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Pathophysiology of brain injury. F. Della Corte – C. Maestrone Intensive Care Unit – University of Novara -School of Medicine. Objectives. -To describe which are the common pathophysiological features shared by head injury and stroke -To define the mechanisms of hypoxic-ischaemic

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Pathophysiology of brain injury l.jpg

Pathophysiology of brain injury

F. Della Corte – C. Maestrone

Intensive Care Unit –

University of Novara -School of Medicine


Objectives l.jpg
Objectives

-To describe which are the common pathophysiological

features shared by head injury and stroke

-To define the mechanisms of hypoxic-ischaemic

damage at neuronal level

-To stress the importance of ischemia in the determination

of severity in the outcome in head injured patients

-To define the consequences of ischemic events

in the adult


Ischemic stroke vs head injury l.jpg
Ischemic stroke vs Head injury

Central core

Peripheral penumbra

In most of the presentations molecular mechanisms are basically the same though operating in:

-different sequences

-different time courses

-different intensities


Factors contributing to the increase of irreversibly damaged brain parenchyma l.jpg

Deterioration of CBF

due to progressive

damage of arterial

blood supply

Activation of cytotoxic

processes secondary to

formation and/or release

of neurotoxic mediators

compound and development

of tissue acidosis

Factors contributing to the increase of irreversibly damaged brain parenchyma


Slide5 l.jpg

Cellular injury during ischemia

  • Inadequate Energy supply

  • Deterioration of Ion Gradients

  • Consequences of calcium overload


Slide6 l.jpg

Mild to moderate ischemia

Severe ischemia

Advanced ischemia

Loss of function

causes accumulation

of glutamate

and aspartate

which bind to

NMDA receptors

Insufficient oxygen

and glucose

Influx of water

Na+ Cl-

Cytotoxic edema

Inadequate energy

supply

Influx of Ca2+

Influx of water

Na+ Ca2+

Irreversible cellular injury

Failure of neuronal activity

Regional brain dysfunction

Anaerobic

metabolism

Destruction of cell

components

Formation of

free radicals,

eicosanoids and

leukotrienes

Accumulation of lactic acid and H+

compromises neuronal integrity


Slide7 l.jpg

Cellular injury during ischemia - Inadequate energy supply

Ischemia ( O2,glucose)

ATP

Lactic acid

Depolarisation

Failed homeostatic

mechanisms

[H+]

[Na+] i

[K+] i

[Cl-] i

VCR

[Ca2+] i

Neurotransmitters

Free Fe2+

LCR

Glutamate

NA DA

Free radicals

Lipolysis

NO synthesis

Auto-oxidation

Arachidonic acid

Proteolysis

Glial injury

Free radicals

IRREVERSIBLE INJURY


Ischemia and brain injury l.jpg
Ischemia and brain injury

Prognosis in head injury has been strictly correlated with:

-the degree

-the duration of the ischemia

More than 90% of authopsies on HI pts showed ischemic

lesions of different severity

Graham D.I., Adams J.H. Ischemic brain damage in fatal head injuries. Lancet 1:265-266, 1971


Slide9 l.jpg

Vasospasm

Intracranial

hypertension

Arterial

hypotension

Posttraumatic cerebral ischemia

Focal tissue compression

from intracranial hematomas

Brain edema and

swelling


Slide10 l.jpg

CBF

ml/100g/min

Time course and CBF in head injury

50

.

.

.

45

.

40

.

.

.

.

.

.

35

30

Phase

I II III

25

Day

0 1 2 3 4 5 6 7 8 9 10 11 12 13

Martin NA, Patwardhan RV, et al: Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm. J Neurosurg 87: 9-19, 1997


Slide11 l.jpg

CBF

ml/100g/min

%

ischemia

Time course and CBF in head injury

.

.

40

40

.

.

.

.

30

35

.

.

.

20

30

10

25

.

20

0

6 12 18 24 30 36 42 48

hours after injury

Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 75: 685-693, 1991


Slide12 l.jpg

Motorscore

= 1,2

= 3,4,5

AJDO2

ml/100ml

9.0

Time course and CBF in head injury

.

8.0



.

7.0

.

6.0

.

.

5.0

.

4.0

3.0

hours



Bouma GJ, Muizelaar JP, Choi SC, et al: Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg 75: 685-693, 1991


Slide13 l.jpg

Time course and CBF in head injury

%

100

90

CBF

(ml/100g/min)

80

70

60

> 55

35 to 55

< 35

50

40

30

20

10

0

I II III

Phase

Martin NA, Patwardhan RV, et al: Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm. J Neurosurg 87: 9-19, 1997


Sequential activation of cerebrovascular responses l.jpg
SEQUENTIAL ACTIVATION OF CEREBROVASCULAR RESPONSES

Survival

CBF (ml/100g/m)

Ischemic threshold

Death

50

40

30

20

10

0 1 2 3 4 5 6 7 8 9 10 days post injury

Bullock MR et Al J. Neurotrauma 1996; 13; 643-5


Sequential activation of injury processes l.jpg
SEQUENTIAL ACTIVATION OF INJURY PROCESSES

ICP mechanisms

Cytotoxic edema

Vascular engoargement

Vasogenic edema

0 1 2 3 4 5 6 7 8 9 10 days post injury

Bullock MR et Al J. Neurotrauma 1996; 13; 643-5


Slide16 l.jpg

Time course of jugular venous desaturations

Gopinath SP: J Neurol,Neurosurg and Psy 1994; 57:717-723

%

desaturations

(SjO2 < 50%

for ten minutes or more)


Cbf and incidence of jugular venous desaturations l.jpg
CBF and incidence of jugular venous desaturations

Gopinath SP: J Neurol,Neurosurg and Psy 1994; 57:717-723

ml/100g/min


Oxygen and glucose metabolism after head injury l.jpg
Oxygen and glucose metabolism after head injury

100

50

0

%

Metabolicratio =

CMRO2/CMRglu

Bergsneider: J Neurosurg 86; 241-251, 1997


Slide19 l.jpg

Cerebral Blood Flow

  • 39.9 + 11.2 (Schroeder, 1995)

  • 42.5 + 15.8 (Mc Laughlin, 1996)

    • Vasoreactivity 0.4-9.1%

29.3 + 16.4

Mc Laughlin, 1996

Contusion

Perilesional edema

CT-normal tissue


Brain oxygen tension l.jpg
Brain oxygen tension

Van den Brink, Neurosurgery 46; 868-878, 2000


Glutamate l.jpg
Glutamate

Days after injury

mM

Yamamoto: Acta Neurochir S75: 31-34


Potassium l.jpg

Potassium

Potassium

  • Contusion

  • No contusion

mM

hours

Doppenber EMR: Determinants of cerebral extracellular potassium after severe human head injury. Acta Neurochir 1999; S75: 31-34


Framework of stroke l.jpg
Framework of stroke

Stroke

Infarction

85%

Hemorrhage

15%

Cerebrovascular

disease

80%

Intracerebral

Cardiogenic

embolism

15%

Subarachnoid

Other

unusual

5%


Slide24 l.jpg

Atherosclerosis and thrombus formation

Physiological subtypes of thrombotic-related ischemic stroke

Primary large vessel

occlusive disease

Embolism

-arterial atherothrombosis

-cardiogenic

atrial fibrillation

myocardial infarction/

mural thrombus

cardiomyopathy

prosthetic valves

-”paradoxical”

(deep vein thrombosis)

-atherothrombosis

-dissection

-arteritis

-migraine

-drug-induced

-etc

Thrombosis

Primary small vessel

occlusive disease

-”lacunar” (i.e. microatheroma/lipoyalinosis

-arteritis

-eclampsia

-drug-induced

-antiphospholipid antibodies

Rotthrock JF In Hemostasis and Thrombosis:

Philadelphia, JB Lippincott Company, 1994


Slide25 l.jpg

Atherosclerosis and thrombus formation

Oxydation of LDL cholesterol

Monocyte/Macrophage

Smooth muscle cells

Endothelial cells

Free radical release

Oxidize LDL cholesterol

Scavenger receptor

Cytotoxicity

Foam cell

formation

Promote endothelial

injury

Recruit monocytes

Inhibit macrophage egress

De Graba TJ in Barnett (eds): Stroke:Pathophysiology,

Diagnosis and Management - New York - Churchill Davidson, 1992


Slide26 l.jpg

Atherosclerosis and thrombus formation

Minimal endothelial injury

Role of Monocytes and T Lymphocytes

in the transformation to foam cells

Smooth muscle cell migration

and proliferation

Platelets adhesion


Slide27 l.jpg

Atherosclerosis and thrombus formation (2)

Plaque fissuring and Formation

of platelet thrombus

I - Platelets activation

II - Platelets adhesion

III - Activation of coagulation cascade

Thrombus formation


Slide28 l.jpg

Atherosclerosis and thrombus formation

Potential outcome of plaque fissuring

1)fibrotic organization

2)intraintimal and intraluminal thrombosis

3)occlusive thrombosis


Slide29 l.jpg

Evolution of

Cerebral Atherothrombosis

The ischemic penumbra


Slide30 l.jpg

Cerebral Embolism formation

I

II

III

Cardiac Sources


Any question from the floor l.jpg
Any question from the floor ?

  • Short !!

  • Easy to understand!!!

  • …and to be

    replied !!!!

Please


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