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Oral med > Cranial nerve disorders > Flashcards

Cranial nerve disorders Flashcards

1
Q

What are the twelve cranial nerves?

A

 I – Olfactory (S)
 II – Optic (S)
 III – Oculomotor (M)  IV – Trochlear (M)
 V – Trigeminal (S/M)  VI – Abducens (M)

 VII – Facial (S/M)
 VIII – Vestibulocochlear (S)  IX – Glossopharyngeal (S/M)  X – Vagus (S/M)
 XI – Accessory (M)
 XII – Hypoglossal (M)

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2
Q

What does cranial nerve 1 do?

A
  • Smell perception.
  • Olfactory receptor cells found in the mucous membrane of the nasal cavity

 CN I passes through the cribiform plate of the ethmoid bone and continues to reach the cerebral cortex

 Collateral fibres to amygdala and hippocampus

 To be perceived as an odour an inhaled substance must be soluble in water

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3
Q

How do you test cranial nerve one?

A

 Ask if any problems with smell
 Use of an odorous object e.g. an orange, coffee to test each nostril

individually

 Further investigation may involve CT/MRI brain or other appropriate neurological investigations

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4
Q

What pathology can occur with problems with CN1?

A

Anosmia ( loss of smell)

Dysosmia (smell alteration)

olfactory halucinations

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5
Q

What can cause anosmia?

A

 Congenital absence of receptors – Kallman Syndrome, Albinism
 Psychogenic (taste usually intact)
 Nasal obstruction/rhinitis
 Cribiform plate pathology – Head injury/skull fracture, Cranial surgery, SAH  Central pathology – Tumours, Aneurysms, Meningitis, Sarcoidosis, MS

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6
Q

What can cause dysosmia?

A

 Depression
 Local nasopharyngeal conditions

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7
Q

What can cause olfactory halucinations?

A

 Temporal lobe disease - Epilepsy (complex partial seizures)

 Psychiatric disease – Depression, Schizophrenia

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8
Q

What can cause reduced odour recognition?

A

Alzeihmers

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9
Q

How does the visual pathway work?

A

Retinal nerve cells converge at the optic disc to form the optic nerve

 At the optic chiasm lateral fibres continue in the ipsilateral optic tract, however medial fibres decussate (cross) into the contralateral optic tract

 Fibres run to the visual cortex in the occipital lobe of the brain

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10
Q

What will occur with left optic nerve compression?

A

Defect on left side

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11
Q

1) What visual defects will occur with chiasm compressions from pituitory tumour?
2) What visual defects occur with a left cerbrovascular event?

A

1) bitemporal hemianopia
2) homonymous hemianopia

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12
Q

How do you test CN2?

A

Visual acuity – Snellen chart

Visual fields

Pupillary reflexes – (PERLA) (Note CN III involvement)

 Light

Accommodation

Fundoscopy

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13
Q

What CN2 pathology is there?

A

Eye lesions – Cateracts, Glaucoma, Migraine, Vitreous haemorrhage, Infarction, Infection e.g. Choreoretinitis (CMV)

 Optic nerve/chiasm/tract
 Ischaemia – Giant cell arteritis, Thrombus /Embolism, Systemic hypotension, other

connective tissue disorders

 Demyelination – MS (optic neuritis)

 Pressure – Tumour –a pituitary adenoma in particular can cause pressure on the optic chiasm, Grave’s disease, Paget’s disease, Aneurysms

 Raised intracranial pressure

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14
Q

Cranial nerves 3,4 6, what are their functions?

A

They are motor nerves that supply the extraocular muscles and elevators of the upper eyelid.

Muscle action is coordinated to give both rapid eye movements (saccades) and smooth pursuit eye movements. The cerebellum plays a role in this coordination.

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15
Q

What muscles move your eyes?

A
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16
Q

What muscles do CN3 (occulomotor) innervate?

A

All the muscles around the eye except Lateral rectus and superior oblique

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17
Q

What nerve supplies lateral rectus?

A

abducens

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18
Q

What nerve supplies superio oblique?

A

Trochlea nerve.

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19
Q

What pathology is associated with CN3,4,6?

A

 Any pathology affecting the brainstem, cavernous sinus, superior orbital fissure

or orbit can cause dysfunction of these cranial nerves.

 Nystagmus is a pattern of involuntary eye movement that can be physiological or pathological. Cerebellar and vestubular pathology often presents with nystagmus.

 Ptosis is drooping of the upper eyelid. It may be seen in CN III lesions, stroke, myaesthenia gravis, muscular dystrophies and Horner’s syndrome.

 Horner’s syndrome occurs when there is damage to the oculosympathetic pathway. It presents as unilateral ptosis, miosis and anhidrosis.

Most common presenting complaint is diplopia

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20
Q

What is cranial nerve5? What are the different branches and what do they innervate?

A

Trigeminal Nerve

Va) Opthalmic division- Innervates, scalp and forehead, cornea and nose (including corneal reflex)

Vb)Maxillary division

 Sensation of skin over lower eyelid, cheek and upper jaw, midlateral nose and lateral part of

alar, upper lip, upper teeth and palate

 Passes to the trigeminal ganglion via the foramen rotundum

 Vc Mandibular division

 Sensation of skin over temple, lower jaw (sparing the angle of the mandible C2/3 nerve roots),

lower lip, anterior tongue, lower teeth and floor of mouth

 Motor supply to muscles of mastication

 Enters/exits the skull via the foramen ovale

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21
Q

How can you test CN5 function?

A

To test the sensory element-

  • Have the patient close their eyes and use cotton wool to touch the three sensory areas on both sides, asking the patient to say if/when they feel something
  • Corneal reflex test – use a wisp of cotton wool to touch over the cornea (over the iris). Normal response is a blink on both sides.
22
Q

How to test the motor element of CN5?

A

Feel the masseters and temporalis muscles with the teeth clenched. Ask the patient to open their mouth passively (jaw may deviate to the affected side) and then against resistance (looking for general weakness)

23
Q

What are the signs of CNV pathology?

A

 Unilateral sensory loss over the face/tongue/buccal mucosa

 Absent corneal reflex

 Jaw deviation on opening towards the affected side

 Wasting of muscles of mastication

 Trigeminal neuralgia

 Sudden, severe, recurrent stabbing pains in the distribution of one or more branches of the Vth cranial nerve.

24
Q

What CNV pathology can be present?

A

 Brainstem lesions – MS, Infarction, Syringobulbia

 Cerebellopontine angle lesions – Acoustic neuroma, Meningioma

 Cavernous sinus lesions – Thrombosis, ICA aneurysm

 Peripheral lesions – Orbital cellulitis/trauma, Maxillary or Mandibular infection or tumour, Skull fracture, Peripheral neuropathies.

 Trigeminal neuralgia

25
Q

What does Cranial nerve 7 supply

A

Intracranial branches:
 Greater petrosal nerve  Nerve to stapedius mm.  Chorda tympani

 Extracranial branches:
 Posterior auricular nerve
 Nerve to stylohyoid and posterior belly of digastric mm.  5 major facial branches

26
Q

What are the 5 extra oral facial branches?

A

Temporal

Zygomatic

Buccal

Mandibular

Cervical

27
Q

How to tes cranial nerve VII?

A

 Ask patient to:
 Scrunch up their eyes

 Raise eyebrows
 Blow out cheeks
 Show teeth

 Schirmer’s test to evaluate lacrimal function

28
Q

What is CNVII main actions?

A

 Motor supply to muscles of facial expression and stapedius muscle.

 PSNS to salivary and lacrimal glands
 Sensory from skin around the EAM
 Taste from anterior 2/3rds of the tongue

29
Q

What CNVII pathology can be present?

A

 Cerebral cortex – Stroke, Tumour
 Brainstem – Stroke, Tumour, MS
 Cerebellopontine angle – Acoustic neuroma, Meningioma
 Geniculate ganglion – Herpes zoster (Ramsey Hunt syndrome)
 Facial canal – Bell’s palsy
 Petrous temporal bone – Skull fracture
 Facial nerve branches – Parotid tumour/infection, Facial trauma/lacerations
 Facial mononeuropathy – Vasculitis, Sarcoidsis, Behcets’s syndrome, Sjogren’s syndrome, DM

30
Q

What is an upper motor neurone?

A

UMN

A motor neurone that originates in the motor cortex or brainstem and carries motor information down to LMNs

31
Q

What is a lower motor neurone?

A

Originate in the spinal cord or brainstem nuclei and carry motor information to effector organs

32
Q

What facial weakness do you get with a) upper motor neurone pathology or B) lower motor neurone pathology

A
33
Q

What is bells palsy?

A

A unilateral, lower motor neurone facial paralysis that is thought to be due to acute viral inflammatory demyelination of the facial nerve, causing swelling and secondary nerve ischaemia within the facial canal.

34
Q

What are the clinical features of bells palsy?

A
35
Q

How do you treat Bell’s palsy?

A

 Can resolve fully without any treatment
 Prednisolone 50mg PO for 5 days
 Aciclovir
 Avoidance of complications – eye patch, lubricating eye drops

36
Q

What is the prognosis of bells palsy?

A

60-80% make a full recovery

Recovery usually begins within 8 weeks and is complete by 6-12 months

Residual defects may include facial weakness, ‘crocodile tears’ (gustatory crying) and synkinesias including ‘jaw winking’

Poor prognostic factors are

  •  Profound facial weakness  Reduced tearing
     Hyperacusis

 Older age
 Systemic hypertension, diabetes or psychiatric illness

37
Q

What is ramsey hunt syndrome?

A

A reactivation of the herpes varicella zoster virus (shingles) affecting the facial nerve.

Symptoms/signs

Otalgia

Hearing loss

Vesicles in the external ear canal and

palate

Ipsilateral facial paralysis

Possible tinnitus or vertigo

Treatment: antiviral medication

38
Q

WHAT IS CNVIII’s function?

A

Vestibular nerve – Sensory nerve involved with balance, carrying information from the vestibular apparatus

 Cochlear nerve – Sensory nerve involved with hearing, carrying information from receptor hair cells in the organ of corti within the cochlear

39
Q

What is the CNVIII pathology?

A

Brainstem - MS, Stroke, Tumour
Cerebello-pontine angle – Acoustic neuroma, meningioma
Base of skull – Paget’s disease, nasopharyngeal carcinoma, meningitis

 Peripheral pathology

Ototoxins – Furosemide, Aminogylcoside antibiotics (gentamicin)

Benign Paroxysmal Positional Vertigo (BPPV) – episodic vertigo of brief duration induced by head movements. Usually due to cupulolithiasis of the semicircular canals. Treated with Epley head manoeuvres

Vestibular neuronitis- acute, usually non-recurrent vertigo without hearing loss or tinnitus

 ** Menieres disease** – recurrent severe vertigo with unilateral hearing loss and tinnitus

40
Q

What are the clinical features of CNVIII pathology?

A

 Deafness (sensorineural deafness)  Tinnitus
 Vertigo

 Nystagmus – (rapid involuntary movement of the eyes) horizontal or rotatory nystagmus, fast beats away from the side of the lesion

41
Q

How to test CNVIII?

A

Testing of hearing:
 Vocal distraction testing - a general screen
 Tuning fork testing (512Hz) – to distinguish sensorineural and conductive deafness

 Weber – tuning fork held at midline forehead
 Rinne – tuning fork held by each ear and then on the mastoid process.

Normal = Air conduction is louder than bone conduction

 Testing of balance:  Turning test

42
Q

Function of glossopharyngeal nerve?

A

 Sensation from middle ear, pharynx and posterior 2/3rds of the tongue  Taste from posterior 2/3rds of the tongue
 Motor to stylopharyngeus muscle
 PSNS to the parotid gland (via the otic ganglion)

43
Q

What is the function of the vagus nerve?

A

 Sensation from larynx, pharynx, EAM, tympanic membrane

 Visceral sensation from many body organs
 Motor to muscles of the larynx, pharynx and soft palate
 PSNS to various viscera

44
Q

What pathology can occur with Vagus nerve pathology?

A

 Ipsilateral palatal/pharyngeal weakness – nasal speech, regurgitation of food into nose, dysphagia, asymmetric palatal movement (uvula moves away from side of lesion)

 Ipslateral vocal cord weakness – hoarseness, dysphonia, weak (bovine) cough, asymmetric vocal cord weakness

 Loss of sensation over the EAM

 Systemic issues such as cardiac arrhythmias, constipation, incontinence

45
Q

What pathology can present with the glossopharyngeal nerve?

A

CN IX lesions present with ipsilateral loss of pharyngeal sensation.

46
Q

How do glossophayngeal and vagus combined lesions present?

A

They have the symptoms of isolated gloospharyngeal and vagus in addition to loss of gag reflex

47
Q

The recurrent laryngeal nerve is a branch of the Vagus, which side is more commonly assosciated with pathology? and what causes RLN pathology?

A

The left RLN loops under the aortic arch and is more commonly damaged than the right RLN.

48
Q

How do you test the function of nerves 9 and 10?

A

 Look at the uvula and ask the patient to say ‘ahh’. Deviation to one side suggests a CN X lesion on the opposite side

 Assessment of cough and swallow

 Gag reflex

49
Q

What does the accesory nerve (CNXI) supply?

A

Spinal part- comes from C1-C5 anterior horns and supplys the trapeziusand sternocleidomastoid

cranial part- motor supply of muscles to larynx,pharynx and soft palate.

50
Q

How to test the accesory nerve?

A

 Shrug their shoulders (Trapezius)
 Turn their head to each side against resistance (SCM)

51
Q

What does the hypoglossal nerve supply?

A

Motor supply to the muscles of the tongue.

It contributes to speech and swallowing

52
Q

How do you test CN12 function?

A

Assess the tongue at rest in the mouth for fasciculations and atrophy

 Ask the patient to stick out their tongue. The tongue may deviate to the side of any lesion present.

Oral med (18 decks)

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