CNS Flashcards
CNs made up of?
Brain(Cerebrum,cerebellum,brainstem and spinal cord)
Functions of CNS
Patterns of action potentials encode information leading to:
1.Sensory perception
2.Information processing, 3.integration, & storage
Motor and Behavior
Required terms
White matter: High density of myelin covering axon pathways (and very few neurons)
Gray matter: High density of neurons and dendrites (Axons also present).
Nucleus: cluster of neurons within the CNS
Ganglion: cluster of neurons outside the CNS
Cortex: dense layers of neurons
Tract: axons within the CNS traveling as a group/usually named based on region of origin & termination (i.e. spinocerebellar tract)
Pathway: similar to tract however it relates more to synaptically connected neurons performing a function
grey matter externally,white matter internally
Cytology of the CNS
Neuron…cell to cell communication or signaling
Neuroglia….
CNS
Astrocytes…maintain extracellular environment…buffer…glutamate
Oligodendroglia…myelin sheaths
Microglia (latent phagocytes)…..removing infectious agents
Ependymal cells (line ventricles/CSF production)
PNS
Schwann cells
Satellite cells…similar to astrocytes
BAsic functional unit of the neuron
Dendrite,cell body,axon,synapses,spinal cord,
What does Excitatory synapses focus on dendrites or Axon?
Dendrites
Axonal dendritic communications
What does Inhibitory synapses focus on dendrites or Axon?
Axosomal communication
Contents of the Axon Hilux is
High density of sodium Chanel that moves in 1 direction after Excitation(its activated a refractory phase)…greatest probability of generating an action potential
Characteristics of Uni-polar cell type
invertebrates have these.
axon and a dendrite coming out as a sngular process
Characteristics of pseudo-uni-polar cell type
Primary sensory neurons.
cell body,axon and bifurcates to receive sensory inputs and the other end to spinal cord
Characteristics of bipolar cell type
Sensory organs to the eyes, dendritic sites at the and
internurones
middleman
Characteristics of Multi-polar cell type
cell body and 2 ends of dendrite sites
Axonal Transports
powered by ATP:
Kinesin: anterograde Dynein: retrograde
Motor Neurone-axon to the toe.
.presynaptic terminal relies on generation of protein in the cell body…
active axonal transport allow for energy and ca use for movement of substance from soma to the axon and synaptic terminal
Micro filament and neuro filament
Atp and calcium used by protein for transport..
A lot Atp calcium dependent….
Kinesin…antegrade…to the presynaptic region
Dynein..retrograde..from the presynaptic neurone
expensive
lysosomal degradation as an example.
Neuroglia components
Astrocytes --projection everywhere. Epindymal cells….produce csf… Astrocytes may regulate csf production since its connected to Epindymal cells Can pick up potassium ions Management of glutamate concentration
Oligodendrocyte…produces myelin
AP
they are the same size,needs frequency altered to be able to use more or less
Myelination
produced by Oligodencrocytes
Greater conduction velocity
Increases the effective membrane resistance (length constant)
Decreases the capacitance
Restricts action potential generation to the Nodes of Ranvier
Nodes are rich in sodium and potassium channels
+ and – forces attract each other ,blocks the charges from seeing each other so capacitance is decreased.
Ap regeneration does not need to happen throughout the axonal length.
Minimize Atp,conduction at nodes of Ranvier
Myelination benefits
Fast reflexes
“Complex mental processing”
Metabolic Advantage
Types of fibres
A fibers (myelinated) 1 to 22 microns Subdivided into: α β γ δ in order of decreasing
B fibers (myelinated) 1 to 3 micrometers C fibers (unmyelinated fibers) 0.1 to 2.5 micrometers
Peripheral nerve fibres and thier reactions
A-alpha fibers: motor & proprioception
A-beta fibers: motor, touch, pressure
A- gamma fibers: motor/muscle tone (muscle spindle)
A-delta fibers: pain, temperature,touch
B-fibers: PREganglionic autonomic
C- fibers: dull pain, temperature, touch, POSTganglionic autonomic– NO MYELIN
Synaptic Signaling
-Classic Neuron-Neuron Junction
Electrical ..found in brain astrocytes neurons,fast signal transmission
Gap Junctions(cell to cell communication through open channels) -Chemical
Neurotransmitter mediated
-Neuron-Glial(neurons and astrocytes)
-Extra-synaptic – we now know NT released at a synapse can have actions at locations distal to the original synapse.
Receptors outside synapse
Electrical synapses/Gap junctions
found in brain astrocytes neurons,fast signal transmission
Low-resistance pathway between cells that allows current to flow directly from one cell to another
Allows the exchange of small molecules between cells.
Fast & bidirectional
Synchronization of network activity/Electronically coupled neurons
Gap junctions regulated by voltage, intracellular pH, Ca++, and G protein—coupled receptors
Chemical synapsis
ACh—nicotinic(NMJ)
Nicotinic(GAnglia site)
Neuropeptide
Neuropeptides. In Neuron dense vesicles…co released with something else
Gaseous transmitter
nitric oxide…Direct transmission.
Characteristics of a neurotransmitter
Criteria
Present in presynaptic terminal
Cell must be able to synthesize the substance
Released upon depolarization of presynaptic membrane
Specific receptor on the postsynaptic membrane (+/- extrasynaptic locations) to respond to it
Differencies between peptide and non peptide neuro transmitters
Non peptide or classic neurotransmitter/Peptide transmitter.
Synthesized and packaged in the nerve terminal/Synthesized and packaged in the cell body; transported to the nerve terminal by fast axonal transport
Synthesized in active form/Active peptide formed when it is cleaved from a much larger polypeptide that contains several neuropeptides
Usually present in small, clear vesicles/Usually present in large, electron-dense vesicles
Released into a synaptic cleft/May be released some distance from the postsynaptic cell
There may be no well-defined synaptic structure
Action of many terminated because of uptake by presynaptic terminals via Na+-powered active transport/Action terminated by proteolysis or by the peptide diffusing away
Typically, action has short latency and short duration (msec)/Action may have long latency and may persist for many seconds
Classic neurotransmitters examples(small molecules)
Class I Acetylcholinexx Class II: Biogenic Amines Norepinephrine xx Epinephrine Dopamine Serotonin Histamine Class III: Amino Acids Gamma-aminobutyric acid (GABA) Glycine…inhibitory….spine Glutamate….excitate…brain Aspartate
Classes of neuro peptides and peptide transmitters
- Hypothalamic-releasing hormones…Luteinizing hormone
- Pituitary peptides
- Peptides that act on gut and brain…Substance P…increase the number of pain signal coming to brain .opiod will reduce that signal.
- Other tissues…
Examples Gaseous Neurotransmitters
Are NOT released from “vesicles”
Nitric oxide (NO)(Blood vessels and in the Brain)
Carbon monoxide
Nmda stimulate NO production(Brain)…….Ca from NMDA…calmodulin….activates endothelial nitric oxide synthase which promotes…arginine to convert into….NO
Cerebral vessel tone influenced
Glutamate Activity
major excitatory….
Brought into the vesicle by Vglut…..
Glutamatergic neuron stimulated by AP…
after VGCC opens and releases calcium.
..
Glutamate released and stimulates a lot of other receptors
Ligand gated ion channels(NMDA,AMPA, Kainate and gprotein coupled receptors
Metabotropic glutamate receptors.
Glutamate levels are controlled by EAAT1,2,3,4,5(Excitatory Amino Acid transporters)
Excitotoxicity happens because we have glutamate hanging around for too long ..
Major TBI release glutamate into the brain and stimulate glutamate receptors to release calcium too much calcium may cause Apoptosis.
Astrocytes(express these transporters EAAT 1 and 2 that take up glutamate and they contain an enzyme called glutamine synthase which convert glutamate to glutamine that is not active at glutamate receptors.
Glutamine can be excreted from cell and taken back up by presynaptic terminals and in the presynaptic terminal there is an enzyme glutaminase which will convert glutamine back to glutamate.
Post-synaptic responses to neurotransmitter
EPSP (or IPSP) occurs when neurotransmitter binds to a post-synaptic receptor
ligand gated ion channel (“fast” transmission)
G-protein coupled receptor (“slow” transmission)
Gaba is main Inhibitory
EPSP…depolarize…….Glutamate NeurotransmitTer(AMpA receptor)…..passess …na and will depolarise
IPSP…
hyperpolarize…….Gaba NT(Gaba receptor) ..passes chloride for increase chloride conductance which then comes in and hyper polarize the cell and cause IPSP
between excitation and inhibitory, the one the happens depends on the membrane potential
the nernst potential of the ions involved..
EPSP excitatory response
Increased Na+ influx
Decreased Cl- influx or K+ efflux
Change in receptor expression or enzymatic/metabolic activity (delayed effect)
potassium channel closes or potassium stays in the cell.
IPSP inhibitory response
Increased Cl- influx or K+ efflux
pre-synaptic
post-synaptic
Change in receptor expression or enzymatic/metabolic activity (delayed effect)
in IPSP 1 synapse chnahges membrane potential by how much
*Each EPSP changes membrane potential by 0.5-1mV at most for <15ms.
What magnitude of change is generally required to reach threshold?
so we need multiple synapse to reach threshold easily by multiple firing
must be done with 15Ms
Spatial and Temporal Summation is Required to Reach the Threshold Potential
It is the sum total of all synaptic activity that determines if threshold is reached and and if an action potential is triggered
Facilitation (sub-threshold stimulation)
Function of reverbatory circuit
used for short term memory
Most synaptic events occur at the ?
Dendrites.
Majority of Synapses are dendritic.
ALkalosis and acidosis does what to neuronal excitability
Alkalosis greatly increases neuronal excitability
Acidosis greatly depresses neuronal activity;
What does Hypoxia do to neuronal excitability
Decreases.
Drugs can increase or decrease excitability.T or F
T
Cerebral cortex
Cranial nerve 1 Fine tune lower brain functions Sensory perception Cognition Learning Large “memory storehouse” Motor planning & voluntary movement Language Essential for “higher level thought”
2 hemispherer connected by the Corpus Colusum
Fontal lobe
Planning and carrying out motor behavior (motor, premotor, cingulate motor, and supplementary motor areas, frontal eye field)
Speech (Broca’s area, inferior frontal gyrus of the dominant hemisphere)
“Intellectual activities”
Personality and emotional behavior (rostral frontal lobe)
MOTOR
Broca’s area
Parietal Lobe
Sensory perception and processing (somatosensory cortex/parietal association cortex)
Projections to the frontal lobe carrying somatosensory information modulates voluntary motor behavior
Parietal association cortex processes visual information from the occipital lobe and then sends projections to the frontal lobe to influence motor behavior.
In dominant hemisphere sends somatosensory information to Wernicke’s area.
Establishment of spatial context (non-dominant hemisphere)
Occipital LoBe
Visual perception and processing
Projections to the frontal eye fields influence motor behavior of the eyes
Projection to the midbrain modulates convergent eye movements, pupillary constriction, and accommodation.
Temporal lobe
Processing and perception of sound and vestibular information.
Higher-order visual processing (i.e. facial recognition)
Optic pathways transverse the temporal lobe.
A portion of Wernicke’s area (posterior region of the temporal lobe).
Emotional behavior (medial temporal lobe: limbic system)
Autonomic nervous system regulation (medial temporal lobe)
Learning and memory (hippocampus).
Somatosensory Cortex feature,primary motor cortex.
density of receptors and its specifically organised to the regions of the body
Premotor area features
coordination of multiple muscle group ….high conc of mirror neurons…learning a motor task…learning things from watching someone perform a motor movement
Cerebellum features
Associated nerves: Cranial nerve VIII
Primary functions:
Coordination & Equilibrium
(somatosensory input from spinal cord, cerebral cortex, vestibular organs inner ear)
Sensory association/language
Essential for complex highly coordinated muscular movements (playing tennis, talking, typing, etc.)
Sequencing of motor movement
Makes corrective adjustments to movement in real time based on continuous sensory information from the periphery
Motor learning/muscle memory “learns from its mistakes”
Balancing antagonististic muscle group
Adjust muscle tone
Fine tune movements
Receives input from spinal cord
Basal Ganglia features
Primary functions:
Influences thalamocortical motor inhibition
Control of fine motor movements and relative intensity, direction, and sequencing of complex movement patterns
Includes the striatum, globus pallidus, substantia nigra, & subthalamic nucleus
No input from the spinal cord, but does receive direct input from the cerebral cortex via the thalamus.
Lesions produce abnormal movement and posture.
The brainstem
Medulla,pons,midbrain
Associated Nerves: 12 cranial nerves
Primary functions:
Sensation from & motor control of the head neck & face
Input of several special senses (hearing, balance & taste)
Mediate ANS functions (cardiac output, BP, peristalsis of the gut, & pupillary constriction)
Conduit of ascending and descending pathways that carry sensory and motor information to other areas in the CNS
Reticular formation receives a summary of much of the information that enters the spinal cord and brain stem, filters information (excludes irrelevant stimuli) & regulates arousal
Medulla
Associated nerves: Cranial nerves VIII-XII
Primary functions:
Subconscious CV & respiratory control
Early relay nuclei in auditory, balance/equilibrium, gustation, head and neck control input
Brainstem reflexes
Pons
Associated nerves: Cranial nerves V-VIII Primary functions: Respiratory control Urinary control Motor control of the eye Sensation and motor control of the face Ventral: Pontine nuclei relay movement and sensation info from cortex to cerebellum Dorsal: Taste & Sleep
Midbrain
Associated nerves: Cranial nerves III-IV
Primary functions:
Acoustic relay & mapping
Eye movement, lens & pupillary reflexes
Pain modulation
Contains nuclei and relay pathways critical for motor coordination (i.e. substantia nigra)
Thalamus
Associated nerves: Cranial Nerve II
Primary functions:
Sensory & motor relay/coordination between cerebral hemispheres and lower CNS regions
Sensory modulation and gating
Regulation of cortical activation (attention & consciousness)
Visual input
Need a functional thalamus to get to a higher level brain function
Hypothallamus
Associated nerves: Cranial Nerve II
Primary functions:
Sensory & motor relay/coordination between cerebral hemispheres and lower CNS regions
Sensory modulation and gating
Regulation of cortical activation (attention & consciousness)
Visual input
Drive to eat and drive to do things for reward.
Amygdala and hypocampus
Amygdala primary function:
Social behavior and expression of emotion
Hippocampus primary functions:
Memory
Spinal cord Consist of?
Associated Nerves: Dorsal ....Sensory Ventral ...Motor Primary Functions: Sensory input Reflex circuits Somatic and autonomic motor output
Whats the work of the sensory receptors
Transduce changes in environmental energy into electronic signals
How do sensory receptors send the environmental enery received to the brain and spinal cord
Via action potential
Where are the primary afferent neuron cell bodies housed
Dorsal root
crainial nerve ganglia
Features of the of primary afferent neuron cell body
a peripheral process that extends distally within a peripheral nerve to appropriate sensory receptors & (2) a central process that enters the spinal cord/brain through a dorsal root or a cranial nerve
Dermatomes are determined by?
Embryonic development
Groups of Info from the environment is grouped as follows.
Exteroceptive information: interaction of the skin with the environment
Fine discriminatory touch …mechanoreceptors
Pain and temperature…pain receptors/thermal receptors
Proprioceptive information: body and limb position informing movement…receptors located in our joints .muscle and tendons..
Enteroceptive information:From different organs in our body.. internal status of the body
In all receptor instances,ehats the common underlying fact that is happening
Permeability of membrane to ions is changed in all instances by the receptors
Sensory Transduction: Receptor Activation
Mechanical (Mechanoreceptor) Chemical (Chemoreceptor) Thermal (Thermoreceptors) Pain (nociceptors) Electromagnetic (detect photons) lights hitting the eyes. Etc.
Sensory receptors adapt but pain do not adapt…T/F
T
Ways to change memebrane potential by Receptors
(1) by mechanical deformation (2) by chemical activation (3) by alterations in temperature (4) by the effects of electromagnetic radiation
3 major types of mechanosensitive Afferent fibres
Tactile fibers Fast (FA)
FAI….adapts fast but
able to pinpoint where stimulus is coming from.
or Slow Adaptation (SA)..they continue to fire as long as stimulus is there.(SA1) continue to fire as long as stimulus is there but small receptive field
Type I fibers: small receptive field..tell what exact point with a pin prick
Higher density type I fibers= better two point discrimination
small receptor field
Type II fibers: large receptive field ..tell something stuck ur finger but not specific spot
How does receptor density affect info received
More receptors u have more clarity of image and information and info received.
Stimulus Intensity VS Receptor Potential graph
Low stimulation ..u can tell the diff be heavy and light stimuli.
Mild stim we will tell discrete difference
When signal strength is high we will have the ability to diff pressure at the top range
there is no maxing out
IN a Linear relationship between Stimulus Intensity VS Receptor Potential graph what will happen
There will be a maxing out and pain and thermal receptors are linear and they max out.
How do we perceive stimulus
Spatial summation
-Multiple receptors firing in a small area at the same time and this depends on receptor density.
Temporal Summation
….how often does a fibre fire…
Stimulus interpretation requires sensory coding
Sensory modality
Touch, pressure, flutter, vibration, cold, hot, pain, etc.
Taste, smell, position, vision, etc.
Spatial location
Population of neurons within a receptive field
Stimulus intensity
Frequency of AP, # of sensory receptors involved
Stimulus frequency
Temporal and spatial sumation
Interstimulus interval
Stimulus duration
Explain the labeled line principle
Each nerve tract terminates at a specific point in the CNS and carries a selective sensory modality (i.e. low-threshold mechanoreceptors VS pain)
Sensation is perceived when a specific stimulated nerve leads to specific areas in the CNS (i.e. “separate dedicated cell populations in the thalamus and somatosensory cortex”)
Alteration of the specific nerve tracts activity will only change the intensity of the stimulus (quantitative)amount of pressure felt will b changed. VS changing the type of stimulus perceived (i.e. qualitative)
For example the sensation of pressure will change in intensity but it will not “turn into” the sensation of pain ( a different set of afferents will carry the nociceptive afferents).
Sensory info is carried by 2 alternative pathways namely?
- Dorsal column- Medial Lemniscal
2. Anterolateral System
Dorsal Column-Medial Lemniscal features
Highly Localized Touch sensations
Touch sensations (fine gradations of intensity)
Phasic sensations (vibratory)
Skin contact sensation
Joint position
Pressure sensations (fine gradations of intensity)
Composed of large myelinated fibers transmit
signals at rate of 30-110 m/sec
More spatial orientation
mechanofibres
Anterolateral system
features
Pain Thermal sensations (warm/cold)
Crude touch and pressure
Tickle & itch
Sexual sensations
Composed of smaller myelinated fibers that transmit signals at a rate of 40m/sec
Less spatial orientation
Dorsal Column Medial Lemniscal Pathway action
Transmits signals upward to the medulla via the dorsal columns of the spinal cord in somatotopic fashion. Signals synapse synapse in dorsal column nuclei Nucleus gracilis (lower body/leg) Nucleus cuneatus (upper body/arm) 2nd order neuron axons (internal arcuate fibers) then cross to the opposite side of the medulla and project to the thalamus (3rd order neurons) via the medial lemniscus (pons, midbrain).
The ANterolateral System
Spinothalamic
Enters the spinal cord from the dorsal spinal nerve roots, immediately synapses in the dorsal horns
Cross to the contralateral cord
Travel upward through the anterior and lateral white columns
Tracts terminate at all levels of the lower brain stem and in the thalamus
Spinocerebellar Proprioceptive Pathway
Perception of position, conscious awareness of body movements & local reflexes
These pathways carry both cutaneous and proprioceptive information to cerebellum and cerebral cortex
Central pain pathways
Aδ (fast, well localized pain) & C fibers (slow, dull, less localized) synapse in the gray matter of the dorsal horn of the spinal cord
Aδ at lamina I, V, and X
C at lamina I, and II
Central pain pathways
Spinothalamic
Spinoreticular
Spinomesencephalic
Mechanism of Action of Moro Neurons
Function is Dependent on Intact Efferent Cellular Circuits.
Behavior (reflective & voluntary muscle movement or glandular secretion) is triggered by central neurons which activate motor neurons .
Upper motor neurons (brain) synapse on lower motor neurons (spinal cord or anterior root) whose axons leave the CNS to affect the periphery.
What location is the motor neuron controlling somatic musculature located
Ventral horn of the spinal cord
What location is the inter-neuron of the motor neuron located
Intermediate/lateral horn.
if they supply the axial muscle they are located in the medial ventral horn
Descending Motor Pathways are ?
Lateral and Medial
Lateral descending motor pathways
Lateral corticospinal, lateral corticobulbar tract, rubrospinal tract
Terminate in the lateral portions of the spinal cord gray matter. Excite interneurons (primary) but can also excite motor neurons directly.
influence reflex arcs that control fine movement of the distal ends of limbs, as well as those that activate supporting musculature in the proximal ends of limbs.
Medial descending motor pathways
Pontine/medullary reticulospinal tracts, vestibulospinal tracts, tectospinal tract
Terminate in the medial ventral horn on the medial group of interneurons
These interneurons connect bilaterally with motor neurons that control the axial muscles (balance and posture) and help control of proximal limb muscles.
Corticospinal (pyramidal Tract)
Very fast signals Betz cells 70m/sec
Controls the limbs
voluntary skeletal movement controlling muscle in the trunk and proximal limb
ventral …trunk muscles
lateral…control limbs
Blood supply to the brain are
2 vertebral arteries and 2 carotid arteries
allows collateral circuation
Spinal cord blood supply
Lack of collateralization in the spinal cord
Artery of Adamkwitz can be cut off and there will be a problem
Components of CSF
CNS “lymphatic system” & protection from mechanical force
Cavity enclosing the brain & spinal cord has capacity of ~ 1600-1700ml
~ 125ml is CSF (remainder brain & spinal cord)
~ 30 ml of CSF is in cerebral ventricles
Formed from choroid plexuses @ 0.35 ml/min
Reabsorbed by arachnoid villi – function like one way valves
fluid flows when CSF pressure is 1.5mmHg > than venous pressure
naCsf > nablood
148/145
Kcsf
CSF flow
Fluid from lateral ventricles passes through intraventricular foramina (of Munro) to the third ventricle additional fluid is added and then it flows downward along the aqueduct of Sylvius into the fourth ventricle, more fluid is added and then it passes out of the fourth ventricle through three small openings two lateral foramina of Luschka, and a midline foramen of Magendie entering the cisterna magna ( a large fluid space that lies behind the medulla and beneath the cerebellum) which is continuous with the subarachnoid space surrounding the spinal cord
Blood brain barrier structure
Tight junctions between CNS capillary endothelial cells.
Fenestrations in brain 1/8th size of fenestrations in other areas
Astrocytes also restrict movement (ex. by taking up potassium ions) and provide structural support.
Exists in tissue capillary membranes in all areas of the brain parenchyma except hypothalamus, pituitary, and area postrema
Movement across BBB depends on what?
Movement across BBB depends on size, charge, lipid solubility, and degree of protein binding in the blood
Permeable/slightly permeable and Impermeable things to the blood brain barrier
Permeable: H20, C02, O2, lipid soluble substances (anesthetics, ETOH)
Slightly permeable: Na, Cl, K, Ca, Mg
Impermeable: polar molecules, plasma proteins, glucose (facilitated diffusion only), non-lipid soluble large organic molecules (mannitol)
ICP range
8-12
What makes up the ICP
Rigid cranial vault fixed volume
Brain (cellular and ICF) (80%)
Blood (arterial and venous)(12%)
CSF (8%)
calculate CPP
MAP-ICP or CVP
80-100(Normal)
grey matter flow is higher than white matter flow…more metabolic activity here.
below 50 is bad.
Factors that will influence cerebral blood flow
Normal Adult 50ml/100g/min =750ml/mi
Factors impacting CBF Level of arousal/neural metabolism Temperature Concentration of CO2 and H+ ions O2 (only when extremely low) Blood Viscosity Decrease in hematocrit will increase CBF but decrease O2 carrying capacity of the blood Severe polycythemia can reduce CBF
WHAT is Flow metabolism coupling
more activity…more action potential…na/k pump and Atp use…so blood flow higher.
Neuronal Activity (metabolism) and Local CBF
Metabolic by-products (glial, neuronal, vascular)
CBF to localized brain regions change up to 100-150% within seconds in response to local neuronal activity changes (sensory input/arousal)
CBF and relationship with CO2
CO2 + H20 = carbonic acid
Carbonic acid disassociates into H+
H+ ions cause “almost” proportional vasodilation of cerebral vessels
Each 1 mmHg change in PaCO2
CBF changes approximately 1-2ml/100g/min
CBV changes 0.05ml/100g brain tissue
= 10 ml difference for 15 mmHg change
Effect lasts ~ 6hrs and then in will return to normal despite maintenance of altered CO2 levels (bicarb transport)
Blood and co2 level relate linearly…..
Co2 goes up….neuronal activity goes up.
Brain metabolism
Only 2% of total body mass, 15-20% of total body metabolism and cardiac output
Cerebral Metabolic Rate (CMRO2) =
3-3.8ml/100g/min = 50ml/min of O2
Pediatric patients =5.2ml/100g/min
Brain not capable of much anaerobic metabolism (high metabolism coupled with low local glycogen and oxygen stores)
Brain glucose consumption 5.5mg/100g/min
FYI
Energy consumption of teh brain is high,it is used mainly for used to support electrophysiologic function - meaning the depolarization repolarization (ionic gradient maintenance) and synthesis, transport and reuptake of neurotransmitters. The other 40% is just to maintain cell integrity.
If PO2 of brain tissue drops below 30mmHg (35-45mm Hg normal) or PaO2 drops below 50-60mmHg
CBF increases
How does the Auto-regulation of CBF & Arterial Blood Pressure happen
CBF auto-regulated really well between MAP of 70-150mmHG or 50-150
Cerebral vasculature adjusts to changes in CPP/MAP after 1-3 minutes
HTN will shift auto-regulatory range to higher minimum values and maximums of 180-200mmHg
Review SLide 45
green,blue ,orange
Does the autoregulation mechanism always override?
Yes,Neither transection of these nerves or mild to moderate stimulation causes much change
When does The SNS kick in
May shift the auto-regulation curve to the right
SNS minor role unless sudden extreme BP rise (stroke prevention) or hemorrhagic shock
Whats is the effect of temp with CBF
CBF changes 5-7% per 1 degree C change
Hypothermia decreases CBF and CMRO2
Hyperthermia opposite effect
