ANATOMY AND

NEUROPHYSIOLOGY OF
THE BRAIN
Dr Muh Ramli,
Department of Anesthesiology University of
Hasasnuddin
Makassar INDONESIA

OTAK MANUSIA
OTAK MANUSIA
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Seberat + 1 kg
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tangan
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HARTA KARUN YANG BESAR

RAKSASA TIDUR
ANUGERAH YG PALING BERHARGA DARI TUHAN

Normal brain

Normal Brain and Scalp

CEREBRAL VEINS

CT SCAN

Anterior cerebral
arteries
ACoA
Middle cerebral
artery

A1

Internal carotid
arteries

PCoA

P2

P1

basilar artery

Vertebral artery

NEUROPHYSILOGIS
C

BF
ICP
CMR O2
BBB

( Cerebral blood Flow )

( Intra cerebral Pressure )
( Cerebral Metabolism Rate )
( Blood Brain Barrier )

CEREBRAL BLOOD

Varies

FLOW

with metabolic activity

Regional CBF 10 300 ml / 100 g / min
Total CBF averages 50 ml / 100 g / min
< 20 25 ml/100 g/min cerebral
impairment
< 10 ml/100 g/min Irreversible brain
damage
Total

CBF averages 750 ml / min

( 15 20 % CO )

Physiology

Cerebral Blood Flow

Mean

CBF~50 mL/100g/m
Coupled to CMRO2{~3.5
mL/100g/m}
CBF = CPP/CVR
Autoregulated bet CPP 50-150
mmHg

CEREBRAL BLOOD FLOW

CBF = CPP / SVR
CPP = MAP - ICP

REGULATION OF CBF
A.
B.
C.

CEREBRAL PERFUSION PRESSURE

AUTOREGULATION
EXTRINSIC MECHANISM
1.
2.
3.
4.

Respiratory Gas tension

Temperature
Viscosity
Autonomic influences

CBF (mL/ 100 g/ min)

Cerebral Blood Flow (CBF)

50

60

120

160

200

MAP (mmHg)

Cerebral autoregulation curve

Cerebral Blood Flow (CBF)

Relationship between CBF and arterial respiratory gas tensions

CBF (mL/ 100 g/ min)

125
PaCO2
75
PaO2
25
0
25

75
125
Partial pressure (mmHg)

175

Cerebral Perfusion Pressure

CPP = MAP ICP
( Mean Arterial Pressure Intracranial Pressure )
CPP normally 80- 100 mmHg
CPP primarily dependent on MAP because ICP
normally less than 10 mmHg
Increases ICP ( > 30 mmHg ) can
compromise CPP and CBF even in normal MAP
CPP < 50 mmHg slowing EEG
CPP 25 50 mmHg flat EEG
CPP < 25 mmHg irreversible brain damage

Physiology

Cerebral Perfusion Pressure

Pressure

that drives blood to the brain

CPP = MAP ICP
Normal is ~80-100 mmHg

Physiology

Monroe-Kellie doctrine
Changes

in any of the brain

component may necessitate
compensatory changes in volume of
one or more of these components so
as to maintain a constant ICP

Autoregulation

CBF remain constant between MAP 60 160

mmHg
Cerebral vasculature rapidly ( 10 60 sec )
adapts to change in CPP
CPP vasodilatation
CPP vasoconstriction

2 mechanisms to explain cerebral autoregulation

1. Myogenic mechanism
intrinsic response of smooth muscle cells in cerebral
arterioles to changes in MAP
2. Metabolic mechanism

cerebral metabolic demands determine arteriolar tone

tissue demand release tissue metabolites vasodilatation
and increase flow
ion H+, NO, adenosine, prostaglandins may play a role

Cerebral autoregulation

Physiology

Pressure volume curve

Cerebral autoregulation

Extrinsic Mechanism
1. Respiratory Gas Tension
The most important is PaCO2
Acute

change PaCO2 affect CBF

CBF directly proportionate to PaCO 2 20 80 mmHg
CBF changes 12 mL/100g/min per mmHg change
PaCO2
Marked hyperventilation ( PaCO 2 < 20 mmHg )
shift oxy-hemoglobin dissociation curve to the left

Only marked changes in PaO2 alter CBF

Severe

hypoxemia ( PaO2 < 50 mmHg ) increases CBF

. Extrinsic Mechanism
2. Temperature

CBF changes 5 7 % per oC

Hypothermia CMR and CBF
> 42 oC O2 activity cell damage

3. Viscosity

hematocrit viscosity improve CBF, but can

potentially impair O2 delivery
Optimal cerebral O2 delivery occur at Hct 30 34 %

4. Autonomic Influences

Intracranial vessel innervated by sympathetic

( vasoconstrictive ), parasympathetic ( vasodilatory ), and
noncholinergic nonadrenergic fibers
Especially innervation large cerebral vessels by
sympathetic fiber. Increses sympathetic stimulation
limit CBF

Modulation of the autoregulatory range

from Textbook of Neuroanesthesia, 1997

Arteriolar diameter and cerebrovascular resistance in

the regulation of CBF during changes in CPP
From Textbook of Neuroanesthesia, 1997

CARBON DIOXIDE
Inhalation of 5% CO2

50% CBF

Inhalation of 7% CO2

100% CBF

The influence of blood pressure on the CBF

response to PaCO2

The influence of PaCO2 on pressure

autoregulation of CBF
From Young & Ornstein, 1994

CO2 and the Cerebral Circulation

Anesthesiology 88, 1998

CO2 and the Cerebral Circulation

Anesthesiology 88, 1998

CO2 and the Cerebral Circulation

Anesthesiology 88, 1998

CO2 and the Cerebral Circulation

Anesthesiology 88, 1998

Changes in CBF as function of arterial carbon

dioxide tension and oxygen tension.

The relationship of CBF to perfusion pressure,

PaCO2, and PaO2.
Michenfelder

Physiology

Factors affecting autoregulation

pH
PaCO2
PaO2
Chronic

HT
SNS activity
Low pH causes vasodilatation
High pH causes vasoconstriction

CBF, CPP, PaCO2 and PaO2

Cerebral Metabolism

Neuronal
electrical
activity

Cellular
integrity

60%
40%
Normal brain oxygen requirement

CEREBRAL METABOLISM
Brain responsible for 20% of total body
oxygen consumption
Cerebral Metabolic Rate ( CMR ) usually
expressed in terms of Oxygen Consumption
( CMRO2 ) 3 3,8 ml/100gr/min
Brain is High Oxygen Consumption ,

interruption in 10 seconds ( O2 tension rapidly drops

below 30 mmHg ) Unconsciousness
If Blood Flow not reestablished within 3 8 min
ATP stores depleted Irreversible cell injury
Hippocampus and cerebellum most sensitive to
hypoxic

Cerebral Metabolism
Glucose as primary energy source
Brain glucose consumption:
5 mg/100g/min over 90% metabolized
aerobically
CMRO2 parallels with glucose consumption
Acute hypoglycemia as devastating
hypoxia
Hyperglycemia accelerating cerebral
acidosis and cellular injury exacerbated
global hypoxic brain injury

Oxidative and Non-oxidative

Pathway

BLOOD-BRAIN BARRIER

Unique blood vessels that the

junction between vascular
endothelial cells nearly fused
Paucity of pores is responsible
for term BBB
This lipid barrier :
allow CO2, O2, lipid-soluble
substances ( most anesthetics )
enter the brain freely
Penetrate poorly ions, proteins,
large substance ( mannitol )
penetrate poorly

Continuous vs Fenestrate
Capillary

Continuous capillary
Specialized continuous capillary
throughout most CNS bound
together by tight junction
Cytoplasmic extension of
astrocyte end in expanded feet
wrap around capillaries

Fenestrate capillary
Are capillaries that contain
windows , or pores, that span
the endotelial lining, permits
rapid exchange of water and
large solute

BLOOD-BRAIN BARRIER

Endothelial cells of capillaries

in the brain are different to
peripheral tissues :

Brain endothelial cells are joined

by tight junctions of high
electrical resistance providing an
effective barrier against
molecules.
There is no such movement in
brain endothelial cells.
Brain capillaries are in contact
with foot processes of astrocytes
which essentially separate the
capillaries from the neurones.

BLOOD-BRAIN BARRIER
Blood-brain

by

barrier may be disrupted

Severe hypertension
Tumors
Trauma
Strokes
Infection
Marked hypercapnia
Hypoxia
Seizure activity

Cerebrospinal Fluid

Cerebrospinal Fluid
Dynamic
Major function to protect CNS against

trauma
Found in cerebral ventricles and cisterns
and subarachnoid spaces
Formed by choroid plexuses of the
cerebral ventricles ( mainly lateral )
CSF production about 21 ml/hr ( 500
ml/day ) but total CSF volume about 150
ml