Neuro Flashcards
How many neuones in somatic vs autonomic pathways
2 vs 3
What are the emergent properties of the brain?
Properties the whole system has but individual components do not. e.g. consciousness, sensory awareness, thought process, sensory attention
What is a Brodmann area?
Area of cortex classificed on histological appearence and subsequently function
Explain rostral caudal in CNS
Different for brain stem and cerebrum
Explain evolution of brain - out to in
Neocotex - complex function
Paleocortex - memory and emotion e.g. cingulate gyrus, archicortex e.g. brainstem, olfaction
What structure separates the anterior lateral ventricles?
Septum pellucidum
What is the fornix
Band of nerve fibres within the limbic system which connects the hippocampus, mammillary bodies and the anterior nuclei of the thalamus
Where is the calcarine sulcus?
Sagital view- occipital lobe
Where is the lateral fissure/ sulcus
Between temporal and frontal/ parietal lobes
What is the insula?
Infolding of brian deep
Responsible for consciousness, emotion and homeostasis
What is the corona radiata
Neural traffic from cerebral cortex
What is the caudate nucleus
Part of basal ganglia.
Involved in voluntary movement.
Loops around the putamen/ globus palidus, lateral to thalamus and medial to insula
What is the lenticular nucleus
Lens shaped, formed from the putamen and globus pallidus (medial).
What is the corpus striatum?
striatum plus globus pallidus/ caudate + lenticular
What is the (neo)striatum?
Caudate nucleus and the putamen.
Responsible for reward, motivation, motor and action planning
What composes the basal ganglia
Corpus striatum, substantia nigra and subthalamic nucleus
What are the cerebellar peduncles
Fibres from cerebellum to brain stem. L and R sup, mid and inf (6)
Briefly explain drainage on the brain
Centrally via the superior and inferior sagittal sinuses. Into confluence with occipital.
Transverse sinuses to sigmoid to IJV
What is the conus medullaris
Tapering end of spinal cord T12-L1
What is the filum terminale
Delicate strand of fibrous tissue from apex of conus medullaris - continuation of pia. Travels within a dural sac before adhering to the dural and then fusing to the coccyx
What are the denticulate ligaments?
Ligaments either side of the spinal cord which attach to the arachnoid and dura maters to provide support (between them) extension of Pia.
Describe lumbar puncture
L3/4 by finding the PSIS and going medially- feel above and below for largest space
Safe Lumbar puncture in kids?
L5/S1
Where is the substantia gelatinosa and what is found there?
Rexed lamina 2. Part of spinothalamic trunk. C fibres pain gate control theory of pain. Fibres from Lissauer’s synapse here. 2nd order neuones then deccusate in the anterior white commissure.
Where is the substantia nigra and what is found there?
Parts of rexed lamina III-V form. Pain and temperature from spinthalamic. Fibres from Lissauer’s synapse here. 2nd order neuones then deccusate in the anterior white commissure.
Difference between ataxia and apraxia
Apraxia = inability to perform complex movements despite having the capability to bring about movement Ataxia = a loss of full control of body movements
Aphasia vs aphonia vs dysarthria
aphasia = speech and language disorder
aphone = pysical inability to produce sound e.g. bilateral recurrent laryngeal nerve damage
Disarthria - disruption of articulation of speech e.g. movement of tongue
What is paraplegia
Loss of sensory and motor functions of lower limbs
What is Chorea
Involuntary jerky movements of hips shoulders face e.g. Huntington’s
Describe features of spasticity
hypertonia, hyperreflexia and paralysis
What is a neuropore
End of neral tube as it fuses away from cervical region
How can spina bifida be detected before birth?
alpha-fetoprotein in blood test or amniocentesis
USS
Types of spina bifidal
Occulta - just vertebrae affected often asymptomatic
meningocoele - meningeal involvement
Myelomeningocoele - neural tissue outside the body
Symtoms of spina bifida
Anywhere along length of cord by normally lumbosacral.
Weakness in lower limbs.
Blader control
Orthopaedic problems
Pressure sores
Hydrocephalus
Neurological development - behaviour, problem solving and memory
Neural tube defect cranially
Anencephaly
Rachischisis - failure of neural fold elevations = motor and sensory deficits, chronic infections, and disturbances in bladder function or anencephaly
How can hydrocephalus be treated? What happens if no treatment?
Peritoneal/ jugular shunt
causing convulsion, tunnel vision, and mental disability.
headaches, vomiting, nausea, papilledema, sleepiness or coma
Describe the dilations/ development of brain
3 cranial dilations in neural nube.
Prosencephalon becomes telencephalon (cerebrum) and diencephalon (thalamus).
Mesencephalon becomes mesencephalon (midbrain).
Rhombencephalon becomes metencephalon (pons) and myelencephalon (medulla oblongata)
Location of ventricles in respect to enbryology
Lateral in tele
third in Di
Aqueduct in mes
Forth in Met/ myel
Describe the flexures of the CNS
Cervical at spinal cord/ medulla juntion
Cephalic at midbrain
Describe the growth of the neural tube into CNS structures
Thickening around central canal = neuroepitheal layer
Mantal around that into dorsal/ alar (sensory) and ventral/ basal plates being motor. Around that is marginal layer which is white matter
Descrbe neural crest cells in CNS developemtn
Migrate Undergo epithial to mesenchyme tranisition. Include: Cranial nerve ganglia Spinal/ dorsal root ganglia Sympathetic ganglia Schwanne cells Leptomeninges
How can alcohol affect developing CNS?
Neural crest cell migration
What is Hirschsprung’s disease
Aganglion megacolon - failure of migration
Describe the functions of astrocytes
Provides structural support
Provides blood brain barrier
Removes (uptakes) neurotransmittors
Provides nutrient to neurones e.g. glucose-lactate shuttle as no glycogen store
Maintains ionic environment e.g. buffers K
Describe the functions of microglia
Phagocytose foreign material and debris - becomes activated. Can APC and activate t cells although inflam is limited as CNS is immune privileged (not to raise ICP). Immune privileged means they can tolerate antigens without an inflam response.
Describe components of the BBB
Tight endothelial cell junctions, basement membrane and astrocyte foot processes.
Types of neurotranmittors
Amino acids e.g. GABA, glycine, glutamate. Biogenic amine e.g. dopamine, na, 5HT, histamine. Peptides e.g. dynorphin, somatostatin, CCK. Others e.g. purines
Describe Glutamate as a neurotransmittor
70% of all synapses. Excitatory.
Ionotropic or metabotropic
Explain ionotropic glutamate receptors
AMPA -fast K Na
Kainate- K Na
NMDA - slow K Na Ca (glycine also agonises) Causes depoalrisation EPSP
Explain metabotropic glutamate receptors
G protein coupled, linked to IP3/ Ca/ cAMP. known as mGluRs. Can upregulate AMPA
Upregulation of Glutamate receptors? Signidicance?
From NMDA and mGluRs upreg AMPA.
Long term potentiation. Ca through NMDA is important however too much can lead to excitotoxicity
Decribe GABA and glycine and their receptors
Inhibitory (IPSP).
Binding to receptors with integral Cl- causes hyperpolarisation.
GABA can also bind to modulatory GPCRs.
GABA is main ihibitory. Barbiturates and Benzos work here.
Glycine mostly in the spinal cord and brainstem - inhibitory interneurones in reflex pathways
General action of biogenic amines and Ach
Mostly neuromodulators confined to specific pathways.
Describe Ach neurotransmission effects and clin sig
Autonomic functions
Mostly excitatory
Often present on pre synaptic terminal to enhance the release of other transmitters.
Also nicotinic and muscurinic in CNS.
Neurones originate in basal forefrain and brainstem spread diffusely to cortex and hippocampus (hence learning and memory).
Within the corpus striatum.
Degen in Alzheimers
Dopamine pathways
Nigrostriatal = motor control (parkinsons)
Mesolimbic (psychotic treatment in schitzo D2) and mesocortical = mood, arousal and reward
tuberoinfundiblar = prolactin release and endocrine function
Describe Na pathways
Brainstem = neurone bodies.Most from locus coeruleus in pons.
Release of Na throughou cortex, hyothalamus, amygdala and cerebellum.
Inactive during sleep and increases with arousal.
Deficiency linked with depression
Describe 5HT pathways
Similar to NA. From Raphe nuclei also in pons. Functions: Sleep Wakefullness Mood Vomiting centre
Origin of superior cerebellar artery
Basilar artery just posterior to superior cerebellar artery
Origin of inferior cerebellar artery
Lateral off vertebral artery
Origin of anterior spinal artery
Anastomosis between vertebral arteries
Origin of pontine arteries
Basillar artery
Origin of opthalmic arteries
ICA just before it becomes middle
Describe blood supply to the spinal cord
Ant and 2 post in SAS. From anastomostes with segmental medulary arteries.
Radicular and intercostal arteries from abdominal aorta. Disruption of artery of Adamkiewicz can cause infarction e.g. AAA surgery
Supply of anterior posterior and middle cerebral arteries
Medially - mostly anterior (almost all of cingulate gyrus and corpus callosum) the posterior for occipital lobe.
Middle = lateral surface (not feet of precentral gyrus.
Middle and posterir share temporal lobe
How does CSF cushion brain?
Isotonic
Causes of subarachnoid
Berry aneurysm
How does CSF get removed and where?
Arachnoid granulations at superior sagittal sinus
CSF from forth to subarachnoid space via?
foramen magendie
What drives flow of CSF
Pressure and chorid epithelia villi
What causes a communicating hydrocephalus
Factors external to ventricular system e.g. scarring of meninges at arachnoid granulations
How is CSF different from blood?
Lower conc of glucose, Ca, protein, K but higher Na, Mg and Cl. Very low immune cells
State the foramen of the cranial nerves as they leave the skull base
1 Cribiform plate 2 Optic canal 3 Superior orbital fissure 4 Superior orbital fissure 5i Superior orbital fissure 5ii Foramen rotundum 5iii Foramen ovale (post sphenoid) and foramen spinosum just lateral to in 6 Superior orbital fissure 7 Facial canal (internal acoustic meatus then stylomastoid foramen) 8 Internal acoustic meatus 9 Jugular foramen 10 Jugular foramen 11 Jugular foramen 12 Hypoglossal canal
Describe sensory neuones
Free nerve endings in temp
Encapsulated for pressure
Specialised cell cuch as pacinian corpuscle for pressure and vibration
What is a quality
Subset of a modality e.g. salt, sweet, sour
Types of receptors found in muscle
Proprioceptors in muscle spindle = length
Golgi tendon organ = tension
Are receptors specific to one modality
Generally yes but punch in the eye
How are stronger stimuli recognised?
More AP frequency
Neibouring cells activated
Whats the difference between tonic and phasic receptors
Tonic - slowly adapting, continually firign
Phasic - raidly adapting, respond maximally and briefly to a stimulus
How is sensory acuity achieved? What is it?
Precision by which a stimulus can be located Laterally inhibiting interneurones 2 point discrimination Synaptic convergence (decrease) and divergence (increase
What is two point discrimination and what factors influence it?
Minimum distance required to percieve two simultaneously applied skin indentations.
Dependant on size of receptive field and density of sensory receptors.
How is the percieved loaction of a stimulation based on?
Crude thalamic localisation. Proetion into cortex.
Somatosensory cortex sharply localises the stimulus. Somatotropic representation.
Relays to other cortical and sub-cortical areas to chose how to respond
What is perception?
Ability to sense stimuli and discriminate between different types
What is the result of a lesion of the sensory cortex?
Epleptic events, loss of two point discrim, astereognosis (3D) touch
L and R of the spinal cord are divided by what?
Dorsal median sulcus and the ventral median fissure
What fibres do the dorsal columns carry
Light touch and proprioception
Describe the fasciculi of the dorsal column
Gracile = medial (thinner) above T6
Cuneate lateral below T6
Describe the two corticospinal tracts’ modalities
Lateral = limb
Ventral = axial
motor descending
Describe the spinothalamic tracts’ modalities
Lateral = pain and temp Anterior = crude touch
Describe the Medial lemniscus pathway
=Dorsal column.
1st ganglion = dorsal root ganglion.
Secondary neurones in the cuneate and gracile nuclei in the medulla.
Decussate to become the internal arcuate fibres to become the medial lemniscus pathway in the Pons and midbrain.
Terminate in Ventral posterolateral nucleus in the thalamus 3rd.
THese terminate in the post centra gyrus (proproception in the sensory-motor cerebral cortex).
Describe the spinothalamic tract pathway
Lissauer’s fasciculus for 1-3 levels. 1st cell body = dorsal root.
Terminate in dorsal horn in Sub gel or nucleus proprius
Deccussate in same level.
Ascends to thalamus at the ventra posteriolateral nucleus.
Tertiary to post central gyrus via internal capsule.
Ascend somatotropically Caudal = dorsolateral.
What is Syringomyelia?
cyst (syrinx) in spinal cord from rugby/ spinal injury e.g. high tackles. Causes pain, paralysis, weakness, loss of temp sensation.
Filled with CSF into spinal cord
Describe Brown- Sequard syndrome
Hemisection of the spinal cord. Loss of ipselateral dorsal column = ipsilateral proprioception and fine touch.
Couterlateral = temp and pain.
(spinothalamic)
Causes include tumour, trauma, ischemia, infection and inflammation
B12 deficiency neuro?
Also B6 -pyroxidine
Dorsal root column degeneration
Effect of syphillis on spinal cord?
Tabes dorsalis.
Demyelination of dorsal column
What is Freidrich’s ataxia?
Heridatary.
Sclerosis and degeneration of dorsal root ganglion, spinocerebellar tracts, lateral corticospinal tracts, and posterior columns.
5-15
Describe Shingles pathology
Reactivation. Dormant in dorsal root ganglion. Infects PNS neurones.
Increased sensitivity and rash.
Postherapeutic neuralgia = chronic pain
Explain conscious and unconscious proprioception pathways
Concious = Dorsal column spinal tract. Unconscious = Dorsal and ventra spinocerebellar tracts and the Cuneo-cerebellar tract.
Describe the Spinocerebellar tracts
1st order from muscles terminate in Clarke’s nucleus/ column. Cell body in dorsal root ganglion.
2nd order trvel in lateral funiculus 3.
Dorsal remains ipsilateral.
Anterior decussates in the cord but the recrosses in the cerebellum and is ipsilateral
Direct of fall in cerebellar damage
= ipsilateral fall and coordination
Vermis damage = fall backwards
Define a motorneuone
A somatic efferent that displaces limbs and sets muscle tone.
Upper and lower motor neuone
Upper motor neurone lesion signs.
Hyper reflexia Hyper tonia Hypokinesia (regidity) Spastic Paralysis Chorea if extrapyradimal Pyradimal = Babinski
Lower motor neurone lesion signs
Paralysis Flaccid weakness Hypotonia or atone Hyporeflexia or areflexia Atrophy Fasciculations
Origin of LMN?
Rexed laminae VIII and IX. Cranial nerve motor nucleus = CNVII not in spinal cord?
What is a motor unit?
A-motorneurone and all the mucle fibres it supplies = minimal functional unit.
What is a strecthc relfex
An involuntary, unlearned, repeatable, automatic reaction to a specific stimulus that does not require the brain intact.
Name the 5 components to a strectch relex
A stretch receptor (e.g. golgi organ or muscle spindle) Afferent fibre Integration cetre An efferent fibre An effector
What is a myotatic reflex?
Monosynaptic stretch reflex. Sets motor tone
Muscle tone in utero and new born?
Low in utero and supressed in new born and returns within months
Muscle tone during sleep and exceptions?
Increased inhibition during sleep apart from resp, extraocular muscles and sphincters.
What do gamma motor neuones do?
Adjust sensitivity of muscle spindles, allow a motorneurones to continue to discharge
Signs of an extra pyradimal lesion e.g. cerebellum or basal ganglia
Tardive dyskinesia, parkinsonism (tremor, rigidity, dyskinesia), akathisia (muscle restlessness), dytonia e.g. spasms
Corticospinal = fine movements.
Extra pyradimal = way they are carried out
Two pyradimal tracts?
Corticobulbar and corticospinal tract
Describe the cortico-bulbar tract
Fibres from Motor cortex/ pre centra gyrus to nuclei of motor cranial nerves - 5, 7, 9,10,12 (not Occulomotor).
Descrube the corticospinal tract
Pre central gyrus (primary motor cortex).
Through internal capsule to brain stem.
Travels in anterior medulla in medullary pyramids.
Limb motor fibres deccasate at bottom of medulla and become lateral corticospinal tract.
Synapse directly in ipsilateral anterior horn (VIII, IX).
Ant = axial, no decussation in anterior white commissure then synapse in ant horn also.
Describe the non-cortical/ extrapyradimal descending tracts
Rubero = voluntary skeletal contraction e.g. hand. Reticulospinal = Autonomic control, posture and locomotion, modulation pain Tectospinal = automatic reactions to visual and auditory stimuli (cervical) Vestibularspinal = Posture maintainance, damage = loss of righting reflex, ataxia of gait and postural instability
Decorticate appearence
Flexors- Cs = spinal tract or cerebral. Relative strength of flexors and extensors
Decerebrate appearence
Extensors Es = pons or midbrain e.g. reticulospinal
Why do you get fasciculations?
Upregulation of Ach receptors. Ach remnants in the blood.
What is spinal shock?
Damage to descending tracts.
Areflexia and flaccid.
Gradually turns to UMN signs.
Explain the functional zones of the cerebellum
Vestibulocerebellum (archicerebellum): balance and ocular relfexes
Spinocerebellum (Paleocerebellum)- error correction (recieves proprioceptive and visual imputs
Cerebrocerebellum (neocerebellum) - motor planning, memory and coordination
Signs of Cerebellar dysfunction
Dysdiadochokinesia, Dysmetria (past pointing) Ataxia Nystagmus Intention tremor Scanning dysarthia (monotone) Hypotonia
No atrophy or weakness
Positive Romberg test and uses?
Causes of gate-
ataxia = sensory
Suggests cerebellar damage
Causes of Cerebellar dysfunction?
Tumour, stroke, genetic e.g. friedreich’s ataxia
Briefly explain the direct, indirect and hypodirect pathways throught the basal ganglia
Direct = Cerebral cortex - striatum, inhibits GPi/ SNr, activates thalamus. - more movement. (Dopamine from SNc increases).
Indirect - striatum inhibits GPe, inhibits STN, activates GPi/ SNr, inhibits thalamus- acts to dampen direct and give finer control. (Dopamine inhibits)
Hypodirect - Cerebral cortex activates STN - activates GPi/ SNreticulata, inhibits thalamus. = breaks
Explain pathophysiology of parkinsons
Progressive degeneration of dopaminergic neurones of the substantia nigra/ nigrostriatal pathway.
Less contol of movements
Describe signs and symotoms of Parkinson’s
Tremor at rest reduced by movement and increased by distraction ‘pill roll’
Hypertonia - lead pipe/ cog wheel rigidity
Bradykinesia
PD gait - small shuffle, pedestal turn, tremor only in upper body
Define pain
An unpleasant and emotional experience involving actual or potential tissue damage.
Has autonomic, somatic, endocrine and emotional responses
What is nociception and some things that can affect it
The perception of physical pain
Modified by experience, expectation, immediate context, culture
Threshold and tolerance to pain.
Threshold is all the same
Tolerance is our variable reaction to a painful stimulum. Increases with age, placebo effect, ongoing pain ect.
Difference between direct and indirect lateral STT
Fasts vs Slow
Intensity loation, quality (somatotopic) vs affective e.g. arousal, emotion
no synapse vs synapse in BS
Corical target vs hypothalamus, RF, Limbic, autonomic centres
Describe the stages of nociception
Transduction - activation of nociceptors
Transmission - replay of action pertentials along nociceptive fibres to CNS
Modulation - By other peripheral nerves or CNS
Perception - Interpretation
Difference in stimulation of Adelta and C fibres
Ad = mechanical C = mechanical, thermal, chemical (polymodal)
Perception of Ad, C and visceral fibres?
Ad = stabbing sharp, ow, well localised, first pain, lower threshold, withdrawral reflex
C = Dull throbbing ‘ooh’, poorly localised, second pain, higher threshold, tissue damage occuring.
Visceral fibres share somatic nociceptive fibres
Rexed lamina of Ad, C and cisceral fibres
Ad = I, V C = Substantia gel (i, II) and V. Visceral = V
Describe transduction of pain
Lesion = K, prostaglandins, 5HT, bradykinin which activate.
AP fired and substance P released from nerve endings.
P increases cap permeability and contributes to inflam.
P (and CGRP - calcitonin gene replated peptide) causes rast cells to release histamine (further nociceptive activation).
Actionn of drugs on transduction
NSAIDS -prostaglandin
Steroids - IL
How can transmission be blocked
Local anaesthetic e.g. lignocaine, inhibits VGSC
What is analgesia and what can cause it?
Inability to perceive pain when tissue damage is occurring. Hypnosis, morphine, TENS (transcutaneous electrical nerve stimulation), natural childbirth techniques and placbos
Describe pain modulation in spinal cord
Exogenous methods e.g. analgesics.
Gate control theory
Endogenousour opioid peptide analgesics (and others) from centtral and decending spinal systems.
Mediated by the periaqueductal grey matter (PAG) in midbrain via feedback from thalamus, cortex, hypothalamus.
Act on nucleus raphe magnus
Why does rubbing help?
Stimulates cutaneous inhibition which increases descending inhibition
Describe perception of pain
Thalamus and the cortex Varies hugely Thalamocortical projection = info about pain. Emotional via limbic Stress via hypo
What is chronic pain
Pain >3 months. Unknown cause/ underlying problem or pain disorder.
Describe the gate control theory of pain
Between SG (via interneuones) around the synapse of C/A fibres in dorsal horn
What is hyperalgesia
Increased pain at a normal threshold stimulation.
Results from peripheral and central sensitisation
What is allodynia
Pain from stimuli not normally painfull.
Also from an area not stimulated (not referred)
Signs of pain
Brow lowers, lids tighten, nose wrinkles, lips tighten
Describe ‘winding up’
Tissue injury causes nerve damage and pain
Repeated C stimulus
Excess Glutamate and NMDA.
Upregulation so these neurones become hyperexcitable (lower threshold) and hyperalgesia.
Can lead to receptive field expansion or allodynia.
Pain decreases after stimulus but does not reach zero before another (same stimulus).
Changes in somatosensory mapping
Types of chronic pain
Nocicpetive, Neuropathic (central and peripheral), Visceral (organ disease inflam), mixed e.g. cancer, lower back, FMS (fibromyalgia)
Explain nocicpetive chronic pain e.g. RA
Wind up Inflam Synovia damage C and A delta Hyperalgesia
Explain neuropathic pain
Neuronal origin
Not explained by a single location/ disease.
Central e.g. thalamic lesion presenting as somatic sensation, not responsive to opioids.
May be burning, shooting, pins and needles.
Causes usual decreased in thrshold, increased fields, prolonged stimulus (hyperpathia).
Spontaneous activity.
Includes hantom limb pain
Describe complex regional pain syndrome types
Type 1 - no lesion but after illness e.g. RSD (reflex sympathetic dystrophy)
Type 2 - identifiable nerve lesion e.g. causalgia - burning in limb caused by peripheral nerve lesion
What is RSD/ CRPS symptoms
Reflex sympathetic dystrophy
Sensory - severe, continuous burning pain, hyperalgesia,
Vasomotor -
Sudomotor/oedema
Motor/ trophic - decreased range of motion, dysfunction, trophic (skin) changes
Stages of CRPS
1 - acute
II dystrophic - thickening of skin, muscle wasting, oedema
III atrophic - limitation of movement, contractures, waxy skin
Opiod receptor info
GPCRs, close VOCC, open K, inhibit cAMP and neurotransmittior release
Opioids and their receptors
Endomorphins = MOP
Dynorphins = KOP
Enkephalns =DOP
Give common weak opiods
Codeine
Give strong opiod examples
Morphine, Fentanyl
Who analgesic ladder
1 non opiod +/- adjuvant
2 weak opiod adjuvant
3 strong oioid adjuvant,
Non = Paracetamol, NSAID
Definition of adjuvants and examples
A pharmacological agent fiven to increase or aid a drug’s effect. Not analgesics in their own right.
AEDs and Steroids e.g. prednisolone
Central pain and opiods?
May be opiod insensitive so antidepressants, AEDs, local anaesthetics and opiod mixtures are given
Describe the development of the ear
Otic placodes arise laterally
Grow and invaginate
Pinch off to become auditory vesicle
Changes shape to form membranous labyrinth: Utricle and saccule/
Utricle becomes semi lunar canals and saccule become choclear. Ossicles from 1st and 2nd arches.
Pouch and cleft forms meatus.
Mandible grows and the ears ascend to be in line with eyes
Define placode
Thickened ectoderm patches on developing head
Congenital causes of middle ear deafness?
Problems with 1/2 branches
Causes of inner ear deafness
Tetratogenic agents and infection e.g. rubella
Describe development of the eyes to shreks ear
Lens placode invaginates and pinches off. Shreks ear. Choroid fissure in the middle.
Whats inside the choroid fissure and its fate
Hyaloid artery- degenerates distally to become the central artery of the retina
Fate of the optic cup?
Retina (pigment and sesnory/ neural) in to layers which fuse, iris and ciliary body (from the rim)
Where do muscles of the eye come from?
Preoptic myotomes from the surrounding region
How does coloboma arise?
Failure of fusion of the edges of the optic stalk around choroid fissure inferio-medially
Future pathology associated with the optic cup?
Retinal tear = separation of the layers
What is the iris?
A contractile diaphragm with a central aperture
Features of rubella?
Microcephaly, PDA, cataracts
Where does the optic tract start and terminate?
Starts at the optic chiasm and terminates at the lateral genicular nucleus
Temporal lobe optic rediation lesion = what?
Superior visual field defect (ST elevation) so an inferior retinal field problem.
Where is Meyers loop?
Temporal optic radiation
Describe differences in rods and cones
Not in fovea vs fovea
Photosensitive vs high acuity
Dark adapted vs day vision
Converge on bipolar cells vs blue, red and green.
Describe the three main functional classes of neurones
Photoreceptors
Interneurones
Ganglion cells
Describe interneurones
Bipolar, horizontal and amacrine.
Combine photoreceptor signils
Describe Magnocellular ganglion cell pathways
No sensitive to colour
Sesnsitive to luminescence contrast and fast motion. Magnum = fig e.g. foramne magnum - looks at big picture? Via the dorsal stream to the posterior parietal cortex
dESCRIBE pARVOCELLULAR GANGLIIONIC CELLS
bETTER AT COLOUR CONTRAST, NOT LUMINANCE AND FINE DETAIL HOWEVER LESS SENSITIVE TO MOTION.
Goes via the ventral stream to the inferior temporal cortex
Describe the primary visual cortex
Separated by the calcarine fissure
Occipital lobe
Each quarter of VF is represented, larger area for macula/ fovea.
Interpretation by cortex e.g. comparison of things so some may seem bigger.
Explain the development of cones
Take ages to mature.
Can be seen via Optical coherence tomography (OCT) - images the retina.
Can see development of the outer nuclear layer still at 5 years. Fovea only has an outer nuclear layer
Sign of fovea hyperplasia?
Nystagmus
What is ambyopia?
Diminished vision in one eye and a result of disuse in childhood.
Causes of ambyopia
Strabismus - inability to focus both eyes on one object = lazy eye
Anisometropia = refractive difference in botheyes
Deprivation e.g. congenital cataracts, ptosis, media opacies
Types of anisometropia
Emmetropia = normal Myopia = infront of retina Hyperopia = behind retina
Types of Stabismus
Esotropia = In
Exotropia = out
Left hypertropia = up
hypotropia = down
Treatment of ambyopia
Glasses/ patch when yound due to brain plasticity but poor comliance
What is glaucoma
High intraocular pressure, damage to optic nerve, peripheral field defect which is often unnoticed and gradual
Sympathetic innervation of eye pathway
Hypothalamus to T1, To Superior cervical ganlion under SCA to dilator pupillae
Abduction and adduction movements
SR and IR are opposite
SR and SO are inverse.
SO abduct = intorsion
Appearance of VI nerve palsy
Esotropia
IV nerve palsy
Hypertrophia
III
Exotropia and hypotropic
Also ptosis and mydriasis
Describe the properties of sound
Compressive wave, frequencey and amplitude
Level of conversation and painful sound
60dB vs 120dB
Describe the travelling wave theory
Basillar membrane resonates and machanically amplifies sound with progressively lower frequencies along its length.
What is Tonotopy
Place on basillar membrane = frequency
Describe the structure of the basillar membrane
One row of inner hair cells and 3 rows of outer hair cells.
Functions of inner and outer hair cells
Inner sense sound
Outer amplify sound
Mechanically tuned by location and electrically tuned by expression of particular ion channels .
Both contain stereocillia to sense sound
What is the tectorial membrane?
attached to the hair bundles. Not sure of function. When basilar moves?
Exlain How bending of stereocillia triggers a nerve AP
Bending opens K channels = depolarisation as endolymph at high conc. Larger if more displacement.
Ca influx
Triggers transmitter release onto spiral ganglion neurones (SGN) - afferent axons of CNVIII
What is the olivocochlear system?
Regulates OHC amplification via efferent feedback
How are loud sounds interpreted and location
More APs from SGN, recruitment of neighbouring fibres. Goes to choclear nucleus in the auditory brainstem. Goes to Medial nucleus of trapezoid body on both sides. Delay allows left/ right and difference in volume/ amplitute.
What constitutes the auditory brainstem?
Lateral and medial superior olives and the medial nucleus of the trapezoid body.
The auditory pathway
Cochlear SGN Dorsal and ventral cochlear nuclei Suppeior olive Inferior colliculus Medial geniculate nucleus The auditory cortex
Causes of hearing impairment
Age, presbyacusis Infection Congenital Loud noises Gentamicin TraumA
Explain the assessment of hearing
Otoscope
Audiograph - sensitivty against frequency (higher lost with age)
Otoacoustic emissions (sound generated by OHC - test in babies)
Auditory brainstem response - electrodes on the brain
Treatments fr hearing loss
Hearing aid
Cochlear implant
Cochlear nucleus
implant.
Congenital causes of hearing loss
DFN - X linked
DFN - AD
AFNB AR
Hair hells, tectorial ….
Where do most strokes occur?
Middle cerebral artery
Describe the vertebral arteries
Tortuous
Posterior ineferior cerebellar artery is the largest branch.
Also the spinal arteries
Describe the Basilar artery
Supplies most of brainstem. Located over pons.
Superior and anterior inferior cerebellar arteries. supplies most of PCA
Describe PCA distribution
Occipital, midbrain, thalamus, half on temporal
Define stroke
Abrupt loss of brain function lasting more than 24 hours or causing death due to inadequate blood supply or spontaneous haemorrhage
Causes of cerebral infarct
Atheroma, embolism, idiopathic, arterititis, blood disorder
Describe intracerebelar haemorrhage causes
Primary or Secondary
Haemorrhagic transformation of infarct
Hypertensive, microaneurysms, lipophyalinosis (wall problem), AV or aneurysm, amyloid, haemostatic, cocain, amphetamines, tumour, venous thrombosis
Define TIA
Sudden focal disturbance of brain functioning (global or local) which resolves within 24 hours
Temporal lobe stroke signs
CNVIII, taste and smell
Wernicke’s area
Memory
Optic radiation - superior quadrantanopia
Pariatal lesion
Primary sensory cortex
Neglect
Speech
Optic radiation either inferior or hemianopia
Describe TACS - total anterior circulation stroke
Proximal occlision Contralateral hemiparesis/ hemianaesthesia Higher dysfunction Hemianopia High mortality
Describe PACs
Occlusion of MCA or restricted infarct
2 signs from TACS or restricted motor deficit (one thing e.g. face) or isolated cortical signs
High early recurrence
Describe LACS (lacunar stroke)
Single perforating artery in the basal ganglia or pons.
Pure motor, sensory, sensory motor, ataxic or hemiparesis.
Silent and underdiagnosed
Describe POCS
Brainstem, cerebellar or occipital involvement.
Complex presentation
Atypical symptoms of stroke
Delerium, confusion, collapse, incontinence
Write note for telangiectasia
k
Investigations for stroke
BM HAematology Biochem CT/ MRI Carotid US ECG Echocardiogram
Treatment for stroke
IV thrombolysis - alteplase
Early asprin
Acute stroke unit
Damage to spinal cord blood supply
Aortic damage Vasculitis - giant cell arteritis Sickle cell Hypotension Cardiac emboli Disc Herniation
Symptoms of spinal artery occlusion
Spinal shock. (seen in urinary spincter too)
Normal ant so dorsal is fine (proproception and touch)
Normally motor
What is a flaccid bladder? (same as areflex)
Lesion at S2-4 lower motor neurone
Describe reflex bladder
UMN lesion.
Works fine but detrusor is more sensitive.
No control.
Increased muscle tone.
Describe motor and sensory areflexic bladder
Aware on unaware of filling - no release in response. Lesion of the sacral spinal cord or sensory nerve or detrusor
Describe the management of head trauma
ABCD (disability)
History
Examination
RAS control
dd
What is a coup and contrecoup injury
Coup = front Contrecoup = rebound`
What are contusions?
Damaged blood vessels around the brain (like bruising)
Describe primary and secondary insult in brain
Primary = haematoma, contusion, haemorrhage, diffuse axonal injury Secondary = preventable, hypoxiam hypoperfusion, oedema, ICP.
BBB disruption?
More permeable so vasogenic oedema.
What is cytotoxic oedema?
Inflam mediatorys and oxiditive stress. NA retention
ICP compensation?
CPP = MAP-ICP. Venous blood and CSF can move out of brain to lower ICP. MAP increases (mean arterial pressure) via Cushings.
Uses of propofol
Decreases Cerebral metabolic rate of O2 (CMRO2) like hibernation.
Dose dependent
USe of Thiopentone (barbiturate)
Decrease CMRO2
Hypotension
EEG monitoring - birst suppression.
Vary heavy = seizures- very bad as high O2 requirement
Describe use of opiods
Pain relief
Reduces stress response
Reduce cough so can intubate
Can exacerbate hypotension
Benefits to ketamine? and disadvantages?
No effect on BP
Predictable
No loss of airway relfexes, semi conscious, hallucinations/ terrors.
Use of neuromuscular blocking agent
Need for intubation
Use of mannitol
Potent osmotic diuretic to remove cererbral oedema but can worsen if passes the BBB
Explain vasopressors
Adjust BP
Invasive BP monitoring
given IV (impair venous drainage?)
MEasures in medically induced coma?
EEG
Bispectral index - depth of anaethesia 1 number from many imputs
ITU nurse and wakefullness
Evidence and reasoning behind medically induced comas?
Relieve swelling and brain decrease brain damage.
Mixed evidence.`
Describe the reticular formation
Central core of brain stem, includes raphe and nucleus coeruleus.
Sleep regulation
Motor control
Cardio/ Resp control
Autonomic functions
Motivation and rewards.
Ascending reticular activating system = consciousness
Imputs on the reticular formation
Senses, hypothalamus, drugs and alcohol. Activate/ inhibit arousal/sleep.
Outputs of RF
Motor system (make more sensitive), autonomic, thalamus, cortex. Many different neurotransmittors. Ach sensitises thalamus to sensory stimuli but quiet during sleep.
RF in sleep
Ach silent.
Cortex can inhibit RF if wanting sleep- waves on EEG. e.g. whilst driving
Describe EEG and waves
Algebraic sum of electrical activity.
Less info when eyes are shut so higher amplitude and lower frequency. Hihger frequency when open and wavees cancel each other out.
Describe specific wave forms
Delta large - deep sleep and brain conditions
Theta intermediate Parietal and temporal children concentrating or meditating adults
Beta like theta but irregular = awake parietal and frontal
Alpha small = awake occipital
Describe locked in syndrome
Loss of RAS descending pathways e.g. lesion below the mid pons - patient is alert and aware but quadriplegic and mute.
What is persistent vegative state?
loss of cortex PVS different from coma as they show some signs of consciousness. Brain death is the irreversible loss of all features of the brain
What is a coma?
State of unconsciousness from which a patient cannot be roused using pain, sound, light. No voluntary movement.
Describe the purpose of sleep
Allows CNS to reset and memories to process
What controls the sleep wake cycle?
RF and hypothalamus (by inihibiting the RF)
Describe a sleep cycle
Quickly into stage 4 (1 hour), straight back to REM, then cycle between stage 3 and REM with progressively more REM
Describe REM sleep
Active brain, inactive body EEG as if awake Waves from pons to thalamus to occipital = dreaming Difficult to disturb Irregular HR and RR Increased BMR Descending inhibition of motorneurones Penile erection Reduced by alcohol Na and 5HT inhibited - explains memory without emotion
Describe non REM sleep
Slow wave sleep Active body, inactive brain e.g. sleepwalking 3/4 stages Waves decreasein amplitude to stage 3 then become delta waves- slows. Restorative Neuroendocrine Decreased cerebral bloodflow, O2 consumption, temp, BP, RR, lower BMR
Describe waking
Na and 5HT start to be released. Ach from brainstem sensitises thalamus and allows wakefulness - thalamo-cortical neurones and communication
What is parasomnia
Sleep paralysis
What is hypersomnia
Day time sleepiness e.g. OSA
What is Narcolepsy
Disorder of arousal - constant hypersomnia
Conditions that affect RAS?
Parkinsons and Schizophrenia, PTSD, Depression(NA, 5HT), Alzheimers (Ach)
Loss of consciousness, where is damage?
Not cortex but RF
Initial management of loss of consciousness?
ABCD
Airway - jaw thrust- not neck extension. Nasopharyngeal better tolerated with suction in mouth. High conc O2
Breathing - mist mask, chest, breast sounds, indicator mask, assist e.g. bag valve mask (BVM) and intubation
Circulation - pulse, breathing effort, cough, movement, ETCO2 (end tidal vol) if ventilated, cap refill, IV access BM stix.
Disability - GCS
Monitor
Treatment loss of consciousness
High flow O2 if hypoxic
Hypoglycaemia - glucose IV
If fitting then Lorazepam IV
Explain the Glasgow coma scale (not score)
Eye 1-4:
None, pain, speech, spontaneous
Verbal 1-5
None, incomprehensible, inappropriate words, confused, orientated
Motor 1-6
None, extension pain, flexion, flexion pain, localise pain, obey command
Use to find pattern of change - if decreasing then bad..
Extradural presentation
Trauma, torn MMA, slow onset, decline in GCS
Subdural presentation
Trauma- brain move in skull/ (boxing).
Slower onset - days to weeks but can be acute, alcohol, age, atrophy of brain (dementia
Subarachnoid presentation
Thunderclap - berry aneurysm
Decorticate response in terms of RF
Intact. Thalamus and cortex connection lost. Unconscious but respond to pain.
Decerebrate response
Rigidity, lower brain/brainstem injury
Inhibition of RF on motor tracts removed
Relexive extension to pain
