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Md ophth neurophysiology

The document summarizes key aspects of physiology of the nervous system. It discusses: 1) Functional subdivisions of the nervous system including sensory, motor, integrative, and autonomic functions. 2) Topics covered including action potentials, nerve impulse transmission, neuromuscular junction, and physiology of sensory and motor functions. 3) Excitable tissues having a more negative resting membrane potential than non-excitable tissues due to ion distributions and channels that facilitate potassium efflux and sodium/potassium pumping. 4) Generation of action potentials relies on voltage-gated sodium and potassium channels opening and closing to cause depolarization, repolarization, and hyperpolarization for signal propagation along myelinated and un

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Physiology of the nervous system Prof. Vajira Weerasinghe Professor of Physiology, Faculty of Medicine University of Peradeniya & Consultant Neurophysiologist, Teaching Hospital, Peradeniya www.slideshare.net/vajira54
Functional Subdivisions • Sensory functions • feeling, eg. pain • Motor functions • movement, eg. walking • Integrative functions • eg. reflexes • Autonomic functions • control of blood pressure • Higher functions • memory, learning
Topics • Action potential • Nerve impulse transmission • Neuromuscular junction • Muscle contraction • Degeneration and regeneration of nerves • Autonomic nerve systems • Neurotransmission • Physiology of sensory nervous system • Physiology of motor function • Physiology of pain and consciousness • CSF composition, formation and drainage
Excitable tissues • Excitable tissues have more negative RMP ( - 70 mV to - 90 mV) excitable Non-excitable Red cell GIT neuron muscle • Non-excitable tissues have less negative RMP -53 mV epithelial cells -8.4 mV RBC -20 to -30 mV fibroblasts -58 mV adipocytes
Resting Membrane Potential • This depends on following factors • Ionic distribution across the membrane • Membrane permeability • Other factors • Na+ /K+ pump
Ionic distribution Ion Intracellular Extracellular Na+ 10 142 K+ 140 4 Cl- 4 103 Ca2+ 0 2.4 HCO3 - 10 28
Flow of Potassium • Potassium concentration intracellular is more • Membrane is freely permeable to K+ • There is an efflux of K+ K+ K+K+ K+ K+ K+ K+ K+ K+ K+
Flow of Potassium • Entry of positive ions in to the extracellular fluid creates positivity outside and negativity inside K+ K+K+ K+ K+ K+ K+ K+ K+ K+
Flow of Potassium • Outside positivity resists efflux of K+ • (since K+ is a positive ion) • At a certain voltage an equilibrium is reached and K+ efflux stops K+ K+K+ K+ K+ K+ K+ K+ K+ K+
Ionic channels • Leaky channels (leak channels) – Allow free flow of ions – K+ channels (large number) – Na+ channels (fewer in number) – Therefore membrane is more permeable to K+
Na/K pump • Active transport system for Na+-K+ exchange using energy • It is an electrogenic pump since 3 Na+ efflux coupled with 2 K+ influx • Net effect of causing negative charge inside the membrane 3 Na+ 2 K+ ATP ADP
Factors contributing to RMP • One of the main factors is K+ efflux (Nernst Potential: -90mV) • Contribution of Na+ influx is little (Nernst Potential: +60mV) • Na+/K+ pump causes more negativity inside the membrane • Negatively charged protein ions remaining inside the membrane contributes to the negativity • Net result: -70 to -90 mV inside
Action Potential (A.P.) • When an impulse is generated – Inside becomes positive – Causes depolarisation – Nerve impulses are transmitted as AP Depolarisation Repolarisation -70 +30 RMP Hyperpolarisation
• Sub-threshold stimulus No action potential • Threshold stimulus Action potential is triggered • Supra-threshold stimulus Action potential is triggered • Strength of the stimulus above the threshold is coded as the frequency of action potentials
Physiological basis of AP • When the threshold level is reached – Voltage-gated Na+ channels open up – Since Na+ conc outside is more than the inside – Na+ influx will occur – Positive ion coming inside increases the positivity of the membrane potential and causes depolarisation -70 +30 outside inside Na+ Voltage-gated Na+ channel
Physiological basis of AP – When membrane potential reaches +30, Na+ channels are inactivated – Then Voltage-gated K+ channels open up – K+ efflux occurs – Positive ion leaving the inside causes more negativity inside the membrane – Repolarisation occurs -70 +30 outside inside At +30 K+
Hyperpolarisation • When reaching the Resting level rate slows down • Can go beyond the resting level – Hyperpolarisation • (membrane becoming more negative) -70 +30
Role of Na+/K+ pump • Since Na+ has come in and K+ has gone out • Membrane has become negative • But ionic distribution has become unequal • Na+/K+ pump restores Na+ and K+ conc slowly – By pumping 3 Na+ ions outward and 2+ K ions inward
Propagation of AP • When one area is depolarised • A potential difference exists between that site and the adjacent membrane • A current flow is initiated • Current flow through this local circuit is completed by extra cellular fluid
Propagation of AP • This local current flow will cause opening of voltage-gated Na+ channel in the adjacent membrane • Na+ influx will occur • Membrane is depolarised
Propagation of AP • Then the previous area become repolarised • This process continue to work • Resulting in propagation of AP
Propagation of AP
Propagation of AP
Propagation of AP
Propagation of AP
Propagation of AP
Propagation of AP
Propagation of AP
Propagation of AP
AP propagation along myelinated nerves • Na+ channels are conc around nodes • Therefore depolarisation mainly occurs at nodes
Distribution of Na+ channels • Number of Na+ channels per square micrometer of membrane in mammalian neurons 50 to 75 in the cell body 350 – 500 in the initial segment < 25 on the surface of myelin 2000 – 12,000 at the nodes of Ranvier 20 – 75 at the axon terminal
AP propagation along myelinated nerves • Local current will flow from one node to another • Thus propagation of action potential and therefore nerve conduction through myelinated fibres is faster than unmyelinated fibre – Conduction velocity of thick myelinated A alpha fibres is about 70-100 m/s whereas in unmyelinated fibres it is about 1-2 m/s
Skeletal muscle • Skeletal muscle is supplied by somatic nerve • When there is a signal to the muscle it contracts and relaxes • Thus there are two events in the skeletal muscle – Electrical - action potential – Mechanical - contraction
Muscle contraction • Excitation - contraction coupling – Excitation : electrical event – Contraction : mechanical event Mechanical event follows electrical event
Skeletal muscle • Electrical event in a skeletal muscle membrane is exactly similar to nerve action potential • Same duration = 1 msec • Same voltage difference = from -70 to +30 mV
Effect of serum hypocalcaemia • Concentration of calcium in ECF has a profound effect on voltage level at which Na+ channels activated • Hypocalcaemia causes hyperexcitability of the membrane • When there is a deficit of Ca2+ (50% below normal) sodium channels open (activated) by a small increase in the membrane potential from its normal level – Ca2+ ions binds to the Na+ channel and alters the voltage sensor
Effect of serum hypocalcaemia • Therefore membrane becomes hyperexcitable • Sometimes discharging spontaneously repetitively –tetany occurs • This is the reason for hypocalcaemia causing tetany
NMJ function • Pre-synaptic membrane • Ca channels • Acetycholine release • Postsynaptic membrane • Acetylcholine receptors • Ligand-gated channels • Synaptic cleft • cholinesterase
Presynaptic terminal (terminal knob, boutons, end-feet or synaptic knobs) ♦ Terminal has synaptic vesicles and mitochondria ♦ Mitochondria (ATP) are present inside the presynaptic terminal Vesicles containing neurotransmitter (Ach)
Presynaptic terminal (terminal knob, boutons, end-feet or synaptic knobs) ♦ Presynaptic membrane contain voltage-gated Ca2+ channels ♦ The quantity of neurotransmitter released is proportional to the number of Ca2+ entering the terminal ♦ Ca2+ ions binds to the protein molecules on the inner surface of the synaptic membrane called release sites ♦ Neurotransmitter binds to these sites and exocytosis occur
Ca2+ Ca2+
• Postsynaptic membrane contain nicotinic acetylcholine receptor Ach Na+ •This receptor contains several sub units (2 alpha, beta, delta & epsilon) •Ach binds to alpha subunit •Na+ channel opens up •Na+ influx occurs
NMJ blocking • Useful in general anaesthesia to facilitate inserting tubes • Muscle paralysis is useful in performing surgery
Neuromuscular blocking agents • Non-depolarising type (competitive) – Act by competing with Ach for the Ach receptors – Binds to Ach receptors and blocks – Prevent Ach from attaching to its receptors – No depolarisation – Late onset, prolonged action – 70–80% of receptors should be occupied to produce an effect – To produce complete block, at least 92% of receptors must be occupied – Ach can compete & the effect overcomes by an excess Ach – Anticholinesterases can reverse the action – eg. • Curare • Atracurium • Tubocurarine
Neuromuscular blocking agents • Depolarising type (non-competitive) – Act like Ach, but resistant to AchE action – Bind to motor end plate and once depolarises – Persistent depolarisation leads to a block • Due to inactivation of Na channels – Two phases • Phase I – depolarisation phase – fasciculations • Phase II – paralysis phase – Ach cannot compete – Quick action start within 30 sec, recover within 3 min and is complete within 12–15 min – Anticholinesterases cannot reverse the action – eg. • Succinylcholine • Ach in large doses • Nicotine
Anticholinesterases • AchE inhibitors – Inhibit AchE so that Ach accumulates and causes depolarising block • Reversible – Competitive inhibitors of AChE – Block can be overcome by curare • physostigmine, neostigmine, edrophonium • Irreversible – Binds to AChE irreversibly • , insecticides, nerve gases
NMJ disorders • Myasthenia gravis – Antibodies to Ach receptors – Post synaptic disorder • Lambert Eaton Syndrome (myasthenic syndrome) – Presynaptic disorder (antibodies against Ca channels) • Botulism – Presynaptic disorder – Binds to the presynatic region and prevent release of Ach
Differences between sympathetic andDifferences between sympathetic and parasympathetic nervous systemsparasympathetic nervous systems Ach (N) Ach (N) Ach (M) Nor Sympathetic Parasympathetic Adre
Neurotransmitters and ReceptorsNeurotransmitters and Receptors ► Acetylcholine (ACh) and norepinephrine (NE) are theAcetylcholine (ACh) and norepinephrine (NE) are the two major neurotransmitters of the ANStwo major neurotransmitters of the ANS ► ACh is released by all preganglionic axons and allACh is released by all preganglionic axons and all parasympathetic postganglionic axonsparasympathetic postganglionic axons ► Cholinergic fibersCholinergic fibers – ACh-releasing fibers– ACh-releasing fibers ► Adrenergic fibersAdrenergic fibers – sympathetic postganglionic– sympathetic postganglionic axons that release NEaxons that release NE ► Neurotransmitter effects can be excitatory or inhibitoryNeurotransmitter effects can be excitatory or inhibitory depending upon the receptor typedepending upon the receptor type
Nicotinic Receptors (cholinergic)Nicotinic Receptors (cholinergic) ►Nicotinic receptors are found on:Nicotinic receptors are found on:  Motor end plates (somatic targets)Motor end plates (somatic targets)  All ganglionic neurons of both sympatheticAll ganglionic neurons of both sympathetic and parasympathetic divisionsand parasympathetic divisions  The hormone-producing cells of theThe hormone-producing cells of the adrenal medullaadrenal medulla ►The effect of ACh binding to nicotinicThe effect of ACh binding to nicotinic receptors isreceptors is always stimulatoryalways stimulatory
Muscarinic ReceptorsMuscarinic Receptors (cholinergic)(cholinergic) ►Muscarinic receptors occur on all effectorMuscarinic receptors occur on all effector cells stimulated by postganglioniccells stimulated by postganglionic cholinergic fiberscholinergic fibers ►The effect of ACh binding:The effect of ACh binding:  Can be either inhibitory or excitatoryCan be either inhibitory or excitatory  Depends on the receptor typeDepends on the receptor type of theof the target organtarget organ
Adrenergic ReceptorsAdrenergic Receptors ► The two types of adrenergic receptors are alphaThe two types of adrenergic receptors are alpha and betaand beta ► Each type has two or three subclassesEach type has two or three subclasses ((αα11,, αα22,, ββ11,, ββ22 ,, ββ33)) ► Effects of NE binding to:Effects of NE binding to:  αα receptors is generally stimulatoryreceptors is generally stimulatory  ββ receptors is generally inhibitoryreceptors is generally inhibitory ► A notable exception – NE binding toA notable exception – NE binding to ββ receptors ofreceptors of the heart is stimulatorythe heart is stimulatory
Alpha ReceptorsAlpha Receptors ► Alpha 1: adrenergic receptors located onAlpha 1: adrenergic receptors located on postsynaptic effector cells.postsynaptic effector cells.  Smooth muscles of blood vessels: ConstrictionSmooth muscles of blood vessels: Constriction ► Arteriolar constrictionArteriolar constriction  Bladder sphincterBladder sphincter  PenisPenis  UterusUterus  Pupillary muscles of irisPupillary muscles of iris ► Alpha 2Alpha 2  Same as the Alpha 1 but are located in the presynapticSame as the Alpha 1 but are located in the presynaptic nerve terminalsnerve terminals
Adrenergic ReceptorAdrenergic Receptor ►Beta 1Beta 1 ►CardiovascularCardiovascular  Cardiac muscle: increased contractilityCardiac muscle: increased contractility increased force of contractionincreased force of contraction  Atrioventricular node: increased heart rateAtrioventricular node: increased heart rate  Sinoatrial node: increase in heart rateSinoatrial node: increase in heart rate ►EndocrineEndocrine  PancreasPancreas
Adrenergic ReceptorAdrenergic Receptor ►Beta 2Beta 2 ►CardiovascularCardiovascular  Dilation of blood vesselsDilation of blood vessels ►EndocrineEndocrine ►Uterine relaxationUterine relaxation ►Respiratory: dilation of bronchial musclesRespiratory: dilation of bronchial muscles
HeartHeart ►Direct stimulation of receptorsDirect stimulation of receptors  Alpha 1 –Alpha 1 – ►Vasoconstriction of blood vessels which increasesVasoconstriction of blood vessels which increases blood pressureblood pressure ►Pressor or vasopressor effect to maintain bloodPressor or vasopressor effect to maintain blood pressurepressure  Beta 1Beta 1 ►Increased force of myocardial contractionIncreased force of myocardial contraction ►Increased speed of electrical conduction in the heart.Increased speed of electrical conduction in the heart.
Sensory Functions • General Sensations • Special Sensations • Vision • Hearing • Taste • Smell
Receptor Sensory modality Sensory nerve Central Connections Ascending Sensory pathway Sensory area in the brain Touch stimulus AFFERENT
Classification of receptors • Mechanoreceptors • Thermoreceptors • Nociceptors • pain • Chemoreceptors • taste, smell, visceral • Electromagnetic receptors • visual
Mechanoreceptors • Mainly cutaneous • Touch • Pressure • Vibration • Crude or Fine mechanosensations • Others: auditory, vestibular, stretch
What happens inside a receptor? • TRANSDUCTION • Stimulus energy is converted to action potentials • Inside the nervous system signals are always action potentials • Language of the nervous system contains only 1 word: action potentials • At the brain opposite happens in order to feel the sensation • PERCEPTION
Two ascending pathways • Dorsal column - medial lemniscus pathway fast pathway • Spinothalamic pathway slow pathway These two pathways come together at the level of thalamus
Dorsal column pathway Spinothalamic pathway Lateral Spinothalamic tract Anterior Spinothalamic tract
Dorsal column pathway Spinothalamic pathway • touch: fine degree • highly localised touch sensations • vibratory sensations • sensations signalling movement • position sense • pressure: fine degree • Pain • Thermal sensations • Crude touch & pressure • crude localising sensations • tickle & itch • sexual sensations
Dorsal column nuclei (cuneate & gracile nucleus) Dorsal column Medial lemniscus thalamus thalamocortical tracts sensorycortex internal capsule 1st order neuron 2nd order neuron 3rd order neuron
Spinothalamic tracts thalamus thalamocortical tracts sensorycortex internal capsule 1st order neuron 2nd order neuron 3rd order neuron
Abnormalities • Sensory loss • Anaesthesia • absence of sensation • Paraesthesia • abnormal sensation • Hemianaesthesia • Loss of sensation of one half of the body • Astereognosis
Localisation of the abnormality • Peripheral nerve • part of a limb is affected • Roots • dermatomal pattern of sensory loss • spinal cord • a sensory level • internal capsule • one half of the body
What is a reflex? Stimulus Effector organ Response Central connections Efferent nerve Afferent nerveReceptor
Stretch reflex • This is a basic reflex present in the spinal cord • Stimulus: muscle stretch • Response: contraction of the muscle • Receptors: stretch receptors located in the muscle spindle • Importance of stretch reflex • Detects muscle length and changes in muscle length
Ia afferent nerve α motor neuron one synapse muscle stretchmuscle contraction γ Motor neuron
Motor system • Consists of • Upper motor neuron • Lower motor neuron
Medulla m otorcortex internal capsule Upper motor neuron Lower motor neuron anterior horn cell
alpha motor neuron • this is also called the final common pathway • Contraction of the muscle occurs through this whether • voluntary contraction through corticospinal tract or • involuntary contraction through gamma motor neuron - stretch reflex - Ia afferent
• Lower motor neuron lesion causes • flaccid paralysis • Upper motor neuron lesion causes • spastic paralysis
Lower motor neuron lesion • muscle weakness • flaccid paralysis • muscle wasting (disuse atrophy) • reduced muscle tone (hypotonia) • reflexes: reduced or absent • spontaneous muscle contractions (fasciculations) • plantar reflex: flexor • superficial abdominal reflexes: present
Upper motor neuron lesion • muscle weakness • spastic paralysis • increased muscle tone (hypertonia) • reflexes: exaggerated • Babinski sign: positive • superficial abdominal reflexes: absent • muscle wasting is very rare
Cerebellum • Centre of motor coordination • Cerebellar disorders cause incoordination or ataxia • Functions of cerebellum • Planning of movements • Timing & sequencing of movements • Particularly during rapid movments such as during walking, running • From the peripheral feedback & motor cortical impulses, cerebellum calculates when does a movement should begin and stop
Features of cerebellar disorders• ataxia • incoordination of movements • ataxic gait • broad based gait • leaning towards side of the lesion • dysmetria • cannot plan movements • past pointing & overshoot • decomposition of movements • intentional tremor • dysdiadochokinesis • unable to perform rapidly alternating movements • dysarthria • slurring of speech • dysphagia • swallowing difficulty • nystagmus • oscillatory movements of the eye • hypotonia • reduction in tone • due to excitatory influence on gamma motor neurons by cerebellum (through vestibulospinal tracts) • decreased reflexes • head tremor • head tilt
Basal ganglia • These are a set of deep nuclei located in and around the basal part of the brain • Caudate nucleus • Putamen • Globus pallidus • Substantia nigra • Subthalamic nuclei • Basal ganglia disorders • Parkinsonism • Athetosis • Chorea • Hemiballismus
Parkinsonism • due to destruction of dopamine secreting pathways from substantia nigra to caudate and putamen. • also called paralysis agitans • first described by Dr. James Parkinson in 1817. Clinical features: • Rigidity of all the muscles • Akinesia (bradykinesia): very slow movements, sluggish to initiate • Resting tremor • Normal muscle power
• expressionless face • flexed posture • soft, rapid, indistinct speech • slow to start walking • rapid, small steps, tendency to run • reduced arm swinging • impaired balance on turning • resting tremor (4-6 Hz) (pill-rolling tremor) • diminishes on action • cogwheel rigidity • lead pipe rigidity • impaired fine movements • impaired repetitive movements
maintenance of posture • mainly to maintain the static posture • necessary for the stability of movements • involve a set of reflexes • integrated at spinal cord, brain stem and cortical level
Postural reflexes • stretch reflex • positive supporting reaction (magnet reaction) • negative supporting reaction • mass reflex • tonic labyrinthine reflex • tonic neck reflexes • labyrinthine righting reflex • neck righting reflex • body-on-head righting reflex • body-on-body righting reflex • optical righting reflex • placing reactions • hopping reaction
postural adjustments vestibular nuclei cerebellum pressure & other receptors neck receptors Retina Occulomotor system vestibular system complex pathways
idea •premotor area •supplementary motor area motor cortex movement basal ganglia cerebellum cerebellum plan execute memory, emotions
What is pain? • There is an International definition of pain formulated by the IASP (International Association for the study of pain) • Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage IASP – International Association for the Study of Pain 2011
• Nociceptive pain • Neuropathic pain • Psychogenic pain
• Transduction – Process of converting noxious stimulus to action potentials • Perception – Central processing of nociceptive impulses in order to interpret pain
Dual nature of pain fast and slow pain • fast pain – acute – pricking type – well localised – short duration – Aδ fibres are involved – fast conduction 20 m/s – somatic pain • slow pain – chronic – throbbing type – poorly localised – long duration – unmyelinated C fibres are involved – slow conduction 1-2 m/s – visceral pain
lateral spinothalamic tract thalamus sensorycortex C fibre thalamocortical tracts
Descending pain modulatory system • several lines of experimental evidence show the presence of descending pain modulatory system – discovery of morphine receptors – they were known to be present in the brain stem areas – discovery of endogenous opioid peptides • eg. Endorphines, enkephalins, dynorphin
Gate control theory • This explains how pain can be relieved very quickly by a neural mechanism • First described by P.D. Wall & Melzack (1965) • “There is an interaction between pain fibres and touch fibre input at the spinal cord level in the form of a ‘gating mechanism’
Gate control theory central control transmission cell touch Aβ fibre when C fibre is stimulated, gate will be opened & pain is felt pain C & Aδ fibres pain is felt + gate is opened
Gate control theory central control transmission cell when Aβ & C fibres are stimulated together, gate will be closed & pain is not felt pain is not felt touch Aβ fibre pain C & Aδ fibres + - gate is closed
Consciousness • Consciousness is the state of being awake and aware of one's surroundings • Assessed by observing a patient's alertness and responsiveness, and can been seen as a continuum of states ranging from – alert – oriented to time and place – communicative – disorientation – delirium – loss of any meaningful communication – loss of movement in response to painful stimulation • Glasgow Coma Scale (GCS) clinically measures the degree of consciousness
Sleep • A natural periodic state of rest for the mind and body, in which the eyes usually close and there is a decrease in bodily movement and responsiveness to external stimuli • Whether it is a state of unconsciousness is questionable • coma is an unconscious state from which the person cannot be aroused • In general anaesthesia a patient is deliberately put into a state of unconsciousness under the action of centrally acting drugs
Arousal & Reticular Activating System • Keeping in conscious, alert, awake state. Is a function of RAS. • In parallel with the ascending somatosensory tracts through thalamus to cortex. • There is a more diffuse ascending system consisting mostly of the ascending reticular formation and diffuse nuclei of the thalamus. • This RAS is necessary to maintain a general level of excitability in the cortex.
Reticular formation
CSF • Cerebral blood flow: 750 ml/min (15% of cardiac output) • volume of CSF – 150 ml • rate of production – 500 ml/day • formed – mainly in the choroid plexuses of the ventricles – small amounts in the ventricles, arachnoid membranes & perivascular spaces
formation • choroid plexus projects into – horn of lateral ventricle – posterior portion of 3rd ventricle – roof of the 4th ventricle • Mechanism: – active transport of Na through the epithelial cells, Cl follows passively – osmotic outflow of water – glucose moves in to CSF – K and HCO3 moved out of CSF
composition • similar to plasma – CSF Plasma – Na 147 (similar) 150 mmol/l – K 2.9 (less) 4.6 mmol/l – HCO3 25 24.8 mmol/l – Cl 113 (more) 99 mmol/l – Pco2 50 40 mmHg – pH 7.33 7.4 – osmolality 289 (similar) 289 mosm – protein 20 (less) 6000 mg/dl – glucose 64 (less) 100 mg/dl – urea 12 (less) 15 mg/dl • some substances do not pass into CSF
blood brain barrier • tight junctions between capillary endothelial cells & epithelial cells in the choroid prevent some substances entering CSF • small molecules & lipid soluble substances pass through easily • blood-brain barrier exists between blood & brain tissue • blood-CSF barrier is present in choroid • these barriers are – highly permeable to water, CO2, O2, lipid soluble substances (such as alcohol), most anaesthetics, – slightly permeable to electrolytes – impermeable to proteins, large organic molecules – drugs (variable)
blood brain barrier • CO2 & O2 crosses easily • H+ & HCO3- slow penetration • glucose – passive: slow penetration – active transport system by glucose transporter GLUT • Na-K-Cl transporter • transporters for other substances
blood brain barrier – No blood brain barrier in the hypothalamus & posterior pituitary • substances diffuses easily • these areas contain chemoreceptors for various substances to detect changes in conc
brain metabolism – brain metabolism is 15% of total metabolism of the body (although brain mass is 2% of total body mass) – therefore brain has an increased metabolic rate – this is due to increased activity of neurons (AP) – requires oxygen – brain is not capable of anaerobic metabolism – energy supply is by glucose – glucose entry is not controlled by insulin
Nerve degeneration and regeneration • Demyelination • Axonal degeneration • Remyelination • Axonal regeneration
Md ophth neurophysiology

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Md ophth neurophysiology

  • 1.
    Physiology of the nervoussystem Prof. Vajira Weerasinghe Professor of Physiology, Faculty of Medicine University of Peradeniya & Consultant Neurophysiologist, Teaching Hospital, Peradeniya www.slideshare.net/vajira54
  • 2.
    Functional Subdivisions • Sensoryfunctions • feeling, eg. pain • Motor functions • movement, eg. walking • Integrative functions • eg. reflexes • Autonomic functions • control of blood pressure • Higher functions • memory, learning
  • 3.
    Topics • Action potential •Nerve impulse transmission • Neuromuscular junction • Muscle contraction • Degeneration and regeneration of nerves • Autonomic nerve systems • Neurotransmission • Physiology of sensory nervous system • Physiology of motor function • Physiology of pain and consciousness • CSF composition, formation and drainage
  • 4.
    Excitable tissues • Excitabletissues have more negative RMP ( - 70 mV to - 90 mV) excitable Non-excitable Red cell GIT neuron muscle • Non-excitable tissues have less negative RMP -53 mV epithelial cells -8.4 mV RBC -20 to -30 mV fibroblasts -58 mV adipocytes
  • 5.
    Resting Membrane Potential •This depends on following factors • Ionic distribution across the membrane • Membrane permeability • Other factors • Na+ /K+ pump
  • 6.
    Ionic distribution Ion IntracellularExtracellular Na+ 10 142 K+ 140 4 Cl- 4 103 Ca2+ 0 2.4 HCO3 - 10 28
  • 7.
    Flow of Potassium •Potassium concentration intracellular is more • Membrane is freely permeable to K+ • There is an efflux of K+ K+ K+K+ K+ K+ K+ K+ K+ K+ K+
  • 8.
    Flow of Potassium •Entry of positive ions in to the extracellular fluid creates positivity outside and negativity inside K+ K+K+ K+ K+ K+ K+ K+ K+ K+
  • 9.
    Flow of Potassium •Outside positivity resists efflux of K+ • (since K+ is a positive ion) • At a certain voltage an equilibrium is reached and K+ efflux stops K+ K+K+ K+ K+ K+ K+ K+ K+ K+
  • 10.
    Ionic channels • Leakychannels (leak channels) – Allow free flow of ions – K+ channels (large number) – Na+ channels (fewer in number) – Therefore membrane is more permeable to K+
  • 11.
    Na/K pump • Activetransport system for Na+-K+ exchange using energy • It is an electrogenic pump since 3 Na+ efflux coupled with 2 K+ influx • Net effect of causing negative charge inside the membrane 3 Na+ 2 K+ ATP ADP
  • 12.
    Factors contributing toRMP • One of the main factors is K+ efflux (Nernst Potential: -90mV) • Contribution of Na+ influx is little (Nernst Potential: +60mV) • Na+/K+ pump causes more negativity inside the membrane • Negatively charged protein ions remaining inside the membrane contributes to the negativity • Net result: -70 to -90 mV inside
  • 13.
    Action Potential (A.P.) •When an impulse is generated – Inside becomes positive – Causes depolarisation – Nerve impulses are transmitted as AP Depolarisation Repolarisation -70 +30 RMP Hyperpolarisation
  • 14.
    • Sub-threshold stimulusNo action potential • Threshold stimulus Action potential is triggered • Supra-threshold stimulus Action potential is triggered • Strength of the stimulus above the threshold is coded as the frequency of action potentials
  • 15.
    Physiological basis ofAP • When the threshold level is reached – Voltage-gated Na+ channels open up – Since Na+ conc outside is more than the inside – Na+ influx will occur – Positive ion coming inside increases the positivity of the membrane potential and causes depolarisation -70 +30 outside inside Na+ Voltage-gated Na+ channel
  • 16.
    Physiological basis ofAP – When membrane potential reaches +30, Na+ channels are inactivated – Then Voltage-gated K+ channels open up – K+ efflux occurs – Positive ion leaving the inside causes more negativity inside the membrane – Repolarisation occurs -70 +30 outside inside At +30 K+
  • 17.
    Hyperpolarisation • When reachingthe Resting level rate slows down • Can go beyond the resting level – Hyperpolarisation • (membrane becoming more negative) -70 +30
  • 18.
    Role of Na+/K+pump • Since Na+ has come in and K+ has gone out • Membrane has become negative • But ionic distribution has become unequal • Na+/K+ pump restores Na+ and K+ conc slowly – By pumping 3 Na+ ions outward and 2+ K ions inward
  • 19.
    Propagation of AP •When one area is depolarised • A potential difference exists between that site and the adjacent membrane • A current flow is initiated • Current flow through this local circuit is completed by extra cellular fluid
  • 20.
    Propagation of AP •This local current flow will cause opening of voltage-gated Na+ channel in the adjacent membrane • Na+ influx will occur • Membrane is depolarised
  • 21.
    Propagation of AP •Then the previous area become repolarised • This process continue to work • Resulting in propagation of AP
  • 22.
  • 23.
  • 24.
  • 25.
  • 26.
  • 27.
  • 28.
  • 29.
  • 30.
    AP propagation alongmyelinated nerves • Na+ channels are conc around nodes • Therefore depolarisation mainly occurs at nodes
  • 31.
    Distribution of Na+channels • Number of Na+ channels per square micrometer of membrane in mammalian neurons 50 to 75 in the cell body 350 – 500 in the initial segment < 25 on the surface of myelin 2000 – 12,000 at the nodes of Ranvier 20 – 75 at the axon terminal
  • 32.
    AP propagation alongmyelinated nerves • Local current will flow from one node to another • Thus propagation of action potential and therefore nerve conduction through myelinated fibres is faster than unmyelinated fibre – Conduction velocity of thick myelinated A alpha fibres is about 70-100 m/s whereas in unmyelinated fibres it is about 1-2 m/s
  • 35.
    Skeletal muscle • Skeletalmuscle is supplied by somatic nerve • When there is a signal to the muscle it contracts and relaxes • Thus there are two events in the skeletal muscle – Electrical - action potential – Mechanical - contraction
  • 36.
    Muscle contraction • Excitation- contraction coupling – Excitation : electrical event – Contraction : mechanical event Mechanical event follows electrical event
  • 37.
    Skeletal muscle • Electricalevent in a skeletal muscle membrane is exactly similar to nerve action potential • Same duration = 1 msec • Same voltage difference = from -70 to +30 mV
  • 38.
    Effect of serumhypocalcaemia • Concentration of calcium in ECF has a profound effect on voltage level at which Na+ channels activated • Hypocalcaemia causes hyperexcitability of the membrane • When there is a deficit of Ca2+ (50% below normal) sodium channels open (activated) by a small increase in the membrane potential from its normal level – Ca2+ ions binds to the Na+ channel and alters the voltage sensor
  • 39.
    Effect of serumhypocalcaemia • Therefore membrane becomes hyperexcitable • Sometimes discharging spontaneously repetitively –tetany occurs • This is the reason for hypocalcaemia causing tetany
  • 40.
    NMJ function • Pre-synapticmembrane • Ca channels • Acetycholine release • Postsynaptic membrane • Acetylcholine receptors • Ligand-gated channels • Synaptic cleft • cholinesterase
  • 41.
    Presynaptic terminal (terminalknob, boutons, end-feet or synaptic knobs) ♦ Terminal has synaptic vesicles and mitochondria ♦ Mitochondria (ATP) are present inside the presynaptic terminal Vesicles containing neurotransmitter (Ach)
  • 42.
    Presynaptic terminal (terminalknob, boutons, end-feet or synaptic knobs) ♦ Presynaptic membrane contain voltage-gated Ca2+ channels ♦ The quantity of neurotransmitter released is proportional to the number of Ca2+ entering the terminal ♦ Ca2+ ions binds to the protein molecules on the inner surface of the synaptic membrane called release sites ♦ Neurotransmitter binds to these sites and exocytosis occur
  • 43.
  • 44.
    • Postsynaptic membranecontain nicotinic acetylcholine receptor Ach Na+ •This receptor contains several sub units (2 alpha, beta, delta & epsilon) •Ach binds to alpha subunit •Na+ channel opens up •Na+ influx occurs
  • 45.
    NMJ blocking • Usefulin general anaesthesia to facilitate inserting tubes • Muscle paralysis is useful in performing surgery
  • 46.
    Neuromuscular blocking agents •Non-depolarising type (competitive) – Act by competing with Ach for the Ach receptors – Binds to Ach receptors and blocks – Prevent Ach from attaching to its receptors – No depolarisation – Late onset, prolonged action – 70–80% of receptors should be occupied to produce an effect – To produce complete block, at least 92% of receptors must be occupied – Ach can compete & the effect overcomes by an excess Ach – Anticholinesterases can reverse the action – eg. • Curare • Atracurium • Tubocurarine
  • 47.
    Neuromuscular blocking agents •Depolarising type (non-competitive) – Act like Ach, but resistant to AchE action – Bind to motor end plate and once depolarises – Persistent depolarisation leads to a block • Due to inactivation of Na channels – Two phases • Phase I – depolarisation phase – fasciculations • Phase II – paralysis phase – Ach cannot compete – Quick action start within 30 sec, recover within 3 min and is complete within 12–15 min – Anticholinesterases cannot reverse the action – eg. • Succinylcholine • Ach in large doses • Nicotine
  • 48.
    Anticholinesterases • AchE inhibitors –Inhibit AchE so that Ach accumulates and causes depolarising block • Reversible – Competitive inhibitors of AChE – Block can be overcome by curare • physostigmine, neostigmine, edrophonium • Irreversible – Binds to AChE irreversibly • , insecticides, nerve gases
  • 49.
    NMJ disorders • Myastheniagravis – Antibodies to Ach receptors – Post synaptic disorder • Lambert Eaton Syndrome (myasthenic syndrome) – Presynaptic disorder (antibodies against Ca channels) • Botulism – Presynaptic disorder – Binds to the presynatic region and prevent release of Ach
  • 50.
    Differences between sympatheticandDifferences between sympathetic and parasympathetic nervous systemsparasympathetic nervous systems Ach (N) Ach (N) Ach (M) Nor Sympathetic Parasympathetic Adre
  • 51.
    Neurotransmitters and ReceptorsNeurotransmittersand Receptors ► Acetylcholine (ACh) and norepinephrine (NE) are theAcetylcholine (ACh) and norepinephrine (NE) are the two major neurotransmitters of the ANStwo major neurotransmitters of the ANS ► ACh is released by all preganglionic axons and allACh is released by all preganglionic axons and all parasympathetic postganglionic axonsparasympathetic postganglionic axons ► Cholinergic fibersCholinergic fibers – ACh-releasing fibers– ACh-releasing fibers ► Adrenergic fibersAdrenergic fibers – sympathetic postganglionic– sympathetic postganglionic axons that release NEaxons that release NE ► Neurotransmitter effects can be excitatory or inhibitoryNeurotransmitter effects can be excitatory or inhibitory depending upon the receptor typedepending upon the receptor type
  • 52.
    Nicotinic Receptors (cholinergic)NicotinicReceptors (cholinergic) ►Nicotinic receptors are found on:Nicotinic receptors are found on:  Motor end plates (somatic targets)Motor end plates (somatic targets)  All ganglionic neurons of both sympatheticAll ganglionic neurons of both sympathetic and parasympathetic divisionsand parasympathetic divisions  The hormone-producing cells of theThe hormone-producing cells of the adrenal medullaadrenal medulla ►The effect of ACh binding to nicotinicThe effect of ACh binding to nicotinic receptors isreceptors is always stimulatoryalways stimulatory
  • 53.
    Muscarinic ReceptorsMuscarinic Receptors (cholinergic)(cholinergic) ►Muscarinicreceptors occur on all effectorMuscarinic receptors occur on all effector cells stimulated by postganglioniccells stimulated by postganglionic cholinergic fiberscholinergic fibers ►The effect of ACh binding:The effect of ACh binding:  Can be either inhibitory or excitatoryCan be either inhibitory or excitatory  Depends on the receptor typeDepends on the receptor type of theof the target organtarget organ
  • 54.
    Adrenergic ReceptorsAdrenergic Receptors ►The two types of adrenergic receptors are alphaThe two types of adrenergic receptors are alpha and betaand beta ► Each type has two or three subclassesEach type has two or three subclasses ((αα11,, αα22,, ββ11,, ββ22 ,, ββ33)) ► Effects of NE binding to:Effects of NE binding to:  αα receptors is generally stimulatoryreceptors is generally stimulatory  ββ receptors is generally inhibitoryreceptors is generally inhibitory ► A notable exception – NE binding toA notable exception – NE binding to ββ receptors ofreceptors of the heart is stimulatorythe heart is stimulatory
  • 55.
    Alpha ReceptorsAlpha Receptors ►Alpha 1: adrenergic receptors located onAlpha 1: adrenergic receptors located on postsynaptic effector cells.postsynaptic effector cells.  Smooth muscles of blood vessels: ConstrictionSmooth muscles of blood vessels: Constriction ► Arteriolar constrictionArteriolar constriction  Bladder sphincterBladder sphincter  PenisPenis  UterusUterus  Pupillary muscles of irisPupillary muscles of iris ► Alpha 2Alpha 2  Same as the Alpha 1 but are located in the presynapticSame as the Alpha 1 but are located in the presynaptic nerve terminalsnerve terminals
  • 56.
    Adrenergic ReceptorAdrenergic Receptor ►Beta1Beta 1 ►CardiovascularCardiovascular  Cardiac muscle: increased contractilityCardiac muscle: increased contractility increased force of contractionincreased force of contraction  Atrioventricular node: increased heart rateAtrioventricular node: increased heart rate  Sinoatrial node: increase in heart rateSinoatrial node: increase in heart rate ►EndocrineEndocrine  PancreasPancreas
  • 57.
    Adrenergic ReceptorAdrenergic Receptor ►Beta2Beta 2 ►CardiovascularCardiovascular  Dilation of blood vesselsDilation of blood vessels ►EndocrineEndocrine ►Uterine relaxationUterine relaxation ►Respiratory: dilation of bronchial musclesRespiratory: dilation of bronchial muscles
  • 58.
    HeartHeart ►Direct stimulation ofreceptorsDirect stimulation of receptors  Alpha 1 –Alpha 1 – ►Vasoconstriction of blood vessels which increasesVasoconstriction of blood vessels which increases blood pressureblood pressure ►Pressor or vasopressor effect to maintain bloodPressor or vasopressor effect to maintain blood pressurepressure  Beta 1Beta 1 ►Increased force of myocardial contractionIncreased force of myocardial contraction ►Increased speed of electrical conduction in the heart.Increased speed of electrical conduction in the heart.
  • 59.
    Sensory Functions • GeneralSensations • Special Sensations • Vision • Hearing • Taste • Smell
  • 60.
    Receptor Sensory modality Sensory nerve Central Connections Ascending Sensorypathway Sensory area in the brain Touch stimulus AFFERENT
  • 61.
    Classification of receptors •Mechanoreceptors • Thermoreceptors • Nociceptors • pain • Chemoreceptors • taste, smell, visceral • Electromagnetic receptors • visual
  • 62.
    Mechanoreceptors • Mainly cutaneous •Touch • Pressure • Vibration • Crude or Fine mechanosensations • Others: auditory, vestibular, stretch
  • 63.
    What happens insidea receptor? • TRANSDUCTION • Stimulus energy is converted to action potentials • Inside the nervous system signals are always action potentials • Language of the nervous system contains only 1 word: action potentials • At the brain opposite happens in order to feel the sensation • PERCEPTION
  • 64.
    Two ascending pathways •Dorsal column - medial lemniscus pathway fast pathway • Spinothalamic pathway slow pathway These two pathways come together at the level of thalamus
  • 65.
    Dorsal column pathway Spinothalamicpathway Lateral Spinothalamic tract Anterior Spinothalamic tract
  • 66.
    Dorsal column pathwaySpinothalamic pathway • touch: fine degree • highly localised touch sensations • vibratory sensations • sensations signalling movement • position sense • pressure: fine degree • Pain • Thermal sensations • Crude touch & pressure • crude localising sensations • tickle & itch • sexual sensations
  • 67.
    Dorsal column nuclei (cuneate& gracile nucleus) Dorsal column Medial lemniscus thalamus thalamocortical tracts sensorycortex internal capsule 1st order neuron 2nd order neuron 3rd order neuron
  • 68.
  • 69.
    Abnormalities • Sensory loss •Anaesthesia • absence of sensation • Paraesthesia • abnormal sensation • Hemianaesthesia • Loss of sensation of one half of the body • Astereognosis
  • 70.
    Localisation of theabnormality • Peripheral nerve • part of a limb is affected • Roots • dermatomal pattern of sensory loss • spinal cord • a sensory level • internal capsule • one half of the body
  • 71.
    What is areflex? Stimulus Effector organ Response Central connections Efferent nerve Afferent nerveReceptor
  • 72.
    Stretch reflex • Thisis a basic reflex present in the spinal cord • Stimulus: muscle stretch • Response: contraction of the muscle • Receptors: stretch receptors located in the muscle spindle • Importance of stretch reflex • Detects muscle length and changes in muscle length
  • 73.
    Ia afferent nerve αmotor neuron one synapse muscle stretchmuscle contraction γ Motor neuron
  • 74.
    Motor system • Consistsof • Upper motor neuron • Lower motor neuron
  • 75.
  • 76.
    alpha motor neuron •this is also called the final common pathway • Contraction of the muscle occurs through this whether • voluntary contraction through corticospinal tract or • involuntary contraction through gamma motor neuron - stretch reflex - Ia afferent
  • 77.
    • Lower motorneuron lesion causes • flaccid paralysis • Upper motor neuron lesion causes • spastic paralysis
  • 78.
    Lower motor neuron lesion •muscle weakness • flaccid paralysis • muscle wasting (disuse atrophy) • reduced muscle tone (hypotonia) • reflexes: reduced or absent • spontaneous muscle contractions (fasciculations) • plantar reflex: flexor • superficial abdominal reflexes: present
  • 79.
    Upper motor neuron lesion •muscle weakness • spastic paralysis • increased muscle tone (hypertonia) • reflexes: exaggerated • Babinski sign: positive • superficial abdominal reflexes: absent • muscle wasting is very rare
  • 80.
    Cerebellum • Centre ofmotor coordination • Cerebellar disorders cause incoordination or ataxia • Functions of cerebellum • Planning of movements • Timing & sequencing of movements • Particularly during rapid movments such as during walking, running • From the peripheral feedback & motor cortical impulses, cerebellum calculates when does a movement should begin and stop
  • 81.
    Features of cerebellardisorders• ataxia • incoordination of movements • ataxic gait • broad based gait • leaning towards side of the lesion • dysmetria • cannot plan movements • past pointing & overshoot • decomposition of movements • intentional tremor • dysdiadochokinesis • unable to perform rapidly alternating movements • dysarthria • slurring of speech • dysphagia • swallowing difficulty • nystagmus • oscillatory movements of the eye • hypotonia • reduction in tone • due to excitatory influence on gamma motor neurons by cerebellum (through vestibulospinal tracts) • decreased reflexes • head tremor • head tilt
  • 82.
    Basal ganglia • Theseare a set of deep nuclei located in and around the basal part of the brain • Caudate nucleus • Putamen • Globus pallidus • Substantia nigra • Subthalamic nuclei • Basal ganglia disorders • Parkinsonism • Athetosis • Chorea • Hemiballismus
  • 83.
    Parkinsonism • due todestruction of dopamine secreting pathways from substantia nigra to caudate and putamen. • also called paralysis agitans • first described by Dr. James Parkinson in 1817. Clinical features: • Rigidity of all the muscles • Akinesia (bradykinesia): very slow movements, sluggish to initiate • Resting tremor • Normal muscle power
  • 84.
    • expressionless face •flexed posture • soft, rapid, indistinct speech • slow to start walking • rapid, small steps, tendency to run • reduced arm swinging • impaired balance on turning • resting tremor (4-6 Hz) (pill-rolling tremor) • diminishes on action • cogwheel rigidity • lead pipe rigidity • impaired fine movements • impaired repetitive movements
  • 85.
    maintenance of posture •mainly to maintain the static posture • necessary for the stability of movements • involve a set of reflexes • integrated at spinal cord, brain stem and cortical level
  • 86.
    Postural reflexes • stretchreflex • positive supporting reaction (magnet reaction) • negative supporting reaction • mass reflex • tonic labyrinthine reflex • tonic neck reflexes • labyrinthine righting reflex • neck righting reflex • body-on-head righting reflex • body-on-body righting reflex • optical righting reflex • placing reactions • hopping reaction
  • 87.
    postural adjustments vestibular nuclei cerebellum pressure &other receptors neck receptors Retina Occulomotor system vestibular system complex pathways
  • 88.
    idea •premotor area •supplementary motor area motorcortex movement basal ganglia cerebellum cerebellum plan execute memory, emotions
  • 89.
    What is pain? •There is an International definition of pain formulated by the IASP (International Association for the study of pain) • Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage IASP – International Association for the Study of Pain 2011
  • 90.
    • Nociceptive pain •Neuropathic pain • Psychogenic pain
  • 91.
    • Transduction – Processof converting noxious stimulus to action potentials • Perception – Central processing of nociceptive impulses in order to interpret pain
  • 92.
    Dual nature ofpain fast and slow pain • fast pain – acute – pricking type – well localised – short duration – Aδ fibres are involved – fast conduction 20 m/s – somatic pain • slow pain – chronic – throbbing type – poorly localised – long duration – unmyelinated C fibres are involved – slow conduction 1-2 m/s – visceral pain
  • 93.
  • 94.
    Descending pain modulatorysystem • several lines of experimental evidence show the presence of descending pain modulatory system – discovery of morphine receptors – they were known to be present in the brain stem areas – discovery of endogenous opioid peptides • eg. Endorphines, enkephalins, dynorphin
  • 95.
    Gate control theory •This explains how pain can be relieved very quickly by a neural mechanism • First described by P.D. Wall & Melzack (1965) • “There is an interaction between pain fibres and touch fibre input at the spinal cord level in the form of a ‘gating mechanism’
  • 96.
    Gate control theory centralcontrol transmission cell touch Aβ fibre when C fibre is stimulated, gate will be opened & pain is felt pain C & Aδ fibres pain is felt + gate is opened
  • 97.
    Gate control theory centralcontrol transmission cell when Aβ & C fibres are stimulated together, gate will be closed & pain is not felt pain is not felt touch Aβ fibre pain C & Aδ fibres + - gate is closed
  • 98.
    Consciousness • Consciousness isthe state of being awake and aware of one's surroundings • Assessed by observing a patient's alertness and responsiveness, and can been seen as a continuum of states ranging from – alert – oriented to time and place – communicative – disorientation – delirium – loss of any meaningful communication – loss of movement in response to painful stimulation • Glasgow Coma Scale (GCS) clinically measures the degree of consciousness
  • 99.
    Sleep • A naturalperiodic state of rest for the mind and body, in which the eyes usually close and there is a decrease in bodily movement and responsiveness to external stimuli • Whether it is a state of unconsciousness is questionable • coma is an unconscious state from which the person cannot be aroused • In general anaesthesia a patient is deliberately put into a state of unconsciousness under the action of centrally acting drugs
  • 100.
    Arousal & ReticularActivating System • Keeping in conscious, alert, awake state. Is a function of RAS. • In parallel with the ascending somatosensory tracts through thalamus to cortex. • There is a more diffuse ascending system consisting mostly of the ascending reticular formation and diffuse nuclei of the thalamus. • This RAS is necessary to maintain a general level of excitability in the cortex.
  • 101.
  • 102.
    CSF • Cerebral bloodflow: 750 ml/min (15% of cardiac output) • volume of CSF – 150 ml • rate of production – 500 ml/day • formed – mainly in the choroid plexuses of the ventricles – small amounts in the ventricles, arachnoid membranes & perivascular spaces
  • 103.
    formation • choroid plexusprojects into – horn of lateral ventricle – posterior portion of 3rd ventricle – roof of the 4th ventricle • Mechanism: – active transport of Na through the epithelial cells, Cl follows passively – osmotic outflow of water – glucose moves in to CSF – K and HCO3 moved out of CSF
  • 105.
    composition • similar toplasma – CSF Plasma – Na 147 (similar) 150 mmol/l – K 2.9 (less) 4.6 mmol/l – HCO3 25 24.8 mmol/l – Cl 113 (more) 99 mmol/l – Pco2 50 40 mmHg – pH 7.33 7.4 – osmolality 289 (similar) 289 mosm – protein 20 (less) 6000 mg/dl – glucose 64 (less) 100 mg/dl – urea 12 (less) 15 mg/dl • some substances do not pass into CSF
  • 106.
    blood brain barrier •tight junctions between capillary endothelial cells & epithelial cells in the choroid prevent some substances entering CSF • small molecules & lipid soluble substances pass through easily • blood-brain barrier exists between blood & brain tissue • blood-CSF barrier is present in choroid • these barriers are – highly permeable to water, CO2, O2, lipid soluble substances (such as alcohol), most anaesthetics, – slightly permeable to electrolytes – impermeable to proteins, large organic molecules – drugs (variable)
  • 107.
    blood brain barrier •CO2 & O2 crosses easily • H+ & HCO3- slow penetration • glucose – passive: slow penetration – active transport system by glucose transporter GLUT • Na-K-Cl transporter • transporters for other substances
  • 108.
    blood brain barrier –No blood brain barrier in the hypothalamus & posterior pituitary • substances diffuses easily • these areas contain chemoreceptors for various substances to detect changes in conc
  • 109.
    brain metabolism – brainmetabolism is 15% of total metabolism of the body (although brain mass is 2% of total body mass) – therefore brain has an increased metabolic rate – this is due to increased activity of neurons (AP) – requires oxygen – brain is not capable of anaerobic metabolism – energy supply is by glucose – glucose entry is not controlled by insulin
  • 110.
    Nerve degeneration and regeneration •Demyelination • Axonal degeneration • Remyelination • Axonal regeneration