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Neurology Systems > Week 2 > Flashcards

Week 2 Flashcards

1
Q

describe refraction

A
  • bending of light when it passes from one optical medium to another.
  • light rays bend to form a sharp image on the retina
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2
Q

describe accommodation

A
  • we can focus on far off or near objects by changing how much we bend the light rays
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3
Q

which parts of the eye allow for light refraction?

A
  • cornea, aqueous humor, lens and vitreous humour are transparent to allow light to fall on the retina.
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4
Q

which part of the eye is the most powerful ‘bender’ of light?

A
  • cornea is the most powerful ‘bender’ of light (45D), but lens (15D) has the capacity to change its ‘bending power’.
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5
Q

how does the lens (pupil) change when an object becomes closer?

A
  • when an object comes closer, the eye needs more bending power to focus on an object > the lens becomes thicker and hence more powerful, and a clear image is formed on the retina again.
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6
Q

the changes occurring in both eyes as it changes focus from a distant to close object is called?

A

accommodation

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7
Q

which three processes happen simultaneously and comprise accommodation?

A
  • lens changes shape (becomes thicker and more spherical).
  • pupils constrict.
  • eyes converge.
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8
Q

how does the lens thicken during accommodation?

A
  • ciliary body contraction (parasympathetic) causes lens to become thicker and more spherical.
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9
Q

what muscles allow our eyes to converge when focusing on an object up close?

A
  • medial rectus muscles of both eyes to converge (CN III innervation).
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10
Q

what is myopia?
how do objects look?

A
  • a refractive error causing short-sightedness.
  • close objects look clear, distant objects appear hazy.
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11
Q

what is hyperopia?

A
  • a refractive error causing long-sightedness.
  • close objects look hazy, distant objects appear clear.
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12
Q

what is astigmatism?
how do objects appear?

A
  • a refractive error causing non-spherical curvature of cornea (or lens).
  • close and distant objects appear hazy.
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13
Q

what is presbyopia?

A

a refractive error causing long-sightedness of old age

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14
Q

how is myopia corrected?

A
  • bending power needs to be decreased.
  • biconcave lenses > spectacles, contact lenses, lase eye surgery.
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15
Q

how is hyperopia corrected?

A
  • biconvex glasses alleviate the use of cornea and lens for focusing distant objects and ‘rests’ the accommodative power.
  • contact lenses.
  • laser eye surgery.
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16
Q

how is astigmatism corrected?

A
  • special glasses called cylindrical glasses (curved in only one axis).
  • laser eye surgery.
  • special contact lenses called toric lenses.
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17
Q

what causes presybyopia?

A
  • with age the lense gets less mobile/elastic.
  • so when the ciliary muscle contracts, it is not as capable as before to change the shape of the lens.
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18
Q

when does presbyopia usually start?

A

5th decade of life

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19
Q

define phototransduction

A
  • the conversion of light energy to an electrochemical response by the photoreceptors (rods and cones).
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20
Q

how is rhodopsin regenerated?

A

from dietary vitamin A.

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21
Q

what is rhodopsin composed of

A

opsin + 11-cis retinal

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22
Q

what happens when light falls on rhodopsin pigments?

A
  • 11-cis retinal, isomerises to all-trans retinal.
  • all-trans retinal connot fit into the opsin, so rhodopsin splits, resulting in bleaching of the visual purple (rhodopsin).
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23
Q

what role does vitamin A play in the visual pigment rhodopsin?

A

regeneration

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24
Q

in the dark and at rest, what state are the photoreceptor cells in?

A
  • kept in a depolarised state by open Na+/Ca+ channels.
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25
Q

what conditions can cause vitamin A deficiency?

A
  • malnutrition
  • malabsorption syndromes such as coeliac disease, sprue.
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26
Q

what are the consequences of vitamin A deficiency on the eye?

A
  • affects vision > (night) blindness.
  • also essential for healthy epithelium > conjunctiva and epithelium are also abnormal.
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27
Q

what are some physical manifestations of vitamin A deficieny on the eye?

A
  • Bitot’s spots.
  • corneal ulceration.
  • corneal melting > future opacification of the cornea
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28
Q

in what orientation are images shown to the retina?

A

upside down and inverted

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29
Q

all fibres from the eye pass through the optic nerve to the?

A

optic chiasma

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30
Q

what happens at the optic chiasma?

A

the (medial) nasal fibres of the eye cross to the opposite side.

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31
Q

what does the optic tract contain?

A

fibres from the (lateral) temporal half of the ipsilateral eye and the crossed-over nasal fibres from the contralateral eye.
- this corresponds to ALL fibres from the opposite half of the visual field.

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32
Q

where do fibres from the optic tract synapse?

A

synapse at the lateral geniculate body (LGB) of the thalamus.

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33
Q

what do the tracts emenating from the LGB of the thalamus do?

A
  • also called the optic radiation.
  • the optic radiation passes behind the Internal capsule (retro-lentiform fibres) to reach the primary visual cortex in the Occipital lobe (Area 17).
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34
Q

what does the right visual cortex see?

A

the left half of the visual field.

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35
Q

what is the label showing?

A

optic chiasma

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36
Q

label the visual pathway

A
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37
Q

what will a lesion to the right optic nerve cause?

A

blindness in right eye

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38
Q

what will a lesion causing disruption of the optic chiasma in the middle cause?

A

bitemporal hemianopia
- impaired peripheral vision in both eyes.

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39
Q

what will a lesion in the right optic tract cause?

A

contralateral homonymous hemianopia
- loss of left visual field in both eyes

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40
Q

what will happen if there is a lesion on the optic radiation?

A

contralateral homonymous hemianopia
- the inability to see one half of the visual optic on both eyes.
- e.g. both eyes cant see the left half of the visual field.

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41
Q

what is intorsion of the eyeball?

A

when the top of the eyeball rotates towards the nose

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42
Q

what is extorsion of the eyeball?

A

when the top of the eyeball rotates away from the nose

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43
Q

what is the primary action of the medial rectus?

A

adduction of eyeball

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44
Q

what is the primary action of the lateral rectus?

A

abduction of the eyeball

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45
Q

what is the primary, secondary and tertiary action of the superior rectus?

A
  • elevation, adduction and intorsion of the eyeball.
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46
Q

what is the primary action of the superior oblique?

A

intorsion of the eyeball

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47
Q

what is the primary, secondary and tertiary action of the inferior rectus?

A
  • depression, adduction and extorsion of the eyeball.
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48
Q

what is the primary action of the inferior oblique?

A
  • extorsion of the eyeball.
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49
Q

RADSIN mnemonic for actions of individual EOM

A

Recti ADDuctors, Superiors INtortors

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50
Q

label the EOMs allowing these eye movements and their innervation

A
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51
Q

describe strabismus (squint)

A

misalignment of the eyes:
- esotropia (manifest convergent squint).
- exotropia (manifest divergent squint).

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52
Q

what are the functional consequences of strabismus (squint)?

A
  1. Amblyopia (lazy eye) where brain supresses the image of one eye leading to poor vision in that eye without any pathology.
  2. Diplopia (double vision) usually occurs in squints occuring as a result of nerve palsies.
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53
Q

what are the three intrinsic eye muscles called?

A
  • ciliaris muscle in ciliary body
  • constrictor puppillae in iris at pupillary border
  • dilator pupillae > radially running muscle in iris
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54
Q

how are the ciliaris muscle and constrictor pupillae innervated?

A
  • parasympathetic innervation from oculomotor nerve (CN III).
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55
Q

how is the dilator pupillae innervated?

A

sympathetic innervation from plexus around blood vessels

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56
Q

describe the afferent limb pathway of the light reflex

A
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57
Q

describe the efferent limb pathway of light reflex

A
  • from the Edinger-Westphal nucleus (EWN), part of IIIn nucleus:
    > preganglionic sympathetic fibres pass through IIIn into orbit.
    > parasympathetic fibres go to & synapse in ciliary ganglion.
    > postganglionic fibres go through short ciliary nerves to constrictor pupillae.
    > pupillary constriction of both sides.
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58
Q

what is ansicoria? and what is an example of a condition that can cause it?

A
  • pupils are of different sizes.
  • Horner’s syndrome.
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59
Q

what are some common causes of absent/abnormal pupillary reflex?

A
  • diseases of the retina > detachment/degenerations or dystrophies.
  • diseases of the optic nerve such as optic neuritis (frequently seen in MS).
  • diseases of the III cranial nerve (efferent limb).
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60
Q

In a CN III palsy due to a medical cause such as diabetes, there is usually no damage to the parasympathetic fibres. So, if you see a patient with a CN III palsy and the pupillary reflex is absent, what is suspected?

A

suspect a cerebral artery aneurysm > emergency

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61
Q

Horner’s syndrome can occur due to a disruption of sympathetic innervation at which points?

A
  • thoracolumbar outflow of sympathetic fibres
  • sympathetic chain and cervical ganglia.
  • post-ganglionic sympathetic fibres travelling along with blood vessels.
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62
Q

what does nuclear sclerosis cause?

A
  • lens opacification
  • makes objects appear less clear, and also makes patient see more of the red spectrum.
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63
Q

what is conjunctivitis? what are its symptoms?

A
  • self-limiting bacterial or viral infection of the conjunctiva.
  • red, watering eyes, discharge.
  • no loss of vision as long as infection does not spread to the cornea.
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64
Q

what is the treatment for a stye or hordeolym?

A

warm compress
eyelid hygiene
may need surgical incision and curettage

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65
Q

what is an example of an inflammatory pathology of the cornea?

A

corneal ulcer

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66
Q

what is an example of a non-inflammatory pathology of the cornea?

A

dystrophies

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67
Q

how can opacification of the cornea be treated?

A

corneal transplant - keratoplasty

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68
Q

what are the causes of corneal ulcer?

A
  • infectious - viral/bacterial/fungal infection of the cornea > needs aggressive management to prevent spread, scarring.
  • non-infectious ulcers due to trauma, corneal degenerations or dystrophy.
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69
Q

describe corneal dystrophies

A
  1. bilateral
  2. opacifying
  3. non-inflammatory
  4. most genetically determined
  5. sometimes due to accumulation of substances such as lipids within the cornea
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70
Q

what is the clinical presentation of corneal dystrophies

A
  • first to fourth decade
  • most commonly > decreased vision
  • start in one of the layers of the cornea and spread to the others.
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71
Q

what % of people over 65 have some degree of cataract?

A

30%

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72
Q

what are the risk factors for developing cataracts?

A

primary:
- age
- smoking
- diabetes mellitus
- systemic corticosteroid use

secondary:
- alcohol consumption
- UV exposure
- trauma
- previous eye surgery
- radiation exposure

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73
Q

what is the surgical management of cataracts?

A

pseudophakia:
- removal of lens affected by the cataract and its replacement with an artifical lens.
- the most common surgical technique is phacoemulsification, which breaks down the existing lens using ultrasound waves.

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74
Q

what is the second most common global cause of blindness?

A

glaucoma

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75
Q

what is the most commonly seen form of primary glaucoma called?

A

primary open angle glaucoma (POAG)

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76
Q

what causes glaucoma?

A

raised intraocular pressure (IOP)

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77
Q

what are the consequences of raised IOP?

A
  • pressure on nerve fibres on surface of retina > die out > visual field defects.
  • pressure on optic nerve head as nerve fibres die out > optic disc appears unhealthy, pale and cupped.
  • results in altered field of vision.
  • ultimately all nerve fibres are lost > blindness.
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78
Q

what are the triad of signs for the diagnosis of glaucoma?

A
  • raised IOP.
  • visual field defects.
  • optic disc changes on opthalamoscopy > optic disc appears unhealthy, pale and cupped.
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79
Q

what is the management of primary open angle glaucoma?

A

First-line: laser trabeculoplasty

Second-line:
- prostaglandin analogues eye drops
- beta-blocker eye drops
- miotics e.g. pilocarpine
- carbonic anhydrase inhibitors drops

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80
Q

what is the clinical presentation of angle closure glaucoma?

A
  • sudden onset
  • painful
  • vision lost/blurred
  • headaches (often confused with migraine)
  • red eye, cornea often opaque as raised IOP drives fluid into cornea
  • pupil mid dilated
  • AC shallow, and angle is closed
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81
Q

why does the angle close in angle closure glaucoma?

A

AC = anterior chamber

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82
Q

what is the management of acute angle closure glaucoma?

A

Decrease IOP:
- IOP-lowering agents e.g. a combination of beta blockers, pilocarpine, and IV acetazolamide (carbonic anhydrase inhibitor).
- Rarely intravenous hyperosmotics (eg. mannitol) may be added if there is no improvement in IOP
- Analgesia and antiemetics

  • Peripheral iridotomy – a laser is used to make a hole in the peripheral iris to allow free flow of aqueous – the contralateral eye is treated prophylactically as it is predisposed to PACG
  • Surgical iridectomy – rarely used nowadays, but still carried out when a laser iridectomy is not possible
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83
Q

how does POAG form?

A
  • the drainage through the trabecular meshwork is blocked (in most cases).
  • this leads to a gradual, painless build up of intraocular pressure.
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84
Q

how does angle closure glaucoma form?

A
  • In health, aqueous humour, which is produced by the ciliary body, flows through the pupil and leaves the eye via the trabecular meshwork.
    -The trabecular meshwork is a circular structure that lies in the anterior chamber angle, which is where the cornea meets the iris.
  • Primary angle-closure glaucoma occurs when the iris blocks the drainage angle, which causes a rise in IOP and subsequent damage to the optic nerve.
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85
Q

what is the vascular layer of the eye called?

A

uvea

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86
Q

what are different types of uveitis called?

A
  • anterior uveitis - iris with or without ciliary body inflammed.
  • intermediate uveitis - ciliary body inflamed.
  • posterior uveitis - choroid inflammed.
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87
Q

what are causes of uveitis?

A

Autoimmune diseases:
- Ankylosing spondylitis
- Behçet’s disease (associated with HLA-B27 positivity)
- Juvenile idiopathic arthritis
- Multiple sclerosis
- Systemic lupus erythematosus (SLE)
- Inflammatory bowel disease
- Granulomatosis with polyangiitis
- Reactive arthritis

Other causes:
- Infections (e.g., herpes, tuberculosis, syphilis, HIV)
- Trauma
- Iatrogenic causes (e.g., ocular surgery or medications)
- Ischaemic conditions

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88
Q

what is the pathophysiology of anterior uveitis?

A
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89
Q
A

infection has spread through valveless emissary veins leading to cavernous sinus thrombosis.

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90
Q

what do we use to examine the eye?

A

slit lamp
fundoscopy

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91
Q

what are some commonly encountered opthalamic conditions?

A
  • acute red eye (anterior segment)
  • loss of vision (posterior segment)
  • trauma
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92
Q

what are symptoms and signs of infective conjunctivitis?

A

Eye redness
Itching
Irritation
Excessive tearing
Discharge from the eyes, which can vary in consistency based on the cause
Photophobia, which suggests corneal involvement (keratoconjunctivitis)

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93
Q

what is the treatment for infective conjunctivitis?

A
  • viral > symptom relief and hygiene practises
  • bacterial > symptom relief and good hygiene practise, but if severe > topical antibiotics like chloramphenicol may be recommended.
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94
Q

treatment for allergic conjunctivitis?

A
  • topical antihistamine (olopatadine)
  • avoid allergen
  • mast cell stabilisers (sodium chromoglycate)
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95
Q

when presented with acute red eye, what are the three important differential diagnoses to rule out?

A
  • Acute angle-closure glaucoma
  • Anterior uveitis
  • Scleritis
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96
Q

what are symptoms and signs of a corneal ulcer?

A
  • pain
  • red
  • photophobia
  • discharge (purulent/watery)
  • history of contact lens wear
  • corneal defect with surrounding infiltrate
  • +/- cells/pus in the anterior chamber
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97
Q

what are symptoms and signs of a corneal abrasion?

A
  • history of trauma
  • pain
  • red
  • watering
  • blurred vision
  • epithelial defect
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98
Q

what is the treatment for a corneal abrasion?

A
  • topical antibiotics (chloramphenicol/fucidic acid)
  • analgesia
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99
Q

what are symptoms and signs of acute anterior uveitis

inflammation of iris and ciliary body

A

symptoms:
- Painful red eye worsening over several days
- Photophobia
- Blurred vision
- Headache

signs:
- Conjunctival injection
- Hypopyon (fluid level)
- Keratic precipitates
- Posterior synechiae and irregular pupil

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100
Q

what is the treatment for acute anterior uveitis?

A
  • topical steroids (prednisolone 1% hourly)
  • dilating drops (cyclopentolate 1% 3 times daily)
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101
Q

what are symptoms and signs of scleritis?

A
  • severe pain
  • redness (deep scleral vessels)
  • nodule (does not move over sclera)
  • very tender
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102
Q

what is the treatment for scleritis?

A

systemic steroid

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103
Q

what are symptoms and signs of acute angle closure glaucoma?

A
  • severe pain
  • redness
  • blurred vision
  • nausea and vomiting
  • hazy cornea
  • fixed mid-dilated pupil
  • hard eyeball
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104
Q

what is the treatment for acute angle closure glaucoma?

A
  • lower intraocular pressure (carbonic anhydrase inhibitors, beta blockers, prostaglandins).
  • constrict pupil (pilocarpine)
  • laser iridotomy
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105
Q

what is orbital cellulitis?

A
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106
Q

what are symptoms and signs of orbital cellulitis?

A
  • Periocular pain and swelling
  • Fever
  • Malaise
  • Erythematous, swollen and tender eyelid
  • Chemosis
  • Proptosis
  • Restricted eye movements +/– diplopia
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107
Q

what is the treatment for orbital cellulitis?

A
  • admit
  • IV antibiotics
  • CT scan
  • drainage of pus
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108
Q

what are some vascular causes for sudden, complete loss of vision

A
  • central retinal artery occlusion
  • central retinal vein occlusion
  • ischaemic optic neurpathy: arteric
  • giant cell arteritis
  • vitreous haemorrhage
  • retinal detachment
109
Q

what is the appearance of the retina using a fundoscope in a patient with central retinal artery occlusion?

A
  • pale retina
  • cherry red spot > perfusion of fovea or macula by coroidal vessels.
110
Q

what is the treatment for central retinal artery occlusion (CRAO) or branch retinal artery occlusion (BRAO)?

A
  • treat in same way as stroke
  • STAT, aspirin
  • identify and treat cardiovascular risk factors
111
Q

what is the treatment of central retinal vein occlusion

A
  • identify and treat CV risk factors
  • if they have oedema > intravitreal anti Vegf injection.
112
Q

what does a fundus examination in central retinal vein occlusion look like?

A
  • haemorrhages in all areas
  • can develop macular oedema (diagram C)
113
Q

describe giant cell arteritis, symptoms and signs, and management

A
  • Giant cell arteritis (GCA), also known as temporal arteritis, is a condition where the arteries, particularly those at the side of the head (the temples), become inflamed.
  • Symptoms and signs: temporal headache, Jaw claudication, vision loss, systemically unwell.
  • GCA should be treated immediately with high-dose steroids (40–60 mg prednisolone OD) to prevent blindness and stroke.
114
Q

what are some causes of gradual vision loss?

A
  • cataract
  • glaucoma
  • age-related macular degeneration
  • diabetic retinopathy
115
Q

how do we classify glaucoma?

A
  • open or closed angle.
  • chronic or acute.
116
Q

what are symptoms of age-related macular degeneration (AMD)?

A
  • progressive loss of central vision
  • distortion
117
Q

Age-related macular degeneration (ARMD) pathology

A

ARMD describes degeneration of photoreceptors in the central retina (macula) that leads to the formation of drusen, which are visible on slit-lamp biomicroscopy.

118
Q

what are symptoms and signs of age-related macular degeneration (AMD)?

A
  • Reduced visual acuity, worse for near vision and central vision (patients may say they struggle seeing faces)
  • Visual distortion – particularly line perception when tested with Amsler grids.
  • Drusen in dry ARMD – yellow pigmented spots on the retina that are collected around the macula
  • Subretinal or intraretinal haemorrhages in wet ARMD seen as red patches on the retina around the macula
119
Q

what % of age-related macular degeneration is dry vs wet?

A

90% dry
10% wet

120
Q

what is the management of ARMD?

Both WET and DRY

A

Dry ARMD
- Zinc and antioxidant vitamin A, C and E supplements have been shown to reduce progression by up to 30%.

Wet ARMD
- Anti-vascular endothelial growth factor (anti-VEGF) injections limit progression and can even reverse vision loss – typically administered in monthly injections.

121
Q

what are investigations of ARMD?

A
  • Slit-lamp biomicroscopy Allows identification of exudative, pigmentary or haemorrhagic changes in the retina to allow diagnosis of ARMD
  • Colour fundus photography
  • Fluorescein angiography Used to identify neovascular ARMD to guide anti-VEGF therapy
  • Ocular coherence tomography (OCT)
122
Q

what is the most common cause of visual impairment in the working age population?

A

diabetic retinopathy

123
Q

signs and symptoms of diabetic retinopathy

include appearance on fundoscopy

A

Early stages of diabetic retinopathy may be asymptomatic. As the disease progresses, symptoms can include:
- Floaters or dark spots in the vision
- Blurred or distorted vision
- Difficulty seeing at night
- gradual loss of vision
- fundoscopy: microaneurysms, retinal haemorrhages and exudates, neovascularisation.

124
Q

what are investigations in diabetic retinopathy?

A
  • fundoscopy
  • OCT
  • fluorescein angiography
125
Q

what is the management if diabetic retinopathy?

A
  • blood glucose control, cholesterol, BMI etc.
  • Laser photocoagulation
  • Intravitreal injections of anti-vascular endothelial growth factor (anti-VEGF) agents for diabetic macular oedema.
  • Vitrectomy surgery for advanced cases with complications such as vitreous haemorrhage or retinal detachment.
126
Q

regarding signal transduction of sensory nerves, the frequency of action potential is propotional to?

A

the stimulus intensity
- therefore neurotransmitter release varies with the pattern of action potentials arriving at the axon terminal.

127
Q

what determines sensory acuity?

A

density of innervation and size of receptive fields.

128
Q

cutaneous sensation is mediated by which three types of primary afferent fibres?

A
  • Aβ = large myelinated (30-70 m/s) touch, pressure, vibration
  • Aδ = small myelinated (5-30 m/s) cold, “fast” pain, pressure
  • C = unmyelinated fibres (0.5-2 m/s) warmth, “slow” pain
129
Q

proprioception is mediated by which two types of primary afferent fibres?

A

Aα and Aβ e.g. muscle spindles, golgi tendon organs etc.

130
Q

primary afferent nerve fibres enter the spinal cord via the?

A

dorsal root ganglia (or cranial nerve ganglia for head)

131
Q

describe the transmission of sensory information by mechanoreceptive (Aα and Aβ) fibres.

A
  • Project straight up through ipsilateral dorsal columns
  • Synapse in cuneate and gracile nucleiof thalamus
  • The 2nd order fibres cross over midline (decussate) in the brainstem and project to reticular formation, thalamus and cortex
132
Q

describe the transmission of sensory information by thermoreceptive and nociceptive (Aδ and C) fibres

A
  • 1st order fibres synapse in the spinal cord
  • The 2nd order fibres cross over the midline in the spinal cord
  • Project up through the lateral spinothalamic (anterolateral) tract to reticular formation, thalamus and cortex
133
Q

what does Brown-Sequard syndrome cause in the contralateral and ipsilateral side of the body?

A
134
Q

what activates nociceptors?

A
  • low pH, heat (via ASIC, TRPV1 etc.)
  • local chemical mediators (e.g. bradykinin, histamine, protaglandins).
135
Q

how do NSAIDs work?

A
  • Prostaglandins sensitise nociceptors to bradykinin
  • NSAIDs are analgesic (and anti-piretic and anti-inflammatory) because they inhibit cyclo-oxygenase which converts arachidonic acid to prostaglandins
  • So NSAIDs work well against pain associated with inflammation
136
Q

how do local anaesthetics work?

A

block Na+ action potential and therefore all axonal transmission.

137
Q

how do opiates work as analgesics?

A
  • Reduce sensitivity of nociceptors
  • Block transmitter release in dorsal horn (hence epidural administration)
  • Activate descending inhibitory pathways
138
Q

how does trans cutaneous electric nerve stimulation (TENS) work as an analgesic?

A

It uses a low-voltage electrical current to block pain or change your perception of it.

139
Q

explain the gate control hypothesis for pain modulation

A

The concept of the gate control theory is that in the spinal cord, non-painful input closes the gates to painful input, which results in prevention of the pain sensation from traveling to the CNS (i.e., non-noxious input [stimulation] suppresses pain).
- for example if we fall and hurt our knee, small pain fibres travel up the spinal cord and we percieve pain. Often we rub our knee after as a way to possibly reduce pain as now large sensory touch fibres enter the spinal cord and close the pain gate.

140
Q

del

A

del

141
Q

Brainstem nuclei receive control inputs about voluntary movements from?

A

higher centres – from the cerebral cortex (motor, premotor and supplementary motor cortex), the basal ganglia and the cerebellum

142
Q

which four systems control movement?

A
  1. descending control pathways
  2. basal ganglia
  3. cerebellum
  4. local spinal cord/brain stem circuits
143
Q

proximal (shoulder/hip) muscles are mapped to which neurones in the spinal cord?

A

medial motorneurones in medial white matter

144
Q

distal (finger/toe) muscles map to which neurones in the spinal cord?

A

lateral motoneurones

145
Q

describe nociceptors

A

free nerve endings of A-delta and C-fibres that respond to thermal, chemical and mechanical noxious stimuli.

146
Q

where are the cell bodies of primary afferent/1st order neurons found?

A

dorsal root ganglion

147
Q

describe A-delta nerve fibres

A
  • lightly myelinated medium diameter fibres.
  • responsible for fast (first) pain or sharp pain.
148
Q

describe C nerve fibres

A
  • small, unmyelinated fibres.
  • responsible for slow (second), dull pain.
149
Q

what is the major ascending tract for nociception? and which lamina of Rexed does it arise in? where does it end?

A
  • spinothalamic tract > lateral.
  • arises in Rexed Lamina 1, 2 & 5.
  • ends in thalamus
150
Q

del

A

del

151
Q

what is an outcome of peripheral sensitisation to pain?

A

hyperalgesia > increased perception of pain or even non-noxious stimuli as noxious stimuli.

152
Q

describe primary and secondary hyperalgesia

A
  • primary hyperalgesia > hyperalgesia at the site of injury.
  • secondary hyperalgesia > hyperalgesia in surrounding uninjured tissue.
153
Q

describe allodynia

A

type of hyperalgesia causing dynamic mechanical hyperalgesia in response to light touch.

154
Q

what changes to the nociceptor occur in allodynia?

A

decreased threshold for response

155
Q

del

A

del

156
Q

what are the 3 main components of central sensitisation to pain?

A
  • wind-up
  • classical
  • long-term potentiation
157
Q

what are the different classifications of pain?

A
  • duration: acute or chronic.
  • mechanism: nociceptive, neuropathic, nociplastic.
158
Q

what are the differences between acute and chronic pain?

A

acute pain:
- physiological
- presence of noxious stimuli
- serves protective function
- usually nociceptive

chronic pain:
- pathological
- presence of noxious stimuli is not essential
- does not serve any purpose
- nociceptive, neuropathic or nociplastic

159
Q

what is nociceptive pain usually described as??

A

throbbing
aching
stiffness

160
Q

what is neuropathic pain?

A

Pain caused by a lesion or disease of the somato-sensory nervous system

161
Q

describe nociplastic pain

A

Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.

e.g. painful physical symptoms of depression/anxiety, fibromyalgia

162
Q

what is the length of sympathetic preganglionic and postganglionic fibres?

A

short preganglionic (due to close proximity to vertebral column) and long postganglionic fibres

163
Q

sympathetic ganglia are located?

A

in the prevertebral and paravertebral ganglia

164
Q

do sympathetic nerves have craniosacral or thoracolumbar outflow?

A

thoracolumbar

165
Q

which vertebral regions is sympathetic outflow from?

A

T1-12 and L1-2 regions
thoracolumbar

166
Q

which vertebral regions is parasympathetic outflow from?

A

cranial (III, VII, IX, X) and sacral (S2-S4) regions.

167
Q

where do parasympathetic ganglia lie?

A

close to or within target organ

168
Q

cranial nerves that contain parasympathetic outflow include the?

A

oculomotor nerve
facial nerve
glossopharyngeal nerve
vagus nerve

169
Q

in the sympathetic system, the synapses between pre and post ganglionic cells are?

A

cholinergic and nicotinic

170
Q

in the parasympathetic system, the synapses between pre and post ganglionic cells are?

A

cholinergic and nicotinic

171
Q

sympathetic and parasympathetic preganglionic fibres release what which acts on what?

A

release acetylcholine which acts on nicotinic cholinergic receptors

172
Q

in the parasympathetic system the synapses between post ganglionic cells and their targets are?

A

cholinergic and muscarinic

173
Q

sympathetic postganglionic fibres release what which acts on what?

A

noradrenaline which acts on alpha or beta adrenergic receptors

174
Q
A

all of the above

175
Q

whats the ratio of adrenaline vs noradrenaline released into the blood by the adrenal medulla?

A

80:20

176
Q

in the eye, activation of the sympathetic system causes?

A
  • contraction of the radial muscle of the iris > dilation of the pupil.
  • relaxation of the ciliary muscle surrounding the lens > eye focuses far away.
177
Q

what receptors does adrenaline act on in the eye?

A
  • activates alpha-1 receptors on radial muscle of the iris
  • activates beta-2 receptors on ciliary muscle around lens.
178
Q

in the eye, activation of the parasympathetic system causes?

A
  • activates muscarinic receptors on sphincter muscle of the iris > contracts muscle and makes pupil smaller.
  • activates muscarinic receptors on ciliary muscle around the lens > ciliary muscle contracts and eye focuses close up.
179
Q

eye drops used to dilate the pupil of the eye may contain?

A

a muscarinic antagonist or an alpha-1 agonist

180
Q

what is an example of the stretch reflex?

A

patellar tendon (knee-jerk) reflex

181
Q

which afferent sensory fibres are activated during the stretch reflex?

A
  • stretch activates 1a afferent sensory nerves in the muscle spindle.
182
Q

describe a monosynaptic reflex

A
  • direct contact to alpha-motorneurones in the stretched muscle causing rapid contraction of the agonist muscle.
  • one synapse, no interneurones involved.
183
Q

describe reciprocal inhibition

A
  • as the agonist muscle contracts, antagonist muscle relaxes (enabling agonist joint movement).
  • this spindle afferent connection is with inhibitory interneurones, so decreased activation of alpha-motorneurones to the antagonist muscle, which then relaxes.
184
Q

label the events that occur to allow the stretch reflex

A
185
Q

why do we have spinal reflexes?

A

Instead of directly traveling to the brain, sensory neurons of a reflex arc synapse in the spinal cord. This is an important evolutionary adaptation for survival, which allows faster actions by activating spinal motor neurons instead of delaying reaction time by signals first having to go to the brain.

186
Q

describe the golgi tendon organ

A

Golgi tendon organ is a proprioceptor that provides information regarding the changes in muscle tension.

187
Q

describe the inverse stretch reflex (golgi-tendon organ or clasp-knife reflex) and what 3 things it causes

A
  • caused by 1b afferent nerves from the golgi tendon organs (GTO), which monitor muscle tension.
  • muscle contracts and shortens- pulls on tendon and (sensory) 1b afferent nerves from the GTOs increase firing (higher AP frequency).

Causes:
1. activation of inhibitory interneurones to the agonist muscle > decrease in contraction strength.
2. activation of excitatory interneurones to antagonist muscles.
3. as for spindles, info about muscle tension ascends spinal dorsal columns to somatosensory cortex.

188
Q

why do we need the inverse stretch reflex?

A

protective mechanism to prevent muscle damage > avoids muscle contracting so hard tendon is ripped from bone
- reflex is polysynaptic and protective

189
Q

describe the flexor/withdrawal reflex

A

increased action potentials in nociceptive nerves
1. increased activity in flexor muscles of the affected part via numerous excitatory interneurones.
2. simultaneously, via a number of excitatory and inhibitory interneurones, antagonistic extensors are inhibited.

allows hand to be withdrawn from painful stimulus for example

190
Q

describe the crossed extensor reflex

A

(contralateral extension to prevent falling over due to withdrawal reflex)
- excitatory interneurones cross the spinal cord, excite contralateral extensors.
- other interneurones cross the spinal cord, synapse with inhibitory neurones and **inhibit contralateral flexors **
- sensory info ascends to the brain in the contralateral spinothalamic tract.

191
Q

why are the flexor and crossed extensor reflexes slower than the stretch reflex?

A
  • nociceptive sensory fibres are smaller diameter than muscle spindle afferents (conducts more slowly).
192
Q

how can the GTO reflex be over-ridden by voluntary input from the CNS?

A
  • descending voluntary excitation of alpha-motorneurones by the brain overides the inhibition from the GTOs and maintains muscle contraction.
193
Q

how can the stretch reflex be overriden?

A
  • strong descending inhibition (e.g. anxious patient) hyperpolarises alpha-motorneurones > makes stretch reflex hard to evoke.
194
Q

why is it clinically important to test reflexes?

A
  • assessing integrity of the whole spinal cord circuit.
  • can help localisation of spinal level of a problem e.g. segmental trauma to the spine.
195
Q

what are the main lateral pathways called that are involved with movement?

A
  • corticospinal tract (CST).
  • rubrospinal tract (RST).
196
Q

del

A
197
Q

which structures are involved with strategy - the goal and the movement strategy to best achieve this goal?

A
  • association neocortex.
  • basal ganglion.
198
Q

which structures are involved with tactics - the sequence of spatiotemporal muscle contractions to achieve a goal smoothly and accurately?

A
  • motor cortex
  • cerebellum
199
Q

which structures are involved with execution - activation of motor neuron and interneuron pools to generate goal-directed movement?

A
  • brain stem
  • spinal cord
200
Q

what is the function of lateral pathways in movement?

A
  • control voluntary movements of distal muscles - under direct cortical control.
201
Q

what is the function of ventromedial pathways in movement?

A
  • control posture and locomotion > under brain stem control.
202
Q

where does the rubrospinal tract (RST) begin and end?

A
  • starts in the red (=’rubro’) nucleus of the midbrain and recieves inputs from same cortical areas as the CST.
  • synapses in the ventral horn of spinal cord.
203
Q

where does the corticospinal tract begin and end?

A
  • 2/3 of CST originates in areas 4 & 6 of the frontal motor cortex, the rest (1/3) is somatosensory.
  • at medulla/spinal cord junction, the CST crosses over.
  • CST axons synapse on ventral horn motor neurones and interneurones to control muscles voluntarily.
204
Q

what would be the consequences of a lesion to CST and RST?

A
  • fine movements of arms and hands are lost.
  • can’t move shoulders, elbows, wrist and fingers independently.
205
Q

what would be the consequence of a lesion to the CST alone and not the RST?

A
  • same deficits seen as if both had lesion, however, functions reappear after a few months.
  • been taken over by RST.
206
Q

what is the role of the primary motor cortex and pre-motor areas in movement?

A

plan and control precise voluntary movements.

207
Q

where do axons in the medial white matter originate from?

A
  • medial tracts from brainstem control posture, balance and oritenting mechanisms.
208
Q

where do axons in the lateral white matter originate from?

A
  • lateral tracts from motor cortex control precise, skilled voluntary movements.
209
Q

which two somatotopically organised motor maps are present in area 6 of the brain?

A
  • premotor area (PMA)
  • supplementary motor area (SMA)
210
Q

del

A

del

211
Q

del

A

del

212
Q

what generates a mental image of the body in space?

A
  • somatosensory, proprioceptive and visual inputs to posterior parietal cortex (areas 5 & 7).
213
Q

if you only think about moving, which area of the brain is active?

A

area 6 > pre-motor cortex and supplementary motor area

214
Q

why do PMA ‘mirror neurones’ fire?

A
  • specific neurones in area 6 fire when movement is made or is imagined - rehearsed mentally.
  • also fire when others make the same movement (this allows understanding of the actions or intentions of others) = ‘mirroring’
215
Q

where are decision making neurones forund in the motor cortex?

A

cortical PMA

216
Q

describe a feedback mechanism controlling movement

A
  • actual change in body position: initiates rapid compensatory feedback messages from brainstem vestibular nuclei to spinal cord motor neurons to correct postural instability.
  • e.g. flex right bicep > extend left leg.
217
Q

del

A

del

218
Q

describe the basal ganglia motor loop

A
  • major subcortical input to area 6 comes from ventral lateral nucleus in dorsal thalamus (VLo).
  • input to VLo comes from basal ganglia.
  • basal ganglia are targets of frontal, prefrontal and parietal cortex.
  • so loop of info cycles from: Cortex > thalamus and basal ganglia > SMA (cortex area 6).
219
Q

what parts of the basal ganglia ‘predict’ movements, and which movements are they?

A
  • putamen fires before limb/trunk movements.
  • caudate fires before eye movements.
220
Q

where do inhibitory (GABAergic) medium spiny neurones from the putamen and caudate project to?

A
  • globus pallidus
  • substantia nigra pars reticula
221
Q

why does cortical activation of the putamen boost cortical excitation

A

cortical excitation:
1. excites putamen, which
2. inhibits (inhibitory) globus pallidus, which therefore
3. reduces inhibition of VLo cells, so
4. activity in VLo boosts SMA activity

positive feedback loop

222
Q

what is the function of the direct cortical loop through the basal ganglia?

A

selects specific motor actions
- via caudate/putamen

223
Q

what is the function of the indirect cortical loop through the basal ganglia?

A

suppresses other/inappropriate action to allow proper activation of intended motor programs
- via subthalamic nucleus

224
Q

what is the cause of huntingtons disease symptoms?

A

profound loss of caudate, putamen and globys pallidus
i.e. loss of ongoing (tonic) inhibition by basal ganglia

225
Q

the cerebellum is only 10% of brain volume but comprises what % of total CNS neurones?

A

50%

226
Q

what is the role of the cerebellum in movement?

A
  • instructs direction, timing and force of movement based on predictions, calculations and experience.
  • lesions to cerebellum > uncoordinated, inaccurate movements.
227
Q

what processes does sleep support?

A
  1. neuronal plasticity
  2. learning and memory
  3. cognition
  4. clearance of waste products from CNS
  5. conservation of whole body energy
  6. immune function
228
Q

evidence suggests that the activity of sleeping originates in the…

A

reticular formation of the brain stem (pons region).

229
Q

many molecules are believed to contribute to sleep, including:

A
  • (Delta) sleep inducing peptides (DSIP)
  • adenosine
  • melatonin
  • serotonin
230
Q

what is the role of the hypothalamus in sleep?

A
  • activity of the suprachiasmatic nuclei (SCN) of the hypothalamus demonstrates 24 hr circadian rhythm and controls release of melatonin from the pineal gland.
231
Q

how does darkness stimulate melatonin release?

A
  • inhibitory neurons in the suprachiasmatic nucleus (SCN) are stimulated by light and act to inhibit pineal gland.
  • darkness therefore removes inhibition and causes stimulation of pineal gland > melatonin release > sleepiness.
232
Q

describe orexin (AKA hypocretin)

A
  • an excitatory neurotransmitter released from hypothalamus, required for wakefulness.
  • orexin neurons are active during the waking state and stop firing during sleep.
  • defective orexin signalling causes narcolepsy.
233
Q

discuss serotonin and sleep

A
  • many neurons within the reticular formation are serotonergic; drugs that block serotonin formation inhibit sleep suggesting serotonin must be critical to sleep induction.
  • these effetcs may be related to melatonin production as serotonin is a precursor.
234
Q

the wave pattern produced by an EEG recording can be analysed by what factors?

A
  1. amplitude: the size of the wave (ranges from 0-200 uV).
  2. frequency: number of waves per second (ranges from 1-50+).
235
Q

in general, does the frequency of brain waves on an EEG increase or decrease with neuronal excitation?

A

increase

236
Q

does the amplitude of brain waves tend to increase or decrease with neuronal excitation?

A

decrease

237
Q

what are the four main types of wave pattern seen on an EEG?
and what states are they associated with?

A
  1. beta- associated with alert awake state. Very high frequency, low amplitude waves.
  2. alpha- associated with relaxed awake state. High frequency, medium amplitude waves.
  3. theta- associated with early sleep. Low frequency waves which can vary enormously in amplitude.
  4. delta- associated with deep sleep. Very low frequency but high amplitude waves.
238
Q

what are the different stages if the sleep cycle?

A
  1. slow wave, non-REM, S-sleep. Slow eye movements. Light sleep very early in the sleep cycle. Easily roused. High amplitude, low frequency theta waves.
  2. eye movements stop. Frequency slows further but EEG shows bursts of rapid waves called ‘sleep spindles’.
  3. high amplitude, verly slow (2Hz) delta waves interspersed with short episodes of faster waves, spindle activity declines.
  4. exclusively delta waves.
239
Q

which stages of the sleep cycle does deep sleep occur?

A

3 & 4

240
Q

when does REM sleep occur in the sleep cycle? and give features of REM sleep.

A
  • from stage 4 sleep, move back up through stage 3 and stage 2 before entering REM sleep.
  • dreams occur during REM sleep.
  • 25% of sleep is REM.
  • low amplitude, high frequency waves eerily similar to awake state.
241
Q

physiological characteristics of deep, slow-wave sleep

A
  1. deep sleep that occurs in the first hours of sleep
  2. most restful type of sleep
  3. associated with decreased vascular tone (and therefore BP), respiratory and basal metabolic rate.
  4. hippocampus very active- creation of new memories?
242
Q

describe primary insomnia

A
  • chronic insomnia where there is usually no identifiable psychological or physical cause.
243
Q

describe secondary insomnia

A

temporary, in response to pain, bereavement or other crisis.

244
Q

night terrors in relation to sleep cycle

A
  • occur in deep, delta sleep and are common in children 3-8 y/o, typically occurring early in the night.
  • child does not remember episode on waking the following morning.
245
Q

describe somnambulism (sleep-walking) in relation to the sleep cycle

A

occurs exclusively in non-REM sleep, mainly in stage 4 sleep and is more common in children and young adults, probably due to the decline in stage 4 sleep with age.

246
Q

describe narcolepsy in relation to the sleep cycle

A
  • enter directly into REM sleep with little warning.
  • linked to dysfunctional orexin release from the hypothalamus.
247
Q

what is cognition?

A

cognition describes the integration of all sensory information to make sense of a situation.

248
Q

what are the three key components of learning and memory?

A
  • hippocampus - formation of memories.
  • cortex - storage of memories.
  • thalamus - searches and accesses memories.
249
Q

in what system are memories formed?

A

the limbic system > gives events emotional significance which is essential for memory.

250
Q

describe the limbic system

A
  • most primitive part of the cortex.

consists of four distinct areas:
- hypothalamus (assoc. with ANS responses).
- hippocampus (assoc. with memory).
- cingulate gyrus and amygdyla (assoc. with emotion).

251
Q

what is the collective function of the limbic system?

A

responsible for instinctive behaviour e.g. thirst, sex, hunger etc. and emotive behaviour are driven by seeking reward or avoiding punishment.

252
Q

what part of the brain assesses the significance of an event?

A

the frontal cortex and its association with the rewrd/punishment centres in the limbic system assess the significance of an event.
- if deemed insignificant > forgotten.

253
Q

what is the hippocampus essential for?

A

learning and the formation of memories

254
Q

what are the consequences of bilateral hippocampal damage on learning and memory?

A
  • immediate (sensory) memory (seconds in length) and intact long-term meory (from time before damage), but are unable to form new long-term memories.
255
Q

memory can be divided into?

A
  • immediate or sensory memory
  • short-term memory
  • intermediate long-term memory
  • long-term memory
256
Q

describe immediate or sensory memory

A
  • describes the ability to hold experiences in the mind for a few seconds.
  • based on different sensory modalities.
  • bisual memories decay fastest (<1s), auditory ones slowest (<4s).
257
Q

describe short-term memory

A
  • seconds to hours.
  • used for short-term tasks such as dialling a phone number, mental arithmetic, reading a sentence.
  • associated with maintained excitation from reverberating circuits.
258
Q

describe intermediate long-term memory

A
  • hours to weeks.
  • e.g. what you did last weekend.
  • associated with chemical adaptation at the presynaptic terminal > increasing Ca2+ entry to presynaptic terminals, increases neurotransmitter release
259
Q

describe long-term memory

A
  • can be lifelong e.g. where you grow up and your childhood friends.
  • associated with structural changes in synaptic connections.
260
Q

what happens to a short-term memory if it is deemed significant, or insignificant?

A
  • significant > reverberating circuit results in consolidation of the memory into long term storage.
  • insignificant > reverberation fades and no consolidation occurs.
261
Q

what are the two types of amnesia?

A
  1. anterograde - cannot form new memories.
  2. retrograde - cannot access (more recent) old memories.
262
Q

what type of amnesia occurs if the thalamus is damaged but the hippocampus is intact? and what does this suggest?

A

retrograde > suggests thalamus is required for ‘searching’ our existing memory bank

263
Q

what are the structural changes occuring at the synapse that are involved with long-term memory?

A
  1. increase in NT release sites on presynaptic membrane.
  2. increase in number of NT vesicles stored and released.
  3. increase in number of presynaptic terminals.
  4. increased amplitude in EPSP in the post-synaptic cell is often observed > long-term potentiation.
264
Q

what are the two main types of long-term memory?

A
  1. declarative or explicit memory
  2. procedural/reflexive/implicit memory
265
Q

describe declarative or explicit memory

A
  • type of long-term memory
  • abstract memory for events (episodic memory) and for words, rules and language (semantic memory).
  • relies heavily on the hippocampus.
266
Q

describe procedural/reflexive/implicit memory

A
  • type of long-term memory.
  • acquired slowly through repitition.
  • includes motor memory for acquired motor skills such as playing tennis, and rules based learning such as, in the UK, always driving on the lift.
  • mainly based in cerebellum, independent of hippocampus.
267
Q

describe consolidation

A
  • short-term memory is converted to long-term memory through consolidation.
  • involves selective strengthening of synaptic connections through repitition (for minutes to hours).
  • requires attention.
268
Q

describe Korsakoff’s syndrome

A
  • commonly caused by chronic alcoholism.
  • vitamin B1 (thiamine) deficiency leads to damage of limbic system structures.
  • the ability to consolidate memory is impaired.
  • patients have greatly reduced REM sleep which is important for memory.
269
Q

describe the effect of Alzhiemer’s disease on memory

A
  • severe loss of cholinergic neurons throughout the brain, including the hippocampus.
  • causes gross impairment of memory.
  • patients have greatly reduced REM sleep.

Neurology Systems (14 decks)

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