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Central Nervous System Pathology > Cerebrovascular Disease & CNS Trauma > Flashcards

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

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2
Q
  • REGIONAL ischemia to the brain that results in FOCAL neurologic deficits lasting < 24 hours
A

Transient Ischemic Attack (TIA)

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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

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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

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5
Q

Vulnerable cells to Hypoxia/Ischemia

A

Vulnerability: Neurons&raquo_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
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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
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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)
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8
Q
  • artery that branches into the Middle Cerebral Artery & Anterior Cerebral Artery
A

Internal Carotid Artery

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9
Q

Posterior Cerebral Artery Supply, Lesion & Symptoms

A
  • Supplies posterior and inferior surfaces

- Contralateral visual field defect

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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
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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
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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
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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)
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14
Q

Hemorrhagic/Red Infarct

A
  • Reperfusion of necrotic area

- characteristic of embolic infarcts, b/c emboli can be lysed without reformation

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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)
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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)
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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
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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
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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
Q

Intraventricular Hemorrhage

A
  • Extension of Intracerebral Hemorrhage that ruptures the ventricular (ependymal) lining
26
Q

Cerebral Amyloid Angiopathy

A

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
Q

Classification of Cerebral Vascular Malformations, and Presentation

A
  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
Q

Anteriovenous Malformation (AVM)

A
  • 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
Q

Cavernous Hemangioma (Cavernoma)

A
  • 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
Q

Vascular Dementia

A

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
Q
  • parenchymal contusion at site of impact
  • associated with blows to stationary head and falls
  • contusion damage greatest to gyral crowns
A

Coup Injury

32
Q
  • Parenchymal contusion 180 degrees opposite site of impact due to rebound injury
  • associated with falls
A

Contrecoup Injury

33
Q

Laceration

A
  • brain tear from penetrating or perforating injury
34
Q

Diffuse Axonal Injury (DAI)

A
  • 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
Q

Midbrain stroke

A

Weber syndrome:

  • Ipsilateral CN III defect
  • contralateral hemiparesis
36
Q

Pons stroke

A
  • quadriparesis or hemiparesis
  • horizontal gaze paresis
  • facial weakness
  • ataxia
  • Intranuclear Opthalmoplegia: damage to MLF
  • dysarthria
37
Q

Medullary Stroke

A

Wallenberg syndrome:

  • ipsilateral facial numbness
  • contralateral body numbness
  • ipsilateral ataxia
  • ipsilateral horner’s syndrome
  • vertigo, dysarthria, dysphagia, nausea, vomiting
  • NO MOTOR WEAKNESS
38
Q

Cerebellar stroke

A
  • dysarthria
  • ipsilateral ataxia
  • vertigo
  • tremor
  • nystagmus
39
Q

Core of Ischemic Stroke

A
  • area of irreversible ischemia
40
Q

Penumbra of Ischemic Stroke

A
  • 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
Q

Inclusion Criteria for tPA Acute Stroke Therapy

A
  • 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
Q

Exclusion Criteria for tPA Acute Stroke Therapy

A
  • 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
Q

When do you use heparin in the stroke unit?

A
  • 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
Q

When do you use Warfarin/Coumadin in stroke unit?

A

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
Q

When do you treat HYPERTENSION after stroke?

A
  • 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
Q

When do you treat HYPOTENSION after stroke?

A
  • 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

Central Nervous System Pathology (15 decks)

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