
- results in damage of all tissue types of brain parenchyma (neurons, glia, blood vessels) in the distribution of the occluded vessel
Types:
- thrombotic
- embolic
- lacunar
- risk of stroke doubles >55yo
13
Q
Anemic/Pale/Non-Hemorrhagic Infarct
A
- no reperfusion to necrotic area
- typically due to thrombotic stroke (even if the thrombus is lysed, the plaque will reform the thrombus, preventing perfusion)
14
Q
Hemorrhagic/Red Infarct
A
- Reperfusion of necrotic area
- characteristic of embolic infarcts, b/c emboli can be lysed without reformation
15
Q
Acute Infarct
A
Timing: 0-2 days Gross: - Tissue softening - Dusky gray matter discoloration - Blurring of gray/white matter demarcation
Micro:
- Early: RED NEURONS: eiosinophilic change in cytoplasm of neurons, with nuclear collapse
- NEUTROPHILIC INFILTRATION (1-3 days)
16
Q
Subacute Infarct
A
Timing: 2-4 Days
Gross:
- Swelling/edema of tissue with mass effect
- dead tissue begins to crack away from viable tissue
Micro:
- Liquefactive necrosis: red neurons breakup and disappear
- PMNs replaced by lymphocytes and macrophages (3-5 days)
17
Q
Chronic/organized/healed/remote Infarct
A
Timing: 4 days +
Gross:
- early: liquefactive necrosis
- late: cystic cavitation (b/c no fibroblasts)
Micro:
- Cavity formation
- Reactive GLIOSIS: astrocytic processes & capillaries that line cystic space
- Neuronal encrustation: Fe & Ca deposits on neurons in infarct rim
18
Q
Cerebral Venous Thrombosis
“Venous Infarct”
A
- thrombosis of dural venous sinus or cortical vein
- usually bilateral & symmetrical
- blocked venous drainage results in congestion, ischemia and hemorrhagic necrosis
19
Q
Epidural Hematoma
A
Collection of blood between the dural and the skull
- Classically due to trauma: fracture of the temporal bone with rupture of the MIDDLE MENINGEAL ARTERY (high pressure)
- lens-shaped lesion on CT
- lethal (may have lucid interval before neurologic deterioration)
20
Q
Subdural Hematoma
A
- collection of blood underneath the dura, covering the surface of the brain
- due to trauma: tearing of BRIDGING VEINS between the dura and arachnoid
- CRESCENT-shaped lesion on CT
- presents with progressive neurologic signs
- more common in elderly
- lethal
21
Q
Subarachnoid hemorrhage
A
- Bleeding into subarachnoid space
- presents with sudden headache - “THE WORST HEADACHE OF MY LIFE”, with nuchal rigidity
- Lumbar puncture shows XANTHOCHROMIA (yellow hue due to bilirubin breakdown)
- Classically due to rupture of BERRY ANEURYSM
22
Q
Berry (Saccular) Aneurysm
A
- thin walled, saccular outpouchings that lack a media layer (increasing risk of rupture)
- Most common site is at bifurcation of the ANTERIOR COMMUNICATING ARTERY of anterior Circle of Willis (connects L&R ACAs)
- Associated with Marfan’s syndrome, Ehlers-Danlos Syndrome and Autosomal Dominant Polycystic Kidney Disease
- most common cause of non-traumatic subarachnoid hemorrhage
- Rupture (at dome of aneurysm) can cause:
- vasospasm of Circle of Willis (infarct)
- Arachnoid fibrosis, with COMMUNICATING HYDROCEPHALUS
23
Q
Intracerebral Hemorrhage / Chronic Hypertensive Hemorrhage
A
Bleeding into BRAIN PARENCHYMA
- Classically due to rupture of CHARCOT-BOUCHARD MICROANEURYSMS of the LENTICULOSTRIATE VESSELS (undergo hyaline arteriolosclerosis)
- Basal Ganglia (especially Putamen) is most common site
- Other sites: Thalamus, Brainstem, Deep Cerebellar White Matter
- Presents as severe headache, nausea, vomiting, eventual coma
24
Q
Charcot-Bouchard Microaneurysm
A
- Associated with Chronic hypertension
- affects small vessels (e.g., in basal ganglia, thalamus)
25
Intraventricular Hemorrhage
- Extension of Intracerebral Hemorrhage that ruptures the ventricular (ependymal) lining
26
Cerebral Amyloid Angiopathy
Another cause of Intracerebral Hemorrhage, but more superficial (cortical) and lobar (vs. ganglionic)
- Amyloid is deposited in small & medium-sized cortical and leptomeningeal blood vessels
- Beta amyloid (AB amyloid) is derived from AMYLOID PRECURSOR PROTEINS (APP) --> has apple-green birefringence
- Micro: Affected vessels have double-barrel vessel-within-a-vessel appearance
27
Classification of Cerebral Vascular Malformations, and Presentation
1. Anteriovenous Malformation (AVM)
2. Cavernous Hemangioma (Cavernoma)
3. Venous Angioma
4. Capillary Telangiectasia
Presentation:
- if symptomatic (AVM or Cavernoma):
- Intracerebral hemorrhage or subarachnoid hemorrhage
- seizure disorder
- Asymptomatic: incidental radiographic/autopsy finding
28
Anteriovenous Malformation (AVM)
- tortuous, large caliber vascular tangle in parenchyma ("can of worms")
- due to direct AV shunt (arteries have smooth muscle and elastic lamina; veins have smooth muscle, but no elastic lamina), with no capillary bed; flow rates rapid
- commonly involves MCA territory
- reactive changes in surrounding brain: Hemosiderin, Calcium, Gliosis
29
Cavernous Hemangioma (Cavernoma)
- abnormal vessels with thin fibrous walls (no smooth muscle or elastic lamina), without intervening brain tissue
- occurs most often in brainstem, cerebellum, or cerebral subcortical white matter
- Flow rates sluggish
- resembles a hematoma
30
Vascular Dementia
Loss of memory and other cognitive abilities secondary to cerebrovascular disease
1. Multi-infarct dementia: due to bilateral infarcts of gray matter
2. Diffuse white matter disease: arteriolosclerosis affecting the myelination of white matter and axonal loss
31
- parenchymal contusion at site of impact
- associated with blows to stationary head and falls
- contusion damage greatest to gyral crowns
Coup Injury
32
- Parenchymal contusion 180 degrees opposite site of impact due to rebound injury
- associated with falls
Contrecoup Injury
33
Laceration
- brain tear from penetrating or perforating injury
34
Diffuse Axonal Injury (DAI)
- Stretching and shearing of axons in deep white matter (callosal and periventricular white matter and brainstem)
- axons severed at nodes of Ranvier, with swelling proximal to site of interruption
- Patient unconscious from moment of injury, without lucid interval
- Micro: see rounded swellings in white matter neuropil (can silver stain)
35
Midbrain stroke
Weber syndrome:
- Ipsilateral CN III defect
- contralateral hemiparesis
36
Pons stroke
- quadriparesis or hemiparesis
- horizontal gaze paresis
- facial weakness
- ataxia
- Intranuclear Opthalmoplegia: damage to MLF
- dysarthria
37
Medullary Stroke
Wallenberg syndrome:
- ipsilateral facial numbness
- contralateral body numbness
- ipsilateral ataxia
- ipsilateral horner's syndrome
- vertigo, dysarthria, dysphagia, nausea, vomiting
- NO MOTOR WEAKNESS
38
Cerebellar stroke
- dysarthria
- ipsilateral ataxia
- vertigo
- tremor
- nystagmus
39
Core of Ischemic Stroke
- area of irreversible ischemia
40
Penumbra of Ischemic Stroke
- tissue at risk, but salvageable by acute stroke therapy (tPA)
- supplied by same artery as the core of ischemia, but will maintain viability for period of time b/c of collateral supply
41
Inclusion Criteria for tPA Acute Stroke Therapy
- 18 years of age
- Acute ischemic stroke
- Clearly defined time of stroke onset and able to treat WITHIN 3 HOURS; “LAST TIME SEEN NORMAL” (most reliable measure of time); protocol may be expanded to 4.5 hours
- Measurable neurological deficit (measure deficits/risks)
- Baseline CT scan showing NO EVIDENCE OF INTRACRANIAL HEMORRHAGE
42
Exclusion Criteria for tPA Acute Stroke Therapy
- Improving symptoms (may recanalize w/o therapy)
- ANY KIND OF HEMORRHAGE: Stroke or head trauma within 3 months (risk for additional hemorrhage); Major surgery within 14 days; History of ICH; Suspected SAH; GI Bleed or Urinary Tract hemorrhage within 21 days; Arterial puncture at a noncompressible site within 7 days; Use of heparin within 48 hours and elevated ptt
- No defined time of onset ("I DON'T KNOW")
- BP >185/110; aggressive management of BP needed
- Seizure
- Pt > 15 seconds; platelets > 100,000; glucose400
**tPA has 10x increase risk of hemorrhage, but still a small absolute risk
43
When do you use heparin in the stroke unit?
- Heparin is not used regularly in stroke unit due to increased risk of hemorrhage, with no increased benefit
- May be used later for PROPHYLAXIS AGAINST DVT
44
When do you use Warfarin/Coumadin in stroke unit?
CARDIOGENIC CAUSES:
- Atrial Fibrillation
- Mechanical MVR or AVR (mitral/aortic valve replacements)
- Cardiac Thrombus (e.g., mural thrombus)
- MI (usually life-long anticoagulation)
* Coumadin is no better than aspirin for prevention of non-cardiogenic recurrent stroke
45
When do you treat HYPERTENSION after stroke?
- Wait 24/48 hours to treat HTN after stroke
- Treatment only if necessary (>220/120) (MAP >130)
- Hypotension can be even more detrimental than the HTN
46
When do you treat HYPOTENSION after stroke?
- More detrimental than hypertension: want adequate blood flow to vessel that is having difficulty receiving BF
- Seek cause and treat aggressively
- Arterial BP monitoring may be necessary
- Use 0.9 NS first to ensure adequate preload; Then add vasopressors if needed
