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module 6: Neuroanatomy - Coggle Diagram

- - - - MOTOR
        
        CN III: Occulomotor - eyeball movement, sphincter papillae, ciliary muscle
        
        distribution
        
        o emerges from nuclei in the midbrain
        
        o exits through superior orbital fissure
        
        o at this point, divides into
        
        – inferior division (supplies inferior rectus, medial rectus & inferior oblique)
        
        – superior division (supplies superior rectus & levator palpebrae superioris)
        
        o Its parasympathetic distribution will enter ciliary ganglion & eventually supplies sphincter pupillae & ciliary mm.
        
        MOTOR
        
        SOMATIC
        
        controlled by oculomotor nucleus
        
        VISCERAL
        
        parasympathetic
        
        controlled by accessory motor nucleus
        
        course
        
        CN III runs between SCA and PCA at the level of midbrain
        
        Forms vascular triangle with CN III
        
        Risk of compression due to aneurysm/vascular abnormality
        
        DISEASE
        
        Oculomotor nerve palsy
        -Ptosis (drooping) of eye lid (paralysis of Levator palpebrae superioris muscle)
        -Abducted eyeball (paralysis of medial rectus muscle)
        
        CN IV: Trochlear
        
        course
        
        Emerges from the posterior surface of the midbrain
        
        • Pass anteriorly in lateral wall of cavernous sinus
        
        • Pass through SOF
        
        • Supplies the superior oblique muscle
        
        CN VI: AbducenT
        
        DISTRIBUTION
        
        o emerges from pons
        
        o course through cavernous sinus lateral to internal carotid artery
        
        o exits through superior orbital fissure
        
        oto supply lateral rectus muscle
        
        DISEASE
        
        CN VI is very near to internal carotid artery (ICA) within the cavernous sinus.
        
        Prone for compression due to aneurysm of ICA in the cavernous sinus and causes paralysis of the lateral rectus muscle
        
        Right internal squint,-
        
        due to paralysis of Lat rectus (CN6) & effect of Med rectus (CN3)
        
        CN XI: Accessory
        
        FUNC COMP: somatic motor
        
        COURSE
        
        CRANIAL
        
        emerges at dorsolateral sulcus of MO
        
        Joins CN10 temporarily as it passes jugular f.
        
        supplies mm. of pharynx via pharyngeal plexus.
        
        SPINAL
        
        emerges as several rootlets fr. first 5 Cv segments of spinal cords.
        
        supplies trapezius & sternocleidomastoid mm.
        
        CN XII: Hypoglossal
        
        COURSE
        
        emerges as several rootlets from MO.
        
        hypoglossal canal.
        
        supply mm of tongue- (styloglossus, hyoglossus, genioglossus & intrinsic mm. of tongue)
        
        Superior root of Ansa cervicalis
        
        conveyed fibers from C1 / C2
        
        supply infrahoid mm. (omohyoid, sternohyoid, thyrohoid)
      - SENSORY
        
        CN I: Olfactory - smell
        
        originates from the olfactory mucosa in the roof of nasal cavity
        
        o passed through cribriform plate of ethmoid bone
        
        o to enter the olfactory bulb in the anterior cranial fossa
        
        o travel via olfactory tract to several olfactory areas in the brain
        
        DISEASE- ANOSMIA (loss of smell)
        
        Old people – due the reduction in no. of olfactory neurosensory cells
        
        Trauma to cribriform plate – could lead to CSF leakage (rhinorrhea)
        
        CN II: Optic - vision
        
        distribution
        
        o optic tracts emerge from the lateral geniculate nucleus, located in the thalamus, from each hemisphere
        
        o form optic chiasm
        
        o Nasal retinal fibers desiccate to the opposite side
        
        o Temporal retinal fibers remain on ipsilateral side
        
        o the nerve exits through optic canal
        
        o to supply the retina
        
        course
        
        begins at retina
        
        optic chiasma
        
        fiber travel through opic tract
        
        1 more item...
        
        disease
        
        right side blindness - (lesion: section of optic chiasm) - defect at R&L temporal vision field (T)
        
        bitemporal hemianopsia - (lesion: section of the right optic nerve)
        
        left homonymous hemianopsia
        
        (lesion: section of right optic tract)
        
        defect at L temporal vision field (T)
        
        defect at R nasal vision field (N)
        
        CN VIII: Vestibulocochlear
        
        Functional component : special sensory (for hearing & equilibrium)
        
        emerges at junction of pons & medulla,
        
        exits internal acoustic meatus,
        
        SUPPLY-
        a) organ of Corti – within cochlear (for hearing)
        b) semicircular duct, utricle & saccule (for equilibrium)
      - BOTH
        
        CN V: Trigeminal
        
        divisions
        
        1. Ophthalmic division, CN V1
        
        COURSE
        
        originates from trigeminal ganglion in the middle cranial fossa
        
        divides into three branches:
        i. frontal nerve – 2 branches
        ii. lacrimal nerve
        iii. nasociliary nerve – 4 branches
        
        exit cranium via SOF into orbit
        
        NERVE
        
        FRONTAL
        
        LACRIMAL-Pass through supraorbital notch, supplies skin of forehead & scalp
        
        NASOCILIARY-Pass through common tendinous ring
        
        SUPRAORBITAL-Pass through supraorbital notch, supplies skin of forehead & scalp
        
        SHORT CILIARY-Supplies eyeball
        
        LONG CILIARY- Supplies eyeball
        
        ANT. POST. ETHMOIDAL-
        • Sensory fibers to meninges of anterior cranial fossa
        • Supplies upper part of nasal cavity & external nose tip
        • Supplies sphenoid & ethmoid air cells
        
        2. Maxillary division, CN V2
        
        Branches directly from maxillary trunk
        
        POST. SUP. ALVEOLAR N.- Supply the maxillary sinus & molar teeth
        
        ZYGOMATIC N.
        
        INFRAORBITAL N.
        
        MID. SUP. ALV. N.- upply premolar nerve
        
        ANT. SUP. ALV. N.- supply canine & incisor nerve
        
        ZYGOMATICOFACIAL - supply skin of face
        
        ZYGOMATICOTEMPORAL- supply skin of temple
        
        Branches derived from pterygopalatine ganglion
        
        PHARYNGEAL N.- Supply the nasopharynx mucosa
        
        NASOPALATINE N.
        
        GREATER PALATINE N.- Supply the hard plate
        
        LESSER PALATINE N.- Supply the soft plate
        
        COURSE
        
        originates from trigeminal ganglion in the middle cranial fossa.
        
        exit cranium via FORAMEN ROTUNDUM to reach pterygopalatine fossa.
        
        nerve branches are from:
        i. directly from maxillary trunk
        ii. derived from pterygopalatine ganglion
        
        3. Mandibular division, CN V3
        
        SENSORY
        
        o inferior alveolar nerve – give rise to the mylohyoid nerve (motor nerve)
        
        o lingual nerve
        
        o auriculotemporal nerve
        
        o buccal nerve
        
        MOTOR
        
        MASTICATION
        
        4 more items...
        
        OTHER
        
        4 more items...
        
        COURSE
        
        originates from trigeminal ganglion in the middle cranial fossa.
        
        exit cranium via FORAMEN OVALE To reach infratemporal fossa
        
        FUNC:
        o sensory functions >> ophthalmic and maxillary nerves
        o motor & sensory functions >> mandibular nerves
        
        • Emerges from the lateral aspect of pons
        
        CN VII: Facial
        
        CN IX: Glossopharyngeal
        
        Fx Comp: somatic sensory, special sensory (for taste), visceral sensory. somatic motor, visceral motor.
        
        It emerges from lateral aspects of medulla.
        
        Exits cranium via jugular foramen
        
        BRANCH
        
        CAROTID
        = carotid sinus & carotid body of ECA
        
        PHARYNGEAL
        = m.membrane of pharynx, tonsil, soft palate.
        
        LINGUAL
        = general & taste sensation to
        
        CN X: Vagus
        
        Fx Comp: somatic sensory, special sensory (for taste), visceral sensory. somatic motor, visceral motor.
        
        emerges as series of rootlets from lat. aspects of MO.
        
        exits cranium via jugular foramen
        
        gives rise to auricular b. (supplies skin of external ear)
        
        Continues inferiorly in carotid sheath & gives rise to:
        = pharyngeal branch, laryngeal b. palatal b.
        = heart, lungs, esophagus, stomach & intestine.
- - - - NEURON = -70mV
      - CARDIAC MUSCLE = -80mV
      - SKELETAL MUSCLE = -90mV
    - - • Unequal distribution of ions
      - • Large cations being trapped inside cell [K+ is major ICF cation & Na+ is major ECF cation]
      - • Na+ /K+ pump and limited permeability keep Na+ high outside cell
      - • K+ is very permeable and is high inside cell; attracted by negative charges inside
    - - Na-K pump: an active pump
      - because 3 Na+ are pumped out for every 2 K+ taken in, pump is electrogenic.
        • It adds about –3mV to RMP
  - - - • By rapid changes in permeability to ions
        •Neurons and muscles do this to generate and conduct impulses
  - - - Some ions are permitted to cross more easily than others. Ion channels stay open all the time (non-gated).
    - - Gates can be opened or closed in response to a triggering event – change in the protein conformation of the channel.
      - TRIGGER event
        
        VOLTAGE GATED- changes in membrane potential
        
        LIGAND/ chemically gated - binding of a specific extracellular chemical messenger to a surface membrane receptor
        
        MECHANICALLY GATED- stretching or other mechanical deformation
        
        THERMALLY GATED- Local changes in temperature (hot or cold)
        
        A triggering event at some point along the membrane opens some of the sodium channels, allowing some sodium ions to enter the ICF from the ECF. This initiates a graded depolarization of the cell locally where the triggering event occurs.
    - - MP changes occur by ion flow through membrane channels
        
        K+ leak channels are always open
        
        Voltage-gated (VG) channels are opened by depolarization
        
        VG K+ channels are closed in resting cells
        
        • VG Na+ channels are closed in resting cells
    - - POLARISED
        
        has potential due to the charges are separated across the plasma membrane
      - DEPOLARISED
        
        the membrane potential becomes less negative/ less polarized; the inside is less negative than RMP
      - LOCAL POTENTIAL
        
        GRADED POTENTIAL.
        
        Short distance signals. The amount of change in potential is proportional to the intensity of the stimulation.
        
        • Once Ach binds to the ligand gated Na+ channels, channels open, high conc. of Na+ (extracellular) inflow to the cell, K+ outflow from the cell – local depolarisation / local potential.
        • Local depolarisation decays with distance from
        stimulus (from dendrites/body to hillock)
        
        If the stimulus is strong enough or the amount of Ach is enough, the depolarisation reaches hillock, generate local current to invert the polarisation of the entire body of neuron - depolarisation reaches threshold (-55mV)
      - HYPERPOLARISED
        
        membrane potential becomes more negative than RMP.
      - THRESHOLD POTENTIAL
        
        level of stimulation to generate an action potential.
    - - • The action potential causes an electrical current that stimulates adjacent regions.
        • Series of action potentials occur sequentially along the length of the nerve (impulse propagation) .
        • AP is a wave of MP change that sweeps along the axon from axon hillock to synapse
        • Wave is formed by rapid depolarization of the membrane by Na+ influx; followed by rapid repolarization by K+ efflux
      - MECHANISM
        
        DEPOLARISATION
        
        • At threshold, VG Na+ channels open (fast to open)
        
        • Na+ driven inward by its electrochemical gradient
        
        • This adds to depolarisation, opens more channels (+ve feedback loop)
        
        • Causes a rapid change in MP from –70 to +30 mV
        
        REPOLARISATION
        
        • VG Na+ channels close; VG K+ channels open
        
        • Electrochemical gradient drives K+ outward
        
        • Repolarizes axon back to RMP
        
        VG K+ channels slow to open and slow to close – causes the repolarization over shoot the RMP – HYPERPOLARIZATION
      - CHARACTERISTIC
        
        • Once it is formed – will be propagated
        
        • The size, amplitude, and velocity (speed) of an action potential are independent of the intensity of the stimulus that initiated it as long as above threshold.
        
        • size or speed of action potential does not change if the stimulus intensity is above a threshold (supramaximum)
        
        • More intense stimulus causes more FREQUENT firing without changing the magnitude.
        
        • It obeys “All or None” Law
        
        • When MP reaches threshold an AP is irreversibly fired.
        • Because positive feedback opens more and more Na+ channel.
        • Shortly after opening, Na+ channels close and become inactivated until repolarization
        
        • Can’t be summated.
      - PROPAGATION
        
        • Action Potential spreads down the axon in a chain reaction
        
        • Unidirectional in vivo [Refraction prevents spread back across axon]
        
        • Speed of propagation
        
        varies with the axon diameter [Faster with larger and thick axons]
        
        assisted by the myelin sheath
        
        Impulse jumps from one “Nodes of Ranvier” to another
        
        Faster in myelinated axon known as ‘saltatory conduction’
        
        It increases conduction speed up to 15 times
        
        AXON CONDUCTION
        
        • Axon’s properties affect its ability to conduct current
        • Includes high resistance of cytoplasm [Resistance decreases as axon diameter increases]
        
        in an Unmyelinated Axon
        
        • After axon hillock reaches threshold and fires AP, its Na+ influx depolarizes adjacent regions to threshold
        
        • Generating a new AP
        
        • Process repeats all along axon
        
        • So AP amplitude is always same
        
        • Conduction is slow
        
        in Myelinated Axon
        
        • Gaps in myelin are called Nodes of Ranvier
        
        • APs occur only at nodes. VG Na+ channels are present only at nodes
        
        • Current from AP at 1 node can depolarize next node to threshold
        
        • Fast because APs skip from node to node
        
        • Called saltatory conduction
  - - - Na+ channels are inactivated and no matter what stimulus is applied they will not re -open to allow Na+ in & could not depolarise the membrane to the threshold of an action potential.
      - • Membrane cannot produce another AP because Na+ channels are inactivated
    - - Some of the Na+ channels have re-opened but the threshold is higher than normal making it more difficult for the activated Na+ channels to raise the membrane potential to the threshold of excitation.
      - occurs when VG K+ channels are open, making it harder to depolarize to threshold
- - - - DEFINE
        
        • Is a functional connection between a neuron (presynaptic) and another cell (postsynaptic)
        
        • There are electrical and chemical synapses
        
        • Electrical synapses are rare in nervous system
        
        • Synaptic transmission at chemical synapses is via neurotransmitters (NT)
      - ELECTRICAL
        
        • Depolarisation flows from presynaptic into postsynaptic cell through channels called gap junctions
        
        GAP JUNC
        
        • formed by connexin proteins
        
        • very fast conduction
        
        • found in smooth and cardiac muscles, brain, and glial cells
      - CHEMICAL
        
        • Synaptic cleft separates terminal bouton of presynaptic from postsynaptic cell
        
        • Pre synaptic terminal releases neurotransmitter
        
        • Synthesis of neurotransmitters
        
        • Ca2+ Influx triggers release of neurotransmitters
        
        • NTs are in synaptic vesicles
        
        • Vesicles fuse with bouton membrane; release NT by exocytosis
        
        • Neurotransmitter across synaptic cleft
        
        • Amount of NT released depends upon frequency of AP
        
        • Postsynaptic cell has specific receptors for neurotransmitter
    - - • Synaptic potentials are graded and can depolarize or hyperpolarize the receiving cell membrane.
      - • Excitatory postsynaptic potential (EPSP) opens Na+ channels and depolarizes the membrane.
      - • Inhibitory postsynaptic potential (IPSP) opens K+ channels and hyperpolarizes the membrane.
    - - • Acetylcholine: Autonomic ganglion, stimulates muscle contractions
        
        •Has nicotinic and muscarinic receptor subtypes.
        • These can be excitatory or inhibitory
        • Used in brain and ANS; used at all neuromuscular junctions
      - • Monoamines: norepinephrine, epinephrine, dopamine, serotonin
      - • Amino acids: glycine, glutamic acid, GABA
      - • Peptides: enkephalins, substance P
      - NEUROPEPTIDES
        
        • Enkephalins: bind to opiate receptors and relieve pain.
        
        • Beta-endorphin: binds to opiate receptors and lasts longer.
        
        • Substance P: helps perceive pain.
    - - LIGAND-GATED
        
        •Contain both a NT receptor site and an ion channel
        • Open when ligand (NT) binds to its receptors
      - NICOTINIC ACh
        
        • Formed by 5 polypeptide subunits
        • 2 subunits contain ACh binding sites
        
        • Opens when 2 AChs bind
        
        • Permits diffusion of Na+ into and K+ out of postsynaptic cell
        
        • Inward flow of Na+ dominates
        
        • Produces EPSPs
      - G Protein-Coupled
        
        • Is a 1 subunit membrane polypeptide
        • Activates ion channel indirectly through G-proteins
      - MUSCARINIC ACh
        
        • Binding of 1 ACh activates G-protein cascade which affects gated K+ channels
        
        • Opens some, causing hyperpolarization
        • Closes others, causing depolarization
      - Acetylcholinesterase- Inactivates ACh, terminating its action; located in cleft
    - - CONVERGENCE
        
        a single neuron receives impulses from two or more fibers, allows collection and processing of information.
        
        SUMMATION
        
        Their graded potential are all below threshold
        
        Graded potential arrives at the trigger zone and summate to create an AP
        
        SPATIAL
        
        • EPSPs fade quickly over time and distance
        • Spatial summation takes place when EPSPs from different synapses occur in postsynaptic cell at same time
        
        TEMPORAL- Temporal summation occurs because EPSPs that occur closely in time can sum before they fade
      - DIVERGENCE- an impulse from one neuron stimulates two or more fibers. This may amplify a response
        
        AMPLIFYING TYPE- corticospinal pathway in controlling skeletal muscle
        
        MULTIPLE TRACT- impulse transmission in the dorsal column of spinal cord
      - EPSP
        
        • Graded in magnitude
        
        • Have no threshold
        
        • Na+ or Ca2+ influx cause depolarisation
        
        • Summate
        
        • Have no refractory period
    - - POSTSYNAPTIC
        
        • GABA and glycine produce IPSPs
        
        • IPSPs dampen EPSPs
        
        • Making it harder to reach threshold
      - PRESYNAPTIC
        
        • Occurs when 1 neuron synapses onto axon or bouton of another neuron, inhibiting release of its NT
        • K+ efflux or Clinflux causes hyperpolarisation
  - - - • Neuromuscular junction : the synapse between motor neuron and muscle fiber
      - • Motor neurons : are the nerves that innervate muscle fibers
      - • Motor unit : single motor neuron and the muscle fibers it innervate
      - • Single synaptic ending of the motor neuron innervating each muscle fiber and underlying specializations of sarcolemma
      - • NT released from presynaptic terminal is ACh, postsynaptic membrane contains a nicotinic receptor.
    - - • As axon approaches muscle , it divides into many terminal branches and loses its myelin sheath
      - • Each of these axon terminal forms special junction ,a neuromuscular junction with one or more muscle fiber
      - • The axon terminal is enlarged into a knoblike structure ,the terminal bouton, which fits into shallow depression in underlying muscle fiber
    - - • Ca2+ uptake into the terminal causes release of the neurotransmitter acetylcholine into synaptic cleft , which has been synthesized and stored into synaptic vesicles
        • ACh travels across the synaptic cleft to postsynaptic membrane which is also known as motor end plate.
      - • Motor end plate contains nicotinic receptors for ACh, which are ligand gated ion channels
      - • ACh binds to the alpha subunits of nicotinic receptors and causes conformational change.
      - • When conformational changes occurs ,the central core of channels opens & permeability of motor end plate to Na+ & K+ increases
      - END PLATE POTENTIAL
        
        • When the ion channel on post synaptic membrane opens both Na+ & K+ flow down their concentration gradient.
        
        • At resting potential net driving force for Na+ is much greater than K+ ,when ACh triggers opening of these channels more Na+ moves inwards than K+ out wards, depolarizing the end plate. This potential change is called end plate potential (EPP).
        
        • EPP is not an action potential but it is simply depolarization of specialized motor end plate
        
        • Small quanta (packets) of ACh are released randomly from nerve cell at rest, each producing smallest possible change in membrane potential of motor end plate, the MINIATURE EPP.
        
        • When nerve impulse reaches the ending, the number of quanta release increases by several folds and result in large EPP.
        
        • EPP then spread by local current to adjacent muscle fibers which are depolarized to threshold & fire action potential
      - ACETYLCHOLINESTERASE ENDS ACh
        
        • To ensure purposeful movement ,muscle cell electrical response is turned off by acetylcholinesterase (AChE), which degrade ACh to choline & acetate
        
        • About 50%of choline is returned to the presynaptic terminal by Na+choline transport to be reused for ACh synthesis.
        
        • Now muscle fiber can relax, if sustained contraction is needed for the desired movement another motor neuron AP leads to release of more ACh
    - - BLACK WIDOW SPIDER VENOM
        
        the venom of black widow spider exerts its effect by triggering explosive release of ACh from the storage vesicles, not only at NMJ but all cholinergic sites. all cholinergic sites undergoes prolonged depolarization.
        
        • Respiratory paralysis – depolarisatiom block – VG Na+ channels trapped in inactivated state – no new AP – inhibit contraction of diaphragm
        
        • The most harmful result is respiratory failure
      - BOTULINUM TOXIN
        
        botulinum toxin exerts its lethal effect by blocking the release of ACh.
        
        • Clostridium botulinum poisoning (botulism) most frequently resulted from improper canned food contaminated with clostridia bacteria
        
        • Death is due to respiratory failure caused by inability to contract diaphragm.
      - CURARE
        
        competitively binds to ACh receptor sites on motor end plate, so ACh can not combine with these sites to open ion channels, no EPP and muscle paralysis.
        
        • Curare does not alter membrane permeability nor inactivated by AChE.
        
        • In severe poisoning person dies of respiratory failure caused by inability to contract the diaphragm.
        
        • In past it was used as deadly arrowhead poison.
      - ORGANOPHOSPHATE
        
        • Irreversibly inhibiting AChE – prevents the inactivation of release ACh
        
        • Death resulted from respiratory failure
        
        • Depolarisation block, no new AP
        
        • Lethal action at nicotinic receptors of respiratory muscles; other symptoms related to the effect of build up at muscarinic receptors, e.g. drooling, vomiting, diarrhoea; ACh overstimulation in the brain leads to seizure
        
        • Examples: pesticides (malathion – mosquito control), military nerve gas (chemical weapon sarin gas)
      - MYASTHENIA GRAVIS
        
        • A disEase involving NMJ is characterized by the extreme muscular weakness (myasthenia=muscular & gravis=severe)
        
        • It is an auto immune condition (autoimmune means immunity against self) in which the body produces antibodies against its own motor end plate ACh receptors.
        
        • Thus not all ACh molecules can find functioning receptors site with which to bind.
        
        • As a results ,AChE destroys much of ACh before it ever has a chance to interact with receptor site & contribute to EPP.
        
        • Treatment : It is treated with long acting anticholinesterase inhibitor pyridostigmine or neostigmine. Which maintains the ACh levels at NMJ at high levels thus prolonging the time available for ACh to activate its receptors.
- - - - Anterior temporal lobe
      - Posterior orbital frontal cortex
      - Anterior cingulate gyri & subcallosal gyr
      - Fx as cerebral assoc area for control of behaviour
    - - Includes portions of the hypothalamus and other forebrain structures that encircle brain stem
      - Responsible for:
         Emotion (preparing for attack, crying, laughing, joy satisfaction, pleasure, fear)
         Plays important role in motivation and learning and memory
      - Amygdala recognises angry or fearful facial expressions
      - Hippocampus involved with learning, long-term memory and storage
    - - Located in the central gray area surrounding the aqueduct of Sylvius and extending into periventricular zone, amygdala & hippocampus
      - • Can inhibit the reward centres
      - • Strong stimulation causes a pattern of rage
        
        • Defence posture
        
        • Piloerection
        
        • Wide-open eyes, dilated pupils
    - - Basolateral nuclei are highly developed in human and plays many behavioural activities
      - • It receives neuronal signals from all portions of limbic cortex, neocortex esp auditory & visual assoc areas
      - • It transmits signals back to the same cortical areas, hippocampus, into the septum, thalamus & hypothalamus
      - • Behavioural awareness areas that operate at a semiconscious level
      - Effects of stimulating the amygdala:
        
        Through hypothalamus cause change in:
        
        • BP, HR, GI motility & secretion
        
        • Defecation & micturition
        
        • Pupillary dilation
        
        • Piloerection
        
        • Secretion of various ant pit hormones
        
        Other involuntary movements
        
        A pattern of rage, escape, punishment, severe pain and fear
        
        Sexual activities
  - - - superior
        
        thalamus
      - inferior
        
        Continues with tegmentum of midbrain
      - lateral
        
        Internal capsule
      - medial
        
        Lateral wall of 3rd ventricle
    - - Autonomic
      - Endocrine
      - Neurosecretion
      - Temperature regulation
      - Regulation of food & water intake
      - Emotion & behaviour
      - Control of circadian rhythm
  - - - posterior end
        
        expanded to form pulvinar, which overhangs the superior colliculus.
        
        Pineal gland
      - medial
        
        connected to the opposite thalamic by interthalamic adhesion.
        
        Lateral wall of 3rd ventricle (transverse section)
      - anterior end
        
        narrow and rounded
      - INTERNA MEDULLARY LAMINA
        
        Y-shaped structure containing nerve fibres.
        
        separates reticular nucleus from thalamic mass
        
        contains thalamocortical & corticothalamic fibers
      - lateral
        
        internal capsules
      - superior
        
        Floor of lateral ventricle [coronal section]
      - inferior
        
        Hypothalamus [coronal section]
    - - Transmit general & special sensory to sensory cortices
      - • Receive impulses from cerebellum & basal ganglia and interface with motor regions in frontal lobe
      - • Have connections with associative & limbic areas of cortex
  - - - Medially: caudate nucleus & thalamus
        Laterally: lentiform nucleus
    - - Medially: lentiform nucleus
        Laterally: claustrum
    - - Claustrum, Putamen, Internal & External globus pallidus
  - - - CAUDATE NUCLEUS
        
        HEAD
        
        ✓large
        ✓in frontal lobe
        
        BODY
        
        ✓tapered curve
        ✓in occipital lobe
        
        TAIL [in temporal bone]
        
        ✓terminates in amygdaloid nucleus
        ✓roof of inferior horn of lateral ventricles
      - PUTAMEN
      - GLOBUS PALLIDUS
    - - ventricle of the brain, thalamus, subthalamic nuclei & substantia nigra
    - - i. Part of extra-pyramidal motor system
      - ii. Facilitate behaviour & movement – required and appropriate
      - iii. Inhibit unwanted & inappropriate motor actions or behaviour
      - The balance between the cerebellum and the basal ganglia allows smooth, coordinated movement, and a disturbance in either system will show up as movement disorders.
    - - PARKINSONISM
        
        degeneration of dopamine-producing cells in substantia nigra (depletion of dopamine in striatum)
      - HUNTINGTON'S
        
        hereditary disease of unwanted movement results from degeneration of the caudate and putamen, and produces continuous dance-like movements of the face and limbs
      - HEMIBALISM
        
        flailing movements of one arm and leg (one-sided), caused by damage (i.e., stroke) of the subthalamic nucleus
- - - - A rapid, involuntary sequence of actions occurring in response to a STIMULUS
      - FUNC
        
        • To maintain muscle length
        
        • To protect from injury
        
        • To maintain body balance and posture
      - INTEGRATING CENTRE
        
        • Spinal cord (e.g. knee jerk, inverse stretch reflex, withdrawal reflex)
        • Brainstem (e.g. pupillary light reflex, gag reflex, coughing reflex)
      - COMPONENT (DEEP monosynaptic)
        
        Sensory receptor (muscle spindles)
        
        • Are found in almost all skeletal muscles esp. in those that exert fine motor control
        
        • Functions: to maintain muscle length and muscle tone and posture
        
        • 3 Main components:
        
        INTRAFUSAL F.
        
        • Provide regulation of muscle spindle stiffness – variable sensitivity to stretch
        
        PRIMARY SENSORY AXON
        
        • Ia and II fibres send impulses to spinal cord
        • Type Ia detects muscle length and rate of change in muscle length
        • Type II detects muscle length
        
        GAMMA MOTOR N.
        
        • Innervate the contractile end of intrafusal fibres
        • Regulates muscle spindle tension (stiffness)
        
        Stimulation of γMN causes the contractile ends of intrafusal fibres to shorten.
        • Therefore, nuclear bag portion stretches.
        • This leads to reflex contraction of the skeletal muscle.
        
        Increased γMN activity increases spindle sensitivity during stretch.
        • Input from various brain regions to γMN influences the sensitivity of the muscle SPINDLES
        
        CO-ACTIVATION OF gamma & alpha MN
        
        RELAXED MUSCLE
        
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        CONTRACTED MUSCLE in hypothetical sit.
        
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        CONTRACTED MUSCLE IN NORMAL
        
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        FACTORS to increase its discharge.
        [causes hyperactive of stretch reflex]
        
        PHYSIOLOGICAL
        
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        PATHOLOGICAL
        
        1 more item...
        
        Sensory neuron (group Ia and group II afferents)
        
        Integrating center (spinal cord)
        
        Motor neurons (α- and γspinal motor neurons)
        
        Effector (the same muscle (homonymous) of muscle spindles)
      - STRETCH [Monosynaptic reflex]
        
        Stimulus: stretching of the skeletal muscle
        
        Stimulation of intrafusal fibre/muscle spindle (stretch rec.)
        
        Impulses sent via Ia/II fibre
        
        Integration centre: spinal cord(L2-4), monosynapse.
        
        Impulse sent to effector via α-MN fibre
        
        Effector & response: extrafusal fibres (the same muscle) contract
        
        SIGNIFICANCE
        
        ▪ They help maintain a normal posture
        
        ▪ They function to oppose sudden changes in muscle length
      - WITHDRAWAL [polysynaptic]
        
        RECIPROCAL INNERVATION
        
        Sensory neurons conduct AP from pain receptors to s. cord
        
        sensory neurons synapse w/ excitatory inter n. (that are part of withdrawal reflex)
        
        collateral branches of sensory neurons also synapse w/ inhibitory inter n. (that are part of reciprocal innervation)
        
        the inhibitory inter n. synapse w/ alpha MN supplying the extensor muscles -> causing them to relax and not oppose the flexor muscles of withdrawal reflex, which are contracting
        
        CROSS EXTENSOR- To stabilise the body.
        - FLEXOR - to allow rapid withdrawal of appendage from dnger stimuli
        - GOLGI TENDON ORGAN- to detect muscle tension -> prevent mm damgae
        
        INVERSE STRETCH
        
        Stimulus: excessive muscle contraction
        
        Receptor: Golgi tendon organ (GTO)
        
        Afferent nerve: Ib fibre (myelinated)
        
        Integration centre: spinal cord
        
        • Ib synapses with inhibitory interneuron to αMN supplying agonist muscle and excitatory interneuron to antagonist muscle
        
        Efferent nerve: αMN (inhibited)
        
        Effector/response: muscle (agonist) relaxation
    - - Function – protective
      - • Normal response [• Plantar flexion]
      - • Clinical importance.
        • In UMNL – extension of toes (Babinski sign)
    - - Loss of inhibitory commands from UMN.
        • Receptor involved is GTO
    - - voluntary UMN innerv. of arm overflows to increase excitability of LMN pool of lower extremities -> make easier to elicit reflex
  - - - PAIN- an unpleasant sensory & emotional experience associated with actual or potential tissue damage [The International Association for the Study of Pain (IASP)]
        
        occurs when tissues are being damaged, and it causes the individual to react to remove the stimulus
        
        • is a symptom
        
        • is subjective, protective, and modified by developmental, behavioural, personality and cultural factors
        
        • associated signs are crying, sweating, increased HR & BP, behavioural changes.
      - • Definition of nociception:
        • Neural response related to potentially tissue damage stimuli
      - TYPES
        
        FAST
        
        • Also called sharp pain, pricking pain, acute pain and electric pain
        
        • Felt within 0.1 sec after the stimulus is applied
        
        • Well localised
        
        • Not felt in most deeper tissues of the body
        
        STIMULUS= mechanical & thermal
        
        SLOW
        
        • Also called slow burning pain, aching pain, throbbing pain, nauseous pain and chronic pain
        
        • Felt only after 1 sec or more and then increases slowly over many seconds or even minutes
        
        • Poorly localised
        
        • Usually associated with tissue destruction
        
        • Can lead to prolonged, almost unbearable suffering
        
        STIMULUS= all 3 types
    - - Free nerve ending
        
        • Widespread in the superficial layers of the skin, somatic tissues and certain internal tissues, except brain tissue and lung parenchyma
        
        • E.g. periosteum, arterial walls, joint surface and etc.
      - TYPE OF STIMULUS
        
        mechanical
        
        thermal
        
        chemical-
        
        bradykinin, serotonin, K+
        
        ions, histamine, H+
        
        , lactic acids, ACh,
        
        proteolytic enzymes, leucotrienes, cytokines, capsaicin
      - Non-adapting nature of pain receptors
        
        Adapt very little and sometimes not at all
        
        • As the pain stimulus continues, esp. for slow, aching, nauseous pain, excitation of pain fibres becomes progressively greater – increase the sensitivity of pain receptor (hyperalgesia)
        
        Rate of tissue damage as a stimulus for pain
        
        • Pain resulting from heat (>45°C) is closely correlated with the rate at which damage to the tissues is occurring and not with the total damage that has already occurred
        
        • Intensity of pain is also closely correlated with the rate of tissue damage from causes other than heat (bacterial infection, tissue ischemia, tissue contusion)
      - NEUROTRANSMITTERS
        
        PROSTAGLANDIN & BRADYKININ- sensitize nociceptors to activation by low-intensity stimuli
        
        HISTAMINE & 5-HT- cause pain when directly applied to nerve endings
        
        HYDROGEN IONS & 5-HT - act directly on ion channels on cell, but mostly binds to membrane receptors and activate 2nd mess. sys. via G proteins
    - - TISSUE DAMAGE
        
        • Bradykinin thought to be the agent most responsible for causing pain following tissue damage
        
        • Intensity of pain felt correlates with local increase in K ion concentration or increase in proteolytic enzymes
      - TISSUE ISCHEMIA
        
        • When blood flow is blocked, the tissue often becomes very painful and the greater the rate of metabolism, the more rapidly the pain occurs
        
        • May be due to the large accumulation of lactic acid (anaerobic metabolism) as well as bradykinin and proteolytic enzymes (cell damage)
      - MUSCLE SPASM
        
        • Results partially from the direct effects of muscle spasm in stimulating mechanosensitive pain receptors
        
        • Also the indirect effects of muscle spasm to compress blood vessels and cause ischemia
        
        • Spasm increases the rate of metabolism making the relative ischemia even greater – release of chemical pain-inducing substances
  - - - • Neospinothalamic tract is used for transmission of fast pain (Aδ fibre)
      - • Mechanical and acute thermal pain
      - • First order neuron (pain fibre) terminate lamina I (lamina marginalis) of the dorsal horns, then excite second order neuron of the neospinothalamic tract
      - • Glutamate is the primary neurotransmitter, secreted by Aδ fibre in the spinal cord
      - • Second order neuron decussates to the opposite side of the cord through the anterior commissure and then turn upward to the brain via the anterolateral columns - lateral spinothalamic tracts
      - • Most terminate in the thalamus (ventrobasal complex and posterior nuclear group), a few fibres terminate in the reticular formation of brain stem, and then third order neuron transmits signals to the basal areas of brain and somatosensory cortex.
    - - Pain signals enter the spinal cord (first order neuron)
      - • First synapse is present in the dorsal horn of the spinal cord
        
        • Afferent fibre (C fibre) enters the spinal cord
        
        • Synapses at the laminae II & II of the dorsal horns (substantia gelatinosa)
        
        • Neurotransmitter at the first synapse of the pain pathway is substance P (chronic pain)
      - Cross over (decussate) through the anterior commissure to the opposite side
      - • The second order neuron travels through (ascends up) the lateral spinothalamic tracts
      - • Pain perception at the thalamus (10-25%), most terminate at reticular nuclei, tectal area & periaqueductal gray region
      - • The third order neuron sends impulses to the somatosensory cortex for the localisation of pain
      - • Localized only to a major part of the body
  - - - MODULATION
        
        • Pain modulation means pain perception variability which is influenced by endogenous & exogenous mechanism, that can increase or decrease pain threshold.
        
        PAIN SUPPRESION. analgesia system – block pain signals
        
        has 3 components:
        
        Periaqueductal gray and periventricular areas of mesencephalon and pons
        
        • Raphe magnus nucleus in the pons and the nucleus reticularis in the medulla
        
        • Pain inhibitory complex in the dorsal horns of the spinal cord
        
        Transmitters substances
        
        • Enkephalin – causes both pre- and post-synaptic inhibition of incoming pain fibres (Aδ, C)
        
        • Serotonin – released from the dorsal horn and causes the release of enkephalin
        
        OPIOID
        
        Brain’s opiate system (endogenous opioid peptides)
        • Endorphin (hypothalamus & pituitary)
        • Enkephalins, dynorphin (brain stem)
        
        ACTION
        
        • Endogenous opioid peptides: endorphin, enkephalin, dynorphin
        
        • Exogenous opioid peptides: morphine, codeine, fentanyl, pethidine, opium (poppy plant), heroin
        
        • Act presynaptically or postsynaptically
        
        • Blocks Ca2+ channels and inhibits Ca2+ influx and thereby prevent pain neurotransmitter release (glutamate, substance P) from presynaptic membrane
        
        • Open up K+ channels and causes K+ efflux and resulting in hyperpolarization of the membrane and prevents pain neurotransmitter activity
        
        • Inhibits cAMP activity and alters pain neurotransmitter activity
        
        • Activates descending pain modulatory (inhibitory) pathway
        • Inhibit GABA-mediated inhibition of descending pathway activity
        
        Enhancement and inhibition all levels of the nervous system. Modulation at the peripheral nerve, spinal cord, brain sites influences pain perception.
        
        GATE CONTROL THEORY
  - - - PULPAL ORIGIN
      - PDL ORIGIN
- - - - WHAT?
        
        Largest part of the brain.
        
        2 hemispheres- separated by longitudinal fissure
        
        Connected by each other by corpus callosum
        
        SURFACE= Gray matter.
        
        white matter covered with layer of neural cortex (gray)
        
        FISSURE
        
        longitudinal
        
        contain- falx cerebri, ant cerebral arteries, corpus colossum
        
        SULCI
        
        central, parieto-occipital, calcarine, cingulate
        
        LOBES
        
        frontal,
        
        precentral gyrus, ant to PCG
        
        pars triangularis, pars opercularis
        
        mid frontal gyrus
        
        ant. part
        
        ant part of paracentral lobule-medial
        
        occipital,
        
        Walls of calcarine sulcus
        
        Close to visual area
        
        parietal
        
        postcentral gyrus
        
        su[. parietal lobule
        
        inf. parietal lobule
        
        lower end of PCG
        
        temporal
        
        Lower end of central sulcus & sup temporal gyrus
        
        Uncus & anterior part of parahippocampal gyrus
        
        FUNC
    - - WHAT?
        
        “Little brain”
        
        Divides into hemispheres
        
        Unconsciously control voluntary muscles to produce coordinated and smooth action.
        
        Each cerebellar hemisphere controls ipsilateral side of the body
      - LOCATION
        
        within posterior fossa,
        
        straddles the brainstem &
        
        forms roof of 4th ventricle
        
        Separated from cerebral cortex by TENTORUM CEREBELLI
      - PARTS
        
        VERMIS (join 2 hemisphere)
        
        HEMISPHERE
      - DIVISION/LOBES
        
        ANTERIOR- neocerebellum (coordination)
        
        POSTERIOR- paleocerebellum (posture)
        
        FLOCCULONODULAR- archicerebellum (equilibrium).
        [flocculus + nodule of inferior vermis]
        
        PRIMARY FISSURE devide ant. & post. lobe
      - DISEASE
        
        VERMIS SYN.- -loss of postural control
        
        CEREBELLAR HEMISPHERE SYN- – ipsilateral incoordination of limb, may fall to the side of lesion
        
        DYSARTHIA- speech
        
        NYSTAGMUS- eye movement
    - - TYPE
        
        DURA MATER- - strong, "tough mother"
        e.g: falx cerebri , falx cerebelli, tentorium cerebelli, diaphragma sella
        
        ARACHNOID - spidery, holds blood vessels
        
        PIA MATER - "delicate mother"
      - STRUCTURE
        
        FALX CEREBRI
        
        TENTORIUM CEREBELLI
        
        FALX CEREBELLI
        
        DIAPHRAGM SELLAE
      - CEREBRAL HAEMORRHAGE
        
        traumatic posterior displacement of brain.
        
        may tear superior cerebral veins
        produces a subdural hematoma
        
        Symptoms ; headache, confusion & disturbance of memory
        
        (Subarachnoid haemorrhage)
        
        Rupture of arteries that lie within Subarachnoid space, causes blood to contaminate the CSF
        e.g: aneurysms near the circle of Willis at base of brain
        
        Symptoms: Increased intracranial pressure 🡪Headache, LOC, Possibly followed by coma & death
  - - - ARTICULATION
        
        Muscular movements of the mouth, tongue, larynx, vocal cords
        
        • Facial & laryngeal regions of motor cortex activate the respective muscles
        
        • Cerebellum, BG & sensory cortex help to control the sequences and intensities of muscle contraction
      - BROCA'S AREA
        
        Word formation
        
        • Plans motor patterns to form WORDS
        
        • Lesion causes nonfluent aphasia (motor aphasia)
      - WERNICKE'S AREA
        
        Interpretation of language
        
        • Closely assoc with primary & secondary hearing of temporal LOBE
        
        • Lesion causes fluent aphasia
      - ANGULAR AREAS
        
        Lesion causes word blindness (dyslexia)
        
        Interpretation of visual info
      - SPEAKING
        
        A HEAR WORD
        
        primary auditory area
        
        wernicke's area
        
        broca's area
        
        motor area
        
        A WRITTEN WORD
        
        primary visual cortex
        
        angular gyrus
        
        wernicke's area
        
        broca's area
        
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    - - ASSOCIATED - classical conditioning
      - NON-ASSOCIATED
        
        HABITUATION
        
        • Neutral stimulus is repeated many times
        
        • 1 st time is novel & evokes reaction
        
        • By repetition, it evokes less and less electrical response
        
        • Eventually, subject becomes habituated to the stimulus and ignores it
        
        • It helps us distinguish meaningful information from the background
        
        • E.g. fire alarms in preclinical blocks
        
        SENSITISATION
        
        • Is opposite of habituation
        
        • Progressive amplification of a response
        
        • When a stimulus has become habituated, it is paired with noxious stimulus
        
        • Subsequently, subject will react more strongly to the 1st stimulus
    - - BRAIN REGION
        
        HIPPOCAMPUS
        
         Short-term memory & consolidation for long-term memory.
        
         Important for declarative memory (facts).
        
        MEDIAL TEMPORAL LOBE-  Memory consolidation
        
        LIMBIC SYSTEM-  Emotional memory
        
        CEREBELLUM-  motor & sensory regions
         procedural memory (skills).
        
        PREFRONTAL CORTEX-  temporary storage memory site.
         Important for short-term memory.
      - SHORT TERM
        
         Holding about 7-12 pieces of information.
        
         Last for seconds to hours.
        
         Involve transient strengthening of pre-existing synapse.
        
         Stored in hippocampus and prefrontal cortex.
      - LONG TERM
        
         Days to years
        
         Involves activation of specific gene (camp response element binding, CREB) that controls protein synthesis to form new synapses (structural changes).
        
         Stored in various parts of cerebral cortex.
      - STAGES
        
        ACQUISITION
        
        CONSOLIDATION
        
        RETRIEVAL
        
         Process of transferring short-term memory into longterm memory
        
         Involves long-term potentiation (LTP)
        
         LTP is a prolonged increase in the strength of existing synaptic connections following repetitive stimulation
        
         In LTP, there is accumulation of Ca2+ in postsynaptic terminals and increase sensitivity of receptors to neurotransmitter
        
         This process occurs in hippocampus (mainly) and medial temporal lobes of the cerebral cortex
      - MEMORY LOSS
        
        RETROGRADE amnesia – inability to recall recent past events.
        
        ANTEROGRADE amnesia – inability to store new memory in long-term storage.
        
        ALZHEIMER'S- degeneration of cholinergic neurons &
        monoaminergic systems in cerebral cortex and hippocampus
    - - TYPES
        
        SLOW WAVE (NON-REM)
        
        • Deep, slow wave
        
        • Restful
        
        • Decrease in peripheral vascular tone & other vegetative fx
        
        • Divided into 4 stages
        
        RAPID EYE MOVEMENT, REM
        
        paradoxical sleep
        
        • Active form of sleep, assoc with dreaming and muscle movement
        
        • HR & RR become irregular
        
        • Muscle tone is depressed
        
        • The brain is highly active
      - STAGES
        
        • NREM sleep passes through stage 1 & 2, 70-100 min in stage 3 and 4
        
        • Sleep then lightens and REM period follows
        
        • This cycle is repeated at intervals of 90 min throughout the night
        
        • Toward morning, there is less stage 3 & 4, and more REM sleep
        
        • REM sleep occupies 50% of total sleep time in neonates
        
        • In adults, REM sleep declines and plateau at ~25%
      - IMP.
        
        NERVOUS SYS.
        
        • To restore normal levels of brain activity & balance among the different functions of CNS
        
        • Learning & memory consolidation
        
        • Neural maturation
        
        • Cognition
        
        FUNC SYS OF BODY
        
        • To maintain metaboliccaloric balance, thermal equilibrium & immune competence
        
        • Clearance of metabolic waste products generated by neuronal activity
        
        • Conservation of metabolic energy
- - - - 2 LATERAL VENTRICLES (each cerebral hemisphere)
        
         Roughly C shaped
        
        4 PARTS
        
        1. Central part of the body
        
        Location: in the parietal lobe
        
        • Roof: trunk of corpus callosum
        
        • Floor: from medial to lateral;
        
        superior surface of thalamus,
        
         body of caudate nucleus
        
         the stria terminalis
        
        Medial wall: septum pellucidum
        
        Anterior horn
        
        Location: within frontal lobe
        
        • Roof: trunk of corpus callosum
        
        • Floor:  Rostrum of corpus callosum
         Head of caudate nucleus
        
        • Medial wall: septum pellucidum
        
        Posterior horn
        
        Location: in the occipital lobe
        
        • Roof & lateral wall: formed by tapetum (fibers from corpus callosum)
        
        • Medial wall: shows 2 elevations:
        
        Upper elevation -> bulb of posterior horn (forceps major)
        
         Lower elevation -> calcar avis (calcarine sulcus)
        
        Inferior horn
        
        Location: in the temporal lobe
        
        Roof: formed by
        
         Caudate nucleus (tail)
        
         Amygdaloid nucleus
        
         Stria terminalis
        
        FLOOR
        
         Hippocampus
        
         Alveus
        
         Collateral eminence
        
        LATERAL WALL-  Tapetum of corpus callosum
        
        Filled with CSF approx. 7-10ml
      - 3RD VENTRICLE (in diencephalon)
        
        DESCRIPTION
        
        Narrow funnel-shaped cavity of the brain
        
         Located in the midline, comprising the central part of the ventricular system
        
        ROOF- : formed by fornix
        
        ANTEROR WALL
        
         Parts of fornix
        
         Anterior commissure
        
         Lamina terminalis
        
        FLOOR
        
         Mammilary bodies
        
         Infundibular stalk (infundibulum)
        
         Optic chiasma
        
        POSTERIOR WALL-  Pineal gland & Posterior COMMISURE
        
        LATERAL WALL- Thalamus , Hypothalamus
        
         Cavity within diencephalon
        
         Communication: o Foramen of Monro  lateral ventricles
        o Cerebral aqueduct  fourth ventricle
        
        Described as cuboidal structure
        
        RECESSES
        
        • Infundibular recess – extends downwards into infundibulum (stalk of the pituitary gland)
        
        • Optic (chiasmatic) recess – situated at the junction of anterior wall & floor of the ventricle
        
        • Anterior recess – extends anteriorly in front of interventricular foramen
        
        • Suprapineal recess – extends posteriorly above the stalk of pineal gland
        
        • Pineal recess – extends posteriorly between the superior & inferior laminae of the stalk of the pineal gland
      - 4TH VENTRICLE (in the hindbrain)
        
        DESCRIBE
        
         Tent/diamond shaped cavity
        
         Between cerebellum & brainstem
        
         Superior end receives cerebral aqueduct
        
         Inferior end continuous with central canal of spinal cord
    - - cerebral aquaduct / foramen of Sylvius
      - INTERVENTRICULAR/ Foramen of Monro
      - CENTRAL CANAL
  - - - CSF is normally clear
      -  Volume: 150mL
      -  Rate of production: 0.5mL/minute
    - -  Protein: 15-45mg/100mL
      -  Glucose: 50-85mg/100mL
      -  Chloride: 720-750mg/100mL
      -  Number of cells: 0-3 lymphocytes/ mm3
    - - Serve as a protective fluid cushioning & lubricating the spinal column
      -  The cushioning helps prevent injury to the brain
      -  Serve as a nutrient & metabolic waste exchange fluid
    - - Ependymal cells called choroid plexus [in LV, 3rd ventricle & 4th ventricle]
    - - LV choroid plexus produced & secrete CSF
      - Flows through Foramen of Monro into 3rd ventricle
      - Choroid plexus in 3rd ventricle add more CSF
      - Flows down the Foramen of Sylvius into 4th ventricle
      - Choroid plexus in 4th ventricle add more CSF
      - CSF flows out the lateral aperture & median aperture
      - CSF fills the subarachnoid space & bathes the external brain & s.cord
      - CSF is reabsorbed into venous blood of the dural venous sinuses at arachnoid villi/ granulation
  - - -  Leakage of CSF into nose
      -  May be clear fluid or mixed with blood
      -  Trauma is the most common cause. Either:
        
        o accidental
        
        o surgical such as endoscopic sinus surgery, nasal polypectomy, skull base surgery
    - - Dilation of the cerebral ventricular system due to:
        
         Obstruction of CSF flow
        
         Overproduction of CSF
        
         or Reabsorption failure
      - Excessive accumulation of CSF in the brain create harmful pressure on the tissues of the brain
      - Congenital – present at birth due to genetic abnormalities or developmental disorder.
        [Congenital stenosis of cerebral aqueduct ]
        Or acquired – develops later at some point afterward
- - - - FUNC
        
        centre of perception,
        
        site of integration of sensory info
        
        initiation and coordination of motor activity
      - ORGANIZATION OF NERVOUS TISSUE:
        
        collections of neutrons are called nuclei.
        
        collection of axons are called tracts
    - - Extension of CNS
      - 12 CRANIAL NERVE- emerge from brain
      - 31 PAIRS SPINAL NERVE - arise from s. cord
      - FUNC
        
        conveys neural impulses.
        
        from CNS as outputs to muscles & glands
        
        to CNS as input from sensory receptors
      - DIVISION
        
        MOTOR
        
        SENSORY
      - ORGANIZATION OF NERVOUS TISSUE:
        
        collection of neutrons are called GANGLIA.
        
        collection of axons are called NERVES
  - - - imp to furnish microenvironment suitable for neuronal act. (since nerv tiss. has no intercellular matrix)
      - TYPES
        
        EPENDYMAL CELL- specialised epithelium lining s. cord & ventricles
        
        ASTROCYTES- provide media for exchange of metabolites (nutrition)
        
        OLIGODENDROCYTES
        
        MICROGLIA CELLS- defense/ immunological func
    - - free nerve endings.
        
        merkel discs (touch).
        
        Krause end bulbs (touch).
        
        Meissner corpuscles (touch).
        
        Pacinian corpuscles (pressure).
        
        Ruffini endings (pressure)