Neuro Flashcards
(82 cards)
Cranial nerves general inspection
Speech abnormalities: may indicate glossopharyngeal or vagus nerve pathology.
Facial asymmetry: suggestive of facial nerve palsy.
Eyelid abnormalities: ptosis may indicate oculomotor nerve pathology.
Pupillary abnormalities: mydriasis occurs in oculomotor nerve palsy.
Strabismus: may indicate oculomotor, trochlear or abducens nerve palsy.
Limbs: pay attention to the patient’s arms and legs as they enter the room and take a seat noting any abnormalities (e.g. spasticity, weakness, wasting, tremor, fasciculation) which may suggest the presence of a neurological syndrome).
Medical paraphernalia of neuro disease
Walking aids: gait issues are associated with a wide range of neurological pathology including Parkinson’s disease, stroke, cerebellar disease and myasthenia gravis.
Hearing aids: often worn by patients with vestibulocochlear nerve issues (e.g. Ménière’s disease).
Visual aids: the use of visual prisms or occluders may indicate underlying strabismus.
Prescriptions: prescribing charts or personal prescriptions can provide useful information about the patient’s recent medications.
Causes of anosmia
Mucous blockage of the nose: preventing odours from reaching the olfactory nerve receptors.
Head trauma: can result in shearing of the olfactory nerve fibres leading to anosmia.
Genetics: some individuals have congenital anosmia.
Parkinson’s disease: anosmia is an early feature of Parkinson’s disease.
COVID-19: transient anosmia is a common feature of COVID-19.
Causes of decreased visual acuity
Refractive errors
Amblyopia
Ocular media opacities such as cataract or corneal scarring
Retinal diseases such as age-related macular degeneration
Optic nerve (CN II) pathology such as optic neuritis
Lesions higher in the visual pathways
Relative afferent pupillary defect
When the afferent limb in one of the optic nerves is damaged, partially or completely, both pupils will constrict less when light is shone into the affected eye compared to the healthy eye. The pupils, therefore, appear to relatively dilate when swinging the torch from the healthy to the affected eye.
sign of retinal damage: optic neuritis, CRVO, CRAO, larger retinal detachment, unilateral advanced glaucoma, compression secondary to tumour or abscess.
Unilateral efferent defect
commonly caused by extrinsic compression of the oculomotor nerve, resulting in the loss of the efferent limb of the ipsilateral pupillary reflexes. As a result, the ipsilateral pupil is dilated and non-responsive to light entering either eye (due to loss of ciliary sphincter function). The consensual light reflex in the unaffected eye would still be present as the afferent pathway (i.e. optic nerve) of the affected eye and the efferent pathway (i.e. oculomotor nerve) of the unaffected eye remain intact.
Colour vision deficiencies
Optic neuritis: results in a reduction of colour vision (typically red).
Vitamin A deficiency
Chronic solvent exposure
Visual neglect/inattention
= deficit in awareness in one side of visual field
usually parietal lobe injury after stroke
differentiate between true visual field loss (optic nerve) and inattention (cerebral hemisphere)
Visual extinction
patient can’t identify one of the moving fingers when a finger on both hands is wiggling simultaneously. They can, however, identify each of them when they’re wiggled individually.
Visual field defects
bitemporal hemianopia
homonymous field defects
scotoma
monocular vision loss
Bitemporal hemianopia
loss of the temporal visual field in both eyes resulting in central tunnel vision.
result of optic chiasm compression by a tumour (e.g. pituitary adenoma, craniopharyngioma).
Homonymous field defects
affect the same side of the visual field in each eye and are commonly attributed to stroke, tumour, abscess (i.e. pathology affecting visual pathways posterior to the optic chiasm). These are deemed hemianopias if half the vision is affected and quadrantanopias if a quarter of the vision is affected.
Scotoma
an area of absent or reduced vision surrounded by areas of normal vision. There is a wide range of possible aetiologies including demyelinating disease (e.g. multiple sclerosis) and diabetic maculopathy.
Monocular vision loss
total loss of vision in one eye secondary to optic nerve pathology (e.g. anterior ischaemic optic neuropathy) or ocular diseases (e.g. central retinal artery occlusion, total retinal detachment).
Causes of ptosis
Oculomotor nerve pathology
Horner’s syndrome
Neuromuscular pathology (e.g. myasthenia gravis)
Oculomotor nerve palsy
The oculomotor nerve supplies all extraocular muscles except the superior oblique (CNIV) and the lateral rectus (CNVI). Oculomotor palsy (a.k.a. ‘third nerve palsy’), therefore, results in the unopposed action of both the lateral rectus and superior oblique muscles, which pull the eye inferolaterally. As a result, patients typically present with a ‘down and out’ appearance of the affected eye.
Oculomotor nerve palsy can also cause ptosis (due to a loss of innervation to levator palpebrae superioris) as well as mydriasis due to the loss of parasympathetic fibres responsible for innervating to the sphincter pupillae muscle.
Trochlear nerve palsy (CN IV)
innervates is the superior oblique muscle. As a result, trochlear nerve palsy (‘fourth nerve palsy’) typically results in vertical diplopia when looking inferiorly, due to loss of the superior oblique’s action of pulling the eye downwards. Patients often try to compensate for this by tilting their head forwards and tucking their chin in, which minimises vertical diplopia. Trochlear nerve palsy also causes torsional diplopia (as the superior oblique muscle assists with intorsion of the eye as the head tilts). To compensate for this, patients with trochlear nerve palsy tilt their head to the opposite side, in order to fuse the two images together.
Abducens nerve palsy (CN VI)
The abducens nerve (CN VI) innervates the lateral rectus muscle. Abducens nerve palsy (‘sixth nerve palsy’) results in unopposed adduction of the eye (by the medial rectus muscle), resulting in a convergent squint. Patients typically present with horizontal diplopia which is worsened when they attempt to look towards the affected side.
Facial nerve palsy
Facial nerve palsy caused by a lower motor neuron lesion presents with weakness of all ipsilateral muscles of facial expression, due to the loss of innervation to all muscles on the affected side. The most common cause of lower motor neuron facial palsy is Bell’s palsy.
Facial nerve palsy caused by an upper motor neuron lesion also presents with unilateral facial muscle weakness, however, the upper facial muscles are partially spared because of bilateral cortical representation (resulting in forehead/frontalis function being somewhat maintained). The most common cause of upper motor neuron facial palsy is stroke.
Rinne’s test
Normal result: air conduction > bone conduction (Rinne’s positive)
Sensorineural deafness: air conduction > bone conduction (Rinne’s positive) – due to both air and bone conduction being reduced equally
Conductive deafness: bone conduction > air conduction (Rinne’s negative)
Weber’s test
Normal: sound is heard equally in both ears.
Sensorineural deafness: sound is heard louder on the side of the intact ear.
Conductive deafness: sound is heard louder on the side of the affected ear.
Conductive vs sensorineural hearing loss
Conductive hearing loss occurs when sound is unable to effectively transfer at any point between the outer ear, external auditory canal, tympanic membrane and middle ear (ossicles). Causes of conductive hearing loss include excessive ear wax, otitis externa, otitis media, perforated tympanic membrane and otosclerosis.
Sensorineural hearing loss occurs due to dysfunction of the cochlea and/or vestibulocochlear nerve. Causes of sensorineural hearing loss include increasing age (presbycusis), excessive noise exposure, genetic mutations, viral infections (e.g. cytomegalovirus) and ototoxic agents (e.g. gentamicin).
Hypoglossal nerve palsy
causes atrophy of the ipsilateral tongue and deviation of the tongue when protruded towards the side of the lesion. This occurs due to the overaction of the functioning genioglossus muscle on the unaffected side of the tongue.
Vagus nerve lesion
asymmetrical elevation of palate
uvula deviation away from lesion
inability to close glottis (weak cough)
absence of gag reflex (+glossopharyngeal)
change to voice quality (+glossopharyngeal)
