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ESA 5 > Nervous System > Flashcards

Nervous System Flashcards

1
Q

List the divisions of the nervous system

A
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2
Q

Name the coverings, myelin cells and tumours of the CNS

A
  • Covered by meninges
  • Myelin by oligodendrocytes
  • Only tumours of glia can be malignant
    • Tumours of neruones are benign but cause increased intra cranial pressure
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3
Q

Name the coverings, myelin cells and tumours of the PNS

A
  • Covered by endo/peri/epineurium
  • Myelinated by Schwann cells
  • All tumours in PNS are benign
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4
Q

What are emergent properties?

A

The complex behaviours of neruonal networks not seen in individual neurones. Responsible for:

  • Consciousness
  • Sensory awareness
  • Thought processes
  • Sensory attention
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5
Q

What are sutures?

A

Immovable fibrous joints between bones in the cranium

  • Sagittal, coronal and lambdoid

Meet at important points

  • Sagittal and coronal = Bregma point
  • Sagittal and lambdoid = Lambda point
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6
Q

Describe the 3 different types and functions of neurones

A
  • Afferent
    • Arise from a sense organ and diverge into CNS
    • Sensory input
  • Efferent
    • Cell bodies in CNS - many other neurones converge
    • Motor
  • Interneurones
    • Entirely within CNS
    • Integrate input with output
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7
Q

List the different types of glial cells

A
  • Astrocytes
  • Oligodendrocytes
  • Microglia
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8
Q

Give the function of the meningeal layers in the CNS

A
  • Support and mechanically stabilise contents of cranium
  • Provides blood supply to skull and brain
  • Provides a space for flow of CSF
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9
Q

Describe some functions of the CSF

A
  • Cushions brain against mechanical injury
  • Reservoir for metabolic substrates for the brain
  • Chemical stability - dissolves and carries away products of metabolism from the brain
  • Buoyancy - reduces net weight of the brain to 25g
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10
Q

How are links formed between neurones?

A
  • Genetically
  • Sensory experience
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11
Q

What is the notochord and what is it’s role?

A

A solid cord of cells formed by prenotochordal cells migrating through the primitive pit.

  • Basis for midline, axial skeleton and neural tube
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12
Q

Describe the production of the neural tube

A
  • Day 18-23
  • Induction of neural plate from ectoderm
  • Elevation of lateral edges of neural plate
  • Neural folds fuse with eachother in the midline
    • Begins in the future cervical region and proceeds in both a caudal and cranial direction
    • Tube forms with anterior and posterior neuropores
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13
Q

Describe some neural tube defects

A
  • Spina bifida = incomplete closing of the spine and spinal cord membranes which can lead to posterior herniation of the meninges or spinal cord
    • Mainly occurs in lumbosacral region
    • Hydrocephalus can occur - cognitive delay if untreated
  • Ananecephaly = failure of neural tube to close cranially which leads to absence of cranial structures
    • Not compatible with life
  • Rachischisis = failure of neural fold elevation
    • Not compatible with life
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14
Q

How can neural tube defects be diagnosed and prevented?

A
  • Diagnosed using maternal serum α-fetoprotein and ultrasound scan
  • Can be prevented using folic acid (vit B9) 3 months pre-conception and during 1st trimester
    • Reduces incidence by 70%
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15
Q

Describe the formation of the spinal cord

A
  • 3rd month - same length as vertebral column
  • After, vertebral column grows faster
    • Spinal roots must elongate as they still exit at the same intervertebral foramen
    • Forms cauda equina
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16
Q

Describe the formation of the brain

A
  • Neural fold formation in 4th week produces 3 primary brain vesicles
    • Fore/mid/hind brain
  • In 5th week - 5 secondary brain vesicles form
    • Telen/dien/mesen/meten/myelencephalon
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17
Q

Name the primary and secondary vesicles of the brain and their adult derivatives

A
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18
Q

Describe the formation of flexures in the brain and why this happens

A
  • Growth at cranial neural tube exceeds available space
  • Cervical flexure at spinal cord-hindbrain junction
  • Cephalic flexure at midbrain region
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19
Q

Describe the formation and function of the ventricular system

A
  • Persistence of tubular structures = Interconnected ‘resvoirs’ filled by CSF from cells of ventricular lining
  • Cushions brain and spinal cord within their bony cases
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20
Q

Describe the consequences of disruption to the formation of the ventricular system, when this occurs and how it can be treated

A

Disruption to fluid circulation = hydrocephalus

  • Occurs in spina bifida, tumours, infections
  • Treated using a shunt
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21
Q

What is the neural crest? Describe it’s formation

A

Cells of the lateral border of the neuroectoderm tube

  • Become displaced and enter mesoderm
  • Undergo epithelial to mesenchymal transition
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22
Q

Why is the neural crest vulnerable to injury? Describe some neural crest defects

A
  • Vulnerable to environmental insult or genetic disease due to complex migratory pattern
  • SINGLE - Hirschsprung’s disease (aganglionic megacolon) = no enteric nervous system in GI tract
  • MULTIPLE - DiGeorge Syndrome = thyroid deficiency, cardiac defects, abnormal facies (CATCH 22)
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23
Q

Describe the early organisation of the neural tube

A
  • Addition of neuroblasts - dorsal and ventral thickening
  • Ventral thickening = basal plates (motor)
  • Dorsal thickening = alar plates (sensory)
  • Dorsal and ventral midline portion = roof/floor plates
    • Pathway for nerve fibres
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24
Q

What is the function of astrocytes?

A
  • Structural support
  • Provide energy to neurones
    • Neurones do not store or produce glycogen
    • Astrocytes convert glycogen from blood supply into lactate
    • Transport into neurone via glucose-lactate shuttle
  • Remove neurotransmitters
    • Re-uptake of glutamate by transporters
  • Maintains ionic environment
    • Via Na-K-ATPase and NKCC2 channels
  • Helps to form blood brain barrier
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25
Q

What is the function of oligodendrocytes?

A
  • Myelinate axons in the CNS
    • Scwann cells in PNS
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26
Q

What is the function of microglia?

A
  • Recognise foreign material and activates
  • Phagocytosis to remove debris and foreign material
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27
Q

What is the role of the blood brain barrier?

A
  • Limits diffusion of substances from the blood to the extracellular fluid
    • Transports glucose, amino acids and potassium to control concentrations
  • Maintains correct environment for neurones
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28
Q

Describe the structure of the blood brain barrier

A
  • TIght junctions between epithelial cells
  • Basement membrane of capillary
  • End feet of astrocyte processes
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29
Q

Describe the immune mechanisms in the brain

A
  • Rigid skull cannot tolerate inflammatory response
  • Microglia act as antigen presenting cells to T cells
    • T cells can enter CNS
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30
Q

Name the different types of neurotransmitter with examples

A
  • Amino acids
    • Glutamate - excitatory
    • GABA - inhibitory (brain)
    • Glycine - inhibitory (spinal cord/brainstem)
  • Biogenic amines
    • Acetylcholine
    • Noadrenaline
    • Dopamine
  • Peptides
    • Enkephalins
    • Neuropeptide Y
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31
Q

Describe the different types of glutatmate receptors

A
  • Inotropic = ion channel (mainly K+ and Na+)
    • AMPA, kainate, NMDA
      • NMDA also Ca2+
    • Activation causes depolarisation and increased excitability
  • Metabotropic = GPCR
    • mGLuR1-7
    • Change in IP3/Ca2+ mobilisation or inhibition of adenylate cyclase and decrease cAMP
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32
Q

Describe the inhibitory amino acid neurotransmitters. Which drugs enhance this response?

A
  • GABA/glycine receptors = Cl- ion channels
    • Opening causes hyperpolarisation due to IPSPs decreasing action potential firing
  • Barbituates and benzodiazepines enhance response to GABA
    • Sedative and anxiolytic effects
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33
Q

Briefly describe some dopmaine dysfunctions and how to treat them

A
  • Parkinson’s = loss of motor dopaminergic neurones
    • Treated with levodopa - converted to dopamine by DOPA decarboxylase
  • Schizophrenia = release of too much dopamine
    • Treated with dopamine D2 receptor antagonists
    • Amphetamines produces similar behaviour by releasing dopamine and noradrenaline
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34
Q

Which arteries supply the Circle of Willis?

A
  • Internal carotids (from carotid canal)
    • Anterior cerebrals - medial surface of frontal and parietal lobes
    • Middle cerebrals - lateral surface of cerebral cortex
  • Vertebral arteries (from foramen magnum)
    • Basilar - cerebellum and brainstem
      • Posterior cerebrals - inferior brain and occipital lobes
  • Anterior/posterior communicating arteries - collateral circulation
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35
Q

Name the main causes of cerebrovascular accident

A
  • Thrombosis - obstruction by a locally formed clot
  • Embolism - obstruction by an emboli found elsewhere
  • Hypoperfusion - due to systemically low blood pressure
    • Shock/sepsis
  • Haemorrhage - accumulation of blood in the cranium
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36
Q

Describe the venous drainage of the brain

A

Cerebral veins + venous sinuses → internal jugular

  • NB: cerebral veins cross the subarachnoid space where they are prone to rupture after head trauma
    • Subarachnoid haemorrhage
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37
Q

Describe the blood supply to the spinal cord

A

Supplied by segmental arteries from or near the Aorta

  • Single anterior spinal artery = anterior 2/3rds
  • Paired posterior spinal arteries = posterier 1/3rd
  • Anastamosis = arterial vasocorona = lateral spinal cord
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38
Q

What do the vessels of the Circle of Willis supply?

A
  • Ext carotid = face, scalp, mouth, jaw
  • Int carotid
    • Opthalmic
    • Anterior choroidal = internal capsule, thalamus, optic chiasm
    • Anterior cerebral = medial frontal/parietal lobes
    • Middle cerebral = lateral frontal/pareital/occipital lobes
  • Vertebral (from subclavian)
    • Basilar = brainstem
    • Posterior inferior cerebellar = cerebellum
    • Posterior cerebral = midbrain, thalamus, temporal and occipital lobes
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39
Q

Name the meningeal layers and spaces formed between them

A
  • Dura mater
    • Periosteal layer
      • Extradural space
    • Meningeal layer
      • Subdural space
  • Arachnoid mater
    • Subarachnoid space
  • Pia mater
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40
Q

Where are the most likely places for an intracranial haemorrhage? Arterial or venous?

A
  • Extradural space = arterial
  • Subdural space = venous
  • Subarahcnoid space = arterial
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41
Q

Where is the CSF produced?

A

Ependymal cells (cuboidal epithelium) which line the ventricles form the choroid plexus which produces CSF

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42
Q

Describe the passage of CSF

A
  1. Left and right lateral ventricles
  2. Third ventricle (between thalamus)
  3. Fourth ventricle (between pons and medulla oblongata)
    • Via cerebral aqueduct
  4. Central spinal canal
  5. Subarachnoid cisterns (between arachnoid and pia mater)
  6. Drainage into dural venous sinuses via arachnoid granulations
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43
Q

Describe hydrocephalus including different types, consequences and treatment

A

Abnormal collection of CSF within the ventricles of the brain

  • Causes raised intracranial pressure which can lead to cerebral atrophy
  • Communicating (non-obstructive) = absence of flow obstruction
    • Subarachnoid haemorrhage = fibrosis and atrophy of arachnoid granulations
  • Non-communicating (obstructive) = flow obstruction
  • Treated by reversing cause or with a shunt
    • Drains fluid into right atrium or peritoneum
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44
Q

Describe a lumbar puncture, including what it is used to detect

A
  • Patient in a foetal position
  • Insert needle between L3/4, L4/5 or L5/S1
  • Into subarachnoid space
  • Used to detect CNS infections (meningitis) or subarachnoid harmorrhages
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45
Q

Describe the organisation of the somtosensory system

A
  • 1st order neurone (primary afferent)
    • Dorsal root ganglion to medulla
  • 2nd order neurone
    • Medulla to midbrain to thalamus
    • Decussation in medulla
  • 3rd order neurone
    • Thalamus to primary somatosensory area of cerebral cortex
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46
Q

What is sensory modality?

A

The variety of stimuli that sensory neurones are responsive to

  • Heat, light, chemical change, mechanical pressure
  • Receptors respond preferentially to one modality
    • Exceptions = sensation depends upon type of receptor activated
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47
Q

Describe receptor adaptation

A
  • Tonic receptors = slowly adapting receptors that keep firing action potentials as long as the stimulus lasts
    • Pain receptors
  • Phasic = rapidly adapting receptors that respond maximally and briefly to a stimulus
    • Action potential frequency decreases during a maintained stimulus
    • Touch receptors
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48
Q

What is sensory acuity? List 3 ways that sensory acuity is achieved

A

The precision by which a stimulus can be located

  1. Lateral inhibition
  2. Two point discrimination
  3. Convergance/divergence
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49
Q

Describe lateral inhibition

A

When inhibitory interneurones inhibit adjacent 2nd order neurones to the 1st order neurones that received the initial stimulus. This allows greater sensory acuity.

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50
Q

Describe two point discrimination

A

The minimum interstimulus distance required to perceive two simultaneously applied skin indentation.

  • Fingertips have a higher density of receptors and, therefore, smaller receptive fields so two point discrimination is greater than in the forearm
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51
Q

How does convergence or divergence change sensory acuity?

A
  • Convergence decreases acuity (many neurones converge onto one neurone)
    • Visceral pain fibres merging with somatic pain fibres (MI)
  • Divergence amplifies signal (one neurone diverging onto many neurones)
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52
Q

Where do we feel sensation?

A
  • Thalamus
    • Crude localisation and discrimination of stimuli
    • Highly organised projections to cortex
  • Somatosensory cortex (post-central gyrus)
    • Sharp localisation and recognition of qualities of modalities
    • Somatotropic represntation = each body area has specific cortical representation
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53
Q

Describe shingles in relation to sensory distribution

A
  • Herpes zoster virus infects dorsal root ganglia neurones
    • Reactivated after lying dormant
  • Increases sensitivity of dorsal root neurones
    • Burning/tingling/painful
  • Skin becomes scaly and blistered
  • Virus restricted to 1 or 2 dorsal root ganglia so affected areas reflect dermatomal distribution
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54
Q

What is perception?

A

Awareness of stimuli and ability to discriminate between different types of stimuli

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55
Q

Describe how the property, modality, rate of change, location and intensity of stimuli are coded

A
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56
Q

What are ascending tracts?

A

Fibre tracts by which sensory information is conveyed to the brain

  • Conscious = pain, temperature, crude touch, tactile sensation
  • Unconscious = muscle length/tension, joint position/angle (unconscious proprioception), light touch
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57
Q

Describe the first stage of spinal sensation

A
  • Spinal sensory neurone cell bodies in dorsal root ganglion
  • Travels in posterolateral Tract of Lissauer in the spinal cord
  • Terminates in dorsal horn
    • Pain in Laminae III and IV (Nucleus Proprius)
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58
Q

Describe secondary stage of spinal sensation

A
  • Secondary sensory neurone sends axon ventrally underneath spinal cord
  • Decussates into opposite lateral funiculus
  • Ascend medulla, pons, midbrain and terminate in thalamus
    • Ventral posterolateral nucleus
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59
Q

Describe third stage of spinal sensation

A
  • 3rdorder sensory neurones ascend in post-central gyrus of cerebral cortx
    • Via internal capsule
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60
Q

Name the ascending tracts of conscious sensation and their function

A
  • Dorsal column - medial lemniscal
    • Fine touch and conscious proprioception
  • Lateral spinothalamic
    • Pain and temperature
  • Anterior spinothalamic
    • Crude touch and pressure
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61
Q

Name the ascending tracts of unconscious sensation and their function

A
  • Dorsal/anterior spinocerebellar tract
  • Ventral/posterior spinocerebellar tract
  • Cuneo-cerebellar tract

ALL unconscious proprioception from muscle and joint receptors

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62
Q

Describe the dorsal column - medial lemniscal tract including function, location of 1st, 2nd and 3rd order neurone cell bodies, decussation and termination

A
  • Fine touch, conscious proprioception and vibration
  • 1st order neurones from upper limb (via fasciculus cuneatus) or lower limb (via fasciculus gracilis)
    • Bodies in dorsal root ganglion
  • 2nd order neurone bodies in nucleus cuneatus/gracilis
    • Decussate in medulla
  • 3rd order neurone bodies in thalamus (ventral posterolateral nucleus)
  • Terminate in sensory cortex (post-central gyrus) via internal capsule
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63
Q

Describe the lateral spinothalamic tract including function, location of 1st, 2nd and 3rd order neurone cell bodies, decussation and termination

A
  • Pain and temperature
  • 1st order cell bodies in dorsal root ganglion
  • 2nd order cell bodies in substantia gelatinosa in the dorsal horn
    • Decussate in spinal cord into lateral spinothalamic tract
  • 3rd order cell bodies in thalamus (ventral posterolateral nucleus)
    • Travel through internal capsule and terminate in sensory cortex
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64
Q

Describe the anterior spinothalamic tract including function, location of 1st, 2nd and 3rd order neurone cell bodies, decussation and termination

A
  • Crude touch and pressure
  • 1st order cell bodies in dorsal root ganglion
  • 2nd order cell bodies in substantia gelatinosa in the dorsal horn
    • Decussate in spinal cord into anterior spinothalamic tract
  • 3rd order cell bodies in thalamus (ventral posterolateral nucleus)
    • Travel through internal capsule and terminate in sensory cortex
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65
Q

Describe the spinocerebellar tracts including individual function and decussation

A
  • Anterior spinocerebellar - unconscious proprioception from lower limbs to cerebellum
    • Decussate twice in spinal cord = ipsilateral
  • Posterior spinocerebellar - unconscious proprioception from lower limbs to cerebellum
    • Fibres do not dessacate = ipsilateral
  • Cuneocerebellar tract - unconscious proprioception from upper limbs to cerebellum
    • Fibres do not dessacate = ipsilateral
    • 2nd order neurone bodies in nucleus cuneatus
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66
Q

Describe the consequences of an injury to dorsal column medial lemniscal pathway and some possible causes

A
  • Loss of proprioception and fine touch
    • Some tactile fibres in anterolateral system so patient is still capable of touch
  • If injury in spinal cord = ipsilateral side
  • If injury in medulla or above = contralateral side
  • Occurs in Vit B12 deficiency and tabes dorsalis (neuro disorder seen in neurosyphilis)
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67
Q

Describe the consequences of an injury to anterolateral pathway and some possible causes

A
  • Loss of pain and temperature sensation
  • Will always be contralateral side affected as fibres decussate immediately when entering spinal cord
  • Brown-sequard syndrome = hemisection of spinal cord
    • Contralateral loss of pain and temperature
    • Ipsilateral loss of fine touch and proprioception
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68
Q

Describe the consequences of an injury to spinocerebellar pathway

A
  • Loss of muscle coordination (unconscious proprioception)
  • Ipsilateral (decussating twice/not decussating at all)
  • Very rarely isolated - usually accompanied by damage to descending motor tracts so muscle weakness and paralysis also
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69
Q

What are the functions of neuronal cell bodies?

A
  • Local function of a neuronal segment
    • Local reflexes
    • Sensory function (dermatomes)
    • Supplying muscle of local neuronal segment (myotome)
    • Receive/carry out commands to enact movements
  • Relaying sensory information to the brain
    • Via collections of axons (fibre tracts/fasciculi)
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70
Q

What are the functions of axonal fibres?

A
  • Carry sensory information from body surfaces and muscles to the brain
    • Via ascending tracts
  • Carry motor commands from the brain to cell bodies of spinal motoneurones
    • Via descending tracts
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71
Q

What is grey matter? How is it divided up?

A

Collections of neuronal cell bodies

  • Divided into dorsal, ventral and lateral horns
  • 10 discrete layers of cell bodies (rexed laminae)
    • Laminae I-VI in dorsal horn
    • Laminae VII = intermediate nucleus
    • Laminae VIII-X in ventral horn
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72
Q

What is the definition of a motoneurone? How are they catergorised?

A

Somatic efferent that supplies skeletal muscle to produce movement and set muscle tone

  • Upper motoneurone = supplies muscles indirectly
  • Lower motoneurone = supplies muscles directly
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73
Q

What is a lower motoneurone?

A

A somatic motor efferent with a cell body in either lamina IX (spinal motor nucleus) or cranial nere motor nucleus

  • Its axons supplies skeletal muscles directly
  • Normally synonymous with alpha-motoneurones
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74
Q

What is the function of lower motoneurones?

A
  • Generates muscle stiffness through force development
  • Evokes voluntary movements when commanded by upper motoneurones
  • Evokes reflex movements when recruited by spinal motor circuits
    • Without involvement of the brain
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75
Q

Describe the signs of a lower motoneurone lesion

A
  • Flaccid muscle weakness
  • Hypo/atonia
  • Hypo/areflexia
    • Absent babinski reflex
  • Denervation muscle atrophy
  • Fasciculations
    • Increased/hypersensitive receptors at NMJ to compensate for lack on innervation
  • Muscle wasting
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76
Q

What is a motor unit?

A

A lower motoneurone and all the muscle spindles it supplies

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77
Q

Define a reflex

A

An involuntary, unlearned, repeatable, automatic reaction to a specific stimulus that does not require the brain to be intact

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78
Q

List the 5 components of a reflex

A
  • Receptor
  • Afferent fibre
  • Integration centre
  • Efferent fibre
  • Effector
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79
Q

What is a monosynaptic stretch reflex?

A

A hard-wired connection between a lower motoneurone and afferent fibre of a muscle-length sense organ

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80
Q

How does the stretch reflex work? What is its function?

A
  • Muscle spindles = length receptor within muscle fibres
  • Spindles detect stretch and fire action potential to:
    • Brain via dorsal columns
    • Cerebellum via spino-cerebellar tracts
    • Spinal motoneurones which causes the reflex contraction of muscle
  • Aims to prevent overstretching and injury to muscle
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81
Q

What is motor tone? What is it’s function?

A

Background electrical impulses from lower motoneurones, causing minimal/background contraction to a muscle

  • Maintenance of body posture
  • Allows head to be held upright
  • In all skeletal muscles of the body
  • Inhibited during deep (REM) sleep
    • Except respiratory and extra-ocular muscle, urinary and anal sphincters
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82
Q

What is the role of y-motoneurones?

A
  • Keep muscles spindles taut
    • Allows firing of a-motoneurones to continue discharging and leading to muscle contraction
  • Adjust sensitivity of muscle spindles
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83
Q

What is the role of the interneurone pathways in reflexes?

A
  • Smoother movement (no single jerk)
  • In case one pathway is damaged
  • Introduce more signals into the circuit
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84
Q

What are descending tracts?

A

Pathways by which motor signals are sent from the brain (motor strip in pre-central gyrus) to lower motoneurones to produce resting motor tone or limb movement.

  • Pyramidal - voluntary movement of muscles of body and face
  • Extrapyramidal - involuntary/automatic control of musculature
    • Originate in brainstem
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85
Q

Name and briefly describe the pyramidal tracts

A
  • Corticospinal tract = supplies musculature of the body on the contralateral side
    • Lateral = decussate in meddulla
    • Anterior = decussate in ventral horn on contralateral spinal cord of intended target
  • Corticobulbar tract = supplies musculature of the head and neck on the contralateral side
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86
Q

Describe the pathway of the corticospinal tracts

A
  • Receives input from pre-motor cortex, supplementary motor cortex and primary motor cortex
  • Descends through internal capsule, midbrain, pons and medulla
    • Divides into two at inferior medulla
  • Lateral decussates and descends into spinal cord and terminates in contralateral ventral horn
  • Anterior remains ipsilateral in spinal cord and only decussates at cervical/thoracic level of target
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87
Q

Describe the pathway and organisation of the corticobulbar tract

A
  • Input from lateral aspect of primary motor cortex
  • Descend through internal capsule into brainstem
  • Terminate on motor nuclei of cranial nerves
  • Usually bilateral innervation
    • Fibres from left can innervate both left and right
  • Some exception
    • Facial nerve is contralateral
    • Hypoglossal nerve is contralateral
88
Q

Name and briefly describe the extra-pyramidal tracts

A

Originate in brainstem and carry motor fibres to the spinal cords via interneurones

  • Rubrospinal
  • Reticulospinal
    • Medial/lateral
  • Tectospinal
  • Vestibulospinal

Responsible for muscle tone, balance, posture, locomotion

89
Q

Describe the vestibulospinal tract including origin, termination and function

A
  • Originates from vestibular nuclei (brainstem)
    • Receive inputs from the organs of balance
  • Terminates in ipsilateral spinal cord
  • Controls balance and posture by innervating ‘anti-gravity’ muscles (arm flexors/leg extensors) via lower motoneurones
90
Q

Describe the reticulospinal tract including origin, termination and function

A
  • Medial orginiates in Pontine Reticular Formation
    • Facilitates voluntary movements
    • Increases muscle tone
    • Terminates in lamina VII and VIII
  • Lateral originates in Medullary Reticular Formation
    • Inhibits voluntary movements
    • Decreases muscle tone
    • Terminates lamina VII and IX
  • Damage leads to unopposed extension of head and limbs
91
Q

Describe the rubrospinal tract including origin, decussate and function

A
  • Originates in red nucleus
  • Immediately decussate in midbrain
    • Travels in lateral funiculus
  • Responsible for control of hand movements
92
Q

Describe the tectospinal tract including function, origin, termination and decussation

A
  • Originates in superior colliculus (visual tectum) or inferior colliculus (auditory tectum)
  • Decussates in midbrain
  • Terminates in contralateral cervical cord
  • Mediates postural reflex movements of the head to auditory and visual signals
93
Q

Describe the causes and consequences of damage to the corticospinal tracts

A

Causes:

  • Trauma - susceptible due long length
  • CVA through internal capsule

Consequences (all contralateral):

  • Hypertonia
  • Hyperreflexia
  • Clonus (decreased descending inhibition)
  • Babinski sign
  • Muscle weakness
94
Q

Describe the consequences of damage to the corticobulbar tracts

A
  • Most muscles receive bilateral innervation so lesion on one side results in generalised muscle weakness
  • Exceptions:
    • Facial nerve - contralateral spastic paralysis
    • Hypoglossal nerve - contralateral spastic paralysis
95
Q

List the signs of an upper motoneurone lesion

A
  • Muscle weakness
    • Upper limb extensors and lower limb flexors (pyramidal weakness)
  • Spasticity
  • Hyperreflexia
  • Hypertonia
  • Babinski sign present
  • Pronator drift
96
Q

What is the scientific basis behind hyperreflexia and hypertonia in UMN lesions?

A

Normally, reflexes and muscle tone are inhibited by the extra-pyramidal tracts via descending inhibition. If this inhibition is absent due to a UMN lesion, the reflexes will increase activity and motor tone will increase.

97
Q

Describe the function of the different parts of the cerebellum

A
  • Vestibulo = balance and ocular reflexes
    • Input from vestibular system
  • Spino = error correction
  • Cerebro = movement planning and motor learning
    • Visually guided movements
    • Coordination of muscle activation
98
Q

Describe some signs of cerebellar disease

A

DANISH

  • Dysdiadochokinesis = inability to perform rapid, alternating movements
  • Dysmetria = overshoot of hand due to lack of coordination
  • Dysarthria = ‘scanning’ speech (monotonous/slurred)
  • Ataxia = poor balance
  • Nystagmus = involuntary eye movements
  • Intention tremor = tremor at the end of movements
  • Slurred speech
  • Hypotonia
99
Q

Name some causes of cerebellar disease

A
  • Tumours/SOL
  • Cerebrovascular disease
  • Genetic - Friedreich’s ataxia = degeneration of cerebellar pathways
  • Coeliac disease (gluten intolerance)
  • Thiamine / Vit E / zinc deficiency
  • Infections - HIV, toxoplasma, CJD
  • Trauma
100
Q

What are the basal ganglia?

A

Multiple nuclei that are interconnected with the cerebral cortrx, thalamus and brainstem. They are found at the base of the forebrain and surround the ventricles. Function:

  • Control of voluntary motor movements
  • Procedural learning
  • Routine behaviours (bruxism etc)
  • Eye movements
  • Cognition
  • Emotion
101
Q

Name the components of the basal ganglia and their respective functions

A
  • Striatum
    • Caudate nucleus = voluntary movement
    • Putamen = regulate movement, influence learning
  • Globus pallidus = regulate voluntary movements
    • External/internal
  • Substantia Nigra = reward, addiction and movement
    • Pars Compacta = fine motor control
    • Pars Reticulata = eye movements
102
Q

What is Parkinson’s disease?

A

Progressive degeneration of the dopaminergic neurones of the Substantia Nigra (nigro-striatal pathway)

103
Q

What are the main signs and symptoms of Parkinson’s?

A
  • Hypertonia
    • Lead pipe/cog wheel rigidity
  • Hypo/bradykinesia = slowness of voluntary movement and reduction in automatic movement
    • Arm swing
  • Resting tremor
    • Pill roll
    • Worse with stress but better with movement
  • Festinating gait = small steps
    • Unsteady changing direction
104
Q

How does polio affect the CNS?

A
  • Invades motoneurones of the brainstem and spinal cord, causing them to die
  • Presents with lower motoneurone paralysis of affected segments
  • No sensory loss
105
Q

Discuss the ascending pain pathways

A
  • Spinothalamic tract (anterolateral) ascending
    • Decussates at level of spinal cord in dorsal horn
  • Direct (fast) = discriminative (quality/intensity/location)
    • Contralateral with somatotropic organisation
    • Lamina I, IV and V
  • Indirect (slow) = arousal
    • Bilateral with no somatotropic organisation
    • Synapses in brainstem
106
Q

Name the stages of nociception

A
  1. Transduction = activation by a stimulus
  2. Transmission = relay of action potentials along nociceptive fibres to CNS
  3. Modulation = by other peripheral nerves or CNS
  4. Perception = interpretation by the brain of the sensation as painful
107
Q

Describe the difference between nociceptive fibres

A
  • A delta - mechanical
    • Fast
    • Sharp and stabbing pain
    • Myelinated
    • Lower threshold
    • Laminae I and V
  • C - mechanical, thermal and chemical
    • Slow
    • Dull and throbbing pain
    • Higher threshold
    • I, II (Sub. Gel.) and V
108
Q

Describe the transduction stage of nociception

A
  • Tissue damage increases K+, prostaglandin, serotonin and bradykinin release to activate nociceptor
  • Nerve endings release Substance P
    • Increases capillary permeability
    • Contributes to inflammation
    • Causes mast cells to release histamine which increases sensitivity further
  • Changes stimulus into action potentials
  • Steroids and NSAIDs (cox-inhibitors) prevent this
109
Q

Describe the transmission stage of nociception, including how this is treated with pain relief

A
  • Impulses through noceiceptive (A delta/C) fibres
    • Terminate in dorsal horn on rexed laminae
  • Local anaesthetics (lignocaine) inhibit voltage dependent Na+ channel activity in these fibres
    • Lipid soluble so diffuse through membrane
  • Visceral fibres converge on spinal cord 2nd order neurones shared by somatic nociceptive fibres (lamina V)
    • Referred pain
110
Q

Describe the modulation stage of nociception

A
  • Gate Control Theory of Pain
    • Massage closes gate by activating touch fibres which inhibit same synapses as pain fibres
    • TENS, acupuncture, pain killers etc
  • Central and descending spinal systems - employ endogenous opiod peptide analgesics / neurotransmitters (enkephalins/endorphins etc)
    • Block neurotransmitter release by inhibiting calcium influx
    • Open K+ channels to hyperpolarise neuron
    • Regulated by fibres in Periaqueductal Grey Matter in mid-brain
111
Q

What is the role of enkephalinergic neurones?

A
  • Inhibit pain pathway in Substantia Gelatinosa
  • Tissue damage stimulates C fibres which inhibit cells of SG
    • Pain sensation
  • Descending serotinergic pathways can reactivate SG
    • Modulation of pain
112
Q

Describe the perception stage of nociception

A
  • In the thalamus/cortex
  • Thalamocortical projections carry information on location, intensity and nature of pain
  • Primary and association areas
    • Secondary somtosensory cortex
  • Emotional response via limbic system
  • Stress response via hypothalamus
113
Q

What is a nerve conduction study?

A
  • Apply an electrical stimulus and measure response distally
  • Different amplitudes stimulate different nerve types
    • Unmyelinated C fibres require higher stimulus
  • Work out which nerves aren’t working based on response
114
Q

What is hyperalgesia?

A

Increased pain at normal threshold due to peripheral and/or central sensitisation

115
Q

What is allodynia?

A

The experience of pain from a non-painful stimulus

  • Can occur in areas other than stimulated area
  • Not synonymous with referred pain
116
Q

What is the difference between acute and chronic pain?

A
  • Acute
      • Cause usually known
  • Chronic
    • Continues after removal of stimulus
    • > 3 months
    • Cause not usually known
117
Q

Describe neuropathic pain

A

Pain caused by damage to somatosensory nervous system (neuronal origin)

  • Difficult to treat - cannot be explained by a single disease process/location
  • Caused by ‘wind-up’:
    • Decreased threshold of nociceptor activationI
    • Increased receptor field of nociceptorsP
    • Prolonged post-stimulus sensations (hyperpathia)
    • Development of abnormal sodium channels which fire off dysfunctionally
118
Q

What is Complex Regional Pain Syndrome? How is it caused?

A

Sympathetically-mediated pain of the extremities

  • No identifiable lesion (Type 1) or identifiable (Type 2)
  • Caused by trauma, fracture, surgery, stroke, MI
119
Q

What are the signs/symptoms of CRPS?

A
  • Sensory - burning, hyperalgesia, allodynia
  • Vasomotor - temperature asymmetry, skin colour changes/asymmetry
  • Sudomotor - oedema, sweating changes/asymmetry
  • Motor - weakness, tremor, dystonia, trophic changes (skin, hair etc) decreased range of motions
120
Q

What is the mechanism behind CRPS?

A
  1. Original injury initiates pain impulse by sensory nerves → CNS
  2. Pain impulse triggers sympathetic impulse which returns to original site of injury
  3. This triggers an inflammatory response
    • Vessels spasm which causes swelling and increased pain
  4. This pain triggers another response which establishes a cycle of pain and swelling
121
Q

What are the stages of CRPS?

A
  1. Pain/burning/aching/sensitivity in a limb following an event or without apparent cause
    • Not compatible with a single peripheral nerve / root
    • Vasomotor disturbances
  2. Progression of soft tissue oedema
    • Muscle wasting
    • Trophic changes (skin/nails/bone/hair)
  3. Limitation of movements
    • Contracture of digits
    • Brittle ridged nails
    • Bone demineralisation (x-ray)
122
Q

What are the side effects of opioids?

A
  • Analgesia
  • Respiratory depression
  • Constipation
  • Itching
  • GI disturbance
  • Antitussive (stop coughing)
  • Euphoria
  • Dependence
123
Q

What are the different opioid receptors? What is their mechanism of action?

A
  • Mu - MOP
    • Close V-G calcium channels
  • Delta - DOP
    • Open K+ channels to hyperpolarise cell
  • Kappa - KOP
    • Inhibit cAMP formation

ALL inhibit neurotransmitter release

124
Q

Name some weak and strong opioids?

A

Weak:

  • Codeine
  • Dihydrocodeine
  • Tramadol

Strong:

  • Morphine
  • Fentanyl
  • Diamorphine (heroin)
125
Q

Describe the WHO analgesics ladder for treating pain

A
  1. Non-opioid - NSAIDs etc
  2. Weak opioid (+/- non-opioid)
  3. Strong opioid (+/- non-opioid)
126
Q

What is opioid insensitive pain? How is it treated?

A
  • Does not respond to increasing opioid dose
    • Nerve compression
    • Nerve destruction
  • Treat with adjuvant analgesics:
    • NSAIDs
    • Paracetemol
    • Ketamine
    • Cannabinoids
127
Q

What is the inner ear? Describe it’s development

A

Sensory organ comprised of semicircular canals and cochlea, encased in bone

  1. Otic placode thickens
  2. Invaginates and pinches off to form the otic vesicle while surface ectoderm closes over
  3. Formation of membranous labyrinth
    • Saccule coils up to form cochlea
    • Utricle changes shape to form semi-lunar canals
128
Q

What is the function of the middle ear? Describe it’s development

A

Conducts sound from external acoustic meatus to inner ear

  • Ossicles develop within cartilage bars 1 and 2
    • Meckel’s (1) - malleus and incus (and mandible)
    • Reichart’s (2) - stapes (and styloid, hyoid)
  • Tympanic cavity and auditory tubes from 1st pharyngeal pouch
    • Expands distally - tympanic cavity
    • Remains narrow and horizontal proximally - Eustachian tube
129
Q

What is the function of the external ear? Describe it’s development

A

Funnels sound into middle ear

  • External auditory meatus from 1st pharyngeal cleft
  • Auricles/pinna from 1st and 2nd pharyngeal arches
    • From 6 auricular hillockes
130
Q

What is the innervation of the ear?

A
  • Inner - vestibulocochlear (8)
  • Outer = trigeminal (V3)
  • Tensor tymapni = V3
  • Stapedius = Facial (7)
131
Q

Describe some causes of congenital deafness

A
  • Middle ear deafness = 1st/2nd pharyngeal arch problems
  • Inner ear deafness = maldevelopment of Organ of Corti
    • Due to teratogenic/infectious agents during pregnancy
132
Q

Describe the formation of the eyes

A
  • Out-pocketings of forebrain (optic vesicles) grow out to make contact with ectoderm (lens placode)
  • Lens placode invaginates and pinches off
  • Tissue folds over and causes choroid fissure to close
    • Connected to forebrain via optic stalk
  • Hyaloid artery in choroid fissure degenerates distally
    • Proximal portion = central retina of the eye
  • Optic vesicle froms optic cup and divides further
133
Q

List the embryological origins of lens, retina, iris, ciliary body, optic stalk and central artery of retina

A
  • Optic placode - lens
  • Optic vesicle:
    • Retina (neural and pigmented layers)
    • Iris = contractile diaphragm with central aperture
    • Ciliary body = muscular/vascular structure connecting choroid to lens
  • Optic stalk - optic lens
  • Hyaloid artery - central artery of the retina
134
Q

Describe how the eyes and ears and positioned during formation

A
  • Ears - initally develop in neck and ascend to the side of the head with growth of the mandible
  • Eyes - initally positioned on the side of the head and move to the front when facial prominences grow
135
Q

Describe some eye abnormalities

A
  • Coloboma = failure of the choroid fissure to close
  • Congenital cataracts = opacity of the lens due to genetics or teratogens (rubella etc)
  • Detached retina = failure of the intraretinal space to be obliterated when retinal layers normally fuse
136
Q

Describe the development of the extraocular muscles?

A

Form from preotic myotomes that develop in the region of the eye

137
Q

List the components of the visual pathway

A
  • Eye (retinal neurons)
  • Optic nerve
  • Optic chiasm - crossing over of fibres
  • Optic tract - hemifields of vision
  • Lateral geniculate nucleus - termination of retinal axons
  • Optic radiation
  • Primary visual cortex
138
Q

Describe the different types of retinal neurons

A
  • Photoreceptors
    • Rods (not in central retina) = photosensitive, dark adapt
    • Cones (in forea) = high acuity, day and colour vision
  • Interneurones = combine signals from photoreceptors
  • Ganglion cells
    • Magnocellular = luminance contrast, motion
    • Parvocellular = colour contrast, fine detail
139
Q

What is Optical Coherence Tomography?

A

Uses light waves to take cross-section pictures of the retina. It can detect:

  • Fovea hypoplasia
  • Retinal dystrophy
140
Q

What is amblyopia? How is it treated?

A

Lazy eye caused by abnormal binocular input early in life

  • Strabismus
    • Divided into esotropia (in) exotropia (out) hypertropia (up) hypotropia (down)
    • Double vision
    • Caused by anisometropia = uncorrected difference in refractive power between the two eyes
  • Treat with glasses/patches
    • Poor adherence
141
Q

What investigations are there for eye abnormalities?

A
  • Slit lamp examination - cataracts
  • Fundoscopy
    • Fovea (centre) = high density of photoreceptors
    • Optic disc (nasal) = where ganglion cells exit (blind spot)
  • Visual field measurement
142
Q

What is glaucoma? What can cause it?

A

High intraocular pressure that causes optic nerve damage and peripheral field defects

Causes:

  • Ocular hypertension
  • Genetics
  • Steroids
  • Diabetes
  • Trauma
  • Race (east asian)
143
Q

Describe the sympathetic and parasympathetic control of the pupil?

A
  • Parasympathetic = constriction via sphincter pupillae
    • Crossing = consensual pupillary reaction
  • Sympathetic = dilation via dilator pupillae
    • Horner’s Syndrome = miosis, ptosis and anhydrosis
144
Q

How can a pituitary tumour causes visual disturbances

A
  • Lesion of the optic chiasm
  • Causes bitemporal visual field defect (hemianopia)
145
Q

Describe the eye muscles, their innervation and consequences of damage

A
  • CN VI (abducens) = lateral rectus
    • Esotropia with reduced abduction
  • CN IV (trochlear) = superior oblique
    • Hypertropia with elevated adduction
  • CN III (trigeminal) = levator palpebrae, medial/inferior/superior rectus, inferior oblique, sphincter pupillae
    • Exotropia and depression with reduced adduction, elevation and depression
146
Q

What properties of sound can be detected by the cochlea?

A
  • Frequency - Hertz (Hz)
  • Volume - Decibels (dB)
147
Q

What is the Organ of Corti?

A

The location of vibration-sensitive hair cells in the cochlea

148
Q

What is tonotopy?

A

Where different regions of the basilar membrane (cochlear) vibrate at different frequencies due to variations in thickness and length

149
Q

Describe the different roles of inner and outer hair cells in the cochlea

A
  • 1 row of inner hair cells = sound sensors
  • 3 rows of outer hair cells = amplifiers
    • Regulated by olivocochlear system (efferent feedback to hair cells)
  • Mechanically tuned by location along the cochlea
    • Tonotopy
  • Electrically tuned by expression of particular ion channels
150
Q

Describe the molecular events that occur in the cochlea during sound transmission

A
  • Bending of stereocilia opens K+ channels
    • Depolarisation which opens V-G Ca2+ channels
    • Triggers transmitter release onto spiral ganglion
  • High extracellular concentration of K+ in cochlea
    • Otherway round to normal cells
151
Q

What are Spiral Ganglion Neurons?

A

Afferent axons of the Vestibulocochlea Nerve (CN VIII)

152
Q

Describe how inner hair cells can transmit the sound to brainstem

A
  • Inner hair cells are primary sensing organ
  • Transmitter release onto spiral ganglion
  • Triggers action potential
    • Louder sound = more APs in more axons
  • Action potentials propogate to brain via CN VIII
  • Innervate Cochlear Nucleus and auditory brainstem
153
Q

List some causes of hearing impairment

A
  • Loud noises
  • Congenital
  • Infections (rubella)
  • Ototoxic substances (aminoglycosides)
  • Trauma to the temporal bone
154
Q

How would you assess hearing?

A
  • Visual inspection via otoscope
  • Audiograms - plot sensitivity against frequency
  • Otoacoustic emissions - tests amplifier function
    • Microphone fitted into ear canal
  • Auditory brainstem response
155
Q

Describe the different types of hearing damage?

A
  • Conductive = blockage / ruptured ear drum / otitis media / otosclerosis
  • Sensory
    • Hair cell destruction (physical or noise-related)
    • Hair cell death (ototoxicity - kanamycin/aminoglycosides)
  • Neural = age / spiral ganglion damage / tinnitus / neuropathy (jaundice) / monaural deafness
156
Q

What are the treatments for hearing loss?

A
  • Hearing aides
  • Cochlear Implants - direct electrical stimulation of spiral ganglion
  • Hair cell regeneration?
    • Further research needed
  • Cochlea Nucleus Implants - direct stimulation of neurons in first nucleus of auditory pathway
157
Q

Describe the auditory pathway

A
  • Cochlea
  • Superior Geniculate Nucleus
  • Cochlear Nucleus
  • Superior Olivary complex
  • Inferior Colliculus
  • Medial geniculate Nucleus (auditory thalamus)
  • Auditory cortex
158
Q

What is a stroke? How do TIAs differ?

A

An abrupt/sudden loss of focal brain function lasting ? 24 hours due to spontaneous haemorrhage or inadequate blood supply.

TIAs resolves completely within 24 hours

159
Q

Name some causes of stroke

A

INFARCT

  • Atheroma/emboli
  • Arteritis
  • Blood disorders

HAEMORRHAGE:

  • Hypertensive microaneurysm
  • Thrombocytopenia
  • Tumour
  • Cocaine/amphetamines
160
Q

Describe the symptoms of stroke in different areas of the brain

A
  • Frontal - motor deficit, Broca’s aphasia (expressive) behaviour/emotion changes
  • Parietal - sensory deficit, visuospatial (neglect) inferior quadrant/hemianopia - sup. optic radiation
  • Temporal - auditory/vestibular deficit, taste, smell, Wernicke’s aphasia (receptive) memory, superior qudrantanopia
  • Occipital - visual disturbance (visual fields, homonymous hemianopia)
  • Cerebellum/brainstem - balance/coordiantion, motor/sensory tracts, CN nuclei
161
Q

Describe the classifications of stroke and their symptoms

A
  • TACS (total anterior circulation stroke) - ICA / MCA
    • contralateral hemiparesis/anopia, cerebral dysfunction
  • PACS (partial..) - branch of MCA
    • Restricted motor deficit
  • LACS (lacunar..) - single perforating artery
    • Pure motor/sensory/ataxia/hemiparesis
  • POCS (posterior..)
    • Brainstem, cerebellar or occipital signs
162
Q

What are the risk factors for developing stroke?

A
  • Non-modifiable = age, gender, genetics, previous stroke
  • Modifiable = smoking, alcohol, diet, sedentary lifestyle
  • Medical = hypertension, hypercholesterolaemia, diabetes, arrhythmia
163
Q

What is the treatment for stroke?

A
  • IV thrombolysis (300mg alteplase) within 3 hours
    • Only if no bleeding risk (warfarin, thrombocytopenia etc)
    • Only for ischaemic stroke
  • Aspirin if not thrombolysed
  • Rehabilitation therapy, education, carer
164
Q

How can strokes be prevented?

A
  • Antithrombotic medication
    • Aspirin
    • Warfarin / heparin
  • Treat risk factors
    • Hypertension/cholesterolaemia
    • Diabetes
  • Lifestyle changes
  • Medication compliance
165
Q

What investigations would be carried out if a stroke was suspected?

A
  • BM!
  • FBC / INR
  • ECG - AF
  • Lipid/ U+E / LFT
  • MRI - bleeding? Cannot thrombolyse
  • Carotid ultrasound - > 50% occlusion = carotid endarctectomy
166
Q

How can the spinal blood supply be compromised?

A
  • Aortic disease / surgery
  • Vasculitis
  • Sickle cell disease
  • Hypotension
  • Disc herniation
  • Tumour/abscess
  • Intraspinal haemorrhage
167
Q

What are the symptoms of lack of blood supply to the spinal cord?

A
  • Flaccid weakness
  • Areflexic
  • Anaesthesia
  • Anterior = loss of pain/temperature
  • Posterior = loss of proprioception (dorsal columns)
  • Can progress to UMN signs
    • Atrophy
    • Sphincter failure
168
Q

Describe some causes of acute intracranial events

A
  • Lack of substrate
    • Blood - blockage in vessels, systemic hypotension, raised ICP
    • Glucose - systemic hypoglycaemia, impaired cerebral circulation
    • Oxygen - airway/breathing problems, CO poisoning
  • Abnormal activity
    • Fitting - Reticular activating system damaged
    • Head injury - RAS damaged
  • Local damage - injury/bleed
169
Q

What are the consequences of raised intracranial pressure?

A
  • Compensation = blood/CSF/brain squeezed out
    • Coning = brainstem compression = death
  • Internal Herniation
  • Secondary brain injury:
    • Hypoxia
    • Hypotension
    • Clot
170
Q

What are the clinical signs of raised ICP?

A
  • Behaviour change
  • Drop in GCS
  • Pupil reaction change
  • BP, pulse, breathing rate change
171
Q

Name some causes of raised intracranial pressure

A
  • Brain swelling
    • Injury
    • Infection (meningitis / encephalitis)
  • Blood
    • Coughing
    • Impaired venous drainage (neck constriction)
  • CSF - subarachnoid blood
  • Haematoma
    • Trauma
    • Haemorrhagic stroke
    • Tumour
  • Tumour - primary/secondary
172
Q

Describe the 3 main types of cerebral hernias and their consequences

A
  • Subfalcine = cingulate gyrus pushed under falx cerebri
    • Same side as mass
    • Compression on anterior cerebral artery = ischaemia of medial and parietal lobes
  • Tentorial = uncus through tentorial notch
    • Damage to oculomotor nerve on same side = pupil dilation
    • Occlusion of posterior cerebral and superior cerebellar artery
    • Secondary haemorrhage into brainstem
  • Tonsilar = cerebellar tonisls into foramen magnum
    • Compresses brainstem = coma
173
Q

What is a contusion and diffuse axonal injury?

A

Contusion = bruise of the brain associated with microvascular damage and multiple microhaemorrhages

Diffuse axonal injury = extensive lesions in white matter tracts over a widespread area (also called shearing)

174
Q

Describe the consequences of traumatic brain injury

A
  • Primary insult
    • Haematoma / haemorrhage
    • Contusions
    • Diffuse axonal injury
  • Secondary insult (target of treatment)
    • Hypoxia
    • Hypoperfusion
    • Oedema
    • Raised intracranial pressure
175
Q

Describe the events occurring after brain injury

A
  1. Disruption to tight junctions = increases permeability
  2. Injury - oxidative stress - inflammatory mediators
    • Vasodilators
    • Coagulation pathway activation
  3. Possible change in expression of ion channels
176
Q

How is cerebral oedema classified?

A
  • Cytotoxic = movement of ions and water
  • Vasogenic = disruption of vessels
    • Blood brain barrier breaks down
177
Q

What is the Monroe-Kellie-Hypothesis?

A

The pressure-volume relationship between ICP, volume of CSF/blood/brain tissue and cerebral perfusion pressure

  • Cerebral perfusion pressure= mean arterial volume - ICP
  • Increase in ICP = decrease in venous volume and CSF volume
    • Compensation ability during increase in ICP
178
Q

What are the responses to metabolic disturbances in the brain

A

Hypoxia / hypercapnia = vasodilation and cerebral oedema

179
Q

What are the advantages of inducing a medical coma?

A
  • Reduce metabolic rate
  • Reduce cerebral blood flow
  • Reduce swelling
  • DECREASE ICP
180
Q

Name some drugs used for inducing a medical coma

A
  • Propofol = decreases cerebral metabolic requirement for O2 and decreases airway reflexes to stop coughing/choking
    • Can cause hypotension
  • Thiopentone = decreases CMRO2
    • High volume of distribution → seizures
    • Can cause hypotension
  • Opioids = pain relief, reduces stress response and airway reflexes
    • Can cause hypotension
  • Ketamine - haemodynamically stable but can cause hallucinations
  • Neuromuscular blocking agents
  • Mannitol - emergency oedema treatment
  • Vasopressors - adjust BP due to aneasthetic-induced drops
181
Q

How can you measure brain function during a coma?

A
  • EEG
  • Bispectral index - monitor depth of anaesthesia using EEG
  • Physiological markers
  • ICP probe into ventricles
182
Q

What is the reticular formation? What is it’s function?

A

A network of cells and nuclei (Raphe etc) in central core of brainstem that receives a wide sensory input to control the level consciousness and awareness

  • Informs hypothalamus to change autonomic signals
  • Alters sensitivity of motor nuclei in ventral horn
  • Controls:
    • Sleep regulation
    • Motor signals
    • Cardio/respiratory centre signals
    • Autonomic signals
    • Reward/motivation
183
Q

What is the ascending reticular activating system? Name it’s inputs and outputs

A
  • Formed by reticular formation projections
  • Raises level of consciousness by filtering out incoming signals
  • Inhibited by hypothalamic sleep centres
  • Input = auditory, nociceptive, visual, visceral
  • Output via thalamus and cortex:
    • Motor - increases tone and activity
    • Autonomic - fight or flight
    • Habituation = filtering out signals if constantly stimulated
184
Q

What is an EEG? What is it used for?

A

Electroencephalogram = measures the algebraic sum of electrical activity of neurones, from the scalp.

Used in epilepsy, dementia, encephalitis and general damage

185
Q

Name some neurotransmitters projecting in the CNS and the disease it can contribute to

A
  • NA - depression
  • 5-HT - depression
  • ACh - Alzheimers
  • DA:
    • Parkinson’s (decreased)
    • Schizophrenia (increased in limbic system)
186
Q

Describe the different types of waves found in an EEG

A
  • Alpha - mainly occipital
  • Beta - parietal / frontal
  • Theta - parietal / temporal (children and concentrating adults)
  • Delta - cortical
187
Q

Describe some conditions with impaired consciousness

A
  • Locked-in syndrome = intact cortex but damaged reticular activating system
    • Only move eye up but aware of surroundings
  • Persistent Vegetitive State = intact brainstem (RAS) but damaged cortex
  • Brain death - no EEG activity in either cortex or RAS
188
Q

What is a coma? Include cause and investigations

A

A state of unconsciousness from which a person cannot be roused using pain, sound or light and does not initiate voluntary movement

  • Causes = intoxication, metabolic (hypoxia/hypothermia) stroke, trauma
  • Investigations = EEG, scans, GCS, history
189
Q

What is the function of sleep? What is it controlled by?

A
  • Resetting of CNS
  • Energy conservation
  • Memory

Controlled by reticular formation and hypothalamus (inhibits RF)

190
Q

What is the difference between REM and non REM sleep?

A
  • Non-REM = slow wave sleep (4 stages)
    • Active body, inactive brain (neurological rest)
    • Neuroendocrine activity (mainly pituitary)
    • Decrease in cerebral blood flow, O2 consumption, temperature, BP, RR = reduced BMR and energy consumption
  • REM = active EEG (waves from pons to thalamus to occipital)
    • Active brain, inactive body due to descending inhibition
    • Irregular HR and RR
    • Increased BMR
    • Penile erection
191
Q

Describe the differences in neurotransmitter released during the stages of sleep

A
  • Waking = active 5-HT, NA, ACh
  • Non-REM = inactive 5-HT, NA, ACh
  • REM = inactive 5-HT and NA but active ACh
192
Q

Describe some sleep disorders

A
  • Insomnia = difficulty sleeping due to increased adrenaline and stress hormone
  • Parasomnia = abnormal movements, behaviours, emotions and dreams
  • Hypersomnia = excessive daytime sleeping
    • Narcolepsy
    • Obstructive Sleep Apnoea = loss of tone of upper respiratory tract muscles that causes closure of airways and reduction in arterial pO2
    • Snoring, wakefulness (no deep sleep)
    • Risks = obesity, age, drugs/alcohol, NM
    • Treatment = continuous positive airway pressure (CPAP) oral appliances, surgery
193
Q

Describe the initial assessment of consciousness

A
  • Airway
    • Nasopharyngeal airway - better tolerated, easily inserted
    • High concentration oxygen
    • Head tilt / jaw thrust
  • Breathing - mask misting / indication mask / chest movement
    • Assistance? Intubation / bag value mask
  • Circulation - pulse, coughing, movement
    • Capillary return
    • IV access
    • BM
  • Disability - AVPU / GCS
194
Q

Describe some immediate treatments for complications during unconsciousness

A
  • Hypoxia = high flow oxygen
  • Hypoglycaemia = IV glucose
  • Fitting = IV lorazepam
  • Opiate OD = IV/IM naloxone
195
Q

What is the AVPU?

A

An immediate indicator of consciousness:

  • Alert
  • Responds to verbal stimulus
  • Responds to painful stimul
  • Unresponsive
196
Q

What is the GCS score?

A

Measurement of consciousness

  • Eye opening /4 = spontaneously / to speech / to pain / none
  • Verbal response /5 = orientated / confused / inappropriate / incomprehensible / none
  • Motor response /6 = obeys command / localises pain / flexion / withdrawal / extension / none
  • Score /15
      • 9-12 moderate
    • >13 minor
197
Q

Describe the symptoms of a lesion in the cerebral hemispheres, brainstem, cerebellum, spinal cord, nerve rotts, peripheral nerves and neuromuscular junction

A
  • Cerebral hemispheres - mental function, motor/sensory loss, visual disturbance
  • Brainstem - cranial nerve damage
  • Cerebellum - DANISH signs
  • Spinal cord - pattern weakness, bladder.bowel dysfunction
    • Brown-sequard / syringomyelia
  • Nerve roots - problems with myo/dermatomes
  • Peripheral nerves - glove and stocking, individual palsies
  • NMJ - ptosis, diplopia, bulbar dysfunction, limb weakness, fatiguability
198
Q

Describe the deficits seen in Brown-Sequard syndrome

A
  • Ipsilateral loss of motor, sensory and proprioception
  • Contralateral loss of pain and temperature
199
Q

What is Syringomyelia? Include symptoms and causes

A

The formation of a cyst or cavity within the spinal cord, which expands over time to destroy the spinal cord

  • Symptoms = chronic pain, loss of sensation (hands) paralysis, abnormal body temperature, sweating
  • Cause = congenital, trauma, meningitis, haemorrhage, tumour
200
Q

Name some causes of loss of consciousness

A
  • Seizure
  • Syncope
    • Vasovagal
    • Postural hypotension
    • Cardiac
  • Hypoglycaemia
  • Head injury
201
Q

Describe some causes of headaches

A
  • Acute:
    • Infections
    • Migraine
    • Subarachnoid haemorrhage (thunderclap)
  • Chronic:
    • Migraine
    • Analgesic abuse
    • Tension
    • Temporal arteritis
202
Q

Describe the different types of epidural haemorrhage, including cause, type of bleed and symptoms

A

Between dura mater and skull

  • Caused by trauma to pterion
  • Rupture of middle meningeal artery
  • Arterial bleed
  • Sudden loss of consciousness, temporary improvement then sudden deterioration
203
Q

Describe the different types of subdural haemorrhage, including cause, type of bleed and symptoms

A

Between dura mater and arachnoid mater

  • Tearing of bridging veins between cerebral cortex and a venous sinus
  • Gradual deterioration over hours
    • Due to raised intracranial pressure
  • Venous bleed
  • Trauma / elderly / alcoholic
204
Q

Describe the different types of subarachnoid haemorrhage, including cause, type of bleed and symptoms

A

Between arachnoid mater and pia mater

  • Due to trauma / ruptured aneurysm / blood thinners / bleeding disorder
  • Arterial bleed
  • Rapid onset = thunderclap headache
205
Q

Name some causes of dizziness

A
  • Vertigo
  • Presyncope
  • Ataxia (cerebellum)
  • Anxiety
  • Anaemia
  • Hypoglycaemia
206
Q

What is vertigo? Include causes and symptoms

A

The sensation of moving objects around a person when they’re stationary

  • Causes:
    • Peripheral - Benign Paroxysmal Positional Vertigo, vestibular neuronitis, Meniere’s
    • Central - migraine, cerebellar disease, drugs
  • Symptoms:
    • Hearing loss / tinnitus
    • Nausea
    • Headache
207
Q

Describe the typical presentation of Myasthenia Gravis

A

Autoimmune attack on post synaptic nAchR

  • Bulbar weakness - swallowing, dysarthria
  • Fluctuating muscle weakness
    • Ptosis
  • General fatiguability
208
Q

What is neuroplasticity?

A

The adaptive capacity of the CNS and its ability to modify its own structural organisation and functioning

209
Q

Describe the regenerative capacity of the nervous system

A
  • Peripheral = Wallerian regeneration = Schwann cells and fibroblasts produce Nerve Growth Factor which promotes regeneration
    • Sprouts from proximal to distal
  • Central = neurogenesis only possible in hippocampus and olfactory bulb
210
Q

Describe the 3 routes of spread of infection into the brain

A
  • Direct spread - middle ear / base of skull fracture
  • Blood - sepsis (emboli → abscess) infective endocarditis
  • Iatrogenic - V-P shunt, surgery, lumbar puncture
211
Q

What is meningitis? Describe the cause, symptoms and complications

A

Inflammation of the leptomeninges (pia and arachnoid)

  • Organisms:
    • Neonates = E. coli
    • 2-5 = H.influenzae type B
    • 5-30 = N. meningitidis
    • >30 = s. pneumoniae
  • Symptoms = headache, neck stiffness, fever, confusion, photophobia, non-blanching rash
  • Complications = RICP, infacraction, abscess, subdural empyema, epilepsy (from scarring)
212
Q

What is encephalitis? Describe the cause, symptoms and consequence

A

Inflammation of the brain parenchyma

  • Cause = cytomegalovirus / toxoplasmosis / rabies / HPV / syphilis
  • Symptoms = fever, headache, confusion, seizures
  • Consequences = Neuronal death caused by replicating virus - inclusion bodies
213
Q

What is prion disease?

A

Prion protein goes through a conformational change (misfolding) which causes other prion proteins to misfold and aggregate together to cause neuronal death

  • Sporadic, familial or ingested
  • Leads to spongiform encephalopathies
214
Q

What is dementia? Describe the different types

A

An acquired global impairment of intellect, reason and personailty without impairment of consciousness

  • Alzheimer’s
  • Vascular = disease/injury to blood vessels in brain
  • Lewy Bodies = clumps of alpha synuclein and ubiquitin
    • Hallucinations, Parkinsonism
  • Frontotemporal = drastic personality changes and language difficulties
215
Q

What is Alzheimer’s? Describe symptoms, treatment and pathology

A

Neurodegenerative dementia (exaggerated aging process)

  • Symptoms = short-term memory loss, language problems, mood swings, disorientation
  • Pathology = atrophy of cortical neurons (white matter) due to increased neuronal damage
    • Neurofibrillary tangles - intracellular Tau protein
    • Senile plaques = foci of enlarged axons, synaptic terminals and dendrites (cotton wool)
    • Amyloid deposition
  • Treated with acetylcholinesterase inhibitors
216
Q

Name some symptoms, causes and consequences of raised intracranial pressure

A
  • Symptoms = headache, vomiting, papilloedema
  • Causes:
    • Expanding local lesions = Tumour, Haematoma, Abscess
    • Global increase = oedema, infection, trauma
  • Consequences:
    • Sulci flattened against the skull
    • Displacement of midline structures
    • Internal herniation
    • Coning
217
Q

Describe the types of damage done from a head injury

A
  • Primary damage = force causing injury
    • Focal = bruising/laceration of brain as it hits skull
      • Tearing of blood vessels = haemorrhage
    • Diffuse = direct tearing to axons/nerves /small vessels/pituitary stalk (diffuse axonal injury)
      • Heals by gliotic scarring
  • Secondary damage = consequences of damage
    • Haemorrhage
    • Infarction
    • Inflammation - oedema
    • Raised ICP

ESA 5 (2 decks)

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