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B&B notes

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Emma O'Bryan

on 23 May 2014

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Transcript of B&B notes

B&B notes
design by Dóri Sirály for Prezi
Brain stem passes through tentorial incisure (between the two tentoria)
the Limbic system is considered the 5th lobe (surrounds diencephalon) does emotion
Basal ganglia = 5 nuclei associated with movement: 1 = caudate nucleus, 2 = putamen, 3 = globus pallidus external, 4 = globus
pallidus internal (5 = substantia nigra in the midbrain
Thalamus = 12 nuclei, either specific or association depending on whether they work with primary or association cortical regions
Hypothalamus = anterior wall of 3rd ventricle
3 types of fibre in white matter: association = link areas in same hemisphere, commissional = link same areas in different hemisphere, projectional = links different parts of the brain (cortex with cerebellum, diencephalon, brainstem, s/c)
And the corpus callosum = 2 ends (anterior = genu, posterior = splendium)

Local circuit current
When stimulating peripheral nerves the graph wll show M-wave, H-reflex and F-wave
M-wave = direct stim of muscle, H-reflex = electrical stretch reflex, F-wave = 'false?' as is antirdromatic (wrong way) AP movement in neighboring amotorneurones.
Lambert-Eaton = autoAb against Ca2+ channels in PREsynaptic.
Myasthenia Gravis = autoAb against ACh in POSTsynaptic
Nicotinic ACh reeceptors permeable to both Na and K+ (EPSPs)
IPSPs rely on GABAa and Cl- ions. The movement of Cl- makes membrane more leaky
CNS NTs = ACh (CNS neurones). Glutamate = excitatory. GABA and glycine = inhibitory. NA, 5HT and dopamine too.
Coma is caused by extensive damage to the brainstem. Can occur even if forebrain (cortex and thalamus) are unharmed.
Midbrain = reflexes (auditory, visual and orientating.)
Pons = movement (coordinate input from vestibular and cochlear apparatus) and masitication and movement and sensation of face
Medulla = visceral... breathing, heart rate, cortical arousal, swallowing, respiration, blood pressure
Gliomas and gliosis = tumour of astrocyte and astocyte prolifferation in wake of injury making a scar
Astrocytes are the reals stars of the CNS, secrete growth factors, look after pH and release cytokines when brain is under inectious attack.
Microglial = small. hoover up debris
Problems with glial cells in part of brain can cause epilepsy there.
Dura mata covers DRG
The epidural space contains fat
Rami communicates = sympathetic. Goes to sympathetic drunk ( noticed this mistake but I like it so I'll leave it in)
Dorsal root ganglia = large, dorsal rami = small... does skin and deep muscles of back. Ventral rami = large... supplies skin and muscle of chest wall and limbs
Radicular arteries follow the nerves once they leave the s/c
31 spinal nerves, 30 vertebrae. There's a nerve above C1 and below Coxygeus therefore somewhere along the collumn a single vertebrae needs two spinal nerves. C8 is the lucky one. Plus C8 doesn't do anything thoracic-like (?) (T1 is however part of the brachial plexus)
Phrenic nerve (C3,4,5) comes off the cervical plexus (C1-4) - cutaneous innervation of head, back, neck AND EAR
Trapezius = exception, like trapezes artists are an exception to human-kind with their ability to fly.... The traps are innervated by spinal accessory (CNXI)
Lumbar plexus...posterior divison = femoral (L2-4) = anterior (annoyingly) skin innervation and quads, anterior division = obturator (L2-4) = medial skin innervation and adducter
Filum terminale = ligament that holds down cauda equina
'Primary afferents' is the bit of the sensory nerve that carries the impulse to the cell body,
Speed of conduction in METRES/second is roughly x6 the width of the axon (though this being measured in microns)
Axon and its accompanying Schwann cell are covered by the endoneurium. These are grouped and wrapped in perineurium to make fasciles. These are then wrapped in epineurium (continuous with dura)
unmyelinated axons are still associated with a Schwann cell (just no myelin) One Scwhann cell can deal with 3-20 unmyelinated fibres
glycoprotien on axon to tell Schwann cell whether it wants myelinating or not
A Alphamotor and A gamma are the motor neurones. Former = general, latter = muscle spindle to maintain tension
A alpha 1a and 1b. Aa1a = sensory to spindle. Aa1b = sensory to GTO
The alphas are fastest and have widest diameter (like alpha gorillas)
Abeta = general sensory afferents
Adelta = fast pain, temperature on skin, muscle, joints
C firbrea = slow pain, temp from skin and muscle
Three mechanoreceptors [all deeper to the epidermis]: Messieners (light touch + thus more superficial) Ruffini's (rough touch + a little deeper) Pacinian (vibrations + thus deeper still)
These are capsulated
Merkel's receptor = in epidermis.
The area innervated by a single sensory nerve ending = receptive field. Sensitive bits of skin have more e.g. fingers
Glabrous skin = that without hair
As so superficial and delicate the sensory afferents will innervate receptive fields that are also innervated by others - this overlap ensures no loss of sensation.
C fibres and Adelta are free nerve endings
After injury, distal nerve axon degenerates, distal Schwann remains as fragments ready to wrap around the axon growth cone from the proximal growing axon
Require both EPSPs and IPSPs for DTRs as need positive flexion and inhibition of extension.
NT = fast, NM=slower, Neurotrophic = slowest
Gylcine is just modulator (inhib)
NA and Dopamine and only NTs (not modulating)
Fast neurotransmission = pentamic C-loop receptors, modulatory = GPCRs
Na+ C-loop receptor = a2byd with 2 ACh bindinding to the two alpha subunits
Neuromodulators that are not fast NTs = substance P (vomiting), inflam mediators e.g. PGE2, bradykinin, also insulin.
FT it's this that is the target of organophosphate nerve agents like sarin
NTs are also reuptaken e.g. glutamate (by neurone and glia) amines too like GABA
Glutamate exploits the energy in the Na+ transmembrane gradient to facilitate its reuptake in pre and post.
Glutamate is the NT for primary afferents (so in DRG)
In terms of pharmacology are target is a well defined molecular entity
Parkinsons = loss of substania nigra
Dopamine cannot pass BBB, L-Dopa can but is broken down into dopamine before it reaches the brain so administed with a drug that inhibits L-Dopa breakdown but cannot pass BBB so L-Dopa can only be converted into dopamine in the brain. Or directly target dopamine receptors with agonists
Schizophrenia can be caused by this parkinsons treatment as it is a case of excessive dopamine. Treatment of schizophrenia is to block dopamine receptors this effects other receptors so has a range of side effects
SE - rise in prolactin (it's release is inhibited by dopamine), allergic, postural hypotension
Depression = inadequate supply of serotonin and noradreneline at the level of the post synaptic receptor.
Treat with SSRIs or tricyclic antidepressants
Tricyclics also have an effect of H1 receptors, muscurinic cholergic receptors, a1 and a2 adrenorecptors. = xerostoma, postural hypotension, diziness, loss of libido
Recreational drugs that cause addiction can: 1. agonise the muscurinic receptors (heroin) 2. antagonise glutamate receptors (ketamine) 3. inhibit amine reuptake (cocaine) 4. agonise nicotinic receptors (nicotine)
Treatment = ween off (methadone for heroin), vaccinate (antibodies for cocaine), induce sickness (alcohol - prevent its breakdown), less toxic alternative (nicotine gum)
Cervical s/c has more white matter because all the tracts have to go through them
Lissauer tract is the tract that takes the STT afferents up a couple spinal levels
97% of nerve cells in the s/c are interneurones. ~1% project in tracts, ~2% are motor neurone
In ventral horn extensor cell bodies are more external.
Ventral horns are enlarged at cervical and lumbar regions as this is where the limbs are so there's lots of efferent muscle fibres
lamina 1 = STT, Lamina 2 = pain, Laminae 3+4 = nucelus proprius.... high conc of myelinated fibres, L. V+VI = median sized fibres
Muscle afferents terminate in L. 1, VI-IX... LI = noicioreceptors (Ad and C-fibres), VI=GTO and muscle spindles (Aa1a+b)
Visceral afferents terminate in I, V and X
CST is sagittally sectioned into C, Th, L and S segments going medially to laterally (like the DCML)
CST tract a.k.a pyramidal as dessucates in pyramids
2 posterior spinal arteries one anterior
Anterior spinal artery divides on each side into sucal and circumflex arteries. It supplies CST (including ventral) and STT and some of SCT and a little gracillus
Posterior supplies majority of DCML

Central lesions are call syringomyelia
Lower motor neurones are that which have their cell body in the ventral horn of the s/c. Upper motor neurones are anything that projects down to these.
Kind of obvious but lower motor neurones can have synapses with either 1) UMN, 2) interneurone, 3) direct afferents e.g. DTRs
UMN can be from the cortex via the CST/pyramidal tract or extrapyramidal (direct from brainstem) these are
by the cortex
Reflex = involuntary response triggered by sensory input.
can be via any of the above listed synapses of LMN
homonygous reflex = what is stimulated contracts e.g. patella reflex
Monsynaptic reflexes are difficult to be supressed by forebrain as no interneurone
'Reciprocal inhibition' = bit with the other muscle
Can't remember what I wanted to write.
A alpha 1a afferents are spontaneously active, relaying info on muscle length.
When the tendon hammer slightly stretches the muscle it causes increased firing the alpha 1a triggering the reflex
But as the quadriceps are such big muscles they have lots of muscle spindle neurones - these all stretch a little bit - it's their summation that causes the large extension reflex
Muscles spindles: contractile elements (actin/mysoin) is contained at ends of spindle - only mitrochondria and stuff in the middle also a lack of connective tissue hence they stretch v easily. This is where the alpha 1a afferents attach. Ay motorneurones attach slightly further out at the contractile elements but still within the fusal or summin... they're 'intra-fusal' Alpha motorneurones on the other hand act on the muscle filaments.
y motorneurones are not activated in the reflex. They'll only fire on stimulation from the CST. They keep the muscle tense keeping it sensitive to stretch
Pathological changes can cause the y motor neurone to apply greater tension in the spindle... this leads to hyperflexia... tendon tax reflex is more sensitive.
The reason for the monosynaptic reflex is muscle fatigue. Cortical stimulous is proportional to what the brain wants doing. If this is say walking at constant speed then cortical stimulous is uniform. But the muscle slowly runs out of glucose and FAs etc. - it fatigues but the brain stays the same. Fatigue reduces the action of the muscle so it will stretch more (as it was being kept short) this is detected by the spindle neurone and it causes (via the monosynaptic reflex) the alpha motor to contract a little more.
When at desired length the y motorneurone has a low level of activity.
The lower limb reflexes are easy to elicit and powerful as we are required to spend so long standing. Also why people with MS need wheelchairs
GTO reflexes are inhibitory (via glycine) and polysynaptic. They fire when the
in the tendon threatens the health of the muscle.
Pain flexion reflexes are polysynaptic so are easy to inhibit.
Crossed extensor reflexes are linked with ^ this, they are polysynaptic and allow weight to be redistrubuted to the nonpainful leg.
Muscle tone is the slight resistance to passive movement due to low level tonic muscle contraction via UMN. UMNL = spascicity LMNL = flaccidity

Afferents that travel in the DCML are not second order they go straight in to the tract
VPL = body somatosensory (VPLs occur on ya bum which is part of the body)
VPM = face somatosensory
Romberg's test is for DCML
TTX channels on free nerve endings of nocioceptors normally closed but opened on inflammation to allow influx of Na+. they remain open as long as the inflam is there.
aleo =
ain and temp (Adelta and C) Neo = pressure and touch (Abeta)
The brain can inhibit pain by activating the inhibitory interneurones of lamina ii. Stop lamina i releasing glutamate by releasing GABA. Opiates mimick this... pain relief. (act on pre and post synaptic membrane
Muscles of mastication are unique in that their ganglia is within the brainstem still (trigeminal nucleus) no peropheral ganglia out of brain stem.
Pupillary light reflex is psNS... light-(optic nerve)-> pretectal nucleus of midbrain -(bilaterally) -> Edinger-Wesphal nuclei -(Oculamotor)--> cillilary body --> sphincter pupilarae
The medial longitudinal fasiculus connects the abducens nucleus of one eye to the oculomotor nucleus of the other. Damage to the MLF results in INO (internuclear opthomalopegia) Presents with monoocular nystagmus
Reticular formation motor/sensory = medial/latera;
Raphe's of reticular formation = serotonin
Substansia nigra and ventral tentorium = dopamine
Pedunculopontine = ACh
Locus coeruleus = NA

Dopamine = reward and pleasure (addiction), serotonin = happiness (depression)
CN XI enters skull via FM, exits via jugular foramen. Nucleus ambiguus hence is in the medulla.
Solitary nucleus is with the vagal nucleus hence it must be in the medulla
Vagus nuclei includes ambiguus (this does to larynx)
Not only is nuc ambiguus in medulla but its in the reticular formation... it holds the respiratory centre.
Vagus has something to do with jugular ganglion
CN IX does
arotid... glosso
Damage to glossopharyngeal = loss of Gag, damage to vagus = loss of Vocal chords
Vestibuloccular reflex = VI and VIII = nystagmus
VIII nuclei by inferior cerebella peduncle
Any damage to brainstem will have vestibullocular symptoms as CNVIII v sensitive to hypoxia.

Taste ends up in the insula after going via the solitary tract of the medulla. Special sensory = CNVII but goes with IX and X

Damage to HYPOglossal is the tongue pointing thing. In direction of damage.
22 bones in the cranium. All but temporomandibular joint are sutures
2x parietal, 2x temporal. the other 8 bones of the skull cap are unpaired
Foramen ovale > foramen rotundum. Both in the sphenoid bone. As is the optic canal
Lamdboid suture between occipital and parietal bones squamous suture between temporal and parietal bones, also occipitalmandibular suture
Facial bones collectively known as viscerocranium
The mandible and vomer are the only unpaired bones in the viscerocranium. Maxillae, Zygomatics, Nasals, Lacrimals, Palatines, Inferior nasal conchae are all paired
Alveolar margains are the bits of the mandible and maxilla that the teeth stick into
Orbit formed of 7 bones: maxilla, palatine, sphenoid, zygomatic, lacrimal, ethmoid, frontal (not temporal, not nasal)

blow out fractures are fractures of the orbit
nasal cavity = 2 bones (+hyaline cartilage), conchae (sup and mid = ethmoid bone)
conchae there to warm air before it travels into lungs - increase its contact with mucosa. Also makes it more turbulent.
Coup injury = brain hits front, countercoup = brain hits back
In concussion = immediate excitatoritoxicity via glutamate release. May last 4 weeks, decreased blood flow. Unconsciousness... something about RF
Double the number of cranial bones at birth - fontanelles seperate them all :)
Retinal ganglion cells --> optic nerve --> optic chiasm --> optic tract -->
Lateral geniculate nucleus (side of thalamus) --> optic radiation --> primary visual cortex
(area 17)

Visual recognition occurs at the lateral geniculate - occipital tract. damage to this results in blindness.
Optic chiasm kind of splits the thalamus from the brain stem
Superior colliculus damage = trouble tracking object with eyes.
Optic info travels in meyers loop before optic radiation on its way to the visual cortex.
Central parts of the eye have bilateral connections to the cortex can be spared in visual cortex lesions
Anton-Babinski = syndrome where blind people think they can see - they fabricate a visual world around them.
NTK 4 visual reflexes: pupilary light reflex, vestibuloccular relfex, accomidation reflex anf blink reflex
PLR blocked by atropine
AR has lens thickening, pupil constriction and orbit convergence. It involves frontal eye fields in premotor cortex to do constriction
FEF is the reason that when we change are fixation we don't see world whizzing past - saccades is the phenomena of rapidly changing point of fixation. Damage to FEF is inability to change point of fixation. The lens thickening is done by the constriction of the cililary muscle. Suspensory ligaments attach this sphincter muscle to the lens at rest when the sphincter is relaxed the ligaments are tight so lens is thin. On constriction therefore the lens can become thick. This is CNIII. It enables one to focus on nearer objects.
Convergence is actiavtion of CN III my cortex to tighten medial rectus in both eyes.
VOR: Afferent = VIII, efferent = VI and III (different in each eye)
Keeps objects in view when head rotates
Direction of nystagmus = direction of fast flick
COWS cold = other, warm = same

The 3 occulomotor nerves are linked via the medial longitudinal fasciculous. The vestibular apparatus feed into this

Blink reflex: in on V1, out on VII (obicularis oculi)
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