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Year 2 - Excess > HNN > Flashcards

HNN Flashcards

1
Q

Name the 3 primary vesicles of the brain

A

Prosencephalon - forebrain
Mesencephalon - midbrain
Rhombencephalon - hindbrain

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2
Q

Name the 5 secondary vesicles of the brain and the primary vesicle they arise from

A

Telencephalon and diencephalon - prosencephalon
Mesencephalon - mesencephalon
Metencephalon and myelencephalon - rhombencephalon

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3
Q

Name the 12 cranial nerves

A

CN I = olfactory
CN II = optic
CN III = occulomotor
CN IV = trochlear
CN V = trigeminal
CN VI = abducens
CN VII = facial
CN VIII = vestibulocochlear
CN IX = glossopharyngeal
CN X = vagus
CN XI = accessory
CN XII = hypoglossal

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4
Q

Discuss testing of the cranial nerves in an UNCONCIOUS patient

A

CN II and III = pupillary reflex
CN V = supra-orbital pressure (do they feel the pain?)
CN V and VII = corneal reflex
CN VIII = caloric test
CN IX and X = gag reflex/cough reflex
CN XII = fasciulation of tongue (often seen when looking for the gag reflex

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5
Q

Discuss primary brain injury and a secondary brain injury (differences between them?)

A

Primary
* occurs at time of impact
* results in axonal shearing or associated haemorrhage
* may be diffuse (axonal damage) or localised
* injury is likely non-reversible
* won’t show improvement/little improvement
Secondary
* occurs from primary insults
* includes hypoxia, hypovolaemia, haematoma, and cerebral oedema
* resultant brain dysfuction is likely reversible
* less likely to be permanent (if ICP is stabilised quickly and treatment is started quickly

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6
Q

Name the structure which marks the change from nasopharynx to oropharynx

A

The tip of the soft palate (draw a horizontal line from there)

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7
Q

Name the structure which marks the change from oropharynx to laryngopharynx

A

The epiglottis

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8
Q

Describe the function of the BBB

A
  • maintain a constant environment
  • protect the brain from foreign substances
  • protect the brain from peripheral transmitters
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9
Q

Discuss the NT GABA

A
  • simple AA
  • acts on chloride channel causing it to open and increase Cl influx
  • less likely to reach threshold to transmit AP - Inhibitory NT
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10
Q

Name the common feature of GABA receptors

A

all composed of 5 sub-units (however the composition of different sub-units is different in different types of GABA receptor)

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11
Q

Discuss glutamate

A
  • main excitatory NT
  • one step removed from GABA (GABA is produced from glutamate breakdown)
  • amino bicarboxylic acid
  • activates sodium and calcium channels causing positive ion influx
  • depolarises cell, more likely to reach potentail - excitatory
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12
Q

Discuss the 3 glutamate receptors

A

AMPA
- ionic channels
- main rapid effect receptor
NMDA
- ionic channels
- sustains depolarization caused by NMDA
Kainate
- G protein coupled receptor
- more long-standing chnages

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13
Q

Discuss serotonin

A
  • 5-hydroxy-trytophan
  • widespread action
  • ALL except 5-HT3 → modulate intracellular activity
    (5-HT3 ~ ionotropic Na+ / K+)
  • inhibitory NT - balances out excessive excitatory NT effects
  • 7 receptor subtypes
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14
Q

Name the serotonin receptor which doesn’t modulate intracellular activity

A

5-HT3

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15
Q

Discuss acetylcholine (in the BRAIN)

A
  • acts on nicotinic receptors
  • acts on potassium and sodium channels
  • causes influx of positive ions - excitatory NT
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16
Q

Discuss dopamine

A
  • either excitatory or inhibitory (D1 and D5 like receptors either E or I, D2 - D4 like receptors are I)
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17
Q

Discuss dopamine receptors

A
  • D1-like (D1 / 5) - ionotropic ~ excitatory / inhibitory
  • D2-like (D2, 3, 4) - GPCR ~ inhibitory
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18
Q

Describe the pathogenesis of Parkinson’s Disease

A
  • degeneration of substantia nigra
  • loss of dopaminergic cells and therefore lack of dopamine
  • therefore excess of ACh activity
  • characterised by tremor, hypokinesia, and rigidity
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19
Q

State the cause of schizophrenia

A

excess of dopamine

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20
Q

State the drug type used in treatment of schizophrenia

A

D2 antagonists

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21
Q

Discuss how prolactin secretion from a secretory adenoma can be decreased by a dopamine agonist

A
  • prolactin secreting cells have D2 receptors
  • dopamine reduced prolactin secretion
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22
Q

State the NT-related theory behind addiction

A

Chasing a dopamine ‘reward’ - via the frontal reward pathway

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23
Q

Discuss the use of D2 antagonists in nausea treatment - hint: it doesnt impact the the brain

A
  • the chemoreceptor trigger zone in the medulla contains D2-like receptors
  • D2 anatgonists can decrease nausea
  • certain dopamine antagonists will not cross the BBB
  • therefore, can decrease nausea without impacting the brain
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24
Q

Name the enzymes with will break down adrenaline in the brain

A

mono-amine oxidases

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25
Q

Discuss general anaesthetic agents

A
  • inhaled or IV
  • IV usually used to get patient to sleep initially, and then gases used to maintain it
  • GASES
  • usually lipophilic
  • absorbed into blood quickly
  • cross BBB
  • rapid action
  • i.e., halothane, isoflurane
  • IV
  • faster action than gases
  • i.e., propofol
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26
Q

Discuss sedatives/anxiolytics

A
  • induce sleep or reduce anxiety
  • act on GABA receptors (action and side effects vary)
  • i.e., barbituates - pentobarbitone, and benzodiazepines - diazepam
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27
Q

Discuss antipyschotics

A
  • used in schizophrenia
  • D2 antagonists
  • i.e., typical - chlorpromazine, haloperidol, and atypical - clozapine and olanzapine
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28
Q

Name the 4 dural folds

A

Falx cerebri
Tentorium cerebelli
Falx cerebelli
Diaphragma sella

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29
Q

Discuss the GCS

A

Eyes
4 - spontaneously open
3 - open in response to voice/sound
2 - open in response to pain
1 - don’t open
Verbal
5 - normal
4 - confused
3 - inappropriate
2 - incoherent sounds
1 - no response
Motor
6 - normal movement (responds to commands)
5 - localises pain
4 - normal flexion
3 - abnormal flexion
2 - extension
1 - no movement
Remember NT i.e, if eyes are swollen shut, patient intubated, suspected spinal injury etc.

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30
Q

State the normal curvature of the spine

A

Cervical - lordosis
Thoracic - kyphosis
Lumbar - lordosis
Sacral - kyphosis

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31
Q

Discuss antidepressants

A
  • incrrease noradrenaline and serotonin action
  • 2-4 weeks theraputic onset
  • e.g. monoamine oxidase inhibitors (phenelzine), tricyclic antidepressants (imipramine), SSRIs (fluoextine)
  • rapid onest example = ketamine (can become a drug of abuse)
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32
Q

Discuss antiseizure medications

A
  • correct the imbalance of excitation and inhibition
  • i.e., Na channel blocker, GABA-pentinoids (act on alpha 2 delta subunit of receptor to reduce neuron activity), drugs which increase GABA action, and barbituates
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33
Q

State a drug used in bipolar disorder treatment

A

lithium carbonate

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34
Q

Discuss caffeine

A
  • blocks adenosine receptors on serotonergic neurons (adenosine is produced when tired - caffeine can reduce sleep quality/quantity)
  • increases energy metabolism in the brain
  • decreases cerebral blood flow
  • boosts adrenaline and dopamine
  • withdrawal causes imbalance a sbrain gets used to the effects (symptomatic)
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35
Q

Discuss alcohol in terms of INTOXICATION

A
  • increased GABA (disinhibition, sedation, and loss of balance)
  • increased adrenaline (high BP)
  • decreased L glutamic acid/glutamate (memory disruption)
  • increased serotonin (sedation and euphoria)
  • increased dopamine (elevated mood)
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36
Q

Discuss the imapct of alcohol on NTs

A

prostate gland

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37
Q

Discuss alcohol WITHDRAWAL

A
  • decreased GABA (anxiety, insomnia, and seizures)
  • increased adrenaline (high BP and tachycardia)
  • increased glutamate (delerium and seizures)
  • decreased serotonin (insomnia and mood disorder)
  • decreased dopamine (dysphoria)
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38
Q

Discuss the PROCESS of alcohol WITHDRAWAL

A
  • continued alcohol use offsets GABA and glutamte balance (more GABA function/less glutamate function)
  • brain adjusts and creates a new normal - downgrades GABA receptors/upgrades glutamate receptors (to try compensate for continued alcohol use)
  • when alcohol is removed NT levels return to normal
  • however, due to the change sin receptor sensitivity changes you get less GABA function and increased glutamate function
  • this causes withdrawal symptoms
  • the more tolerance built up to alcohol, the greater the withdrawal effects
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39
Q

Discuss cannabinoids

A
  • act on multiple receptors
  • cause G protein coupled recpetor changes
  • can have a therapeutic effect in epilepsy, nausea, and spasticity
  • THC - causes mood chnage and sedative effects - high conc. of THC can cause psychiatric symptoms with sustained use
  • cannabidiol - recognised medicinal effects in epilepsy
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40
Q

Discuss drugs of abuse/addiction (cocaine, heroin, ecstasy, LSD, MDMA, amphetamines)

A

cocaine - blocks reuptake of dopamine and serotonin
heroin - an opiod - floods dopamine by blocking GABA release
ecstatsy - reverses reuptake of serotonin, afrenaline and dopamine
LSD - acts on5HT2a receptors (serotonin receptors)
MDMA - blocks monoamine reuptake
amphetamines - releases catecholamines and block monoamine oxidases
THESE DRUGS HAVE A RAPID ONSET WITH VARIOUS EFFECTS AND ARE BEST AVOIDED DUE TO THEIR HIGH TOLERANCE, HIGH SCALE EFFECT, AND HIGH ADDICITION RATE

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41
Q

Discuss cognition enhancers

A
  • aka nootropic drugs
  • improve memory and cognitive performance
  • e.g. ACE inhibitors (used in Alzheimer’s) and piracetam derivatives
  • no effect on normal brain
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42
Q

State the cause of schizophrenia

A

excess dopamine action

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43
Q

State the cause of Parkinson’s disease

A

lack of dopamine action

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44
Q

State the cause of myasthenia gravis

A

lack of ACh action
(autoimmune attack occurs when autoantibodies form against the nicotinic acetylcholine postsynaptic receptors (nAChR) at the neuromuscular junction of skeletal muscles)

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45
Q

State the cause of depression

A
  • lack of serotonin action
  • lack of noradrenaline action
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46
Q

State the cause of epilepsy

A
  • lack of GABA action
  • increased glutamte action
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47
Q

State the cause of migraine

A

lack of serotonin action

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48
Q

Discuss diffuse axonal injury

A
  • can’t be seen in a scan
  • often associated with deep comatose patients
  • damage to axons caused by the brain being ‘shaken’ by head trauma
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49
Q

State the ranges for minor, moderate, and severe GCS scores

A

mild = 14-15
moderate = 9-13
severe = 3-8

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50
Q

Discuss the relationship between GCS score and GOS

A
  • a lower GCS is associated with a lower GOS
  • however, this is a les strict relationship now as we can treat head injuries better - minimising secondary insult
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51
Q

State factors which impact recovery from head injury

A

age, GCS (motor component tends to eb a good indicator for recovery), pupillary response (present is better for recovery), CT features, hypotension, hypoxia, glycaemia, and anaemia

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52
Q

Name the 3 systems of motor control

A

corticospinal (main motor output), basal ganglia (modulator), and cerebellar (modulator)

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53
Q

Discuss the primary motor cortex

A
  • Brodmann area 4
  • located in the posterior frontal lobe
  • works with other regions to plan and execute movement
  • contains large numbers of betz cells (send axons to the spinal cord)
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54
Q

Discuss the supplementary motor area

A
  • Brodmann area 6
  • located on the medial surface of the frontal lobe
  • anterior to primary motor cortex
  • role in motor planning and initiation of movement based on past motor memory
  • can measure anticipation/planning of movement using bereitschaft potential
  • axons sent to premotor and motor cortex
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55
Q

discuss the premotor cortex

A
  • Brodmann’s area 6 (lateral area)
  • modulates posture by optimising joint position/posture for a movement
  • responds to visual and sensory cues
  • major pathway by which fine movements are controlled by vision
  • axons sent to motor cortex and corticospinal tract
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56
Q

discuss the posterior parietal cortex

A
  • assess the context in which movements are made
  • receives sensory, proprioceptive, and visual inputs and uses them to determine the body’s positon in space (and position of the target)
  • produces internal models of the movement to be made before involving the premotor and primary motor cortices
  • works alongisded premotor cortex - together are the highest level of motor control hierarchy
  • sends axons (alongside premotor cortex) to the primary motor cortex which determines the characterstics of the appropriate movement
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57
Q

Discuss the descending corticospinal tract

A
  • descending fibres from the primary motor cortex, supplementary nmotor cortex, and premotor cortex form the cornoa radiata and converge as they pass through the posterior limb of the internal capsule
  • descend through the crus cerebri in the anterior midbrain
  • axons synapse with the brainstem cranial nerve motor nuclei
  • tracts continue into the brainstem and become visible as two pyramids on the ventral surface of the medulla
  • 90% decussate in the medulla
  • axons descend within the lateral corticospinal tract
  • synapse with anterior horn cells
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58
Q

Name the 3 parts of the temporal bone

A
  • Petromastoid
  • Tympanic
  • Squamous
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59
Q

Discuss the protective muscles of the middle ear, including innervation and embryological origin.

A
  • Tensor tympani:
    Largest, attached to malleus
    Contracts in response to loud noise to protect cochlea
    Innervated by mandibular branch of trigeminal nerve (V3)
    Originates from the first pharyngeal arch.
  • Stapedius
    Smaller, attached to stapes, involved in the stapedius reflex
    Innervated by nerve to stapedius (facial nerve)
    Originates from the second pharyngeal arch.
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60
Q

Explain the central processing of sound.

A

Action potentials generated in first-order neurons of the spiral ganglion (cochlea).
Impulse travels in the cochlear part of the vestibulocochlear nerve (CN VIII), which travels in the internal acoustic meatus.
Reaches the cerebello-pontine junction and synapses onto cochlear nuclei (medulla-pons junction)
Continues along olive and trapezoid body of pons to the inferior colliculus of the midbrain.
Reaches medial geniculate body of thalamus
Travels up to superior temporal gyrus (auditory cortex).

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61
Q

Outline the 3 main factors influencing balance.

A
  • Vestibulum
    Vestibulospinal tract: from semicircular canals to vestibular part of vestibulocochlear nerve (CN VIII)
    Then onto vestibular nuclei (pons)
    Upwards to primary vestibular sensory areas of parietal lobe.
  • Vision
    Control and fixation of gaze (stable frame of reference, no jittery vision)
  • Proprioception
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62
Q

Explain the function of the semicircular canals.

A

Detect rotatory acceleration.
3 semicircular canals
- Lateral: tipped up 30º from horizontal
- Superior: sagittal rotation (front roll)
- Posterior: coronal rotation (cartwheel)
* Work in pairs, e.g. left and right lateral canals, left superior & right inferior
* Each canal has a dilatation at one end - the ampulla.
* Ampulla constains crista (sensory organ)
* Crista contains hair cells embedded in a gelatinous cupula
* Movement of endolymph within canal displaces the cupula
* Flow towards the ampulla stimulates lateral canals.
* Flow away from the ampulla stimulates superior and posterior canals.

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63
Q

Explain the function of the otolith organs.

A

Detect linear acceleration.
- Utricle
Larger, more sensitive in horizontal plane
Output mostly to eye muscles
* Saccule
Smaller, more sensitive in vertical plane
Output mostly to postural muscles
Each has a macula containing hair cells
Tips of stereocilia embedded in otolithic membrane, which is weighed down by otoliths (calcium carbonate granules)
Gravity acts on otoliths, displacing the membrane relative to the hair cells, triggering depolarisation

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64
Q

Discuss the innervation of the vestibular system.

A

Vestibular part of vestibulocochlear nerve (CN VIII)
Synapse in vestibular nuclei (pons)
Outputs
* via thalamus to cortex for conscious awareness of position of head in space
* to oculomotor, trochlear and abducens nuclei in brainstem for control and fixation of gaze
* to cerebellum, accessory nerve nucleus and vestibulospinal tract for control of posture

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65
Q

List the branches of the facial nerve (CN VII)

A
  • Temporal
  • Zygomatic
  • Buccal
  • Cervical
  • Marginal mandibular
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66
Q

Discuss the arterial blood supply and venous drainage of the parotid gland.

A

Arterial blood supply: branches of external carotid
- Posterior auricular artery
Gives off superficial temporal artery.
Venous drainage: retromandibular vein
Formed by convergence of maxillary and superficial temporal veins.

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67
Q

Discuss the innervation of the parotid gland.

A
  • Sympathetic
    Superficial cervical ganglion
    Inhibits saliva secretion via vasoconstriction
  • Parasympathetic
    Glossopharyngeal nerve: synapses at otic ganglion
    Auriculotemporal nerve (branch of V3): carries parasympathetic fibres from otic ganglion to parotid gland.
  • Sensory
    Parotid: auriculotemporal nerve
    Fascia: great auricular nerve
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68
Q

List the cutaneous nerves of the head

A
  • Dermatome of ophthalmic nerve:
    Supraorbital nerve
  • Dermatome of maxillary nerve:
    Zygomaticotemporal nerve
    Zygomaticofacial nerve
    Infraorbital nerve
  • Dermatome of mandibular nerve:
    Auriculotemporal nerve
    Buccal nerve
    Mental nerve
  • Back of head: C2 & C3
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69
Q

External carotid artery branches (Some Anatomists Like Freaking Out Poor Medical Students)

A
  • Superior thyroid artery
  • Ascending pharyngeal artery
  • Lingual artery
  • Facial artery
  • Occipital artery
  • Posterior auricular artery
  • Maxillary artery
  • Superficial temporal artery
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70
Q

List the longitudinal muscles of the pharynx and describe their function

A
  • Stylopharyngeus
  • Salpingopharyngeus
  • Palatopharyngeus
    These muscles elevate the pharynx to receive food from the oral cavity
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71
Q

List the skull foramina and the cranial nerves which exit through them

A

Olfactory nerve (CN I) - cribriform plate
Optic nerve (CN II) - optic canal
Oculomotor (CN III), trochlear (CN IV), abducens (CN VI) and ophthalmic nerve (V1) - superior orbital fissure
Trigeminal nerve (CN V)
* Maxillary branch (V2): foramen rotundum
* Mandibular branch (V3): foramen ovale (meningeal branch exits through foramen spinosum)
* Facial ( CN VII) and vestibulocochlear (CN VIII) nerves: internal acoustic meatus
* Glossopharyngeal (CN IX), vagus (CN X), accessory (CN XI): jugular foramen
* Hypoglossal nerve (CN XII): hypoglossal canal

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72
Q

Describe the venous drainage of the spinal cord

A

Vertebral/Batson venous plexus
* In epidural space
* Become continuous with segmental veins that exit via intervertebral foramen

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73
Q

Describe the arterial supply of the spinal cord

A
  • Derived from segmental branches originating from the aorta
  • At the level of the thoracic spinal cord, intercostal arteries project into the spinal cord as:
    2 posterior spinal arteries
  • derived from posterior inferior cerebellar artery or vertebral arteries
    1 anterior spinal artery (Artery of Adamkiewicz)
  • supplies lower third of spinal cord
  • usually arises from left posterior intercostal artery
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74
Q

Describe the flow of CSF through the brain

A

CSF is produced by the choroid plexus (mainly in lateral ventricle, some in 4th ventricle)
Fills lateral ventricles then flows to 3rd ventricle via intraventricular foramen of Munro
Then flows through aqueduct of Sylvius (midbrain) to 4th ventricle
4th ventricle communicates with subarachnoid space via lateral foramina of Luschka and median aperture of Magendie
CSF is resorbed into the venous sytem via arachnoid granulations

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75
Q

Discuss the subcortical blood supply to the brain

A
  • Small perforating arteries arising from the main trunks of the MCA and PCA
  • Deep white matter and basal ganglia are supplied by lenticulostriate arteries
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76
Q

Discuss treatments for ischaemic stroke

A
  • Thrombolysis (within 4.5 hours)
    With tPA (tissue plasminogen activator)
  • Thrombectomy
    For blood clots too large to dissolve with tPA
    Femoral catheter insertion, passed into carotid artery to find clot, deploy stent retriever & remove clot
  • Hemicraniectomy
    Allows reduction in ICP after major stroke, reducing fatality
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77
Q

Myotomes: upper body
(movement, nerve, spinal roots)

A
  • Inspiration
    Diaphragm
    Phrenic nerve (C3-5)
  • Shoulder abduction
    Deltoid
    Axillary nerve (C5)
  • Elbow flexion
    Biceps brachii, brachialis
    Musculocutaneous nerve (C5-6)
  • Elbow extension
    Triceps brachii
    Radial nerve (C7-8)
  • Wrist extension
    Extensor carpi radialis longus & brevis
    Radial nerve (C6,C7)
  • Finger flexion
    Flexor digitorum superficialis & profundus
    Median nerve (C8)
  • Finger abduction and adduction
    Interossei
    Ulnar nerve (C8,T1)
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78
Q

Myotomes: lower body (movement, nerve, spinal roots)

A
  • Thigh adduction
    Adductor longus and brevis
    Obturator nerve (L2-3)
  • Knee extension
    Quadriceps
    Femoral nerve (L3-4)
  • Ankle dorsiflexion
    Tibialis anterior
    Deep peroneal nerve (L4,L5)
  • Great toe extension
    Extensor hallucis longus
    Deep peroneal nerve (L5,S1)
  • Ankle plantarflexion
    Gastrocnemius, soleus
    Tibial nerve (S1-2)
  • Anal contraction
    Sphincter ani externus
    Inferior anal nerve (S2-4)
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79
Q

Describe the causes and presentation of Cauda Equina Syndrome

A
  • Due to bony compression/disc protrusions in lumbar/sacral region
    Presentation
  • Pain: backs of thighs & legs
  • Numbness: buttocks, backs of legs (saddle
    paraesthesia) , soles of feet
  • Weakness: paralysis of legs & feet
  • Atrophy: calves
  • Paralysis: bladder & bowel
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80
Q

Describe the causes and presentation of Hemicord (Brown-Sequard) Syndrome

A
  • Causes:
    Penetrating trauma
    MS
    Tumour
  • Presentation
    Ipsilateral (UMN) weakness (corticospinal)
    Ipsilateral loss of proprioception (dorsal columns)
    Contralateral loss of pain & temperature (spinothalamic)
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81
Q

Discuss spinal modulation of nociception (Gate Control Theory)

A

Dorsal horn level
Under normal circumstances, inhibitory interneurons are actively blocking ongoing nerve input
C fibres block inhibitory interneurons, allowing C fibre input to be transmitted across the synapse from a primary to a secondary afferent
If the inhibitory interneuron is stimulated by a collateral branch of an A beta fibre, the other A beta branch will activate the dorsal column/medial lemniscal pathway to block ongoing transmission of C fibre nociception

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82
Q

Discuss supraspinal modulation of nociception (pain neuromatrix)

A

Engaged under extreme circumstances
Conditioned pain modulation - descending modulation, top-down inhibition
Stimulation of higher structures in the brain activates the peri-aqueductal grey matter (pons) and medullary raphe nuclei (most endogenous opioids found here)
Activates descending nerve fibres going to spinal cord, suppressing pain entering spinal cord
Direct inhibition of projection neurons or enkephalin-containing interneurons reduces activity in nociceptive circuits
Neurotransmitters involved lower down: 5-HT and noradrenaline

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83
Q

Explain the pupillary light reflex

A

Light hits the retina; signal travels through the optic nerve (CN II)
Medial fibres carrying information from the lateral field of vision decussate at the optic chiasm
Fibres subserving the light reflex bypass the lateral geniculate body
They synapse in the ipsilateral pre-tectal nucleus
Then projet to ipsilateral and contralateral Edinger-Westphal nucleus (CN III nucleus)
Synapse in ciliary ganglion
Parasympathetic fibres of CN III innervate sphincter pupillae
Pupillary constriction in both eyes (direct & consensual light response)

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84
Q

Explain the accommodation/convergence reflex

A

Patient is asked to look at a distant object then at an object close to the face
Both pupils should constrict and dilate again when distant gaze is resumed
Fibres from medial rectus travel along CN III
Liaise with mesencephalic nucleus of CN V
Go to convergence centre (tectal/pre-tectal region)
Then go to Edinger-Westphal nucleus
Efferent signal comes out along CN III, synapses at ciliary ganglion
Activates sphincter pupillae

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85
Q

Explain the plantar reflex

A

Tests the integrity of the pyramidal tract to identify corticospinal lesions
Nociceptive afferent signals from S1 dermatome travel in sciatic nerve, reaching the spinal cord
Efferent signals exit via ventral horn
Toe extensors innervated by deep peroneal nerve
Toe flexors innervated by tibial nerve
Loss of descending pyramidal control results in the loss of extensor suppression, leading to an upgoing plantar response
Toe extension, upgoing plantar: positive Babinski sign

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86
Q

Describe posterior cord syndrome.

A

Posterior cord syndrome affects the posterior spinal arteries.
Results in an ipsilateral loss of proprioception and vibration sense below the level of the lesion (pain is intact)
Causes:
B12 deficiency
Copper deficiency
Syphilis
HIV/HTLV1
Extrinsic compression (tumours)

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87
Q

Describe central cord syndrome (syringomyelia)

A
  • Suspended sensory loss at the level of the decussating spinothalamic fibres
  • Weakness may affect arms more than legs
    Causes:
    Syrinx (fluid-filled cyst in spinal canal)
    Slow-growing tumour
    Hyperextension injury
    Anterior cord compression by osteophytes, posteriorly by ligamentum flavum
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88
Q

Describe the corneal reflex

A

Touching cotton wool to the cornea tests trigeminal nerve function (CN V) in the eye being tested, and facial nerve function (CN VII) in both eyes
Signal relayed in ophthalmic branch of trigeminal nerve (V1) synapsing in main sensory nucleus of trigeminal nerve
Then, synapses onto the medial longitudinal fasciculus
Reaches the main motor nucleus of the facial nerve
Facial nerve innervates orbicularis occuli, causing blinking

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89
Q

Describe transverse cord syndrome

A

Deficit (partial or complete) in motor and all sensory modalities
Sensory level associated with transverse cord syndrome
Causes:
Trauma
Tumour
MS/transverse myelitis

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90
Q

Describe the direct pathway (basal ganglia)

A

Increases the amount of movement
Glutamate neurons project from the thalamus to the cortex (excitatory)
Globus pallidus interna and substantia nigra pars reticulata project to the thalamus and release GABA (inhibitory)
To initiate a movement, signals are sent from the cortex to the striatum (corticostriatal pathway)
Activated striatal neurons inhibit globus pallidus interna and substantia nigra pars reticulata, preventing their inhibition of the thalamus and allowing movement
Substantia nigra pars compacta modulates the activity of direct pathway via dopamine release in the striatum, which facilitates the pathway

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91
Q

Describe the indirect pathway (basal ganglia)

A

Reduces amount of movement
GABA neurons project from globus pallidus externa to subthalamic nucleus (inhibitory)
When indirect pathway is activated by signals from the cerebral cortex, GABA neurons in the striatum are activated
These neurons project to globus pallidus externa and inhibit its activity, preventing it from inhibiting the subthalamic nucleus
Subthalamic nucleus neurons are activated by projections from the cortex
These stimulate neurons in the globus pallidus interna and substantia nigra pars reticulata, which will inhibit the thalamus
Substantia nigra pars compacta modulates this pathway via dopaminergic input, which inhibits activity in the indirect pathway, facilitating movement

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92
Q

Describe the embryological development of the spinal cord up until the formation of the mantle, marginal and ependymal layers

A

Neuroepithelial cells in the neural tube give rise to neuroblasts (primitive nerve cells)
As the wall of the neural tube thickens, neuroblasts differentiate
At this point, the wall of the neural tube consists of a cavity, lateral wall and roof plate
Later on during development
> Ependymal layer: ependymal cells (neuroepithelial) lining central canal
> Marginal layer (outermost): future white matter, axons entering & leaving mantle layer
> Mantle layer: future grey matter, contains neuroblasts - future neurons

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93
Q

Describe the embryological development of the spinal cord from the formation of the mantle, marginal and ependymal layers, until the formation of the roof & floor plates

A

Further development (mainly mantle layer), driven by neuroblast differentiation, forms 2 thickenings in dorsal & ventral regions of spinal cord (separated by sulcus limitans)
* Alar plate: sensory region, future dorsal horn
* Basal plate: motor region, future ventral horn
Lumen of neural tube becomes diamond-shaped as a pathway for decussation
>Dorsal: roof plate
> Ventral: floor plate

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94
Q

Describe the embryological development of the spinal cord after the formation of the roof & floor plates

A

Motor nerve fibres arise (week 4) from nerve cell bodies in basal plate of ventral horn
Grow out and form a bundle - ventral root
Sensory nerve fibres arise from cell bodies present outside spinal cord forming dorsal root ganglia (arise from neural crest cells which migrate here)
Processes from dorsal root ganglia grow into dorsal horn
Distal processes of sensory and motor nerve fibres grow together forming spinal nerves
Spinal nerves divide into
> Dorsal rami: dorsal musculature, joints, skin of back
> Ventral rami: limbs & ventral body wall, form plexuses

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95
Q

Differentiate between the different types of axons

A
  • A alpha: largest, fastest, myelinated, proprioceptors of skeletal muscle
  • A beta: 2nd largest, fastest, myelinated, mechanoreceptors of skin
  • A delta, 3rd largest, fastest, myelinated, pain, temperature
  • C, slowest, narrowest, non-myelinated, temperature, pain, itch
96
Q

Discuss regional variations in grey matter in the spinal cord

A

Cervical and lumbar enlargements
- More sensory input and motor output given increased number of muscles in upper & lower limbs respectively, which require finer control
Autonomic regions
- Sympathetic T1-L2
Sympathetic pre-ganglionic cells form the lateral horn
* Parasympathetic S2-S4
Parasympathetic pre-ganglionic cells form an intermediate horn (not visible)

97
Q

Discuss regional variations in white matter in the spinal cord

A

Total amount of white matter is smaller in lumbar segments than in cervical ones
Number of ascending fibres is greater in rostral segments - each level of the cord contains all the ascending fibres from the lower segments
Number of descending fibres is greater in rostral segments - each level of the cord contains all the fibres passing from the brain to more caudal segments

98
Q

Describe the anatomical structure of the Circle of Willis

A

Circle of Willis - anatomical anastomosis formed by:
> Internal carotid: gives rise to anterior and middle cerebral arteries
> Basivertebral system: gives rise to posterior cerebral arteries
> Linked by interconnecting arteries
* Anterior communicating artery
* Posterior communicating arteries
Also supplies cerebellum:
* Posterior inferior cerebellar artery (PICA)
* Anterior inferior cerebellar artery (AICA)

99
Q

Describe the areas of the brain supplied by the 3 main cerebral arteries

A
  • ACA: frontal, pre-frontal and supplementary motor cortex, as well as parts of the primary motor and primary sensory cortex
  • MCA: majority of lateral surface of hemisphere except superior parietal lobe (ACA) and inferior temporal & occipital lobes (PCA); also supplies basal ganglia & part of the internal capsule
  • PCA: occipital lobe, inferior part of temporal lobe, deep structures (thalamus, posterior limb of internal capsule)
100
Q

Explain the ionic basis for the resting membrane potential of excitable cells

A

Resting membrane potential arises due to a difference in charge between the inside and outside of the neuron at rest
More positive ions outside the cell: Na+ and Cl-
More negative ions inside: K+
Concentration gradient moves K+ out of the cell & electric potential gradient forces K+ inside
These forces balance out at equilibrium potential, resulting in a negative resting potential inside the cell (-60mV to -70mV)

101
Q

How is the nerve action potential generated?

A

Voltage-gated ion channels span the neuronal membrane
Nerve impulses depolarise the cell > make charge more positive until it reaches threshold (-55 mV)
Once threshold is reached, rapid depolarisation opens voltage-gated sodium channels & sodium floods the inside of the cell
Positive charge opens voltage-gated potassium channels and repolarisation occurs as potassium exits the cell > potential becomes more negative again
Hyperpolarisation occurs > membrane potential becomes more negative to prevent another action potential from occurring

102
Q

How is nerve conduction affected by myelination of axons?

A

Myelination of axons enables saltatory conduction, where action potentials “jump” from one node to another
The cell is only depolarised at each node of Ranvier, enabling faster neurotransmission

103
Q

Give an example of a condition which arises due to a malfunction in action potential propagation

A

Congenital insensitivity to pain
Loss-of-function mutation affecting voltage-gated sodium channels (Nav 1.7 - only found on nociceptors)
Mutated form means they don’t fire action potentials and patients cannot feel pain
Results in serious injury e.g. self-mutilation

104
Q

Explain the concept of chemical neurotransmission

A
  • AP enters presynaptic terminal
  • Voltage-gated calcium channels open following depolarisation; Ca2+ entry
  • Increase in intracellular Ca2+ allows docking of synaptic vesicles containing neurotransmitters > released via exocytosis
  • Neurotransmitters diffuse across synaptic cleft and bind to & activate receptors on postsynaptic membrane
  • Ions (Na+ or Cl-) enter cell (depolarisation or hyperpolarisation)
  • If total voltage reaches threshold, AP is generated
105
Q

Give examples of conditions resulting from malfunctions in chemical neurotransmission

A
  • Botulism
    Clostridium bacteria produce botulinum toxin which cleaves specialised proteins needed for docking of synaptic vesicles
    Disrupts exocytosis, preventing ACh release
    Clinical features: skeletal muscle weakness, diaphragm paralysis
  • Myasthenia gravis
    Auto-antibody binds to ACh receptor on postsynaptic membrane in motor end plate
    Can induce internalisation or degradation of ACh receptor
    ACh can no longer bind to receptor
    Clinical features: severe muscle weakness, ptosis
106
Q

Compare and contrast temporal and spatial summation of synaptic inputs

A

Excitatory post-synaptic potentials (EPSPs): increase membrane potential & make AP more likely
Inhibitory post-synaptic potentials (IPSPs): decrease membrane potential & make AP less likely
Summation:
* Additive (EPSP + EPSP) = excitatory
* Subtractive (EPSP-IPSP) = no change in membrane potential
> Temporal: increased frequency of postsynaptic potentials from one site
> Spatial: postsynaptic potentials at multiple sites

107
Q

Explain the concepts of divergence and convergence

A

Divergence: enables a single neuron to communicate and affect change in a wider network
E.g. painful stimulus detected by nociceptor, travels to dorsal horn
Information diverges
- Network of interneurons activated to activate motor neurons
- Impulses sent to brain to process pain, localise pain, generate an emotional response, induce learning & memory and engage in protective behaviour
Convergence: neuron receives input from a wide network of neurons & acts to integrate information

108
Q

Summarise methods of localising cerebral function

A
  • EEG: electro-encephalography
    Records electrical activity in the brain
  • TMS: transcranial magnetic stimulation
    Uses electromagnet to stimulate activity in brain; causes depolarisation or interrupted firing
    Interrupt brain activity while performing a task
  • PET: positron emission tomography
    Measures blood flow via a small dose of radioactive material injected into the bloodstream
    Locate brain activity while performing a task
  • fMRI: functional magnetic resonance imaging
    Measures blood flow
    Locate brain activity while performing a task
109
Q

Describe the sensory pathway involved in discriminative touch and tactile sensation

A

Dorsal column/medial lemniscal pathway
First-order neuron
Receptive ending detects stimulus & AP is generated
Axon projects into spinal cord & bifurcates
> One branch projects into dorsal horn
> One branch projects towards brainstem in the dorsal funiculus
Synapses onto second-order neuron in dorsal column nuclei
> Gracile nucleus: lower limb; > cuneate nucleus: upper limbs
Second-order neuron (cell body in dorsal column nuclei)
Axons project out of dorsal column nuclei and decussate to opposite side of medulla via internal arcuate fibres
Project up through brainstem in a bundle of axons (medial lemniscus) terminating in thalamus
Third-order neuron (cell body in thalamus)
Axons project out of thalamus via internal capsule and terminate in appropriate region of somatosensory cortex

110
Q

Describe the sensory pathway involved in crude touch, temperature and pain sensation

A

Spinothalamic pathway
First-order neuron
Noxious stimulus activates free nerve endings; AP generated and projects to spinal cord via primary sensory neuron, reaching superficial dorsal horn
Synapse onto second-order neurons
Second-order neuron
Decussate at level of entry into spinal cord; axons reach anterolateral funiculus
Project up until they reach thalamus via spinal lemniscus; synapse onto third-order neuron
Third-order neuron
Sends axons via internal capsule to terminate in appropriate somatosensory region

111
Q

Describe the corticospinal (pyramidal) pathway

A

Upper motor neurons in primary motor cortex descend via internal capsule to brainstem
Axons project to midbrain via basis pedunculi towards medulla
Axons project down via ventral structures on medulla (medullary pyramids)
85% cross over (pyramidal decussation) to innervate spinal cord
15% ipsilateral
Project down along spinal cord to target lower motor neurons at appropriate spinal segments
Axons which crossed over form lateral corticospinal tract; travel in dorsolateral funiculus and innervate full spinal cord
Axons which stayed ipsilateral form anterior corticospinal tract; travel in ventromedial funiculus and innervate to midthoracic level

112
Q

Describe the corticobulbar pathway

A
  • Allows recruitment of cranial nerve nuclei bilaterally
  • UMN axons project down from primary motor cortex via internal capsule, project down through midbrain via basis pedunculi
  • Reach specific cranial nerve nuclei
  • Recruitment of lower motor neurons bilaterally in pons for trigeminal nerve: muscles of mastication
  • Others project down towards medulla which can innervate vagus (pharynx, larynx, soft palate) or hypoglossal (extrinsic muscles of tongue)
113
Q

Describe the reticulospinal pathway

A

2 principal descending projections that innervate 2 distinct muscle groups
* Pontine tracts: innervate extensor muscles
Ipsilateral oral and caudal pontine reticular nuclei
* Medullary tracts: innervate flexor muscles
Ipsilateral gigantocellular reticular nuclei of the medulla
Bilateral projections (ipsilateral origins)
* Run entire length of cord, conducted in ventral funiculus
* Important in maintenance of balance and posture
* Modulate activity of alpha motor neurons
* Pathology/damage leads to loss of postural control

114
Q

Describe the tectospinal pathway

A

Origin: contralateral superior colliculus (crossed) in midbrain
* Important in balance and posture
* Only projects to cervical spinal segments
* Innervates head muscles to ensure head position is maintained appropriately

115
Q

Describe the vestibulospinal pathway

A

Origin: ipsilateral lateral vestibular (Dieter’s) nucleus of the medulla
* Important in maintenance of balance and posture and runs length of spinal cord in ventral funiculus
* Modulates activity of alpha motor neurons
* Under the influence of the vestibular apparatus in the ear
> Helps coordinate the position of the head with the rest of the body

116
Q

Briefly describe subcutaneous/cutaneous mechanoreceptors (A beta afferents)

A
  • Meissner’s corpuscle: light touch
  • Merkel disk: mechanical deflection
  • Hair follicle receptor: stretch (brushing)
  • Pacinian corpuscle: vibration and deep pressure
  • Ruffini ending: deeper in skin; stretching of skin (slippage)
117
Q

What is a dermatome?

A

An area of skin where sensation is supplied by a single spinal nerve root

118
Q

Describe the systemic effects of pain (acute catabolic stress response)

A
  • CNS: anxiety, depression, sleep impairment
  • Cardiovascular: tachycardia, hypertension
  • Respiratory: hyperventilation and cough inhibition
  • Gastrointestinal: ileus, nausea, vomiting
  • Genitourinary: urinary retention, uterine inhibition
  • Muscle:
    > Restlessness due to pain increases O2 consumption > hypoxia
    > Rigidity due to pain > immobility > DVT risk
  • Metabolic
    > Increased catabolic: cortisone, glucagon, GH, catecholamines
    > Decreased anabolic: insulin, testosterone
    > Decreased plasminogen: increased coagulation, DVT risk
119
Q

Describe the 4 mechanisms involved in the process of nociception

A
  • Transduction: painful stimulus transduced into AP by nociceptors
  • Transmission: AP transmitted through nerve fibres (Ad fibres - fast - and C fibres - slow)
  • Modulation: spinal and supraspinal
  • Perception: conscious - pain is perceived
120
Q

Explain how a TENS machine is thought to modulate the perception of painful stimuli

A

Transcutaneous electrical nerve stimulation (TENS) works by stimulating large A beta fibre input overlapping the area of injury & pain
Suppresses pain as the inhibitory interneuron is stimulated by a collateral branch of an A beta fibre
The other A beta branch will activate the dorsal column/medial lemniscal pathway to block ongoing transmission of C fibre nociception
Useful in treating sciatica, rheumatoid arthritis, multiple sclerosis…

121
Q

Outline the characteristics of nociceptive pain

A

Somatic: skin, muscle, bone
* Site: well-localised
* Radiation: dermatomal
* Character: sharp, aching, gnawing
* Periodicity: constant +/- incident
* Associations: rarely
Visceral: internal organs
* Site: vague distribution
* Radiation: diffuse, to body surface
* Character: dull, cramping, dragging
* Periodicity: often periodic
* Associations: nausea, sweaty, heart rate & BP

122
Q

Outline the characteristics of neuropathic pain

A
  • Common descriptors
    Shooting, electric shock-like, burning, tingling, numbness
  • Examples: post-herpetic neuralgia, painful diabetic neuropathy
  • LANSS Pain Scale > 12/24 implies neuropathic pain
    5 questions:
    Prickling, tingling, pins & needles? Altered colour of skin? Abnormally sensitive? Bursts - electric shocks, jumping? Hot or burning?
    2 signs: cotton wool allodynia, altered pin-prick threshold
123
Q

Identify the parameters to be assessed during holistic pain appraisal

A
  • History, physical, investigations
  • Characteristics: 10
    > Site, radiation, quality, severity, duration, frequency, periodicity
    > Precipitating & relieving factors, associated phenomena
  • Brief Pain inventory (BPI)
  • Impact of pain (physical & mental function), quality of life effects: walking, work, sleep, mood…
  • To assess severity, use numerical rating, verbal rating or visual analogue
  • Short form -36 score for quality of life outcomes
124
Q

List the main components of multi-modal pain management

A

Treatment goals: successful if 30-50% pain relief
* 6 P’s:
> Prevention: back care, exercise, good acute pain control
> Pathology: treat underlying cause
> Physical therapies: maintain activity, physio, TENS
> Pharmacotherapy
> Procedural: regional anaesthesia, nerve blocks, steroid injections, epidurals..
> Psychologically-based: support groups, education, pain management program

125
Q

Describe the WHO ladder for the treatment of nociceptive pain

A

Step 1:
- Paracetamol
Long-term side-effects: increase of all cause mortality, CVS events, GI ulcers and bleeds, decreased GFR
- NSAIDs or COX II inhibitors
Long-term side effects:
Upper GI bleeds
Major vascular events
Renal impairment
Step 2:
Codeine, dihydrocodeine (often as co-analgesics e.g. co-codamol)
Codeine is a pro-drug; metabolised to morphine via first-pass metabolism in liver (CP450 CYP 2D6)
Step 3:
Morphine, oxycodone, tramadol, buprenorphine, fentanyl

126
Q

List the side-effects associated with opioid use

A
  • Nausea (prescribed w/ antiemetic in acute setting)
  • Sedation/cognitive impairment
  • Constipation (long-term)
  • Pruritus (long-term)
  • Respiratory depression
  • Insomnia/decreased libido
  • Addiction/abuse
127
Q

Name different neuropathic analgesics

A
  • Anti-depressants: amitriptyline
  • Anti-convulsants: gabapentin, pregabalin
  • Anti-arrhythmics: lidocaine
  • Others: ketamine, capsaicin, clonidine, cannabinoids
128
Q

Describe how tissues respond to mechanical trauma

A
  • Tissue damage causes release of potassium ions and prostaglandins (activate free nerve endings)
  • Bradykinin is released from plasma, 5HT is released from platelets & damaged capillaries
  • 2 peptides released from free nerve endings
    > CGRP (vasodilation)
    > Substance P (plasma extravasation, oedema, bradykinin release)
    Both activate mast cells, triggering degranulation and histamine release
129
Q

What are the contents of the carotid sheath?

A
  • Internal carotid
  • Internal jugular
  • Common carotid
  • Vagus nerve (CN X)
130
Q

What are the boundaries of the anterior triangle of the neck?

A
  • Apex: jugular notch
  • Superior: inferior border of mandible and a line from its angle to the mastoid process
  • Anterior: median line from chin to jugular notch
  • Posterior: anterior border of sternocleidomastoid
131
Q

What are the boundaries of the posterior triangle of the neck?

A
  • Apex: superior nuchal line
  • Inferior: middle 1/3 of clavicle
  • Anterior: posterior border of sternocleidomastoid
  • Posterior: anterior border of trapezius
132
Q

Describe the contents of the posterior triangle of the neck

A
  • Subclavian artery and vein
  • Suprascapular & transverse cervical arteries
  • Apex of lung
  • Inferior trunk of brachial plexus
  • Spinal accessory, transverse cervical and great auricular nerves
  • Suprapleural membrane
  • Cervical pleura
  • Thoracic duct
  • Superficial cervical and supraclavicular nodes
  • Scalene anterior & medius
133
Q

Describe the boundaries and contents of the root of the neck

A

Boundaries:
T1 vertebra, manubrium, clavicle, upper border of scapula
Contents:
- Apex of lung
- Brachiocephalic trunk
- Subclavian artery and vein
- Thoracic duct
- Vagus nerve and phrenic nerve
- Inferior trunk of brachial plexus (ventral rami of C8 and T1)
-Cervical sympathetic trunk
Cervicothoracic (stellate) ganglion sits against neck of first rib

134
Q

Describe the sympathetic supply to the head

A

Upper thoracic spinal cord supplies head: dilator pupillae muscle, sweat glands, smooth muscle of upper eyelid
Lateral horn (location of cell bodies) > pre-ganglionic sympathetic fibres descend through ventral root into T1/T2 spinal nerves
Bundles go into sympathetic trunk, pass through sympathetic ganglion through middle cervical ganglion
Level of the hyoid bone > synapse onto post-ganglionic fibres in large ganglion
Post-ganglionic fibres leave superior cervical ganglion & pass to common carotid, reaching destination by running onto arteries

135
Q

Explain the meaning of the terms “sick role” and “illness behaviour”

A

The “sick role” implies that an individual is
> Exempt from certain social roles
> Not blamed for their illness
> Responsibilities include trying to get better, seeking help & cooperating when help is offered.
“Illness behaviour” refers to the way in which symptoms are perceived, evaluated & acted upon
> Involves the manner in which people monitor their bodies, define & interpret their symptoms and take remedial action

136
Q

List 5 elements which have been identified as facilitating successful adjustment to chronic illness

A
  • Internal locus of control (greater sense of agency)
  • Flexible
  • Composed (no emotional extremes, no pre-existing psychiatric conditions)
  • Adequate finances
  • Social support
137
Q

List symptoms which may be induced by cytokine activity in chronic illness

A
  • Weakness, fatigue, poor concentration, lethargy
  • Anhedonia
  • Anorexia
138
Q

Explain the meaning of “locus of control” and why it is important in chronic illness

A

“Locus of control” refers to how an individual perceives they have control over their own actions as opposed to events occurring because of external forces
Internal locus of control
* Greater sense of agency, feel empowered to enforce change
* Able to effect change in the world around them
* Take responsibility
External locus of control
* World around the individual effects change on them
* Feels more helpless
* Do not take responsibility

139
Q

Outline the potential for positive experiences of illness & how these are relevant to adjustment

A
  • Enhanced appreciation of life
  • New opportunities
  • Change in life priorities
  • Enhanced sense of purpose
  • Improved relationships
    Improve individual’s ability to adjust
140
Q

Give examples of peripheral nerve disorders that affect motor function

A

Acute: Guillain-Barré syndrome
Genetic: Charcot-Marie-Tooth
Acquired: B12 deficiency

141
Q

Describe how nerve conduction studies are carried out

A
  • Recording and stimulating electrodes
  • Stimulus added leading to a compound muscle action potential (CMAP)
  • Measure time taken from stimulus to AP (latency)
  • Amplitude should stay the same
    Nerve conduction
    > Axonal: CMAP falls
    > Demyelinating: increased latency, change to shape of curve (temporal dispersion)
  • Helps to locate lesion; stimulation of different points allows identification of site of blockage
142
Q

What is electromyography (EMG)?

A

Clinical test which is carried out by listening to sounds of muscle
Identify neurogenic v myogenic lesions
* Allows differentiation of upper v lower motor neuron pathology
* Allows differentiation between myopathic (inflammatory) and polymyositic (destructive) conditions

143
Q

Outline how testing of the neuromuscular junction is carried out

A
  • Nerve conduction studies: repetitive nerve stimulation
  • EMG: single fibre EMG
    May show jitter
144
Q

Discuss the diagnosis of a prolapsed intervertebral disc (IVD)

A

Symptoms
* Sciatica
* Constant ache, throbbing pain in lower back
* Shooting, burning pain in foot
Physical examination
* Straight leg raising (SLR) elicits pain by stretching sciatic nerve
* Hip, back, knee ROM
* Gait, reflexes, strength, testing sensation in relevant dermatomes
Imaging: MRI, CT

145
Q

Explain how the stretch reflex works

A
  • Muscles contain muscle spindles which give information about stretch
  • Information conveyed to CNS by proprioceptive Ia afferents
  • Synapse onto motor neurons supplying the same muscle
  • Excitation of motor neurons causes muscle contraction to prevent excessive stretching/tearing
    Gamma motor fibres: contraction of spinal cells
    Alpha motor neuron fibres: innervate muscles within which muscle spindles are embedded
146
Q

What is a Golgi tendon organ?

A

Sensory ending enclosed in connective tissue that lies near the junction of a tendon with a muscle
Nerve endings associated with collagen fibres within tendons
Provides proprioceptive information which complements information provided by muscle spindles
Prevents excessive tension in muscles; synapse with inhibitory interneuron leads to muscle relaxation

147
Q

Explain why the stretch reflex is important in maintaining posture

A

Helps maintain posture
Slight lean to either side causes a stretch in the spinal, hip and leg muscle spindles on the other side of the body
> Quickly countered by the stretch reflex, which keeps us upright

148
Q

Define spinal shock and explain its effects

A

Spinal shock is the temporary suppression of all reflex activity below the level of a spinal cord injury (SCI), occurring immediately after injury
Autonomic dysfunction appears
* Blood pressure and heart rate instability
* Neurogenic bladder
* Autonomic dysreflexia (T6 and above)
* Temperature control
* Sexual dysfunction

149
Q

Describe the structure of a peripheral nerve

A
  • Contain axons from 2 functionally distinct types of nerve cells: sensory afferent and motor efferents
  • Axons can be myelinated or unmyelinated
  • Within the nerve trunk, fasciculi are found
    > A fascicle is a bundle of axons from individual cells surrounded by perineurium
  • Epineurium, a tough connective tissue, surrounds the peripheral nerve
150
Q

Define neurogenic shock and explain its effects

A

Neurogenic shock is the body’s response to a sudden loss of sympathetic control, resulting in distributive shock
Occurs in SCI above T6, > 50% loss of sympathetic activity
Clinical triad of hypotension, bradycardia and hypothermia

151
Q

Predict the outcomes of a complete high cervical (C1-C4) SCI

A

Symptoms
* Paralysis in arms, hands, trunk, legs
* Tetraplegia or quadriplegia
* Patient may be unable to breathe (C3-C5) or speak
* Control of bladder/bowel movements may be affected
Consequences
* Complete assistance with activities of daily living
* Require indwelling catheter
* Psychological impact
* DVT, pressure areas
* Pain
* Sexual dysfunction & conception issues

152
Q

Predict the outcomes of a complete low cervical (C5-C8) SCI

A
  • Varying degree of arm function
  • Likely able to breathe on their own and speak normally
  • Still very dependent on others for activities of daily living
153
Q

Predict the outcomes of a complete thoracic or lumbar/sacral SCI

A

Thoracic: paraplegic with truncal involvement
Lumbar/sacral: lower limbs affected, little or no control over bladder & bowel

154
Q

Describe how a patient can reinforce a reflex and the physiological basis of this

A

Jendrassik reinforcement manoeuver
* Upper limb: clench teeth
* Lower limb: pulling interlinked fingers in opposite directions
Combination of distraction and cortical inhibition from anterior horn cells reinforces reflexes

155
Q

Explain the concept of the “sensory unit”

A

Single afferent axon with all its sensory receptor endings and the area of skin they are localised to
Each unit has its own receptive field
For sensation to be perceived, the stimulus must fall in a receptive field which recognises that modality

156
Q

What is 2 point discrimination?

A

The idea that for 2 stimuli to be perceived as separate, they must activate different receptors
To activate separate receptors the stimuli must fall within separate receptive fields

157
Q

Describe the development of the neural tube

A
  • Appearance of notochord and mesoderm induces overlying ectoderm to thicken and form a neural plate (cephalic area)
  • Neural plate lengthens and lateral plates elevate, creating neural folds: 19d
  • The depression in the centre is known as the neural groove
  • Folds move towards each other and fuse in the midline, forming the neural tube
158
Q

List the main structures derived from the pharyngeal arches

A

1st arch - maxilla, mandible, zygomatic bone, part of temporal bone, incus, malleus, muscles of mastication, muscles of floor of mouth, tensor tympani
2nd arch - stapes, styloid process, hyoid bone, muscles of facial expression, stapedius
3rd arch - common carotid, stylopharyngeus, hyoid bone
4th arch - subclavian artery, aortic arch, laryngeal cartilages
6th arch - pulmonary arteries, ductus arteriosus

159
Q

Describe the bending of the neural plate

A

Controlled through
* Cell wedging: microtubules and microfilaments changing cell shape, cell cycle
* Hingepoints: median and dorsolateral hinge points
* Extrinsic forces: pushing of the surface ectoderm, adhesion point with notochord

160
Q

Describe the closure of the neural tube

A

Fusion begins in the cervical region and proceeds in cephalic and caudal directions
Open ends of the tube form anterior and posterior neuropores
Closure occurs in week 4
Anterior: day 25
Posterior: day 27

161
Q

Outline cerebral vasomotor reactivity

A

Function: regulation of cerebral blood flow
Blood flow remains constant despite variability in blood pressure (60-100mmHg)
Vessel diameter reduces as blood pressure increases

162
Q

Define stroke and compare the causes and clinical consequences of ischaemic and haemorrhagic stroke

A

A stroke is a focal neurological disturbance that arises due to a disturbance in blood flow to the brain
Ischaemic: blockage of blood vessel
Causes
- Direct damage
- Blood clot lodged in vessel (can arise from carotid artery or heart - AF)
Consequences: can be treated, potentially improving outcomes
Haemorrhagic: burst vessel, blood fills space inside brain
Causes: hypertension, arteriovenous malformation (AVM)
Consequences: treatment is more difficult, poor prognosis

163
Q

Describe the effects of normal aging on hearing

A

Aging results in loss of outer hair cells, loss of “cochlear amplifier”
* Loss of frequency discrimination
* Loss of dynamic range: too quiet to hear then uncomfortably loud
* Affects understanding of speech, mainly high frequencies

164
Q

Describe the different areas of the cerebellum, including their function

A
  • Flocculonodular lobe (aka vestibulocerebellum)
    > Location: vermis
    > Function: balance and spatial orientation
    > Input: vestibular system
    > Output: fastigial nucleus, brainstem vestibular nuclei
  • Spinocerebellum
    > Location: adjacent to vermis
    > Function: fine tune axial and limb movements
    > Input: spinal cord
    > Output: cortex and brainstem via deep cerebellar nuclei
  • Neocerebellum
    > Location: lateral lobes
    > Function: planning movement and evaluating sensory input
    > Input: cerebral cortex/pontine nuclei
    > Output: thalamus, red nucleus (midbrain)
165
Q

Describe the pattern of symptoms and clinical signs in lesions of the cerebellum

A

Symptoms:
* Slurred speech
* Coordination difficulties
* Tremor
* Gait unsteadiness/falls
Signs:
* Nystagmus
* Dysarthria
* Dysdiadochokinesia
* Heel-shin ataxia

166
Q

Explain the role of the blood-brain barrier (BBB)

A

BBB consists of a series of features which prevent harmful substances from entering the brain & spinal cord from the blood
> Capillaries in nervous tissue
- Thick continuous basement membrane, tight junctions, astrocyte processes covering vessel
Ependymocytes: line ventricles & spinal canal, tight junctions restrict movement
Functions:
* Keep out toxins, pathogens
* Prevent fluctuation of ions, nutrients, metabolite concentrations in CNS
* Permeable to substances that can diffuse across (water, gases, small lipophilic molecules)
* Active transport for specific substances e.g. glucose, amino acids

167
Q

Describe the anatomy of the olfactory bulbs and their relationship with the cribriform plate

A
  • Cell bodies of olfactory cells found in olfactory mucosa
  • Axons pass through holes in cribriform plate and enter olfactory bulb (swollen end of olfactory nerve)
  • Olfactory nerve sits under frontal lobe on floor of anterior cranial fossa, above roof of nose
  • Axons from groups of olfactory cells converge on a glomerulus in the olfactory bulb
  • Pattern of glomerular activation encodes which odour has been detected
168
Q

Describe the pathways of olfactory signalling and their cortical representation

A

Olfactory nerve projects centrally without relaying through the thalamus
* Rhinencephalon: “smell brain”
>Anterior olfactory nucleus: olfaction
> Piriform cortex: olfaction
> Olfactory tubercle: intergrates olfaction with other senses (social behaviour, reward, addiction)
> Entorhinal cortex: memory, perception of time
* Limbic system
> Amygdala: memory, decision-making, fear, anxiety, aggresion
> Hippocampus: memory
> Parahippocampal gyrus: memory

169
Q

Describe the knee jerk reflex

A

Striking the patellar tendon causes stretch of the quadriceps muscle
Afferent signal sent through sensory neurons up through dorsal root ganglion, enters dorsal horn (L3/L4) & synapses onto motor neuron
Efferent signal causes contraction of quadriceps
Afferent signal also works through interneuron - has an inhibitory effect on motor neurons going to the hamstrings (antagonist muscles), which relax

170
Q

Describe the anatomy of the nasal cavity

A
  • 3 turbinates (nasal conchae): superior, middle, inferior
  • 3 types of mucosa: nasal, olfactory, respiratory
  • Semilunar hiatus: crescent-shaped groove in the lateral wall of the nasal cavity (middle meatus) - opening for maxillary sinus
  • Opening to Eustachian tube is in the nasopharynx (lateral wall)
  • Posterior nasal aperture (choanae): opens into nasopharynx
171
Q

Name the paranasal sinuses and describe their function

A
  • Ethmoid
  • Frontal
  • Maxillary
  • Sphenoid
    Function: reduce weight of skull, increase resonance of sound, allow circulation of mucus
    Drain into nasal cavity
172
Q

Name the different types of tonsils

A
  • Lingual
  • Palatine
  • Pharyngeal or “adenoid”
  • Tubal
173
Q

What forms the isthmus of the fauces?

A

Right and left palatoglossal folds
The isthmus of the fauces is the boundary between the oral cavity and the oropharynx

174
Q

What is the fossa of Rosenmuller and what is its clinical significance?

A

Pharyngeal recess immediately posterior to the auditory tube
Clinical significance: a mass in the nasopharynx could block the auditory tube
> its middle section is made of cartilage and could be compressed
> Loss of air entry into the middle ear can result in excess mucus production

175
Q

Describe the innervation of the pharyngeal muscles

A
  • All innervated by vagus (CN X) via the pharyngeal plexus
  • Exception: stylopharyngeus, which is innervated by the glossopharyngeal nerve (CN IX)
176
Q

Describe the muscles of the pharynx

A
  • Pharyngeal constrictors: superior, middle and inferior
  • Longitudinal muscles (elevators): lift pharynx to receive food from oral cavity
    > Stylopharyngeus: elevates pharynx & larynx
    > Palatopharyngeus: approximates soft palate and posterior wall of pharynx
    > Salpingopharyngeus: elevates pharynx; opens auditory tube when swallowing
177
Q

Describe the function of the epiglottis

A

Elastic cartilage that closes and covers laryngeal inlet during eating/drinking to prevent entry of foreign substances into lungs

178
Q

What is the vallecula?

A

Depression behind the root of the tongue which serves as a spit trap
* Saliva is held there to prevent the initiation of a swallow reflex

179
Q

Describe the following anatomical features of the larynx:
* Vocal cords
* Vestibular folds
* Rima glottidis

A

Larynx protects the opening of the trachea
* Contains vocal cords (aka vocal folds)
> 2 folds of mucous membrane that vibrate and modulate the flow of expelled air in phonation
* Contains vestibular folds (false vocal cords) - folds of mucous membrane that enclose vestibular ligaments
* Rima glottidis: opening between the true vocal cords and arytenoid cartilages

180
Q

Describe the function of the muscles of the larynx

A
  • Cricothyroid: changes the length of vocal cords to alter pitch of voice
  • Thyroarytenoid: changes the length of vocal cords to alter pitch of voice
  • Posterior cricoarytenoid: opens the vocal folds (abductor)
  • Lateral cricoarytenoid and transverse arytenoid: close rima glottidis (adductors)
  • Oblique arytenoid: acts as a purse-string, contributing to closure of laryngeal inlet w/ aryepiglottic muscle
181
Q

Describe the innervation of the larynx

A

All intrinsic muscles of the larynx are supplied by the recurrent laryngeal nerve except for cricothyroid - supplied by external branch of superior laryngeal nerve
Sensation: (vagus nerve, CN X)
* Above vocal folds: branch of superior laryngeal nerve
* Below vocal folds: branch of recurrent laryngeal nerve

182
Q

Describe the following anatomical features of the larynx:
* Arytenoid cartilages
* Cuneiform tubercle
* Aryepiglottic folds
* Pyriform fossae

A
  • Arytenoid cartilages: pair of small, 3-sided pyramids to which vocal cords attach, enabling movement
  • Cuneiform tubercle: paired cartilages attached to arytenoids; support vocal cords and lateral epiglottis
  • Aryepiglottic folds: 2 ligamentomuscular structures in supraglottic larynx
    > Protect airway while swallowing; lateral border of laryngeal inlet
    > Landmark for intubation
  • Pyriform fossae: one on either side of aryepiglottic fold; common place for food to be trapped
183
Q

What is “glue ear” and how is it treated?

A

Glue ear, also known as otitis media with effusion, is caused by a blockage of the auditory tube
> Leads to the accumulation of fluid within the middle ear due to poor ventilation
Treatment
- Insertion of ventilation tubes: ventilate the middle ear cavity

184
Q

Describe the divisions of the pharynx

A
  • Nasopharynx
    > Base of skull to soft palate
  • Oropharynx:
    > Soft palate to epiglottis
  • Laryngopharynx
    > Epiglottis to bifurcation of oesophagus and trachea
185
Q

Describe the components of attention

A
  • Arousal: general state of wakefulness and responsivity
  • Vigilance: capacity to maintain attention over prolonged periods of time
  • Divided attention: ability to respond to more than one task
  • Selective attention: ability to focus on one stimulus while suppressing competing stimuli
186
Q

Name the term for
1. Breakdown of global attention
2. Impaired arousal
3. Impaired vigilance
4. Impaired divided and selective attention

A
  1. Delirium/acute confusional state
  2. Drowsiness
  3. Impersistence
  4. Distractible
187
Q

Describe the functional anatomy of attention

A
  • Top-down cortical attentional modulation
    > Frontal, parietal and limbic cortices
    > Might be affected by hyperarousal: fear, anxiety, pain
    > Impairs attentional processes: inattention, neglect
  • Bottom-up attentional competition
    > Visual, auditory, somatosensory association cortices
  • Arousal mechanisms: ascending reticular activating system
    > Grey area in brainstem projecting upwards and maintaining arousal
188
Q

How would you test attention in clinical practice?

A
  • 4AT-screen for delirium
    > Alertness
    Ask age, date of birth, place, year…
    Attention (months of the year backwards)
    Acute change or fluctuating course
189
Q

What are the steps involved in learning and memory?

A
  • Registration
    > Alertness
    > Attention-RAS
    > Thalami
    > Frontal cortices
  • Encoding
    > Medial temporal (including hippocampus)
  • Retrieval
    > Reactivation of temporal structures
    > Frontotemporal crosstalk
  • Consolidation
    > Diffuse cortices
190
Q

Describe short-term or working memory

A
  • Holds information temporarily e.g. remembering a phone number
  • Involves active maintenance and manipulation of information in short-term storage
  • Can usually hold 7+/- 2 elements
191
Q

Describe the different types of long-term memory

A
  • Implicit memory/procedural: network involves basal ganglia & cerebellum
  • Episodic memory/declarative: personal experience
    > Extended limbic system (circuit of Papez)
    > Medial temporal lobe: hippocampus & entorhinal cortex
    > Diencephalon: mamillary bodies & thalami
    > Parts of memories e.g. vision, olfaction may be located in regions associated w/ these functions
    > Amygdala is associated with emotional memories
  • Semantic memory: facts - semantic memory network
    > Left hemisphere anterior temporal lobe - key integrative region
    > Anterior temporal cortex (ATC) and angular gyrus (AG) integrate incoming information
  • Verbal v visual
192
Q

Discuss the clinical causes of acute deficits in memory

A
  • Pure amnesia
    > Transient global amnesia: individual knows who they & other people are but keeps repeating things
    > Transient epileptic amnesia: recurrent spells of memory loss, short in duration, happen soon after waking
  • Mixed deficit: delirium
193
Q

Discuss the clinical causes of chronic deficits in memory

A
  • Pure amnesia
    > Hippocampal damage
  • Herpes simplex virus (HSV encephalitis)
  • Anoxia
  • Alzheimer’s disease
    > Diencephalic damage
  • Korsakoff’s syndrome
  • Bilateral thalamic stroke
  • Post subarachnoid haemorrhage
  • Mixed deficit: dementia
194
Q

Which test is used for memory in a clinical setting?

A

Addenbrooke’s cognitive examination - ACE III

195
Q

Describe the inputs and outputs involved in language

A
  • Inputs
    > Comprehension: dysfunction (agraspia)
    > Reading: dysfunction (alexia)
    > Repetition
  • Outputs
    > Speech: dysfunction (aphasia)
    > Sign language/gesture
    > Naming: dysfunction (anomia)
    > Writing: dysfunction (agraphia)
    > Repetition
196
Q

Describe the areas of the brain which may be involved in language dysfunction

A
  • Broca’s area
    > Left frontal: language production
    > Dysfunction:
  • Non-fluent
  • Effortful/difficulty articulation errors
  • Wernicke’s area
    > Left frontal: comprehension
    > Dysfunction:
  • Fluent
  • Nonsense
197
Q

Which structure links Broca’s area and Wernicke’s area?

A

Arcuate fasciculus

198
Q

Describe the area of the brain responsible for judgement and behaviour

A
  • Prefrontal cortex (divided into 3 main areas)
    > Dorsolateral prefrontal cortex
    Executive functions / dysfunction:
  • Sequencing / trouble sequencing
  • Organisation / disorganisation
  • Abstraction / concrete thinking
  • Planning / poor planning
    > Orbitofrontal prefrontal cortex
    Executive functions / dysfunction
  • Social interactions / loss of social niceties
  • Behaviour / loss of table manners
  • Insight / lack of insight
  • Inhibition / disinhibition
    > Ventromedial prefrontal cortex
    Executive functions / dysfunction
  • “Get up and go” / apathetic
199
Q

Define what is meant by a neurodegenerative disorder

A

Progressive and selective dysfunction or loss of neurons associated with deposition of pathologically altered proteins that leads to disruption of functional systems and clinical symptoms

200
Q

Describe the roles of microtubule-associated protein tau (MAPT) and how it can lead to neurodegenerative disease

A

6 soluble isoforms exist
Roles:
* Maintain stability of axonal microtubules
* Protein translation
* Cellular signalling
* Apoptosis
Hyperphosphorylation of tau can lead to neurodegenerative disease
- Formation of insoluble neurofibrillary tangles of helical and straight filaments

201
Q

List examples of tauopathies

A
  • Alzheimer’s disease
  • Frontotemporal dementia
  • Corticobasal degeneration (CBD)
  • Progressive supranuclear palsy (PSP)
  • Chronic Traumatic Encephalopathy (CTE)
202
Q

Describe the pathophysiology of Alzheimer’s disease

A
  • Primarily affects > 65 y/o and co-exists with vascular dementia
  • Clinical presentation
    > Progressive memory loss
    > Executive dysfunction
    > Loss of social and occupational functioning
    > Visuospatial difficulties
    > Personality change
  • Pathology
    > Beta-amyloid plaques
    > Intracellular neurofibrillary tangles of tau
    > Results in neuronal loss, brain atrophy and reduced acetylcholine synthesis
    > Process starts in entorhinal cortex and moves onto hippocampus
203
Q

Describe the pathophysiology of frrontotemporal dementia

A
  • Mean age of onset 53-58y/o
  • Positive family history is common
  • Clinical presentation
    > Change in personality/social conduct
    > Coarsening of personality
    > Indifference to others
    > Disinhibition
    > Parkinsonism
  • Pathology
    > Atrophy in frontal/temporal regions
    > Hypoperfusion in affected regions
    > Intraneuronal and glial tau deposition
204
Q

Describe the pathophysiology of progressive supranuclear palsy (PSP)

A
  • Mean age of onset 63y
  • Clinical presentation
    > Parkinsonism
    > Vertical gaze palsy
    > Dementia
    > Postural instability/falls
    Pathology:
    > Interneuronal and glial cell tau deposition within basal ganglia, brainstem and cortex
    > Midbrain atrophy
205
Q

Describe the pathophysiology of corticobasal degeneration (CBD)

A
  • Mean age of onset 63y
  • Clinical presentation
    > Asymmetric parkinsonism
    > Apraxia and dystonia
    > Alien limb phenomenon
    > Cortical sensory loss
    > Aphasia
  • Pathology
    > Tau deposition within basal ganglia and frontoparietal cortices
    > Ballooned neurons
    > Asymmetrical cortical atrophy affecting superior parietal lobe
206
Q

Describe the pathophysiology of chronic traumatic encephalopathy (CTE)

A
  • Sequelae of chronic repeated head injury
  • Clinical presentation
    > Behavioural change
    > Cognitive difficulties
    > Mood disturbance
    Pathology: widespread cortical tau deposition
207
Q

Describe the structure of alpha-synuclein and its role in the development of neurodegenerative disease

A
  • Unstructured soluble protein encoded by SNCA gene with a role in DNA repair
  • Misfolded alpha synuclein along with ubiquitin and neurofilament proteins form Lewy bodies
  • Lewy bodies: intracytoplasmic inclusion bodies that eventually lead to cell death
208
Q

List examples of alpha-synucleinopathies

A
  • Parkinson’s disease
  • Dementia with Lewy bodies
  • Multiple systems atrophy (MSA)
209
Q

Describe the pathophysiology of Parkinson’s disease

A

Long prodromal period, prevalence increases >65y/o
Clinical presentation
- Motor
> Rest tremor
> Rigidity
> Bradykinesia
> Postural instability
- Non-motor
> Mood disturbance
> REM sleep behaviour disorder
> Hyposmia
> Constipation
Lewy body pathology starts in gut, ascending to brainstem & substantia nigra

210
Q

Describe the pathophysiology of dementia with Lewy bodies (DLB)

A

Clinical presentation:
* Parkinsonism
* Progressive cognitive difficulties
* Visual hallucinations
* Fluctuation in cognition
* Sensitivity to antipsychotic medication
Pathology:
* Lewy body deposition in brainstem and cortex
* Co-existence with Alzheimer’s pathology is common

211
Q

Describe the pathophysiology of multiple systems atrophy (MSA)?

A

Clinical presentation
- Parkinsonism with prominent cerebellar or autonomic features
> Postural hypotension and genitourinary dysfunction
Pathology
- Lewy body deposition predominantly in oligodendrocytes within
> Brainstem
> Striatum
> Cerebellum

212
Q

Give an example of a prion disorder and outline its pathophysiology

A

Creutzfeldt-Jakob disease: rare and rapidly fatal
Prions are tiny misfolded proteins that form aggregates
Clinical presentation
* Rapid onset dementia and behaviour change
* Myoclonic jerks
* Visual disturbances
* Ataxia
Pathology
* Spongiform vacuolation throughout grey matter
* Reactive proliferation of astrocytes & microglia
* Neuronal cell loss
Investigations: lumbar puncture, EEG, MRI shows cortical ribboning

213
Q

Give an example of a trinucleotide repeat disorder and describe its pathophysiology

A

Huntington’s disease: autosomal dominant inheritance
* Caused by expansion of CAG repeats in huntingtin gene (chromosome 4)
Clinical presentation:
* Chorea
* Behavioural change
* Psychiatric disturbance
* Dementia
MRI/CT shows caudate atrophy

214
Q

Briefly describe the anatomy of the following structures in the eye
* Sclera
* Pupil
* Iris
* Choroid
* Cornea
* Anterior & posterior chamber

A
  • Sclera: white of the eye, fibrous elastic tissue, covered by conjunctivae
  • Pupil: darkened hole in the centre of the iris controlling passage of light
  • Iris: coloured part of eye, smooth muscle controls diameter of pupil
  • Choroid: vascular layer in posterior eye between sclera and retina
  • Cornea: avascular transparent structure covering the front of the eye
  • Anterior & posterior chambers: aqueous humour produced by ciliary bodies maintains pressure and provides nutrients
215
Q

Briefly describe the anatomy of the following structures in the eye
* Optic nerve
* Lens
* Retina
* Macula
* Vitreous chamber

A
  • Optic nerve (CN II) carries visual impulses to occipital lobe
  • Lens: focuses visual input to the back of the retina
  • Macula: near the centre of the retina, responsible for detailed central vision
  • Retina: light-sensitive layer of tissue containing rods and cones
  • Vitreous chamber: contains vitreous humour, gel-like structure between lens and retina; contains phagocytes to remove cell debris
216
Q

Describe the sympathetic innervation of the dilator pupillae muscle

A
  • Controlled by hypothalamus
  • Fibres travel ipsilaterally to lateral column of cervical spinal cord, ciliospinal centre (C8-T2)
  • Second-order pre-ganglionic pupilomotor fibres exit spinal cord at T1
  • Enter cervical sympathetic chain synapsing in superior cervical ganglion
  • Post-synaptic fibres travel through internal carotid plexus
  • Enter cranium and join ophthalmic division of trigeminal nerve (V1)
  • Enter orbit through superior orbital fissure, fibres travel with long ciliary and nasociliary nerves
  • Contain alpha adrenergic sympathetic receptors
217
Q

Describe the pathophysiology of non-exudative (dry) age-related macular degeneration (ARMD) as well as its treatment

A

Symptoms: gradual loss of central vision and distortion
Pathophysiology:
* Accumulation of cellular debris (drusen) between retina and choroid
* Atrophy of retinal pigment epithelium and photoreceptors
Treatment:
No cure
Lifestyle advice: diet
Low visual aids, magnifiers, partial sight/blind registration

218
Q

Describe the pathophysiology of exudative (wet) age-related macular degeneration (ARMD) as well as its treatment

A

Symptoms: gradual/rapid loss of central vision and distortion
Pathophysiology:
* Choroidal neovascularization stimulated by VEGF
* Grow under retinal pigment epithelium, cause haemorrhage, leakage and ultimately fibrosis
* Disrupt photoreceptor and retinal function
* Loss of vision is profound if untreated
Treatment:
* anti-VEGF antibodies: intravitreal injection
* Inhibits angiogenesis, reducing leakage & haemorrhage
* Preserve vision/delay visual loss
* Not a cure, repeat monthly for at least 3 months

219
Q

Describe the different types of papillae in the mouth

A
  • Foliate (leaf-shaped)
    > Vertical ridges on side of tongue
  • Filiform (string-shaped)
    > Thread-like structures create rough surface to help with speaking, chewing and cleaning oral cavity
  • Fungiform (mushroom-shaped)
    > Carry 2000-8000 taste buds
    > Distributed across tongue
    > Gustatory receptor cells detect 5 chemicals dissolved in saliva
  • Vallate:
    > Approx a dozen form V-shaped line (boundary between anterior 2/3 and posterior 1/3)
    > Carry some taste buds and minor salivary glands
220
Q

Describe how gustatory receptor cells detect taste

A
  • Substance from food dissolves in saliva
  • Saliva enters taste pore and gustatory receptor cell depolarises
  • Nerve impulse travels along afferent nerve to brain
  • Surrounded by supporting (sustentacular) cells
  • 5 chemicals detected
    > Salty: Na+ ions and others in same group
    > Bitter: protective function e.g. coffee, beer
    > Sour: hydrogen ions
    > Sweet: sugars
    > Savoury/umami: monosodium glutamate
221
Q

Describe the innervation of the tongue

A
  • Anterior 2/3
    > General sensation - pain, temperature, touch: lingual nerve, branch of mandibular division of trigeminal nerve (CN V3)
    > Taste - chorda tympani, branch of facial nerve (CN VII)
    Initially runs in lingual nerve & then passes to chorda tympani
    Chorda tympani travels through middle ear behind TMJ on undersurface of eardrum, joining the facial nerve behind the eardrum
  • Posterior 1/3
    Glossopharyngeal nerve (CN IX) for both general sensation and taste
222
Q

Describe the central processing of taste

A
  • CN IX and CN VII run to brainstem and taste fibres synapse in the nucleus tractus solitarius (NTS) of the medulla
  • Second-order neurons travel to thalamus
  • Third-order neurons project to gustatory cortex
    > Undersurface of frontal lobe, covered by temporal lobe
    > Anterior insula, inferior frontal gyrus
223
Q

Describe the actions and innervation of the extrinsic muscles of the tongue

A
  • Genioglossus: protrusion of the tongue
  • Palatoglossus: elevates root of tongue, depresses soft palate
  • Styloglossus: retracts and elevates lateral tongue
  • Hyoglossus: depression of tongue
    All innervated by the hypoglossal nerve (CN XII) except for palatoglossus (vagus nerve, CN X)
224
Q

Describe the actions and innervation of the extrinsic muscles of the tongue

A
  • Genioglossus: protrusion of the tongue
  • Palatoglossus: elevates root of tongue, depresses soft palate
  • Styloglossus: retracts and elevates lateral tongue
  • Hyoglossus: depression of tongue
    All innervated by the hypoglossal nerve (CN XII) except for palatoglossus (vagus nerve, CN X)
225
Q

Describe the actions of the intrinsic muscles of the tongue

A

Intrinsic muscles change the shape of the tongue
* Vertical: broadens & elongates the tongue
* Transverse: narrows & elongates the tongue
* Longitudinal: retracts & broadens tongue

226
Q

Describe the main steps involved in swallowing (deglutition)

A
  • Buccal phase (voluntary)
    Tongue moves against hard palate to push bolus into pharynx
  • Pharyngeal stage (involuntary)
    Movement of bolus into oropharynx triggers receptors
    Send impulses to deglutition centre (medulla & lower pons)
    Signals sent to uvula and soft palate to close nasopharynx; epiglottis seals larynx
    Upper oesophageal sphincter relaxes to allow passage of bolus
  • Oesophageal stage (involuntary)
    Bolus pushed onwards by peristalsis
227
Q

Name the structures which are drained by the submental and submandibular lymph nodes

A

Submental lymph nodes
* Anterior lower mouth
* Lower lip
* Front of mouth
* Anterior teeth
* Tip of tongue
* Skin of chin
Submandibular lymph nodes
* Cheeks
* Gums
* Upper lip
* Anterior tongue
* Nasocavity
* Maxillary sinus
* Lower part of face

228
Q

List the lymph nodes of the head and neck

A
  • Submental and submandibular
  • Paratracheal
  • Superficial cervical
  • Supraclavicular
  • Jugulo-omohyoid (deep cervical): drains tongue
  • Jugulo-digastric (deep cervical): drains palatine tonsil and tongue
  • Mastoid: drain posterior neck, upper ear & back of external auditory meatus
  • Occipital: drains occipital area of scalp
  • Parotid (pre-auricular): drains superficial areas of face & temporal region
  • Retro-auricular
  • Sublingual
229
Q

Describe the situations in which electroencephalography (EEG) would be indicated

A
  • Episodic events
  • Deteriorating cortical function
    > Coma/altered consciousness
    > Seizures: status epilepticus
    > Encephalitis
    > Encephalopathy: widespread cortical dysfunction, not seizure activity
    > CJD/dementia
    > Prognosis in hypoxic brain injury
    > Rare dementia/cognitive decline
  • Attack disorders
    > First/single seizure: prognosis
    > Firm clinical diagnosis & classification of epilepsy
  • Focal or generalised discharge?
230
Q

What is an evoked potential and how is it used in a clinical setting?

A
  • Measurement of central conduction in the CNS
  • Provide a stimulus and measure the response
  • Categories
    > Visual evoked potentials (VEP)
    Assess macular-cortical pathway’s gross integrity
    P100: discharge that arrives after 100ms at occipital cortex
    > Brainstem auditory evoked potentials (BAEPs)
    Operations around brainstem
    Apply sound stimulus to the ear and relate peaks to aspects of hearing pathway
231
Q

What is the Rinne test?

A

Vibrating tuning fork placed on mastoid bone; ask patient to tell you when sound can not be heard
Then place near auditory canal until they can’t hear it
Used to compare the perception of sounds transmitted by air conduction compared to bone conduction
Screens for the presence of conductive hearing loss: bone conduction is louder than air conduction due to blockage
Normal: air conduction is louder than bone conduction (same with sensorineural hearing loss but they will stop hearing it sooner)

232
Q

Describe the drainage of venous blood in the brain

A

Superior & inferior sagittal sinus, as well as straight sinus, anastomose at internal occipital protuberance
Transverse sinuses emerge from this and form the sigmoid sinuses
Sigmoid sinuses drain into the internal jugular vein via the jugular foramen
Cavernous sinus is located anteriorly & received blood from ophthalmic veins
Drains into superior & inferior petrosal sinuses which drain into internal jugular

233
Q

Which structures, derived from the pia mater, anchor the spinal cord in place?

A

21 denticulate ligaments laterally
Stop movement due to lateral vertebral displacement

234
Q

Describe the falx cerebri

A
  • Sickle-shaped midline fold separating 2 hemispheres
  • Posterior border blends w/ tentorium cerebelli
  • Anterior border attaches to crista galli (ethmoid bone)
  • Upper border attached to vault midline & contains superior sagittal sinus
235
Q

Describe the tentorium cerebelli

A

Tent-shaped fold roofing over posterior cranial fossa
Divides cranial cavity into
* Supratentorial compartment: contains hemispheres, specifically lower aspect of occipital lobes
* Infratentorial compartment: contains brainstem and cerebellum; midbrain passes through tentorial hiatus

236
Q

What makes up the
* Lentiform nucleus
* Striatum

A

The lentiform nucleus consists of the putamen and the globus pallidus
The striatum consists of the putamen, globus pallidus and caudate nucleus

Year 2 - Excess (6 decks)

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