Neurology Seminar
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Transcript of Neurology Seminar
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Neurology Seminar
Cerebral Blood FlowCerebral Perfusion
Cerebral Metabolism
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Outline
Anatomy of the vascular system Arterial Venous
Physiology of the vascular system Cerebral blood flow Cerebral perfusion Cerebral metabolism
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Anatomy of the vascular systemOverview
Brain has two major arterial systems Carotid = cerebral hemispheres Vertebrobasilar = post fossa, occipital lobe, part
of the temporal lobe
Interconnections Circle of Willis
Surface of the neuraxsis= large circumferential arteries
Deep structures = smaller penetrating arteries and arterioles
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Anatomy of the vascular system
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Anatomy of the vascular system
Internal carotids in the cranium Carotid siphon Lies within the cavernous sinus Subarachnoid space->ophthalmic a. Ant. and middle cerebral a.
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Anatomy of the vascular system
Vertebral a. branch of subclavian a. Trans. cervical foramen Foramen magnum Frequent anatomic variation
Lt. vertebral a. directly from aorta Unequal caliber b/n the 2 vertebral a.
Ventrolateral surface of medulla Unite at pons->basilar a. Rt and Lt post cerebral a. at midbrain
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Anatomy of the vascular system
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Anatomy of the vascular systemCircle of Willis
At the base of the brain Surrounds the optic chiasm and pit.
stalk Frequent anatomic variations 50%
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Anatomy of the vascular system
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Anatomy of the vascular systemBlood supply of cerebral hemispheres
Anterior cerebral a. Medial surface of cerebrum Superior border of frontal and
parietal lobe Middle cerebral a.
Most of the lateral surface of cerebral h.
Lateral frontal lobe Sup and lat temporal lobe Deep structures of frontal and
parietal lobe Posterior cerebral a.
Occipital lobe Inferior and medial temporal lobe
Penetrating branches of big a supplydeeper struct.
Lenticulostriate a. of MCA for BG andInt. cap
Perforating br of PCA for thalamus
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Anatomy of the vascular systemAnastomoses and collateral circulation
Circle of Willis Corticomeningeal anastomoses
The 3 major a. on the surface of hemis. b/n extra and intracranial a.
Ophthalmic a. of internal carotid with superficial temporal and facial branch of ext. carotid at face region.
Ext carotid and vertebral a. at the neck
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Anatomy of the vascular systemBlood supply of posterior fossa
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Neurologic signs
Carotid system Hemiparesis
(contralateral body and face) Hemisensory loss
(contralateral body and face)
Homonymous hemianopia
Monocular visual loss Aphasia
Vertebrobasilar Hemiparesis
(contralateral body, ipsilateral face)
Hemisensory loss (contralateral body, ipsilateral face)
Diplopia Dysphagia Dysarthria Dysequilibrium
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Anatomy of the vascular systemVenous system
Superficial and deep system SSS
Superficial v. of sup half of brain Lateral Sinus
Inferior half Deep system (great v. of Galen and inferior sagittal and strait sinus)
Deep white matter & deep brain nuclei Cavernous sinus
Inferior cerebral surface Carotid a., cranial n.,
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Anatomy of the vascular systemVenous system
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Anatomy of the vascular systemVenous system
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Physiology of the vascular system
Cerebral Blood Flow (CBF) Amount of blood that enters the brain. Brain is 2% of body weight About 10% of the intra cranial space About 15% of Cardiac output 50 ml Bl. per 100 gm of brain tissue/min 750 ml/ min About 20% of Ox used at basal state Total Ox used 50ml/min, 3.7ml/100gm There is an oxygen metabolic reserve of only
8-10 seconds
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Physiology of the vascular system
Cortical gray matter has 6X bl. flow than the white matter due to metab.demand
CBF is tightly regulated and maintained within narrow limits
too little blood causes ischemia, results if blood flow to the brain is below 18
to 20 ml per 100 g per minute, tissue death occurs if flow dips below 8
to 10 ml per 100 g per minute Too much blood can raise ICP
CBF > 55 to 60 ml per 100 g per minute
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Physiology of the vascular system
Cerebral Perfusion Pressure (CPP) net pressure of blood flow to the brainCPP = MAP − ICP NL b/n 70-90 mmHg in an adult human, Below 70 mmHg for a sustained period
causes ischemic brain damage Children have pressure of at least 60
mmHg
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Physiology of the vascular system
Autoregulation Physiologic response where by CBF
remains constant and brain maintains proper CPP over a wide range of Blood pressures variations.
to lower pressure, arterioles dilate, and to raise pressure they constrict.
At their most constricted, pressure of 150 mmHg,
At their most dilated the pressure is 60 mmHg.
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Physiology of the vascular system
Autoregulation When pressures are outside 50 to 150
mmHg, the blood vessels' ability to autoregulate pressure through dilation and constriction is lost, and cerebral perfusion is determined by blood pressure alone,
pressure-passive flow
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Physiology of the vascular system
Factors affecting CBF (the ff equation)=Mean arterial pressure - central venous pressure
Cerebro-vascular resistance
Extra cerebral Systemic BP CV function Blood Viscosity
Intra cerebral Cerebral vasculature CSF pressure Auto regulatory mechanisms
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Physiology of the vascular system
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Physiology of the vascular system
Regulation of CBF Metabolic regulation Auto regulation Chemical factors Neurogenic factors
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Physiology of the vascular system
Metabolic regulation CBF is coupled directly to neuronal
metabolic activity Occurs with short latency of 1-2 sec. Strictly regional effect Little effect on the total blood flow E.g.. Sleep, coma, seizure Vasodilator substances
Adenosine, K+, H+, prostaglandin, free radicals, NO
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Physiology of the vascular system
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Physiology of the vascular system
Auto regulation The ability of brain to maintain its blood
flow constant for all but the widest extremes in perfusion pressure
MAP 60-150 mmHg Primarily pressure controlled myogenic
mechanism that operates independently but synergistically with other neurogenic and chemical metabolic mechanism.
Both small and large arterioles Major homeostatic and protective
mechanism.
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Physiology of the vascular system
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Physiology of the vascular system
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Physiology of the vascular systemRegional increase in metabolism
CO2
Local vasodilatationIncreased blood flow
Accommodate metabolic demand
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Physiology of the vascular systemRegional ischemia (occlusive disease)
Intra Luminal pressure
oxygen CO2
lactate Acidotic tissue
Vasodilatation of nearby vessels
Increase blood flow to the area of ischemia
Reduce size of infarct
Reduced cerebro-vascular resistance (infarct zone)
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Physiology of the vascular systemReduced cerebro-vascular resistance
Little change in CVP
Major determinant of BF to the region
of ischemia will be MAP
Proper maintenance of SBP in Mx of
ischemic stroke
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Physiology of the vascular system
Chemical factors Strong influence on CBF Mech= sm ms, NT, pH CO2 readily crosses BBB end product of
cerebral metabolism PaCO2= Vasodilatation & CBF PaO2= Vasodilatation & CBF pH= Vasodilatation & CBF
Lactic acid is a potent vasodilator
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Physiology of the vascular system
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Physiology of the vascular system
Neurogenic control Not as strong as the chem. And metab. Composed of
Extrinsic control Intrinsic control Local components
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Physiology of the vascular system
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Cerebral Metabolism High metabolic activity & high O2 consumption Energy dependant processes
Membrane potential Maintainace of trans-membrane ion gradient Membrane transport Synthesis of cellular constituents
Prot, Nucleic acid, Lipids, NT Energy supplied by high energy phosphate
bond (ATP), synthesized in brain. Glycolytic pathway Krebs cycle 38 moles of ATP/ mole of glucose Respiratory chain (aerobic)
Anaerobic 2 ATP Creatine Phosphate from ADP glycogen
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Cerebral Metabolism
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Cerebral Metabolism, ischemic cascade
in CBF -> in glucose and Ox. Less impaired function at the periphery
Local auto regulatory mech, response to chemical & metab changes is lost
Anaerobic glycolysis Fall in glycogen and pH Rise in lactate Zone of increased perfusion in the
periphery of ischemic zone
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Cerebral Metabolism, ischemic cascade
Substrate depletion->mitoch. failure Leakage of K from cells IC Na, Cl, Ca, free fatty acids Neuronal depolarization
Loss of trans membrane potentialincrease in tissue waterImpaired ATP dependent NT uptake
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Cerebral Metabolism, ischemic cascade
release of excitatory NT glutamate which activates NMDA and AMPA receptors permeability to Na ions Cellular swelling and lysis Massive entry of Ca into post synaptic
neurons ->more release of excitatory NT
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Cerebral Metabolism, ischemic cascade
IC Ca-> activates Phospholipases Protease membrane Endonuclease mitoch. DNA cell Ox free radical microtubular damage
death Nitric oxide
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Ischemic Penumbra
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Ischemic Neuronal Injury (cascade)
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Ischemic Neuronal Injury (cascade)
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Incomplete Ischemia
Local accumulation of AdenosinePotassium
Hydrogen Ion
Lactic acid accumulation
Vasodilatation
Restoration of blood supply
Complete Ischemia
Cell swelling
Infarction
Affection of BBB
Water content of Brain tissue Increases
BRAIN EDEMA
Scavenger cells
Cystic cavity
Enough glucose
Hypoxia
Enough glucose
Lesser degree ofanoxic change
Hypoglycemia
Adequate Ox
Energy maintained By creatinine Phos.
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GENERAL MANAGEMENT Resuscitation – Ox and BP Urgent situations - elevated ICP, (GCS)<8 Monitoring and the decision to treat - ICP <20 mmHg
and CPP between 60 and 75 mmHg Fluid management - avoiding all free water Sedation decrease ICP by reducing metabolic demand, ventilator
asynchrony, venous congestion, and the sympathetic responses of hypertension and tachycardia
Blood pressure control when CPP >120 mmHg and ICP >20 Position 30o to decrease venous outflow Fever Antiepileptic therapy
SPECIFIC THERAPIES Mannitol Corticosteroids (Corticosteroid Randomization After Significant Head
injury) trial enrolled 10,008 Hyperventilation 1 mmHg change in PaCO2 = 3 percent change
in CBF, short-lived (1 to 24 hours) Barbiturates reduce brain metabolism & cerebral blood flow Therapeutic hypothermia Removal of CSF 1 to 2 mL/minute, for two to three minutes at a time Decompressive craniectomy