Sensory Flashcards
What is acute pain?
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
What is chronic pain?
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
What is nociceptive pain?
Arises from the stimulation of specific pain receptors. These receptors can respond to heat, cold, vibration, stretch and chemical stimuli
released from damaged cells
What is neuropathic pain?
Arises from within the peripheral and central nervous system. Specific receptors do not exist here, with pain generated by nerve cell injury
What is wind up?
Frequency dependent increase in excitability due to activity of c fibers
What can be causes of chronic pain?
Badly Managed Acute Pain Emotionally Sensitive Patient Poor Coping Skills Previous Bad Pain Experiences Pain Goes on For Longer Surgical Complications Genetic Predisposition
What model is used to understand chronic pain?
Biopsychosocial model
Name some somatic nociceptive pain conditions
Lower back pain
Myofascial pain
Arthritis
Name some visceral nociceptive pain conditions
Pancreatitis
interstitial cystitis
endometriosis
Functional pain syndrome
Name some neuropathic pain conditions
Post-herpetic neuralgia (shingles) Neuroma Radicular pain (nerve root irritation) CRPS - complex regional pain syndrome Post-amputation pain
Describe malignant pain
80% of cancer patients suffer from pain Psychological component substantial Multiple etiologies Iatrogenic – CT, RT Other psychosocial factors
What are non pharmacological management options for pain?
Exercise
Physiotherapy
What is complementary therapy for pain?
Acupuncture
TENS - transcutaneous electrical nerve stimulation
Describe the WHO analgesia ladder
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
What drugs can act as adjuncts to treating pain?
Anticonvulsants - gabapentin, pregabalin
Antidepressants - amytryptaline
Lidocaine
Baclofen, benzodiazepines
What is the gold standard for cancer pain management?
Opioids
Describe why opioids should be used with caution to treat chronic pain
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
What invasive procedures can be used in chronic pain?
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
What types of sensory receptor exist?
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
What type of adaptation does the discriminative touch modality undergo?
Fast adaptation
What is located in the post central gyrus?
Primary sensory cortex
Receives contralateral sensory input from the body (inc taste)
What is located in the superior parietal lobule?
Integration of sensory inputs, sensory memory, perception of contralateral self & world
What is the internal capsule?
Dense collection of sensory and motor tracts passing to/from the cortex
What is the corona radiata?
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
Describe the structure of the internal capsule
Anterior limb – frontopontine, frontothalamic
Genu - bend
Posterior
Retrolenticular
Head, arm, leg, sensory, vision and hearing arranged somatotopically
How many neurons are involved from sensation up to the cortex?
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
How many Rexed lamina are there?
10
What is a funiculi? And how many are there in the spinal cord?
Bundles of more than 1 tract 3 Dorsal Lateral Ventral
What sensory modalities are carried in the dorsal funiculus?
Fine touch and proprioception from lower body
What modality tracts are carried in the lateral funiculus?
Motor supply to ipsilateral body
What sensory modalities are carried in the ventral funiculus?
Pain and temperature
What sensory modalities are carried by the dorsal column tracts?
Discriminative touch, vibration & conscious proprioception
What are the two parts of the dorsal column tracts?
Fasciculus cuneatus - above ~T6
Fasciculus gracilis - below ~T6
Describe the path that the dorsal columns follow
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
What sensory dysfunction can tertiary syphilis result in?
Tabes dorsalis
Destruction of dorsal columns
What does dorsal column damage cause?
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
What sensory modalities are carried by the spinothalamic tract?
Pain, temperature and simple tactile sensation
Describe the pathway of the spinothalamic tract
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
What is the trigeminal lemniscus?
Carries pain and temperature sensation from to the ventral posterior medial nucleus of the thalamus
What disorder can lead to disruption of the spinothalamic tract?
Syringomyelia - cavitation/expansion of central canal in cervical region Pain and temperature sensation lost in arms and top of chest
What is sacral sparing?
An expanding ventral grey matter tumour can knock out all contralateral pain & temperature sensation except sacral region due to somatotopic organisation of spinothalamic tract
What sensory modalities are carried in the spinocerebellar tract?
Unconscious proprioception to the ipsilateral cerebellum
Dorsal spinocerebellar tract - Muscle spindles, few Golgi tendon organs
Ventral spinocerebellar tract - Golgi tendon organs
Describe the pathway followed by the dorsal spinocerebellar tracts
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
Describe the pathway followed by the ventral spinocerebellar tracts
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
What information is carried by the ventral spinocerebellar tract?
Stretch of the tendon at the muscle tendon interface of the lower limb
What do pure lesions of the spinocerebellar tract cause?
Ataxia / malcoordination of motor action
Wide-based gait
Symptoms normally masked by motor weakness/paralysis
Describe the route of cranial nerve sensory nuclei
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
Describe where trigeminal touch sensation fibres pass
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
What sensory losses would result from a brainstem lesion?
Ipsilateral facial
Contralateral body
What are the thalami?
organised collection of nuclei of sensory, visual, auditory and motor-associated functions
Where do muscle spindle sensory fibres run?
Dorsal column & spinocerebellar pathways
Which afferent neurons carry sensation from muscle spindles?
1a afferents
What is nociceptive pain sensed by?
Free ending on C- and Aδ- fibres
Describe the gate control theory of pain
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
Where are the main output to descending tracts from higher pain centres?
Hypothalamus, periaqueductal gray and brainstem nuclei
Descending inhibition travels to ANS and spinal lamina in dorsolateral
funiculus where 5HT and NA dominant
What drugs are used to treat neuropathic pain?
Tricyclic antidepressants and anti epileptic drugs
Gabapentin+Amitriptyline in combo
Carbemazepine alone - never in combo
How many subclasses of NSAIDs are there?
6
Describe the mechanism of action of NSAIDs as painkillers
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
How do prostaglandins lead to increased pain?
Act on prostaglandin receptor which is GPCR which leads to opening of voltage gated Na channels and therefore increased depolarisation of nociceptors
What are clinical uses of NSAIDs?
Anti-inflammation Anti-pyretic Analgesic Anti-coagulant May delay healing, not used post operatively, post partum
Describe some commonly used NSAIDs
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
List some common side effects of NSAIDs
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
Which drugs can interact with NSAIDs?
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
What is salicylism?
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
What are the 4 main groups of synthetic derivatives of opioids?
Phenylpiperidine series (e.g. pethidine) Methadone series (e.g. dextropropoxyphene) Benzomorphan series (e.g. cyclazocine) Thebaine derivatives (e.g. buprenorphine)
What are pure agonist opioids?
Full agonist activity, may have strong (e.g. morphine, diamorphine,
tramadol) or weak activity (e.g. codeine, dihydrocodeine)
What are partial opioid agonists?
Can be used for addiction rehabilitation
e.g. nalorphine, pentazocine, buprenorphine
What are opioid antagonists?
Used in overdose
e.g.naloxone, naltrexone
What are clinical uses of opioids?
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)
Where are sites of opioid action?
Peri aqueductal gray
Nucleus Raphe Paragigantocellularis in medulla
Dorsal horn
Periphery
Describe the mechanism for opioid drugs
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
Describe opioid metabolism
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
What are some opioid drug half lives?
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
What are advantages and disadvantages of methods of opioid administration?
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
What are side effects of opioid drug use?
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
What are indicators of opioid overdose?
Pupillary constriction
Respiratory depression
Coma (GCS<7)
Describe the management of opioid overdose
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
What are the different categories of headaches?
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!
What is the cribriform plate?
CN I fibres pass from olfactory mucosa to olfactory bulb via cribriform plate
What can be causes of unilateral anosmia?
Meningioma
Anterior cranial fossa tumour
Where does the Olfactory tract carries sensory neurons to?
Orbital and piriform cortexes
Where do Olfactory pathways link to?
Brainstem
Limbic system
Hypothalamus
What can cause a loss of taste or smell?
Viral infection Parkinsons (early sign) Alzheimers (early sign) Meningioma (olfactory groove) Anterior cranial fossa fracture
What are 3 types of tongue papilla?
Fungiform
Filiform - anterior 2/3, no taste buds
Vallate
Which cranial nerve carries taste from anterior 2/3 tongue? And which from posterior 1/3 tongue?
CN VII anterior
CN IX posterior
Describe the pathway of the taste sensation from the anterior tongue
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
What is the region of greatest visual acuity in the eye?
Fovea centralis
What are the 3 layers of the eye?
Retina
Choroid - vascular
Sclera - white
Where is the fovea?
In the centre of the macula densa, yellow spot in eye
Where is the blind spot?
Optic papilla
Where does the left part of the visual field enter the eye?
Right part of both retinas
What are retinal fields?
Region of the retina that is named according to its position relative to the nose or temporal region
What information is carried in the optic chiasma?
Temporal visual field information to contralateral cortex
Where does the stalk of optic radiation run?
Retrolenticular internal capsule
What is Meyers loop?
Optic radiation
Sits inferiorly in temporal lobe & contains upper contralateral visual field
Project to gyri around calcarine sulcus of occipital lobe
Where does the macula project to? And why might it be spared when there is a primary visual cortex lesion?
Occipital pole
Receives different blood supply
What do vascular lesions of the primary visual cortex cause?
Homonymous hemianopia
Blindness or defective vision in right or left halves of visual fields in both eyes
How do you measure visual acuity?
Snellen chart, count digits, movement, light perception
How do you assess someone’s visual fields?
Confrontation with patient staring directly ahead
Examiner compares to their own visual field
Use large red coloured pin
Blind spot mapped (scotoma)
How do you perform fundoscopy?
Examine cornea and lens first
Patient gazes into distance
Disc is a shallow cup with clear margins
Disc = yellow, Fundus = red
What can cause a lack of vision in bilateral temporal visual fields?
Pituitary adenoma
Disrupts optic chiasma
Where are the vestibular and cochlea apparatus housed?
Petrous temporal bone within the bony labyrinth
What fluid is in and around the cochlea?
Surrounded by Perilymph
Filled with Endolymph
Which part of the cochlea is the sensory part for detecting sound?
Organ of corti
Where are vibrations transmitted in the cochlea?
Transmitted from the oval window to the perilymph of cochlea
Then via the vestibular membrane into endolymph
What do cell bodies of the cochlea nerve form? And where do these project to?
Spiral ganglion
Project to the cochlea nucleus in the pons/medulla
Where are high and low frequency sounds detected in the cochlea?
Proximal cochlea - membrane narrow and stiff
Distal cochlea - membrane wide and flexy
How is auditory information distributed in the cortex?
Bilaterally Via trapezoid body which decussates Superior olivary nucleus Inferior colliculus Medial geniculate body of thalamus To primary auditory cortex
What does loss of stereo-placement of sound indicate?
Cortical or thalamic problems
What can cause tinnitus?
Méniere’s Disease, URTI or following exposure to loud sounds
Tensor tympani / stapedius myoclonus can cause tinnitus
Describe the dynamic and static parts of the vestibular system
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
What are the maculae?
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
Where are vestibular nuclei?
Ponto-medullary part of the brainstem
Modulated by cerebellum
Part of vestibulospinal tract
What 3 inputs do we use for balance?
Vestibular
Visual
Proprioceptive
What is Rombergs test and sign?
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
What might be wrong in a Romberg positive patient?
Sensory ataxia
Tabes dorsalis - dorsal column damage
Vestibular system damage
How can you assess visual acuity?
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
What things can reduce visual acuity?
Optic neuritis (infection spread from ethmoid sinus)
Refractive lens error
Parasympathetic
How can you assess a patients visual fields?
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
What could cause bi nasal hemianopia?
Internal carotid aneurysms
What could cause bi temporal Hemianopia?
Pituitary adenoma
What could cause Left Homonymous Hemianopia?
Right sided lesion - post chiasmic
What can cause left upper quadrantopia?
Right temporal lobe tumour/infarct
What can cause left lower quadrantopia?
Right parietal lobe tumour/infarct
What can cause Bilateral central scotoma?
Occipital pole of visual cortex Falls/ impact and contusion
What will you see on fundoscopy if papilloedema is present?
Raised disc
Blurred hyperaemic disc margins
Engorged vessels
Which nuclei are responsible for the consensual light reflex?
Pretectal nucleus
Edinger Westphal nucleus
Where is the ciliary ganglion and what does it do?
Posterior to the eye and acts on the pupil and ciliary body
What is an Argyll Robertson (Prostitutes) pupil?
No pupillary light reflex but accommodation reflex/response OK
Cause: Neuro (3°) syphilis
Damage to pre tectal nuclei due to tabes dorsalis
What does damage to the Edinger-Westphal nuclei result in?
No direct or consensual reflex on damaged side
Pupil dilated and unreactive
Cause: Vascular/tumour/brainstem
What can CN III compression/vascular lesion result in?
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
What can CN III, IV & VI lesions lead to?
Altered resting position of eye
Diplopia
Compensatory head movements
What does Horizontal diplopia indicate?
Medial or lateral rectus issues
What does Vertical diplopia indicate?
Issues with superior/inferior oblique or rectus
What does CN III supply?
x4 muscles that move the eye
x1 that opens eyelid
sphincter pupillae and ciliary body
What can a CNIII nerve lesion produce?
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
Describe the pathway of CN III
Originates in midbrain, exits via interpeducular fossa, passes through cavernous sinus & superior orbital fissure
What can a CN IV lesion produce?
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)
Describe the pathway of the trochlear nerve
Originates in midbrain, exits dorsal surface, decussates & passes through cavernous sinus & superior orbital fissure
What will result from CN VI damage?
No lateral movement of the eye
Eye rests in adducted position, convergent squint
Horizontal diplopia
Diplopia worse when looking toward the affected side
Describe the pathway of the abducens nerve
Originates at pontomedullary junction, passes across base of skull and turns angle to enter the cavernous sinus then passes through superior orbital fissure
When is the abducens nerve at risk of damage?
Raised ICP (compression as it turns into cavernous sinus) Internal carotid aneurysm in cavernous sinus
What results from lesions of the MLF?
Internuclear opthalmoplegia
Cuts interneuron connections between CNVI and CNIII
What is Hypometria (undershoot) a sign of?
cerebellar problems, Parkinson’s, Huntingtons
What is a repetitive eye movement with a fast and slow phase?
Jerk nystagmus
described according to the fast phase
Which side is the problem with a right nystagmus?
Left sided problem
Where is the Trigeminal ganglion?
Petrous temporal bone
Which cranial nerves sit in the cavernous sinus?
III, IV, VI, Va, Vb
Vc passes through foramen ovale in infra temporal fossa
How can you test the trigeminal nerve sensory branches?
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
What is Rogers sign?
Numb chin
Caused by inferior alveolar nerve compression
How can you test the trigeminal nerve motor branch?
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
Describe the pathway of the facial nerve
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
What branches are given off the facial nerve in the facial canal?
Stapedius
Greater petrosal
Chorda tympani
How can you test the facial nerve?
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
Describe the path of the vestibulocochlear nerve
Exits the lateral pontomedullary junction, exits the skull via the internal acoustic meatus with CN VII and passes to the cochlea and vestibular apparatus
How can you test the cochlear component of the vestibulocochlear nerve?
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
How can you test the vestibular nerve?
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
What functions are controlled by the glossopharyngeal nerve?
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
What does the motor branch of the vagus supply?
Supplies pharyngeal constrictors, palatopharyngeus,
salpingopharyngeus, palatoglossus, levator veli palatini, all intrinsic muscles of larynx, cricothyroid & upper oesophagus
How can you test cranial nerves IX and X?
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)
Damage to which nerves can lead to soft palate paralysis?
CN Vc - tensor veli palitini
CN X - levator veli palitini
Palate will be pulled away from the weak side
What does the spinal part of CN XI supply?
Motor supply to trapezius & sternocleidomastoid
How can you test the spinal part of cranial nerve XI?
Shrug shoulders
Axial rotation of neck & feel sternocleidomastoid
SCM weakness can lead to head turned to weak side at rest
What does the Hypoglossal nerve supply?
Supplies all somatic muscle of the tongue - except palatoglossus
How can you test the Hypoglossal nerve?
Protrude tongue – deviates to weak side
Look for wasting & fasciculation
Speed of left-right wiggling
Only LMN lesions lead to unilateral weakness
What 3 things occur during the accommodation reflex?
Vergence
Pupillary constriction
Lens fattening
Describe the process of lens fattening
Ciliary body contraction relaxes suspensory ligaments enabling the lens to recoil thus making it fatter
Describe the pathway of the accommodation reflex that leads to medial vergence of the eyes
Retina to primary visual cortex
To frontal eye field to CN III nucleus to medial rectus muscles
Describe pathway that leads to pupillary constriction and lens fattening in the accommodation reflex
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
What are the 3 muscles that control the eyelid and what is their supply?
Orbicularis oculi = closes (CN VII)
Levator palpebrae superioris = opens (CN III)
Superior tarsal muscle (smooth muscle) = opens (Sympathetic)
What are the 3 axis that the eye can rotate around?
Transverse - look left or right
Sagittal - look up or down
Coronal - torsion, twist
In what 3 ways can the eyes perform tracking movements?
Track target = Target moving
Stabilise target = You are moving target is not
Scan target to target = Saccade (fast movement)
What areas of the brain contribute to control of eye movements?
Vestibular nuclei & parapontine reticular formation
Frontal eye field
Saccade centres (several locations)
Visual association areas
What is the medial longitudinal fasciculus?
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
What can result from lesions to the medial longitudinal fasciculus?
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
Describe the process that brings about voluntary saccades
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
When head is rotating axially in a given direction what makes both eyes look to the opposite side?
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
What 3 things can make you look in the opposite direction?
What happens if any of these are damaged?
Vestibular nucleus
Frontal eye field
Lateral semicircular canal
Eyes drift toward the damaged side if damaged
What is the cold caloric test?
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
What is pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
