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Block 3 AR > Sensory > Flashcards

Sensory Flashcards

1
Q

What is acute pain?

A

The normal, predicted physiological response to an adverse chemical, thermal, or mechanical stimulus associated with surgery, trauma, and acute illness
Time-limited
Responsive to therapy

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2
Q

What is chronic pain?

A

A pain state which is persistent and in which the cause of the pain cannot always be removed or is difficult to treat
May be associated with a long term incurable or intractable medical condition or disease

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3
Q

What is nociceptive pain?

A

Arises from the stimulation of specific pain receptors. These receptors can respond to heat, cold, vibration, stretch and chemical stimuli
released from damaged cells

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4
Q

What is neuropathic pain?

A

Arises from within the peripheral and central nervous system. Specific receptors do not exist here, with pain generated by nerve cell injury

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5
Q

What is wind up?

A

Frequency dependent increase in excitability due to activity of c fibers

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6
Q

What can be causes of chronic pain?

A 
Badly Managed Acute Pain 
Emotionally Sensitive Patient 
Poor Coping Skills 
Previous Bad Pain Experiences
Pain Goes on For Longer 
Surgical Complications 
Genetic Predisposition
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7
Q

What model is used to understand chronic pain?

A

Biopsychosocial model

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8
Q

Name some somatic nociceptive pain conditions

A

Lower back pain
Myofascial pain
Arthritis

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9
Q

Name some visceral nociceptive pain conditions

A

Pancreatitis
interstitial cystitis
endometriosis
Functional pain syndrome

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10
Q

Name some neuropathic pain conditions

A 
Post-herpetic neuralgia (shingles)
Neuroma 
Radicular pain (nerve root irritation) 
CRPS  - complex regional pain syndrome 
Post-amputation pain
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11
Q

Describe malignant pain

A 
80% of cancer patients suffer from pain 
Psychological component substantial 
Multiple etiologies 
Iatrogenic – CT, RT 
Other psychosocial factors
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12
Q

What are non pharmacological management options for pain?

A

Exercise

Physiotherapy

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13
Q

What is complementary therapy for pain?

A

Acupuncture

TENS - transcutaneous electrical nerve stimulation

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14
Q

Describe the WHO analgesia ladder

A

Mild to moderate pain - non opioids, NSAIDs, aspirin, paracetamol
Moderate to severe pain - mild opioids eg codeine with or without non opioids
Severe pain - strong opioids eg morphine with or without non opioids

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15
Q

What drugs can act as adjuncts to treating pain?

A

Anticonvulsants - gabapentin, pregabalin
Antidepressants - amytryptaline
Lidocaine
Baclofen, benzodiazepines

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16
Q

What is the gold standard for cancer pain management?

A

Opioids

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17
Q

Describe why opioids should be used with caution to treat chronic pain

A

Can do more harm than good
Addictive properties
Side effects - constipation etc
Opioid induced hyperalgesia from high dose chronic use
Should be used only for functional rehabilitation

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18
Q

What invasive procedures can be used in chronic pain?

A

Injections: needle techniques to reduce pain in muscle, tendons and joints to reduce inflammation around nerves e.g. trigger point injections, joint injections, acupuncture, epidural steroids
Ablative procedures:permanently interrupt nervous system activity. Chemical: alcohol, phenol Physical: radiofrequency denervation, cryoneurolysis. Used mainly in terminal cancer patients
Implants: continuous catheter techniques, peripheral nerve stimulators
neuromodulations e.g. intrathecal drug delivery, spinal cord stimulators
Nerve blocks: Neuroaxial (epidural, intrathecal), Axial (paravertebral, nerve roots), Peripheral (intercostal, suprascapular, ilioinguinal, upper and lower extremity blocks) Autonomic: stellate ganglion, lumbar sympathetic chain

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19
Q

What types of sensory receptor exist?

A

Free nerve endings - pain and temp
Pacinian corpuscles - mechanoreceptors, deep pressure
Meissner corpuscles - discriminative touch
Muscle spindles - muscle stretch
Merkel cells and disk - light touch
Ruffini ending - touch

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20
Q

What type of adaptation does the discriminative touch modality undergo?

A

Fast adaptation

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21
Q

What is located in the post central gyrus?

A

Primary sensory cortex

Receives contralateral sensory input from the body (inc taste)

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22
Q

What is located in the superior parietal lobule?

A

Integration of sensory inputs, sensory memory, perception of contralateral self & world

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23
Q

What is the internal capsule?

A

Dense collection of sensory and motor tracts passing to/from the cortex

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24
Q

What is the corona radiata?

A

White matter sheet that continues ventrally as the internal capsule and dorsally as the semioval center. Contains both descending and ascending axons that carry nearly all of the neural traffic from and to the cerebral cortex
Associated with the corticospinal tract, the corticopontine tract, and the corticobulbar tract

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25
Q

Describe the structure of the internal capsule

A

Anterior limb – frontopontine, frontothalamic
Genu - bend
Posterior
Retrolenticular
Head, arm, leg, sensory, vision and hearing arranged somatotopically

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26
Q

How many neurons are involved from sensation up to the cortex?

A

3
1st order - Ascend ipsilaterally to nuclei in the medulla
2nd order - Decussate and ascendto thalamus via a lemniscus
3rd order - Ascend to cortex via internal capsule

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27
Q

How many Rexed lamina are there?

A

10

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28
Q

What is a funiculi? And how many are there in the spinal cord?

A 
Bundles of more than 1 tract
3
Dorsal
Lateral
Ventral
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29
Q

What sensory modalities are carried in the dorsal funiculus?

A

Fine touch and proprioception from lower body

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30
Q

What modality tracts are carried in the lateral funiculus?

A

Motor supply to ipsilateral body

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31
Q

What sensory modalities are carried in the ventral funiculus?

A

Pain and temperature

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32
Q

What sensory modalities are carried by the dorsal column tracts?

A

Discriminative touch, vibration & conscious proprioception

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33
Q

What are the two parts of the dorsal column tracts?

A

Fasciculus cuneatus - above ~T6

Fasciculus gracilis - below ~T6

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34
Q

Describe the path that the dorsal columns follow

A

1st order neurons pass into dorsal cord and ascends ipsilaterally to lower medulla where they synapse with 2nd order neuron at nucleus cuneatus or gracilis
2nd order neurons decussate and ascend to ventral posterior nucleus of thalamus & synapse with 3rd order neurons
3rd order neurons travel to primary sensory cortex

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35
Q

What sensory dysfunction can tertiary syphilis result in?

A

Tabes dorsalis

Destruction of dorsal columns

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36
Q

What does dorsal column damage cause?

A

Loss of fine touch, vibration and conscious proprioception below level of lesion ispilateral in cord damage
Sensory ataxia – leads to positive Romberg sign (requires vision to stand steady) & stamping gait
Pseudoathetosis – writhing of digits, hands and feet

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37
Q

What sensory modalities are carried by the spinothalamic tract?

A

Pain, temperature and simple tactile sensation

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38
Q

Describe the pathway of the spinothalamic tract

A

1st order neurons ascend 1-2 vertebral level in dorsal grey matter before synapsing with 2nd order neurons which decussate via the anterior white commissure
2nd order neurons ascend spinothalamic tract to ventral posterior lateral nucleus of thalamus via spinal lemniscus and synapse with 3rd order neurons
3rd order neurons travel to primary sensory cortex

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39
Q

What is the trigeminal lemniscus?

A

Carries pain and temperature sensation from to the ventral posterior medial nucleus of the thalamus

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40
Q

What disorder can lead to disruption of the spinothalamic tract?

A

Syringomyelia - cavitation/expansion of central canal in cervical region Pain and temperature sensation lost in arms and top of chest

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41
Q

What is sacral sparing?

A

An expanding ventral grey matter tumour can knock out all contralateral pain & temperature sensation except sacral region due to somatotopic organisation of spinothalamic tract

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42
Q

What sensory modalities are carried in the spinocerebellar tract?

A

Unconscious proprioception to the ipsilateral cerebellum
Dorsal spinocerebellar tract - Muscle spindles, few Golgi tendon organs
Ventral spinocerebellar tract - Golgi tendon organs

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43
Q

Describe the pathway followed by the dorsal spinocerebellar tracts

A

Lower limb - Clarke’s dorsal nucleus, Sits between C8-L3 1st & 2nd order dorsal spinocerebellar neurons synapse here! Damaged in Freidrich’s ataxia. 2nd order neuron ascends ipsilaterally and passes directly to cerebellum
Upper limb - muscle spindle information passes through the cuneocerebellar tract (runs with fasciculus cuneatus). 1st order neuron ascends to medulla then synapses with 2nd order which goes to cerebellum

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44
Q

Describe the pathway followed by the ventral spinocerebellar tracts

A

Lower limb - 1st order neuron synapses with 2nd order which then decussates and ascends contralaterally before decussating again and entering cerebellum
Upper limb - Golgi tendon information passes through the rostral spinocerebellar tract. 1st order neurons synapse with second order which then enter the cerebellum ipsilateral

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45
Q

What information is carried by the ventral spinocerebellar tract?

A

Stretch of the tendon at the muscle tendon interface of the lower limb

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46
Q

What do pure lesions of the spinocerebellar tract cause?

A

Ataxia / malcoordination of motor action
Wide-based gait
Symptoms normally masked by motor weakness/paralysis

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47
Q

Describe the route of cranial nerve sensory nuclei

A

Send neurons along a route similar to sensory neurons of the body
Most sensory fibres decussate on route to contralateral thalamus
Fibres run from thalamus to primary sensory cortex
Most nociception from CN VII, IX, X passes via CN V’s sensory nucleus

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48
Q

Describe where trigeminal touch sensation fibres pass

A

contralateral thalamus via the trigeminal lemniscus
1st order trigeminal nerve sensory neurons synapse in CN V nucleus
2nd order neurons ascend in trigeminal lemniscus to ventral posterior medial nucleus of the thalamus
3rd order neurons pass to primary sensory cortex

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49
Q

What sensory losses would result from a brainstem lesion?

A

Ipsilateral facial

Contralateral body

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50
Q

What are the thalami?

A

organised collection of nuclei of sensory, visual, auditory and motor-associated functions

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51
Q

Where do muscle spindle sensory fibres run?

A

Dorsal column & spinocerebellar pathways

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52
Q

Which afferent neurons carry sensation from muscle spindles?

A

1a afferents

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53
Q

What is nociceptive pain sensed by?

A

Free ending on C- and Aδ- fibres

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54
Q

Describe the gate control theory of pain

A

Input from pain fibres activates 2nd order cells and inhibit local interneurons in substantia gelatinosa
Pain signal travels onwards
Mechanical stimulation activates inhibitory interneurons
Reduces pain transmission by inhibiting 2nd order cells
Descending control can also increase activity of these interneurons

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55
Q

Where are the main output to descending tracts from higher pain centres?

A

Hypothalamus, periaqueductal gray and brainstem nuclei
Descending inhibition travels to ANS and spinal lamina in dorsolateral
funiculus where 5HT and NA dominant

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56
Q

What drugs are used to treat neuropathic pain?

A

Tricyclic antidepressants and anti epileptic drugs
Gabapentin+Amitriptyline in combo
Carbemazepine alone - never in combo

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57
Q

How many subclasses of NSAIDs are there?

A

6

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58
Q

Describe the mechanism of action of NSAIDs as painkillers

A

Cyclooxygenases break down arachidonic acid to give prostaglandins
NSAIDs Block production of prostaglandins by inhibiting COX enzymes
Three forms of COX: COX 1 – Normal cell function, COX 2 - Inflammation, COX 3 - Fever

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59
Q

How do prostaglandins lead to increased pain?

A

Act on prostaglandin receptor which is GPCR which leads to opening of voltage gated Na channels and therefore increased depolarisation of nociceptors

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60
Q

What are clinical uses of NSAIDs?

A 
Anti-inflammation 
Anti-pyretic 
Analgesic 
Anti-coagulant 
May delay healing, not used post operatively, post partum
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61
Q

Describe some commonly used NSAIDs

A

Aspirin (CV drug)
Ibuprofen (weak action)
Naproxen (strong, low side-effects)
Diclofenac (similar to Naproxen, CV problems)
Indomethacin (strong, high side effects)
COX-2 Inhibitors: Celecoxib, Etoricoxib, Parecoxib (similar to naproxen, lower GI effects)
Paracetamol - antipyretic as COX 3i

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62
Q

List some common side effects of NSAIDs

A

GI problems: vomitting, nausea, diarrhoea, bleeding/ulceration
CV incidents: thrombosis
Headache: drug induced headache
Dizziness, Insomnia, Nervousness, Depression, Vertigo,
Tinnitus: sign of toxic state, reduce dose quickly
Photosensitivity, Renal Impairment, Hypertension
Hypersensitivity: skin rashes and eruptions, angioedema,
bronchospasm
Reye’s syndrome in under 16s - fatty deposits in liver and brain

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63
Q

Which drugs can interact with NSAIDs?

A

Avoid concomitant use of oral NSAIDs
Antidepressants: increased risk of bleeding with SSRIs (e.g. fluoxetine, paroxetine) and venlafaxine
Increased risk of nephrotoxicity with ACE inhibitors and diuretics and also with drugs used for arthritic/skin conditions, e.g. ciclosporin
NSAID can enhance the anti-coagulant effects of many drugs used for CV disorders (e.g. warfarins, heparins and can antagonise the hypotensive effects, e.g when used with alpha and beta-blockers and nitrates

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64
Q

What is salicylism?

A

Salicylate toxicity may occur with high dose acute or chronic ingestion of NSAIDs (1% mortalilty)
Severe toxicity:
Auditory (ototoxicity, tinnitus, deafness)
Pulmonary (apnoea, aspiration pneumonitis, pulmonary oedema,
alkylosis, respiratory arrest)
Cardiovascular (tachycardia,hypotension, asystole, dysrhythmias)
CNS (depression, seizure, encephalopathy, delirium, hallucinations)
GI (pancreatitis, hepatitis (rare in acute cases))
Renal Failure
Coma
Chronic intoxication where plasma levels > 300mg/kg: Fluid replacement, Haemodialysis, Activated charcoal, Lorazepam/diazepam i.v. for seizures

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65
Q

What are the 4 main groups of synthetic derivatives of opioids?

A 
Phenylpiperidine series (e.g. pethidine) 
Methadone series (e.g. dextropropoxyphene) 
Benzomorphan series (e.g. cyclazocine) 
Thebaine derivatives (e.g. buprenorphine)
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66
Q

What are pure agonist opioids?

A

Full agonist activity, may have strong (e.g. morphine, diamorphine,
tramadol) or weak activity (e.g. codeine, dihydrocodeine)

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67
Q

What are partial opioid agonists?

A

Can be used for addiction rehabilitation

e.g. nalorphine, pentazocine, buprenorphine

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68
Q

What are opioid antagonists?

A

Used in overdose

e.g.naloxone, naltrexone

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69
Q

What are clinical uses of opioids?

A

Analgesia – chronic and acute
Anaesthesia (Alfentanil, Fentanil, Remifentanil)
Antitussive (Phlocodine, Dextromethorphan)
Antidiarrhoeal (codeine, loperamide)
Coronary Care (pre-surgical, surgical and post)
Cancer Care (Morphine, Diamorphine, Oxycodone)

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70
Q

Where are sites of opioid action?

A

Peri aqueductal gray
Nucleus Raphe Paragigantocellularis in medulla
Dorsal horn
Periphery

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71
Q

Describe the mechanism for opioid drugs

A

Decrease neuronal transmission by:
Decreasing opening of voltage gated calcium channels
Decreasing Ca2+ release from intracellular stores
Increasing K+ outflow via KATP and KIR channels
Decreasing exocytosis

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72
Q

Describe opioid metabolism

A

Metabolism occurs primarily in liver, possibly in kidney and plasma
Primarily metabolised to morphine and glucoronide metabolites (M6G and M3G)
Other metabolites include ethereal sulphates and normorphines
Metabolites highly water soluble and excreted in urine (~90% of
administered dose) - easy drug test

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73
Q

What are some opioid drug half lives?

A 
Morphine - 3-4 hrs
Diamorphine - converted to morphine
Methadone - over 24 hrs
Codeine - converted to morphine 
Pethidine - 2-4 hrs
Fentanyl - 1-2 hrs
Buprenorphine - 12 hrs
Naloxone 1-2 hrs
Naltrexone - 10 hrs
74
Q

What are advantages and disadvantages of methods of opioid administration?

A

IV: Rapid, Unstable Levels
IM: Control, Pain/irritation
Rectal: less nausea and vomiting, slow
Oral: Easy, Slow, more GI problems
Sublingual: Rapid, less OD, more nausea and vomiting
Intrathecal/Epidural: Rapid, less tolerance, more side effects
Patient controlled administration: Reduced use, Catheter
Patches: Stability, Irritation

75
Q

What are side effects of opioid drug use?

A 
Respiratory depression 
Conscious depression/mood alterations 
Miosis 
Reduced gastric motility 
Nausea and vomiting 
Smooth muscle spasm 
Anaphylaxis 
Psychiatric changes (e.g. Pentazocine, Tramadol - hallucinations) 
Tolerance and dependancy – addiction/withdrawal
76
Q

What are indicators of opioid overdose?

A

Pupillary constriction
Respiratory depression
Coma (GCS<7)

77
Q

Describe the management of opioid overdose

A

Reversed by: Naloxone (i.v., short lasting, ~2-4 hrs), Naltrexone (i.v., longer lasting, ~10 hrs)
If conscious and within 1 hr of OD give activated charcoal and 0.8-2mg naloxone every 2-3 min (≤10mg) for respiratory depression
Coma cocktail: naloxone, O2, glucose and thiamine

78
Q

What are the different categories of headaches?

A

Tension – NSAIDs, diary
Sinus – decongestant, antihistamine, steroid
Migraine – 3 steps, avoid opioids, NSAIDs +/- antiemetic, Rectal NSAIDs + antiemetic, Anti-migraine drugs – triptans: sumatriptan, naratriptan
Prophylaxis – β-blockers, amitriptyline
Cluster – sympathetic involvement, Attacks – sumatriptan, Prophylaxis - verapamil. Around orbit, unilateral, crying and runny nose, autonomic association
Medication overuse headache
Worst ever headache – sub arachnoid haemorrhage – emergency!

79
Q

What is the cribriform plate?

A

CN I fibres pass from olfactory mucosa to olfactory bulb via cribriform plate

80
Q

What can be causes of unilateral anosmia?

A

Meningioma

Anterior cranial fossa tumour

81
Q

Where does the Olfactory tract carries sensory neurons to?

A

Orbital and piriform cortexes

82
Q

Where do Olfactory pathways link to?

A

Brainstem
Limbic system
Hypothalamus

83
Q

What can cause a loss of taste or smell?

A 
Viral infection 
Parkinsons (early sign) 
Alzheimers (early sign) 
Meningioma (olfactory groove)
Anterior cranial fossa fracture
84
Q

What are 3 types of tongue papilla?

A

Fungiform
Filiform - anterior 2/3, no taste buds
Vallate

85
Q

Which cranial nerve carries taste from anterior 2/3 tongue? And which from posterior 1/3 tongue?

A

CN VII anterior

CN IX posterior

86
Q

Describe the pathway of the taste sensation from the anterior tongue

A

Receives taste innervation from CNVII
Taste neurons from anterior tongue (2/3rds) run initially with CN V3
then pass into chorda tympani which travels through middle ear
and into CN VII to the nucleus solitarius in brainstem

87
Q

What is the region of greatest visual acuity in the eye?

A

Fovea centralis

88
Q

What are the 3 layers of the eye?

A

Retina
Choroid - vascular
Sclera - white

89
Q

Where is the fovea?

A

In the centre of the macula densa, yellow spot in eye

90
Q

Where is the blind spot?

A

Optic papilla

91
Q

Where does the left part of the visual field enter the eye?

A

Right part of both retinas

92
Q

What are retinal fields?

A

Region of the retina that is named according to its position relative to the nose or temporal region

93
Q

What information is carried in the optic chiasma?

A

Temporal visual field information to contralateral cortex

94
Q

Where does the stalk of optic radiation run?

A

Retrolenticular internal capsule

95
Q

What is Meyers loop?

A

Optic radiation
Sits inferiorly in temporal lobe & contains upper contralateral visual field
Project to gyri around calcarine sulcus of occipital lobe

96
Q

Where does the macula project to? And why might it be spared when there is a primary visual cortex lesion?

A

Occipital pole

Receives different blood supply

97
Q

What do vascular lesions of the primary visual cortex cause?

A

Homonymous hemianopia

Blindness or defective vision in right or left halves of visual fields in both eyes

98
Q

How do you measure visual acuity?

A

Snellen chart, count digits, movement, light perception

99
Q

How do you assess someone’s visual fields?

A

Confrontation with patient staring directly ahead
Examiner compares to their own visual field
Use large red coloured pin
Blind spot mapped (scotoma)

100
Q

How do you perform fundoscopy?

A

Examine cornea and lens first
Patient gazes into distance
Disc is a shallow cup with clear margins
Disc = yellow, Fundus = red

101
Q

What can cause a lack of vision in bilateral temporal visual fields?

A

Pituitary adenoma

Disrupts optic chiasma

102
Q

Where are the vestibular and cochlea apparatus housed?

A

Petrous temporal bone within the bony labyrinth

103
Q

What fluid is in and around the cochlea?

A

Surrounded by Perilymph

Filled with Endolymph

104
Q

Which part of the cochlea is the sensory part for detecting sound?

A

Organ of corti

105
Q

Where are vibrations transmitted in the cochlea?

A

Transmitted from the oval window to the perilymph of cochlea

Then via the vestibular membrane into endolymph

106
Q

What do cell bodies of the cochlea nerve form? And where do these project to?

A

Spiral ganglion

Project to the cochlea nucleus in the pons/medulla

107
Q

Where are high and low frequency sounds detected in the cochlea?

A

Proximal cochlea - membrane narrow and stiff

Distal cochlea - membrane wide and flexy

108
Q

How is auditory information distributed in the cortex?

A 
Bilaterally
Via trapezoid body which decussates
Superior olivary nucleus
Inferior colliculus 
Medial geniculate body of thalamus
To primary auditory cortex
109
Q

What does loss of stereo-placement of sound indicate?

A

Cortical or thalamic problems

110
Q

What can cause tinnitus?

A

Méniere’s Disease, URTI or following exposure to loud sounds
Tensor tympani / stapedius myoclonus can cause tinnitus

111
Q

Describe the dynamic and static parts of the vestibular system

A

Dynamic Part - Formed from semicircular canals & crista
Acts mainly on eye movements via medial-longitudinal fasciculus
Static Part - Formed from maculae (utricular &saccular)
Acts via vestibulospinal pathway
Excite extensor muscles to keep you upright

112
Q

What are the maculae?

A

Maculae provide information relating to head position relative to trunk
& sense linear acceleration e.g. walking, driving, falling
Utriclar macula - Detect horizontal acceleration (e.g. driving)
Saccular macula - Detect vertical acceleration (e.g. falling)
Active with head in flexion or extension
Extensor activation in a fall (strong extensor thrust)
Active with head held to side

113
Q

Where are vestibular nuclei?

A

Ponto-medullary part of the brainstem
Modulated by cerebellum
Part of vestibulospinal tract

114
Q

What 3 inputs do we use for balance?

A

Vestibular
Visual
Proprioceptive

115
Q

What is Rombergs test and sign?

A

We remain stable if we have 2 out of 3 inputs for balance
If we lose 2 inputs we become unstable
Romberg’s test relies on this: Patient closes eyes, Patient sways/falls in positive test, Patient remains steady in a negative test

116
Q

What might be wrong in a Romberg positive patient?

A

Sensory ataxia
Tabes dorsalis - dorsal column damage
Vestibular system damage

117
Q

How can you assess visual acuity?

A

Snellen chart compares what we see at 6m (20ft)
Wear glasses/contacts
Under 40s should be at least 6/6 (20/20ft)
Acuity of <6/9 needs investigation in elderly
In situations of poor acuity ask patient to count digits, see movement, perceive light

118
Q

What things can reduce visual acuity?

A

Optic neuritis (infection spread from ethmoid sinus)
Refractive lens error
Parasympathetic

119
Q

How can you assess a patients visual fields?

A

Confrontation with patient staring directly ahead
Arms length
Cover one eye - compare Right-Left & Left-Right
Examiner compares to their own visual field
Use large red coloured pin
Blind spot mapped & drawn from patient’s perspective

120
Q

What could cause bi nasal hemianopia?

A

Internal carotid aneurysms

121
Q

What could cause bi temporal Hemianopia?

A

Pituitary adenoma

122
Q

What could cause Left Homonymous Hemianopia?

A

Right sided lesion - post chiasmic

123
Q

What can cause left upper quadrantopia?

A

Right temporal lobe tumour/infarct

124
Q

What can cause left lower quadrantopia?

A

Right parietal lobe tumour/infarct

125
Q

What can cause Bilateral central scotoma?

A

Occipital pole of visual cortex Falls/ impact and contusion

126
Q

What will you see on fundoscopy if papilloedema is present?

A

Raised disc
Blurred hyperaemic disc margins
Engorged vessels

127
Q

Which nuclei are responsible for the consensual light reflex?

A

Pretectal nucleus

Edinger Westphal nucleus

128
Q

Where is the ciliary ganglion and what does it do?

A

Posterior to the eye and acts on the pupil and ciliary body

129
Q

What is an Argyll Robertson (Prostitutes) pupil?

A

No pupillary light reflex but accommodation reflex/response OK
Cause: Neuro (3°) syphilis
Damage to pre tectal nuclei due to tabes dorsalis

130
Q

What does damage to the Edinger-Westphal nuclei result in?

A

No direct or consensual reflex on damaged side
Pupil dilated and unreactive
Cause: Vascular/tumour/brainstem

131
Q

What can CN III compression/vascular lesion result in?

A

Loss of direct and consensual reflex
Compression = loss of all CNIII functions
Vascular lesion = sparing of pupillary functions as parasymp fibers in outer part of nerve and can get alternate blood supply

132
Q

What can CN III, IV & VI lesions lead to?

A

Altered resting position of eye
Diplopia
Compensatory head movements

133
Q

What does Horizontal diplopia indicate?

A

Medial or lateral rectus issues

134
Q

What does Vertical diplopia indicate?

A

Issues with superior/inferior oblique or rectus

135
Q

What does CN III supply?

A

x4 muscles that move the eye
x1 that opens eyelid
sphincter pupillae and ciliary body

136
Q

What can a CNIII nerve lesion produce?

A

Complete ptosis
Divergent squint (down and out position of affected eye)
Horizontal and vertical diplopia
Dilated pupil that’s unreactive to direct or consensual light
Consensual pupil reflex intact in contralateral eye

137
Q

Describe the pathway of CN III

A

Originates in midbrain, exits via interpeducular fossa, passes through cavernous sinus & superior orbital fissure

138
Q

What can a CN IV lesion produce?

A

Upward deviation and extorsion of the eye
Torsional diplopia
Vertical diplopia: worse when descending stairs / reading paper
Tilt head away from lesion to help prevent diplopia (counteracts extorsion produced by inferior oblique)

139
Q

Describe the pathway of the trochlear nerve

A

Originates in midbrain, exits dorsal surface, decussates & passes through cavernous sinus & superior orbital fissure

140
Q

What will result from CN VI damage?

A

No lateral movement of the eye
Eye rests in adducted position, convergent squint
Horizontal diplopia
Diplopia worse when looking toward the affected side

141
Q

Describe the pathway of the abducens nerve

A

Originates at pontomedullary junction, passes across base of skull and turns angle to enter the cavernous sinus then passes through superior orbital fissure

142
Q

When is the abducens nerve at risk of damage?

A 
Raised ICP (compression as it turns into cavernous sinus) 
Internal carotid aneurysm in cavernous sinus
143
Q

What results from lesions of the MLF?

A

Internuclear opthalmoplegia

Cuts interneuron connections between CNVI and CNIII

144
Q

What is Hypometria (undershoot) a sign of?

A

cerebellar problems, Parkinson’s, Huntingtons

145
Q

What is a repetitive eye movement with a fast and slow phase?

A

Jerk nystagmus

described according to the fast phase

146
Q

Which side is the problem with a right nystagmus?

A

Left sided problem

147
Q

Where is the Trigeminal ganglion?

A

Petrous temporal bone

148
Q

Which cranial nerves sit in the cavernous sinus?

A

III, IV, VI, Va, Vb

Vc passes through foramen ovale in infra temporal fossa

149
Q

How can you test the trigeminal nerve sensory branches?

A

Test all 3 divisions (ophthalmic, maxillary, Mandibular) neurotip (sharp or dull), cotton wool
Look at anterior tongue – bite marks, ulceration
Look at eye for ulceration
Corneal reflex (CNVa afferent, CN VII efferent)
Numbness in one division suggests pathology after CN V ganglion
Combined CNVa & CNVb issues indicate cavernous sinus / superiororbital fissure problem

150
Q

What is Rogers sign?

A

Numb chin

Caused by inferior alveolar nerve compression

151
Q

How can you test the trigeminal nerve motor branch?

A

Bite down on tongue depressors look at tooth mark impression
Clench teeth – feel masseter & temporalis
Jaw jerk exaggerated in UMN lesions
Open mandible - deviates toward weak side due to opening action of medial pterygoid muscle

152
Q

Describe the pathway of the facial nerve

A

Exits the lateral pontomedullary junction and exits the skull via the internal acoustic meatus with CN VIII
Passes through the facial canal running close to IAM middle ear –middle ear infection could affect
Exits skull via stylomastoid foramen - risk of compression in baby during forcep delivery
Enters parotid, forms plexus and gives off 5 main branches: Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical

153
Q

What branches are given off the facial nerve in the facial canal?

A

Stapedius
Greater petrosal
Chorda tympani

154
Q

How can you test the facial nerve?

A

Look for facial asymmetry
Test muscle power L-R (resist opening eyes & mouth, show teeth)
Check ear for vesicles (Ramsay-Hunt) & parotid issues
Stapedius affected = complains of hyperacusis
Taste to anterior 2/3 of tongue (not normally tested)
Tears, nasal mucous and saliva (excluding parotid)
Upper motor neurone lesions spare forehead
LMN lesion causes full ipsilateral palsy

155
Q

Describe the path of the vestibulocochlear nerve

A

Exits the lateral pontomedullary junction, exits the skull via the internal acoustic meatus with CN VII and passes to the cochlea and vestibular apparatus

156
Q

How can you test the cochlear component of the vestibulocochlear nerve?

A

Inspect ear & EAM: Blood, Blockage, Polyp, Vesicles, Infection, Secretions
Test hearing in both ears (whispering 68 & 100)
Hearing tests use a 256 Hz tuning fork - Rinne - Tuning fork on mastoid till sound stops then hold in the air by the EAM Air conduction better than bone conduction Conduction deafness leads to no note at EAM (Rinne-negative)
Weber - Tuning fork on forehead ask where patient hears the sound/vibrating & if it is louder on one side (lateralises). Normally there is no lateralisation. Conduction deafness: Sound loudest in affected ear
Sensorineural deafness: Sound loudest in normal ear

157
Q

How can you test the vestibular nerve?

A

Tested if patient complains of vertigo
Hallpike manoeuvre: Start with sitting patient, Hold head between 2 hands, Get patient to lie back to 30° below horizontal, Examiner rotates head by 30° with eyes open, Positive test produces vertigo and rotatory nystagmus toward affected side. Benign paroxysmal positioning vertigo results in no repetition of test result for 10 min. Brainstem lesions have no latent period

158
Q

What functions are controlled by the glossopharyngeal nerve?

A

Sensation from the pharynx, posterior 1/3 of tongue, pharyngotympanic tube & middle ear
Sensation from the carotid body and sinus
Autonomic to parotid gland
Motor to stylopharyngeus

159
Q

What does the motor branch of the vagus supply?

A

Supplies pharyngeal constrictors, palatopharyngeus,
salpingopharyngeus, palatoglossus, levator veli palatini, all intrinsic muscles of larynx, cricothyroid & upper oesophagus

160
Q

How can you test cranial nerves IX and X?

A

Inspect the soft palate and oropharynx for asymmetry
Ask patient to phonate – palate & uvula pulled away from weak side
Touch pharynx to elicit gag reflex
Sensation but no contraction = CN X lesion
Assess character of voice
Assess swallowing (if appropriate)

161
Q

Damage to which nerves can lead to soft palate paralysis?

A

CN Vc - tensor veli palitini
CN X - levator veli palitini
Palate will be pulled away from the weak side

162
Q

What does the spinal part of CN XI supply?

A

Motor supply to trapezius & sternocleidomastoid

163
Q

How can you test the spinal part of cranial nerve XI?

A

Shrug shoulders
Axial rotation of neck & feel sternocleidomastoid
SCM weakness can lead to head turned to weak side at rest

164
Q

What does the Hypoglossal nerve supply?

A

Supplies all somatic muscle of the tongue - except palatoglossus

165
Q

How can you test the Hypoglossal nerve?

A

Protrude tongue – deviates to weak side
Look for wasting & fasciculation
Speed of left-right wiggling
Only LMN lesions lead to unilateral weakness

166
Q

What 3 things occur during the accommodation reflex?

A

Vergence
Pupillary constriction
Lens fattening

167
Q

Describe the process of lens fattening

A

Ciliary body contraction relaxes suspensory ligaments enabling the lens to recoil thus making it fatter

168
Q

Describe the pathway of the accommodation reflex that leads to medial vergence of the eyes

A

Retina to primary visual cortex

To frontal eye field to CN III nucleus to medial rectus muscles

169
Q

Describe pathway that leads to pupillary constriction and lens fattening in the accommodation reflex

A

Retina to primary visual cortex
To frontal eye field to Edinger Westphal nucleus
To ciliary ganglion to ciliary body and sphincter pupillae
Ciliary body causes lens fattening
Sphincter pupillae causes pupillary constriction

170
Q

What are the 3 muscles that control the eyelid and what is their supply?

A

Orbicularis oculi = closes (CN VII)
Levator palpebrae superioris = opens (CN III)
Superior tarsal muscle (smooth muscle) = opens (Sympathetic)

171
Q

What are the 3 axis that the eye can rotate around?

A

Transverse - look left or right
Sagittal - look up or down
Coronal - torsion, twist

172
Q

In what 3 ways can the eyes perform tracking movements?

A

Track target = Target moving
Stabilise target = You are moving target is not
Scan target to target = Saccade (fast movement)

173
Q

What areas of the brain contribute to control of eye movements?

A

Vestibular nuclei & parapontine reticular formation
Frontal eye field
Saccade centres (several locations)
Visual association areas

174
Q

What is the medial longitudinal fasciculus?

A

Neuronal tract that enables conjugate lateral gaze
Connects CNIII, IV and VI with vestibular nuclei, cerebellum & neck muscle lower motor neurons
CN VI nucleus wired up to contralateral CNIII nucleus
Involved in lateral gaze
Under automatic & voluntary control

175
Q

What can result from lesions to the medial longitudinal fasciculus?

A

Inter nuclear opthalmoplegia
Lose conjugate eye activity - medial and lateral rectus don’t work together
Able to converge during accommodation as this involves a different pathway

176
Q

Describe the process that brings about voluntary saccades

A

R Frontal eye field connects to contra L parapontine reticular formation
This connects to L VI nucleus which connects to contra R III nucleus via MLF
R frontal eye field has direct connection to R III nucleus
Overall response is look left

177
Q

When head is rotating axially in a given direction what makes both eyes look to the opposite side?

A

Vestibulo occular reflex
Lateral semicircular canals on same side as the direction the head is moving input to contra VI nucleus and then ipsi III nucleus

178
Q

What 3 things can make you look in the opposite direction?

What happens if any of these are damaged?

A

Vestibular nucleus
Frontal eye field
Lateral semicircular canal
Eyes drift toward the damaged side if damaged

179
Q

What is the cold caloric test?

A

Induce nystagmus & test brainstem function (Cold water cools fluid in lateral SCC causing it to move)
Eyes slowly looking toward cold water side
Fast correction to midline
Nystagmus will be away from side with cold water

180
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

Block 3 AR (8 decks)

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