Module 3C Neurology and Vision - Lectures

Question 1

Ocular anatomy - diagram

Answer 1

Question 2

External eye anatomy - diagram

Answer 2

Question 3

Retina anatomy

Answer 3

Question 4

Measuring visual acuity –> Snellen chart (usually read from 6m)

Answer 4

Question 5

Hyperopia and Myopia

Answer 5

• Hyperopia (farsightedness) = difficulty seeing nearby objects clearly, while distant objects are more in focus
  –> due to the light entering the eye being focused behind the retina (occurs bc eyeball too short OR the cornea or lens is not curved enough to bend light properly)
  .
• Myopia (nearsightedness) = difficulty seeing distant objects clearly, while close objects appear sharp
  –> due to the light entering the eye being focus in front of the retina
  (occurs bc eyeball is too long OR cornea or lens is too curved)

Question 6

Treatment of hyperopia and myopia (that isn’t refractive surgery - eg. LASIK)

Answer 6

• Hyperopia –> Convex (plus-powered) lenses in glasses or contact lenses
• Myopia –> Concave (minus-powered) lenses in glasses or contact lenses

Question 7

Describe how the “pinhole effect” works and how we can use this clinically in the evaluation of refractive errors

Answer 7

• Refractive error = when light rays entering the eye do not focus properly (eg. myopia, hyperopia, asstigmatism)
• Pinhole = a small apperture that elimates the scattered, peripheral rays of light and only allows parallel rays to pass throuhj (this focuses the light more precisely on the retina, improving clarity of vision)
  .
• Clinical use –> we can use this to differentiate between refractive errors and other causes of poor vision (such as disease of the retina or optic nerve)
  –> eg. pt views Snellen chart through a pinhole, if vision improves then likely to be a refractive error (if not then more likely to be due to other pathology (eg. cataracts, macular degenration, or optic neuropathy)

Question 8

Ishihara plates –> what are they used for?

Answer 8

• Ishihara plates are a diagnostic tool used to detect colour vision deficiencies (particularly red-green colour blindness - most common type of colour blindness)
• pt is shown a series of plates in controlled lighting environment (eg. daylight), for each plate pt is asked to identify the number, shape, or path
• they are not as effective for identifying blue-yellow deficiencies or total colour blindness

Question 9

What is red desaturation?

Answer 9

• damage to the optic nerve or pathways affects the processing of colour –> especially red (making it appear less vivid)
• it is often one of the earliest signs of optic neuropathy
• test each eye separately –> a decrease in the perception of red intensity in one eye compared to the other suggests a possible abnormality in the optic nerve of the affected eye (eg. optic neuritis, compression of optic nerve, or ischaemic optic neuropathy)

Question 10

Visual fields digram

Answer 10

Question 11

Oculomotility –> muscles involved + cranial nerve supply to each muscle

Answer 11

Question 12

Ocular movements diagram

Answer 12

Question 13

Pupil pathway –> afferent pathway (sensory input)

Answer 13

1. Light detection –> light enters the eye and is detected by retinal photoreceptors (rods and cones), signal travels via bipolar cells to the retinal ganglion cells
2. Optic nerve (CN II) –> the axons of retinal ganglion cells form the optic nerve
3. Optic chiasm and tract –> at the optic chiasm, fibers from the nasal retina cross to the opposite side (while temporal fibres remain uncrossed), this ensures that input from both eyes reaches both sides of the brain
4. Pretectal nucleus –> light signals are transmitted to the pretectal nucleus in the midbrain (bypassing the lateral geniculate nucleus), bilateral projection occurs - this is where each pretectal nucleus sends signals to both sides of the brain, ensuring a consensual response (both pupils react when one eye is illuminated)

Question 14

Pupil pathway –> Efferent pathway (motor output)

Answer 14

1. Edinger-Westphal Nucleus –> from the pretectal nucleus, signals are sent to the EWN (located in the midbrain), this nucleus provides parasympathetic innervation to the pupils
2. Oculomotor Nerve (CN III) –> preganglionic parasympathetic fibers travel along the oculomotor nerve (CN III)
3. Ciliary Ganglion –> the fibers synapse in the ciliary ganglion, located just behind the eye
4. Short ciliary nerves –> postganglionic parasympathetic fibers travel via the short ciliary nerves to the sphincter pupillae muscle in the iris, causing pupil constriction (miosis)

Question 15

Explain the relative afferent pupillary defect (RAPD)

Answer 15

• RAPD occurs when one eye detects light less effectively than the other due to a unilateral or asymmetrical afferent defect
  –> as a result the affected eye causes a weaker pupillary constriction when exposed to light compared to the healthy eye
  .
  We test for RAPD using the swinging flashlight test:
• Normal response –> both pupils constrict equally when light is shone into either eye
• In RAPD –> when light is shone into the affected eye, both pupils dilate or constrict less than they did when light was shone into the normal eye (this reflects the decreased afferent signal from the affected eye)

Question 16

What is anisocoria?

Answer 16

• condition characterised by unequal size of the pupils –> can be physiological (normal) or pathological (resulting from a dysfunction in the afferent or efferent pathways controlling the iris muscles)

Question 17

What effect does the parasympathetic NS and what does the sympathetic NS have on pupil size?

Answer 17

• Parasympathetic pathway –> controls pupil constriction (miosis) via the sphincter pupillae
• Sympathetic pathway –> controls pupil dilation (mydriasis) via the dilator pupillae

Question 18

What is Adie’s tonic pupil –> include symptoms and diagnosis

Answer 18

• a neurological condition characterised by mydriasis (one pupil is larger than the other) –> usually idiopathic and benign
• Symptoms –> light reflex is absent or sluggish, slow/poor constriction to near objects, diminished tendon reflexes (Holmes-Adie Syndrome)
  .
  Diagnosis –> 0.125% pilocarpine
• Abnomral pupil will constrict
• Normal pupil does not constrict

Question 19

What traid characterises Holme’s-Adie Syndrome?

Answer 19

• Adie’s tonic pupil –> dilated pupil with poor reaction to light and poor constriction to near objects
• Diminished or absent deep tednon reflexes –> most commonly affecting the Achilles reflex
• Occasionally, segmental anhydrosis –> patchy loss of sweating

Question 20

Horner’s syndrome clinical features

Answer 20

• Ptosis –> drooping of the upper eyelid
• Miosis –> constricted pupil
• Anhydrosis –> loss of sweating on the affected side
• Enopthalmos –> affected eye appears sunken
• Loss of ciliospinal reflex –> damage to the sympathetic pathway at any level (central, preganglionic, or postganglionic) prevent activation of the pupillary dilator muscles

Question 21

What is the ciliospinal reflex?

Answer 21

• a sympathetic reflex arc that causes pupillary dilation in response to pain or stimulation of the neck, face, or upper trunk (eg. pinching the skin) –> this is used as a test of the sympathetic innervation to the pupil
  .
  1. Painful stimulation is transmitted via sensory nerves (e.g., cervical spinal nerves).
  2. Signals travel to the sympathetic centers in the spinal cord (C8–T2).
  3. Efferent sympathetic fibers stimulate the pupillary dilator muscles in the iris, causing dilation

Question 22

What are the 4 ways to diagnose Horner’s syndrome (both preganglionic and postganglionic) ?

Answer 22

• 4% cocaine –> normal pupil dilates, Horner’s pupil does not dilate
• 1% hydroxyamphetamine –> pre-ganglionic lesion (both pupils dilate), post-ganglionic lesion (Horner’s pupil does not dilate)
• 1:1000 adrenaline –> pre-gnaglionic lesion (both pupils do not dilate), post-ganglionic lesion (Horner’s pupil will dilate)
• Apraclonidine (0.5% or 1%) –> no effect on normal pupil, Horner’s pupil dilates

Question 23

Fundoscopy anatomy

Answer 23

Question 24

Normal retina VS Diabetic retina (image)

Answer 24

Question 25

Basic anatomy of neuroloigcal system

Answer 25

1. Brain at top 2. Underneath this is the brainstem 3. Cerebellum is tucked behind brainstem 4. Spinal cord goes all the way down 5. Peripheral nerves branch off 6. these meet muscles at the neuromuscular junction

Question 26

Pt has problem down right hand side of body (involves face, arm, leg)

Answer 26

Has to be a brain problem on the left side

Question 27

Pt has problem in right arm and leg, but left side of face is affected

Answer 27

We know that it has to be a brain problem, but we also know that the cranial nerves come out of the brainstem on the same side of the body, but everything comes out and crosses over --> therefore, this has to be a problem with the brainstem (can localise this to the left brainstem)

Question 28

If a pt is cut off from the waist down, what does this tell us?

Answer 28

That this has to be a spinal cord issue, and depending on what level the pt is cut off tells you the level of where the spinal cord problem is + if its involving the arms it has to be the neck

Question 29

If a pt has sciatic for example, where is the problem (basic anatomy)?

Answer 29

- nerve root --> radiculopathy

Question 30

If pt has carpal tunnel for example, where is the problem (basic anatomy)?

Answer 30

This is a mononeuropathy (involves one nerve)

Question 31

Alcoholic neuropathy...

Answer 31

There is damage to all nerves, but peripheral nerves (longest) are damaged first --> generalised peripheral neuropathy (glove and stocking distribution)

Question 32

What does onset tell us about the cause of the problem (neuro)?

Answer 32

- All of these pts will present with right hemiparesis, but the history will tell you the cause!

Question 33

Why should you document smell in head injuries?

Answer 33

Anosmia can indicate damage to the olfactory nerve (CN I)

Question 34

A patient present with transient loss of vision in one eye lasting seconds to minutes, they describe it as a "curtain or shade descending over the vision", you suspect a condition called amaurosis Fugax (acute CN II injury), what 2 vascular causes should you suspect as the cause?

Answer 34

- Carotid artery disease --> imaging - Giant cell arteritis --> ESR

Question 35

If a pt presents with a painful CN III palsy (oculomotor), what should you think of as the cause?

Answer 35

PCOM aneurysm is the most common cause of painful CN III palsy --> do a scan (CT-A), especially if pupil is involved

Question 36

Can you see isolate an isolated CN IV palsy on clinical examination?

Answer 36

Nobody can see an isolated CN IV nerve palsy --> has a very subtle and hard to see effect on eye movements - but what the pt says (history) can tell you a lot - eg. double vision worse when tilt head one way and better the other way

Question 37

Which nerves often gives a false localising sign?

Answer 37

CN VI can give a false localising sign --> this is due to CN VI having the longest cranial nerve course, and therefore lots of things can affect it (eg. pressures/problems within skull can cause a CN VI nerve palsy) - so if you see a new CN VI palsy, then this doesn't mean that it is localised to the 6th cranial nerve, it is can be due to other issues (eg. raised intracranial pressure)

Question 38

Spinal cord tracts anatomy

Answer 38

Question 39

Dermatomes

Answer 39

Question 40

Brachial plexus diagram

Answer 40

Question 41

Which spinal cord level is most likely to be affected?

Answer 41

T7

Question 42

What about in this patient, given the symptoms what is the likely area affected?

Answer 42

- Vibration and proprioception have been spared --> we know that these go through the dorsal column of the spinal tract - Therefore, this is an anterior spinal cord problem

Question 43

Spinal cord blood supply

Answer 43

- Blood supply is split into anterior spinal artery and the posterior spinal arteries - Therefore, if a pt has a stroke that affects the anterior spinal artery then will affect the anterior spinal cord but the posterior spinal cord will be spared as it has a separate blood supply (note: the anterior spinal artery comes off the aorta, so aortic dissection could affect anterior spinal cord only for eg.?)

Question 44

How is the spinal cord affected in this pt + name of condition ?

Answer 44

Brown-Siccard syndrome: - Pain and temperature start in your leg and as soon as they reach your spinal cord they cross over - Power, vibration, and joint position sense, do not cross over --> therefore you get this presentation if one half of the spinal cord is affected

Question 45

CN I --> what is it + what medicolegal implications does it have?

Answer 45

Olfactory nerve --> sense of smell (reported as taste!) - also has medicolegal implications --> eg. cannot smell gas

Question 46

CN II --> what is it + what can be seen in this photo?

Answer 46

Optic nerve - Image shows ptosis and miosis in left eye (Horner's)

Question 47

What does this image show?

Answer 47

Swollen optic disc --> could be cause by raised intracranial pressure (papilloedema)

Question 48

What does this image show?

Answer 48

Atrophic optic disc (on the left) --> a sign of damage to the optic nerve that causes the optic disc to appear pale and have sharp margins

Question 49

Visual fields --> anatomy and what defect is caused by what lesion? (draw it out)

Answer 49

Question 50

Pupillary reflex diagram --> draw it out + mechanism + which cranial nerves are tested

Answer 50

- Shine light in one eye --> testing the integrity of the optic nerve - signals are then sent back out along the outside of the third cranial nerve to cause constriction --> does this direct and also consensual - Tests CN II and CN III

Question 51

Diagram showing how the nerves talk to each other when you look to the right hand side --> what nerves are involved + what connects these nerves + why is this relevant

Answer 51

- Right eye is looking 'out' --> using abducens nerve (CN VI) - Left eye is looking 'in' --> using CN III (oculomotor nerve) - CN VI and CN III 'talk' to each other in the brainstem via the MLF (medial longitudinal fasciculus) --> relevant because the MLF is highly myleinated --> therefore diseases that affect myelin (MS) commonly cause lesions here

Question 52

What does a lesion in the MLF (medial longitudinal fasciculus) cause + mechanism behind this

Answer 52

Internuclear ophthalmoplegia --> this is where the CN III and CN VI don't talk to each other properly - therefore, when the right eye looks 'out' (abducts), the left eye does not move 'in' (adduct), the right eye then wobbles back and forth in response --> therefore, we say that there is failure of abduction of the left eye and a contralateral nystagmus of the right eye

Question 53

CN III palsy --> early/late signs and why this happens + surgical VS medical CN III palsy (and what cause of a surgical CN III palsy do you not want to miss?)

Answer 53

- Early sign --> pupil involvement (dilation) --> this is due to the fact that the constrictor fibres (peripheral parasympathetic fibres) run along the outside of CN III and therefore if there is a tumour/aneurysm pressing on the nerve then these will be the first fibres to be affected - Later sign --> drooping eyelid (ptosis) + eye pointing 'down and out' (shown in the image) . - Surgical CN III palsy --> pupil involving (something from outside pressing in) --> DO NOT WANT TO MISS PCOM aneurysm - Medical CN III palsy --> pupil-sparing (ischaemia of the central motor fibres sparing the peripheral parasympathetic fibres)

Question 54

CN V --> what is it + branches + how to test (subjectively/objectively) + why is it important to identify an issue with the trigeminal nerve?

Answer 54

Trigeminal nerve - can test subjectively with sensation of each branch - can get objectively using corneal reflex . - The trigeminal nerve runs through Meckel's cave --> there can be a metastasis/tumour within this area so if trigeminal pasly suspected then need to image

Question 55

CN VII --> what nerve is this + condition affecting this nerve (+ difference in presentation to stroke)

Answer 55

Facial nerve --> Bell's palsy - Note: relative forehead sparing in a stroke --> but if in doubt then should image to rule out stroke, but weakness of eye closure is pretty indicative of a peripheral nerve lesion (Bell's palsy) as it is very uncommon in a stroke pt

Question 56

Forehead involvement in a peripheral lesion (Bell's palsy - CN VII) and a central lesion (stroke) --> what causes relative forehead sparing in a stroke?

Answer 56

You get relative forehead sparing in a stroke (central lesion) due to the bilateral innervation, so the forehead still receives some signals

Question 57

CN VII --> What is important about the sensory and motor aspects of this nerve (think location of where they meet) + what are the sensory changes seen in a CN VII palsy?

Answer 57

Sensory fibres and motor fibres join together AFTER they have left the brainstem - Sensory changes --> loss of sensation in the mouth, in front of ear, and changes in hearing (CN VII innervates the stapedes muscle in the ear) --> useful to know this

Question 58

CN VIII --> what nerve is this + how do you test?

Answer 58

Vestibulocochlear nerve - Test using Rinne's and Weber's test --> used to see if conductive or sensorineural problem

Question 59

CN IX and X --> what nerves are these + from the image showing uvular deviation, which side is the nerve (CN X) palsy on?

Answer 59

- CN IX --> Glossopharyngeal nerve - CN X --> Vagus nerve . - From this image, the CN X palsy is on the pt's left side --> the uvular deviates away from the side of the palsy (bc that side is paralysed and not pulling the uvula)

Question 60

CN XII --> what is this nerve and how would you test its function?

Answer 60

Hypoglossal nerve - tongue protrusion --> in this case, the tongue will be pushed towards the lesion not away

Question 61

CN XI --> what is this nerve + how would you test its function?

Answer 61

Accessory nerve - Test sternocleidomastoid muscle --> pt turns their head to the side, this works the sternocleidomastoid muscle of the side you are testing (see image - pt turns head to right, left sternocleidomastoid is being tested) - Test trapezius muscle --> pt shrugs their shoulders

Question 62

Role of CT scans

Answer 62

- Acute trauma/crtitically ill pts - Ruling out subarachnoid haemorrhage - Acute stroke (within 48hrs) - TIA - intracranial tumours --> supratentorial mass - Hydrocephalus --> can assess shunt malformations (eg. over/under drainage - as CSF fluid has 0 attenuation so easily seen on scan) - Assess brain prior to lumbar puncture in a pt with focal neurology or elderly pt - Evaluate trauma --> fractures of orbits, temporal bones, skull base - good for looking at sinuses, degenerative disease and spinal stenosis, detection of calcification lesions - when MR contraindicated

Question 63

Contrast agents are drugs and can cause major and minor reactions - give examples of reactions that could occur

Answer 63

- urticaria (mild), bronchospasm, anaphylaxis, nephrotoxicity, seizures

Question 64

Identify the caudate nuclei, lentiform nucleus, and the thalamus on this CT scan

Answer 64

Note: the caudate nuclei and lentiform nucleus are both part of the basal ganglia

Question 65

What does this CT head show?

Answer 65

Subarachnoid haemorrhage

Question 66

Identify these anatomical areas on the CT brain image: - Frontal lobes - Frontal horns - Internal capsule - Caudate - Putamen and Globi Pallidi - Sylvian fissure - Insular lobe - Temporal lobes - Thalamus - Occipital horns - Occipital lobes

Answer 66

Question 67

Why is contrast a useful thing to do sometimes?

Answer 67

- Contrast can make certain vascular abnormalities more visible - Eg. this CT shows the importance of contrast (right image is where contrast has been given) --> shows a large AV malformation clearly

Question 68

CT perfusion studies - what is it and why do we use them in the case of a stroke?

Answer 68

- creates 'perfusion maps' which can tell us about the cerebral perfusion in this case - This CT perfusion study shows that there is an abnormality in the right MCA territory - We can use CT perfusion to assess 'salvageable' brain tissue and guide thrombolysis treatment in the case of a stroke

Question 69

CT VS MRI

Answer 69

- CT is good for assessing bones, but not soft tissues and other structures --> eg. in this case MRI shows spinal cord very well (CT cannot do this)

Question 70

MRI contraindications (eg. due to magnetic environment)

Answer 70

- cardiac pacemakers - MR incompatible vascular clips - electrical stimulator implants or pumps - metallic implants or orbital foreign bodies - severe claustrophobia - caution in pregnancy

Question 71

What is DWI MRI?

Answer 71

- Diffuse-Weighted Imaging is a specialised MRI - Particularly useful in locating an acute infarct where a CT cannot

Question 72

MRI showing a pituitary macroadenoma

Answer 72

Question 73

MRI angiography --> image

Answer 73

Question 74

Which imaging modality is best for viewing intracranial tumours?

Answer 74

MRI !

Question 75

MRI scan showing an AV malformation

Answer 75

- Here, the image shows an AV malformation in the right temporal lobe

Question 76

MR Venography --> image

Answer 76

Question 77

MR showing occlusion of left vertebral artery

Answer 77

Question 78

Answer 78

MRI shows metastasis in spinal cord aswell as a lesion in the frontal lobe - Further MR imaging with contrast shows the spinal cord tumour more clearly

Question 79

MRI is the study of choice for most brain and spine lesions, however, give some situations where a CT would be the better choice of imaging

Answer 79

Question 80

What is myelography and when is it used?

Answer 80

Myelography is a diagnostic imaging technique used to evaluate the spinal cord, nerve roots, and meninges by injecting a contrast agent into the subarachnoid space (the space around the spinal cord that contains cerebrospinal fluid - used when MRI is contraindicated (e.g., due to metal implants or severe claustrophobia) or to provide additional detail in certain spinal conditions

Question 81

Alzheimer's disease

Answer 81

- Conventional MRI can show atrophic changes in posterior parietal regions - PET scan shows changes too (should all be red) - But, using functional imaging we can diagnose certain conditions like Alzheimer's (amyloid is a hallmark of Alzheimer's disease)

Question 82

Overview of nervous system

Answer 82

- Brain - Brainstem - Cerebellum - Spinal cord - Nerve roots - Peripheral nerves - Neuromuscular Junction (NMJ) --> where nerve meets muscle

Question 83

Corticospinal movement ??

Answer 83

Question 84

Upper motor neuron vs Lower motor neuron

Answer 84

Question 85

Normal brain MRI

Answer 85

Question 86

What are the 2 major sensory pathways in the CNS (include function - what signals they carry + when they cross/decussate)

Answer 86

Dorsal Column Medial Lemniscal (DCML) pathway - Fine touch, vibration, proprioception - Cross in the medial lemniscus (a bundle of axons in the medulla oblongata) Spinothalamic Tract - Pain, temperature - Crosses immediately

Question 87

What are first-order neurons, second-order neurons, and third-order neurons and their functions?

Answer 87

First-order neurons: - Primary sensory neurons that detect stimuli from the environment (eg. touch, temperature, pain, or proprioception) - Carry sensory input from the periphery to the CNS . Second-order neurons: - receive signals from firs-order neurons and act as intermediates - relay the sensory signal to the thalamus (or cerebellum in some cases) . Third-order neurons: - receive input from second-order neurons and project to the sensory processing areas in the brain - Deliver the sensory information to the appropriate region of the cerebral cortex for conscious perception and interpretation

Question 88

Where do first-order neurons receive and transmit signals? (+ location of cell bodies + location/route of axons)

Answer 88

First-order neurons: Periphery --> Spinal cord/Brainstem - Cell bodies --> found in dorsal root ganglion of spinal nerves or the ganglia of cranial nerves - Axons --> extend from sensory receptors in the periphery (eg. skin, muscles, joints) to the CNS (spinal cord or brainstem)

Question 89

Where do second-order neurons receive and transmit signals? (+ location of cell bodies + location/route of axons)

Answer 89

Second-order neurons: Spinal cord/Brainstem --> Thalamus (decussate along the way) - Cell bodies --> found in the spinal cord or brainstem (depending on the pathway) - Axons --> decussate (cross to the opposite side of the CNS) and ascend to higher centers like the thalamus

Question 90

Where do third-order neurons receive and transmit signals? (+ location of cell bodies + location/route of axons)

Answer 90

Third-order neurons: Thalamus --> Cerebral cortex - Cell bodies --> found in the thalamus, a major relay center in the CNS - Axons --> project to the primary sensory cortex (in the parietal lobe) via the internal capsule

Question 91

Difference of when second-order neurons cross over (decussate) in the spinothalamic pathway and the DCML pathway

Answer 91

- Spinothalamic pathway --> decussation occurs immediately at level of entry into the spinal cord where the sensory info enters - DCML pathway --> decussation occurs later, in the medulla oblongata (medial lemniscus), after sensory signals ascend ipsilaterally in the spinal cord

Question 92

Spinothalamic tract (aka. anterolateral system) --> what are the two main divisions? + what do these detect? + what are the two types of receptors (nociceptors)?

Answer 92

- Organised into 2 main divisions --> anterior and lateral divisions - Anterior --> crude touch and pressure - Lateral --> pain and temperature . 2 types of nociceptors: - A-delta --> detects fast pain or "pinprick pain" - C-fibers --> pick up slow pain (lasting, enduring pain)

Question 93

Descending pathways --> what are the two main descending tracts and what are the functions?

Answer 93

- Descending pathways are categorised into pyramidal and extrapyramidal tracts --> motor pathways . Pyramidal tracts --> Control voluntary movements (especially fine, precise movements of the limbs): - Corticospinal tracts: Lateral corticospinal tract (fine movements of distal limbs) and Anterior corticospinal tract (controls axial muscles for posture and gross movements) - Corticobulbar tract --> controls head and neck muscles via cranial nerves . Extrapyramidal tracts --> Control involuntary movements, muscle tone, posture, and reflexes, often working with the cerebellum and basal ganglia: - Rubrospinal tract --> influences flexor muscles of upper limbs - Reticulospinal tracts --> controls posture, locomotion, and modulation of reflexes - Vestibulospinal tracts --> controls balance and postural reflexes - Tectospinal tract --> coordinates head and eye movements in response to visual stimuli

Question 94

1st order neurons, 2nd order neurons, and 3rd order neurons diagram showing pathway and locations

Answer 94

Question 95

Ascending and Descending pathways --> diagram showing horizontal cross section of vertebral column and locations of the different pathways

Answer 95

Note: the grey matter in the centre is where synapses occur and info is transmitted, the other areas are basically 'highways' where signals travel up and down

Question 96

Dermatomes

Answer 96

Question 97

Brachial plexus diagram

Answer 97

Question 98

Another brachial plexus diagram

Answer 98

Question 99

Neuromuscular junction --> video + diagram

Answer 99

https://www.youtube.com/watch?v=ApaPlKPb4ek

Question 100

Answer 100

Question 101

Answer 101

Question 102

What are the movements that the eye can do?

Answer 102

Question 104

Extraocular muscles --> innervation

Answer 104

- Superior oblique --> CN IV - Lateral rectus --> CN VI - the rest are supplied by CN III

Question 105

Vertical recti muscles --> what are these muscles, what are their primary actions, and how do you test them?

Answer 105

Superior rectus (SR): - primary action --> elevation of the eye - Test --> isolate SR by positioning the eye laterally (abducted) - ask pt to look outwards - then ask pt to look upwards . Inferior rectus (IR): - Primary action --> depression of the eye - How to test --> isolate the IR by positioning the eye laterally (abducted) - then ask pt to look downwards (Note: by abducting the eye you are isolating the muscle by aligning the muscle with the vertical plane (minimising the effects of other muscles))

Question 106

Obliques --> what are the muscles, what are their primary actions, how to test them

Answer 106

Superior oblique: - Primary action --> Intorsion (also depression and abduction) - How to test --> position the eye medially (adducted) - ask pt to look inward - then ask pt to look downward (in adduction the SO becomes the primary depressor of the eye as the vertical recti muscles are less effective) . Inferior oblique: - Primary action --> Extorsion (also elevation and abduction) - How to test --> position the eye medially (adducted), then ask pt to look upward (Note: Obliques do the Opposite of what they say on the bottle)

Question 107

Why do the oblique muscles do the opposite of what they say on the bottle?

Answer 107

As they attach posteriorly on the eye, rather than anteriorly like the other muscles

Question 108

Yoke muscles

Answer 108

2 muscles work together --> eg. looking left - L lateral rectus and R medial rectus . - Vertical --> eg. right SR and left IO (elevation), right IR and left SO (depression)

Question 109

What is strabismus (squint)?

Answer 109

misalignment of two eyes

Question 110

How is strabismus classified?

Answer 110

- Concomitant --> no limitation of movement - Incomitant --> limitation of movement (paretic vs restrictive)

Question 111

For each term --> what is meant by the term + muscle affected (assuming this muscle isn't working properly rather than the other muscle being overstimulated): - Esotropia - Exotropia - Hypertropia - Hypotropia

Answer 111

- Esotropia --> can they abduct? - lateral rectus - Exotropia --> can they adduct? - medial rectus - Hypertropia --> can they depress? - inferior rectus + superior oblique - Hypotropia --> can they elevate? - superior rectus + inferior oblique

Question 112

Aetiology of types of ocular deviation

Answer 112

Question 113

Differences between comitant strabismus and incomitant strabismus

Answer 113

Question 114

Manifest VS Latent strabismus

Answer 114

- Manifest strabismus --> a constant misalignment of the eyes that is always present during binocular vision - Latent strabismus --> a tendency for the eyes to misalign that is controlled by the brain's fusion mechanim during binocular vision, the eyes are only misaligned when fusion is disrupted (eg. by covering one eye) or if fatigued/stressed

Question 115

How do you test for manifest strabismus, how do you test for latent strabismus, and what further tests do you need to do if it is latent strabismus?

Answer 115

- Cover test --> cover test - Alternate cover test --> latent strabismus - If latent strabismus then need to test individual eye movements to determine which muscle is affected

Question 116

Comitant VS Incomitant

Answer 116

- Comitant = the misalignment remains constant regardless of gaze direction - incomitant = where the misalignment/dysfuncton in eye movement varies on direction of gaze (eg. If the eyes align properly when looking straight ahead but show misalignment or reduced movement in certain directions (e.g., up, down, left, or right), the condition is incomitant)

Question 117

How do you test for an incomitant strabismus? (+ what are versions and what are vengences in this context?)

Answer 117

- Check binocular smooth pursuit --> basically how well the eyes move together in each direction - Versions = both eyes move in the same direction (conjugate movement) - Vengences = the eyes move in opposite directions (disconjugate movement) - eg. convergence (eyes moving inward toward the nose for near focus)

Question 118

Paretic incomitant strabismus VS Restrictive incomitant strabismus + how do we test to tell us the cause of the incomitant strabismus

Answer 118

- Paretic --> results from weakness or paralysis of one or more extraocular muscles due to nerve damage or a neuromuscular disorder (eg. CN palsies, myasthenia gravis) - Restrictive --> occurs when mechanical factors limit the movement of one or more extraocular muscles (eg. trauma, tumours) . Uniocular smooth pursuit (ductions): - used to assess independent range of motion of each eye --> tells us wheteher paretic or restrictive - cover one eye and test eye movements in each eye individually

Question 119

What is meant by the terms ductions and versions?

Answer 119

- Ductions --> movements of a single eye in isolation (evaluates individual extraocular muscles) - Versions --> coordinated movement of both eyes together in the same direction (tests binocular eye movements and evaluates the function of paired extraocular muscles)

Question 120

What does the realtionship between versions (binocular smooth pursuit) and ductions (uniocular smooth puruit) tell us about whether the cause is paretic or restrictive?

Answer 120

- Ductions = Versions --> RESTRICTIVE - Ductions > Versions --> PARETIC

Question 121

What are saccades + why is it useful to test these movements?

Answer 121

- Saccades = rapid, voluntary eye movements that shift the gaze between two points of focus . Useful to test for: - Supranuclear / Internuclear disorders - Spotting subtle paresis - Testing saccadic pathways --> eg. frontal eye fields (FEF) which initiate voluntary saccades

Question 122

What are convergence and divergence and what muscles are used in each?

Answer 122

- Convergence = the inward movement of both eyes towards the nose to focus on a near object (medial rectus muscles of both eyes --> CN III) - Divergence = the outward movement of both eyes when focusing on a distant object (lateral rectus muscles of both eyes --> CN VI)

Question 123

Incomitant - Neurogenic (3rd nerve palsy) --> what are the symptoms

Answer 123

- Ptosis - Down and out - Dilated pupil (if pupil involvement - think more serious cause like aneurysm of PCOM) - Abduction intact . Key: - is it painful - is pupil involved - no improvement

Question 124

Incomitant - Neurogenic (4th nerve palsy) --> what are the symptoms + most common causes

Answer 124

- Torsion (tilt) - Compensatory head tilt - Hypertropia --> type of strabismus where one eye is deviated upwards relative to the other eye - Impaired depression (in adduction) - Trauma (40%), congenital (30%)

Question 125

Incomitant - Neurogenic (6th nerve palsy/lateral rectus palsy) --> what are the symptoms + most common causes

Answer 125

- Esotropia - Reduced abduction - Ipsilateral face turn . - Usually benign

Question 126

What is amblyopia?

Answer 126

Amblyopia (or lazy eye) = refers to a unilateral or bilateral decrease of vision, caused by abnormal vision development in childhood or infancy (one eye will have reduced vision) - most common cause of visual impairment in children

Question 127

When does normal visual develpoment mature?

Answer 127

by 7 years of age

Question 128

What are the 2 main types of amblyopia?

Answer 128

- Refractive amblyopia = caused by significant differences in the refractive error between the two eyes - Strabismic amblyopia = caused by strabismus (eye misalignment)

Question 129

What screening tests are done for amblyopia + When is the school screening age for amblyopia

Answer 129

- Newborn and 6/52 GP test - School screening age is 4-5 yrs (usually spotted by parent/teacher)

Question 130

Management of amblyopia (lazy eye)?

Answer 130

- Glasses (corrective lenses) --> to correct refractive errors - Occlusion therapy (eye patching) --> patching the stronger eye forces the amblyopic eye to work harder, stimulating it to develop better visual acuity . (used if above do not work): - Atropine drops --> can be used in stronger eye to temporarily blurr vision, stimulating the amblyopic eye to work harder - Surgical alignment of eyes (squint surgery)

Question 131

What is the red reflex?

Answer 131

- The red reflex appears as a reddish-orange reflection from the retina, seen when a bright light (usually from an ophthalmoscope) is shone into the eye - The light from the ophthalmoscope enters the eye and is reflected off the retina, which has a rich blood supply, giving the red color. The light is then reflected back through the pupil and is visible to the examiner (an absent red reflex can indicate various eye pathology)

Question 132

Name some causes of an absent red reflex + one condition you do not want to miss

Answer 132

- Ethnic variation - High refractive error - Squint - Cataracts - Retinoblastoma --> cancerous aetiology (do not want to miss)

Question 133

Peter's anomaly

Answer 133

- Peters anomaly is a congenital eye disorder characterized by central corneal opacity and abnormalities in the anterior segment, including the iris, lens, and anterior chamber. - It can cause significant visual impairment and is often associated with other developmental abnormalities.

Question 134

Congenital glaucoma

Answer 134

Question 135

What is nystagmus + some causes

Answer 135

- Nystagmus = involuntary, rapid eye movements - Causes --> Congenital (infantile) - idiopathic, albinism, structural, rod/cone abnormality, Acquired - neurological (CNS / vestibular disease, drugs)

Question 136

Red flags of nystagmus

Answer 136

- Acquired onset ( > 4 months age) - Normal eyes - Oscillopsia ("world shaking") --> if recent then will have 'wobbly' vision, if long-standing then won't have 'wobbly' vision due to compensation - Vertical / Torsional - Other neuro signs/symptoms

Question 137

Which muscle pulls the eye up in abduction? - Inferior rectus - Lateral rectus - Superior rectus - Inferior oblique

Answer 137

Superior rectus

Question 138

Which muscle is supplied by the 4th cranial nerve (trochlear nerve)? - Inferior Oblique - Inferior Rectus - Lateral Rectus - Superior Oblique

Answer 138

Superior oblique

Question 139

Which muscle is the yolk muscle of the Left Superior Rectus? - Right Inferior Oblique - Right Medial Rectus - Left Inferior Rectus - Right Superior Rectus

Answer 139

Right Inferior Oblique

Question 140

What is the key way of separating squints diagnostically? - Acquired v Infantile - Comitant v Incomitant - Intermittent v constant - Manifest v Latent

Answer 140

Comitant v Incomitant

Question 141

What does the Cover test reveal? - If there is a muscle restriction - If there is a nerve weakness - If there is a manifest squint - If there is a latent squint

Answer 141

If there is a manifest squint

Question 142

Why do we test Binocular eye movements (versions?) - To look for incomitant squints - To look for a manifest squint - To assess vision - To assess angle of squint

Answer 142

To look for incomitant squints

Question 143

Why do we test uniocular ductions? - To assess for a squint - To test vision - To see if it is restrictive or paretic - To be complete

Answer 143

To see if it is restrictive or paretic

Question 144

What do we call fast refixation eye movements? - Versions - Dictions - Vergence - Saccades

Answer 144

Saccades

Question 145

Which cranial nerve palsy must be treated with the most urgency with respect to eye movements? - 4th cranial nerve - 6th cranial nerve - 2nd cranial nerve - 3rd cranial nerve

Answer 145

3rd cranial nerve

Question 146

Which of these are adaptive mechanisms for a squint? - Suppression - Anomalous retinal correspondence - Corrected head posture - All of the above

Answer 146

All of the above

Question 147

Which of these are the main cause of amblyopia in children? - Refractive - Strabismic - Sensory deprivation - All of the above

Answer 147

Refractive

Question 148

Which of these are a cause of an abnormal red reflex? - Retinoblastoma - Congenital cataract - Squint - All of the above

Answer 148

All of the above

Question 149

Glasgow coma score --> What is it used for + what 3 things are measured + what score indicates a "comatose" patient

Answer 149

- Assesses level of consciousness - Eye opening response + best verbal response + best motor response (motor score most useful) - < 8 --> comatose patient (note: for pain stimuli --> supraorbital pinch or trapezius squeeze)

Question 150

Glasgow coma scale (GCS) --> Adult and Paediatric

Answer 150

Question 151

What does an abnormal pupil response (fixed and dilated) indicate?

Answer 151

indicates that there is likely pressure somewhere --> uncal herniation (ipsilateral) - the arrow is showing how the medial part of the temporal lobe is being pushed down due to the subdural haematoma above (increased ICP --> brain is pushed downwards) (note: bilateral fixed and dilated pupils is an extremely poor prognostic sign)

Question 152

What does increased intracranial pressure on a CT scan show specifically regarding the cisterns? (+ what are cisterns?)

Answer 152

- Cisterns = enlarged pockets of CSF that are located between the arachnoid and pia mater membranes of the brain - cisterns are compressed when ICP increases as CSF fluid is usually the first thing within the brain to be compensated

Question 153

Monroe-Kellie doctrine

Answer 153

- The skull is a fixed box - 3 intracranial compartments --> Brain, Blood (arterial/venous), CSF - CSF is usually the first compartment to be compensated

Question 154

if ICP gets really high, which direction is the brain pushed and through what structure?

Answer 154

- If ICP is really high then only way brain can be pushed is down ("coming" or tonsillar herniation) - brain is squeezed through the foramen magnum --> a natural opening at the base of the skull

Question 155

What is autoregulation and why is this important for the brain? (+ what 2 things does the brain rely on to survive?)

Answer 155

- Autoregulation = the brain's ability to maintain a constant blood flow despite changes in blood pressure --> this process is important because the brain needs a constant supply of blood and oxygen to function - Brain relies on oxygen and glucose --> doesn't cope well with fats (fatty acids) or proteins (amino acids)

Question 156

Case: - 20yo male brought into Addenbrooke's ED by paramedics on a Friday night - Bystanders say a gang of thieves tried to steal his PhD thesis on theoretical physics (it is Cambridge after all...) and when he valiantly (but unsuccessfully) tried to fight them off he was beaten severely - He was initially conversion normally with his friends about quantum electrodynmaics, then suddenly became very drowsy and an ambulance was called - GCS of 8, R pupil fixed and dilated (not reacting to light), CT scan is shown What is the diagnosis? + What is the treatment?

Answer 156

- Extradural haemorrhage - Treatment --> craniotomy to relieve ICP

Question 157

If right pupil is fixed and dilated, what side is the brain lesion?

Answer 157

Right side

Question 158

These CTs show types of traumatic brain injury, what is shown in each?

Answer 158

- Left --> Subdural haemorrhage ('crescent' shape) - Middle --> Contusion (bruise inside brain) - usually caused by a fall and treated conservatively - Right --> Skull fracture (impacting R frontal lobe)

Question 159

Types of intracranial haemorrhages

Answer 159

Question 160

Types of intracranial haemorrhages --> Diagram

Answer 160

Question 161

Intracranial pressure monitor

Answer 161

- small wire inserted to measure ICP

Question 162

Chronic subdural haematoma --> what age group does this usually develop in and why? + what is the treatment?

Answer 162

- Usually elderly pts --> brain becomes more atrophic as we age, therefore minor trauma can cause this - Treatment --> 2 small holes made to drain blood --> chronic blood is more liquid-like (less viscous) so easier to drain

Question 163

Case: - A 55yo male is brought by his family to ED with sudden onset right facial drooping, arm and leg weakness, and dysphasia 1hr ago - His wife brings you his medications which include atenolol and amlodipine - His CT is shown What is your diagnosis? What is the cause? Which blood vessels are most commonly affected in this type of condition?

Answer 163

- Hx suggests a stroke --> we need to CT first-line to assess - CT shows an acute bleed around basal ganglia --> lateral ventricle is compressed (indicates increased pressure) - High blood pressure has caused this - Lenticulostriate vessels are most likely affected when BP too high --> as these are the smallest and most vulnerable

Question 164

Case: - Student suddenly develops a terrible headache (worst of his life) around the back of his head - His girlfriend brings him to ED and you have the dubious honour of being the duty on call - His CT is shown What is the diagnosis? What would you do if the hx was the same but the CT was normal?

Answer 164

- Subarachnoid haemorrhage - If CT normal --> still suspicious of a SAH due to the hx --> perform a lumbar puncture

Question 165

What is a lumbar puncture + when should a lumbar puncture be performed in regards to a subarachnoid haemorrhage + what are we looking at?

Answer 165

- LP should be performed AFTER 12hrs - No. RBCs --> a normal LP should not contain RBCs (note that can be present due to traumatic tap rather than true SAH) - Appearance --> xanthochromia - CSF appears yellow (caused by the breakdown of Hb) - Spectrophotometry --> to look for bilirubin ( a breakdown product of Hb)

Question 166

What type of imaging is the gold standard to look for vascular abnormalities within the brain?

Answer 166

Cerebral angiogram

Question 167

Where do aneursyms usually form in the brain and what is the treatment?

Answer 167

- Often form at bifurcation points (most vulnerable - exposed to high haemodynamic stresses) Treatment: - Supportive --> Prevent vasospasm (triple H therapy, nimodipine) - Treat cause (prevent rebleed) --> clipping (surgery), coiling (endovascular)

Question 168

Hydrocephalus --> what is it + treatment

Answer 168

- Hydrocephalus = a condition where cerebrospinal fluid (CSF) builds up in the brain, causing pressure to increase and potentially damaging brain tissue - Treatment (CSF diversion therapy) --> need to relieve CSF pressure (VP shunt is most common treatment - drains excess CSF from ventricles into the peritoneal cavity (abdomen) where it is absorbed)

Question 169

Communicating VS Obstructive Hydrocephalus

Answer 169

Question 170

Causes of hydrocephalus

Answer 170

- Causes --> congenital, acquired (meningitis, encephalitis, intraventricular haemorrhage, tumours, TBI ...)

Question 171

Ventriculoperitoneal (VP) shunt - used in treatment of hydrocephalus

Answer 171

Question 172

Case: - 35yo woman, BMI > 35 - 1 week ago while lifting her PhD thesis (very heavy), she developed sudden onset lower back pain which radiates down the back of both of her legs - Now, she has had an episode of urinary incontinence. She also comments that when she wipes herself with toilet paper after using the bathroom the sensation feels 'different from normal' What will you do?

Answer 172

MRI spine --> cauda equina

Question 173

Symptoms of cauda equina

Answer 173

Question 174

What scale is used to measure severity of subarachnoid hemorrhage?

Answer 174

Fisher scale

Question 175

Paediatric brain tumour symptoms

Answer 175

Question 176

What is a supratentorial brain tumour (+ what is the tentorium cerebelli?

Answer 176

a brain tumor that is located above the tentorium cerebelli --> the fold of dura mater that separates the brain stem and cerebellum from the cerebral hemispheres and diencephalon

Question 177

What type of brain tumour (supratentorial or infratentorial) has the potential to cause obstructive hydrocephalus and why

Answer 177

Infratentorial tumour - because it is located in the posterior fossa, beneath the tentorium cerebelli --> where critical structures involved in cerebrospinal fluid (CSF) flow are located - these tumors can block the normal flow of CSF, leading to its accumulation in the brain's ventricles.

Question 178

Symptoms of brain tumour in adults

Answer 178

- Headaches - Memory/cognition/personality change - Seizures - Weakness - Balance issues - Visual disturbance - Hearing/tinnitus

Question 179

Assessment of brain tumour in adults

Answer 179

- CT head - MRI head with contrast - Staging CT - Visual fields/ophthalmology - Hearing test/audiometry - Assess need for steroids (with PPI cover) + assess need for CSF diversion

Question 180

Meninges

Answer 180

- Meningiomas are benign, slowly growing lesions - derived from arachnoid cap cells - inoperable, incurable

Question 181

What is meant by the peripheral nervous system and how is it divided?

Answer 181

- Basically everything outside of the CNS (brain and spinal cord) - the nerves that branch out from the brain and spinal cord (eg. cranial nerves, spinal nerves) Peripheral nervous system is divided into somatic and autonomic: - Somatic: controls voluntary movements and transmits sensory info to the CNS --> composed of motor nerves (control skeletal muscles) and sensory nerves (relay info like touch, pain, and temp. to CNS) - Autonomic: controls involuntary functions (eg. heart rate, digestion, and respiration) --> Sympathetic NS ("fight or flight" response - increased HR, dilation of pupils) and Parasympathetic NS ("rest and digest" - slows HR, stimulates digestion)

Question 182

Nerve and neuron diagram

Answer 182

Question 183

Clinical features of peripheral neuropathy

Answer 183

History: - Sensory --> pins and needles, pain, numbness - Motor --> wasting, weakness (+/- painful cramps)

Question 184

What type of neuropathy is most common? - Motor and sensory - Motor - Sensory - Sensory and autonomic

Answer 184

Motor and sensory

Question 185

Sensory abnormalities --> give an example of a positive symptom and a negative symptom

Answer 185

- Positive symptom --> pain - Negative symptom --> numbness

Question 186

What are the two main types of pathology that can occur with nerves (think anatomy of a neuron)

Answer 186

- Axonal - Demyelinating (2 main parts to a nerve --> axon + myelin) (you can get mixed pathology too)

Question 187

In terms of invetigations, how would you tell the difference between axonal pathology and demyelination pathology

Answer 187

- Axons --> measure size (amplitude) of nerve responses (lower amplitudes than normal = axon loss) - Myelin --> measure speed (velocity) of nerve conduction (slower than normal = myelin damage)

Question 188

What does 'length-dependent' mean in terms of neuropathy?

Answer 188

Simply refers to the fact that the longest nerves will be affected first as they are more vulnerable

Question 189

What is the most common type of mono-neuropathy?

Answer 189

Carpal tunnel syndrome --> median nerve affected

Question 190

What is the most common cause of peripheral neuropathy?

Answer 190

Diabetes

Question 191

What type of neuropathy is sciatica?

Answer 191

Radiculopathy (nerve root - L4/L5)

Question 192

What type of vitamin deficiency is seen in nitrous oxide poisoning?

Answer 192

B12 deficiency

Question 193

What are the 2 main barriers the brain has to protect against infection + what is the most common route of infection?

Answer 193

- Blood-brain barrier --> regulates movement of substances between bloodstream and the brain (selective transport), formed by endothelial cells joined by tight junctions (supported by astrocytes (glial cells)) - Blood-CSF barrier --> comprised of ependymal cells with tight junctions that line the choroid plexus (where CSF is produced) - prevents pathogens in the blood from entering the CSF - blood-borne invasion is the most common route of infection (eg. by polioviruses or Neisseria meningitidis) (invasion via peripheral nerves is less common, but for example Varicella Zoster virus can lay dormant in the sensory ganglia of cranial nerve or the dorsal ganglia)

Question 194

CSF analysis

Answer 194

- Appearance --> clarity, colour - Microscopy --> cell count, WCC, gram stain - Culture - PCR - Serology - Biochemistry

Question 195

Why are glucose lvls low in bacterial infections?

Answer 195

because bacteria likes to eat glucose

Question 196

What type of WBC is seen in the CSF in bacterial infections?

Answer 196

PMN (Polymorphonuclear neutrophils)

Question 197

Meningitis diagram

Answer 197

Question 198

What type of bacteria is Neisseria meningitidis?

Answer 198

Gram-negative diplococcus (closely resembles Neisseria gonorrhoea in structure) - has a polysaccharide capsule which is a key virulence factor

Question 199

Meningococcal capsular groups

Answer 199

Question 200

Meningitis haemorrhagic skin rash

Answer 200

petechial rash

Question 201

Meningitis pathogens table

Answer 201

- Remember Neisseria meningitidis is most common in ages 11-17yrs --> Streptococcus pneumoniae is most common in all other ages --> Haemophilus influenzae is most common in children < 5yrs

Question 202

How are amoebae bacteria transmitted?

Answer 202

lake water

Question 203

Routine vaccination Program: - Babies under 1 year old - Children aged 1 to 15yrs - Adults - Pregnant women

Answer 203

Question 204

Describe how Streptococcus pneumoniae causes meningitis

Answer 204

- Nasopharyngeal colonisation - Bloodstream invasion - Blood-brain-barrier (BBB) crossing --> eg. via infected WBCs - Multiplication in the CSF --> causing inflammation and swelling - Brain damage --> inflammation damages brain and causes symptoms (eg. headache, stiff neck, photophobia)

Question 205

Viral meningitis (more common than bacterial meningitis) --> symptoms + CSF appearance + type of cells found in CSF

Answer 205

- Milder disease than bacterial meningitis --> with headache, fever, and photophobia, but less neck stiffness - CSF is clear in absence of bacteria and the cells are mainly lymphocytes

Question 206

Is encephalitis caused by bacteria or viruses?

Answer 206

Viruses

Question 207

Contact tracing for meningitis

Answer 207

- Exposure to respiratory secretions - Post-exposure vaccination - Antibiotic prophylaxis --> Ciprofloxacin, Rifampicin, Ceftriaxone)

Question 208

Important causes of secondary headaches and primary headaches

Answer 208

Question 209

Red flags for headaches

Answer 209

- New headache - Worst ever headache - Thunderclap onset --> first ever? - Systemically unwell - Symptoms of raised ICP or cancer - Meningism or focal signs

Question 210

Does the brain have sensory neurons?

Answer 210

NO, the brain has no sensory neurons - the pain form seconary headaches come from outside the brain --> eg. brain tumour obstructs CSF flow and stretches the meninges --> eg. haemorrhage causes meningeal inflammation (meningitis)

Question 211

Example of papilloedema --> optic disc is inflamed and bulging

Answer 211

- Papilloedema is a term we use when we know that this is caused by raised ICP --> if we didn't know this then we call it a swollen optic disc - Note: cannot see disc margins (should be crisp and defined)

Question 212

Subarachnoid haemorrhage --> symptoms, investigations, Treatment

Answer 212

- THUNDERCLAP onset worst ever headache (+ never happened before) --> meningitic symptoms - CT --> fantastic early (CT picks up 98% of SAH), rubbish late - LP --> fantastic after 12 hrs and within 2 weeks, useless after this - Treatment --> bedrest, fluids (saline), nimodipine, look for (CT angio) and secure aneurysms (clips/coils)

Question 213

Meningitis

Answer 213

- Same type of headache as SAH, but slower start - Notifiable --> esp. Neisseria menigitidis - Elderly/immunosuppressed --> cover listeria - Steroids for pneumococcus - Antibiotics for all -->

Question 214

Headaches in the Elderly --> GCA

Answer 214

GCA - vasculitis emergency - does not occur under 50 yrs - jaw claudication, amaurosis fugax, scalp, tenderness - palpable pulseless temporal arteries - normal ESR/CRP/Platelets --> excludes GCA as cause - Needs a biopsy to confirm it - Treatment is high dose STEROIDS

Question 215

What is the clinical sign and what is the diagnosis + why + treatment - this is a set piece

Answer 215

- ptosis in left eye (Horner's syndrome) --> caused by traumatic injury to the sympathetic chain (carotid artery dissection) - Treatment is high dose ASPIRIN (rollercoaster in question --> think carotid artery dissection says module lead)

Question 216

What is the diagnosis + what is the visual field defect shown + why thunderclap headache - This is a set piece

Answer 216

- Pituitary adenoma (prolactinoma) --> bitemporal hemianopia - Thunderclap headache --> due to pituitary apoplexy (emergency condition - pituitary gland failure --> Addisonian crisis) - Treatment --> start STEROIDS

Question 217

What is the diagnosis + Treatment - this is a set piece

Answer 217

Venous sinus thrombosis - give HEPARIN

Question 218

Tension-type headache

Answer 218

- most common headache - end of the day, not severe, like a band - no signs on examination - Treatment --> amitriptyline

Question 219

Migraine

Answer 219

- alos very common - blame the parents - recurrent unilateral throbbing gradual onset, hours, nausea, vomiting, photo and motion sensitivity - painkillers don't work - Treatment (holistic, acute/abortive, preventative)

Question 220

Migraine - Diagnostic Criteria (International Headache Society)

Answer 220

Question 221

Migraine treatment

Answer 221

- Important to educate pt that this is treatment and not necessarily curable Abortive treatment: - +/- anti-emetic - Triptan (PO, SC, nasal) --> eg. frovatriptan (long half-life) (if cannot take triptan) - NSAID --> aspirin 600-900mg dispersible

Question 222

Trigeminal neuralgia treatment

Answer 222

- Carbamazepine - Gabapentin - lamotrigine (anticonvulsants)

Question 223

What is Multiple Sclerosis?

Answer 223

a chronic inflammatory demyelinating disease of the brain and spinal cord

Question 224

Diagram of nerves in body

Answer 224

Question 225

Causes of MS?

Answer 225

Genetics: - HLA-associated polymorphisms (HLA-DRB1*15:01) Environment: - Vit D deficiency - Infections --> particularly EBV Smoking exposure Autoimmune: - against myelin and oligodendrocytes (cells that produce myelin)

Question 226

Types of mulitple sclerosis

Answer 226

1. Benign Multiple Sclerosis 2. Relapsing Remitting Multiple Sclerosis (RMMS) --> most common type 3. Secondary Chronic Progressive --> about 50% of RRMS cases progress into this 4. Primary Progressive (10-20% pts)

Question 227

Clinical presentation of multiple sclerosis

Answer 227

Question 228

MS relapse

Answer 228

- a sudden worsening or recurrence of neuro symptoms caused by new inflammation and demyelination in the CNS --> relapses are a hallmark feature of RRMS - new or worsening symptoms lasting at least 24hrs - symptoms are not caused by an infection, fever, or other external factors (eg. heat, stress) - a period of at least 30 days must have passed since the last relapse to be classified as a separate event

Question 229

Optic neuritis in multiple sclerosis

Answer 229

- one of the most common presenting symptoms of MS --> involves inflammation of the optic nerve, leading to visual disturbances and eye pain - 70% unilateral - O/E --> fixed and dilated pupil (does not react to light) - Usually improves over weeks to months, but residual deficits may persist

Question 230

What is Uhthoff's symptom (aka. Uhthoff's phenomenon)?

Answer 230

temporary worsening of neurological symptoms in individuals with MS or other demyelinating diseases, triggered by an increase in body temperature - eg. loses vision R eye for 30 mins in second half of football matches (due to increase in body temperature)

Question 231

Sensory disturbances in multiple sclerosis --> include Lhermitte's sign

Answer 231

Positive symptoms: - paraesthesia --> "pins and needles" - Dyesyhesia --> burning (can be triggered by light touch) Negative symptoms: - Numbness Neuro pain: - Lhermitte's sign (aka. Lhermitte's phenomenon) --> electric shock-like sensation that radiates down the spine, arms, or legs when bending the neck forward (caused by lesions in the cervical spinal cord) Thermosensitivity (Uhthoff's phenomenon) --> symptoms worsen with heat (eg. fever, exercise, or hot weather)

Question 232

Motor symptoms in multiple sclerosis

Answer 232

- Weakness --> usually asymmetrical - Spasticity --> increased muscle tone (limb spasms) - Loss of dexterity --> hands - Fatigue - Impaired coordination and gait --> ataxia (cerebellar involvement) - Spastic paraparesis --> progressive weakness in lower limbs

Question 233

2 eye signs seen in MS

Answer 233

- Relative afferent pupil defect (RAPD) --> sign of disease in the retina or optic nerve (something pressing on it?) causing reduced reactivity to light - Intra-nuclear ophthalmoparesis --> caused by lesion in the MLF, this disrupts communication between the abducens nucleus (controls lateral gaze) and the oculomotor nucleus (controls medial gaze) --> resulting in impaired conjugate horizontal eye movements

Question 234

Diangosis in MS?

Answer 234

Diagnosis requires evidence of at least 2 lesions separated in time and space without a better explanation

Question 235

What is Neuro-myelitis optica spectrum disorder (NMOSD)?

Answer 235

- a chronic, autoimmune, inflammatory condition of the CNS that primarily affects the optic nerves and spinal cord --> causing optic neuritis and transverse myelitis - NMOSD is distinct from MS, but has some overlapping features - often associated with autoantibodies against aquaporin-4 (AQP4)

Question 236

Investigations in multiple sclerosis

Answer 236

Diagnosis is primarily clinical and based on the pt's symptoms and examination, but some tests are useful to confirm diagnosis, rule out other conditions, and assess the extent of disease activity/progression: - MRI --> gold standard, used to identify lesions in the CNS - Lumbar puncture (CSF analysis) --> oligoclonal bands present in CSF, but not serum is a hallmark of MS --> indicate chronic inflammation in the CNS - Visual evoked potentials --> measure the brain's response to visual stimuli (in MS, delayed VEP results can indicate demyelination along the optic nerve or visual pathways)

Question 237

What is the main drug given in the treatment of relapses in Multiple Sclerosis (MS)?

Answer 237

Corticosteroids - suppresses inflammatory response, decreases severity/duration of exacerbations --> IV (3-5 days) or oral 500mg/5 days

Question 238

Prognosis in MS

Answer 238

Question 239

Other treatments used in management of MS

Answer 239

Question 240

Label this diagram + - what is the neurocranium? - which bones are paired? - what is the calvaria?

Answer 240

- Neurocranium = part of the skull that contains the brain - Paired bones --> temporal and parietal bones - Calvaria = the dome-like roof of the neurocranium (made up of parietal, frontal, occipital, and squamous parts of the temporal bone)

Question 241

What are the 3 layers of the meninges?

Answer 241

- Dura mater - outer fibrous layer, blends with periosteum - Arachnoid mater - inner thin delicate layer - Pia mater - microscopic, in direct contact with the brain

Question 242

Meningeal spaces

Answer 242

Note: extradural space is in the brain --> it is called the epidural space in the vertebral column

Question 243

What are the 2 layers of the Dura Mater? + fill in the diagram

Answer 243

- outer periosteal layer - inner meningeal layer - this is the layer that reflects away from periosteal layer to form dural infoldings / reflections --> these separate the brain into compartments

Question 244

Venous drainage of the brain / sinuses + where are all of the sinuses aiming to drain into?

Answer 244

All of the sinuses are aiming to drain into the internal jugular vein - note: the pothalmic veins ar connected t

Question 245

How could picking a spot on your face potentially cause meningitis?

Answer 245

due to the fact that the venous drainage of the face connects with the brain sinuses (as well as draining down into the internal jugular vein) via the cavernous sinus

Question 246

What is the major artery that supplies blood to the dura mater of the brain?

Answer 246

Middle meningeal artery: - a branch of the maxillary artery --> which is a branch of the external cartoid artery - passes through the foramen spinosum

Question 247

What is important about the location of the middle meningeal artery

Answer 247

- located at the pterion - pterion - where four skull bones articulate --> frontal, parietal, sphenoid, temporal - this is a weak spot! --> therefore if there is trauma to the skull then the middle meningeal artery is vulnerable

Question 248

Where will the bleed likely be if there is trauma to the side of the head + which artery is most likely to be affected?

Answer 248

- note: brain pressure will increase - raised ICP

Question 249

Label the diagram + which arteries form the anterior circulation and posterior circulation?

Answer 249

Anterior circulation (internal carotid system): - Anterior cerebral arteries - Anterior communicating artery - Middle cerebral arteries . Posterior circulation (vertebrobasilar system) - Posterior cerebral arteries - Posterior communicating arteries

Question 250

What happens when one of the vessels involved in the circle of willis ruptures + what is the most likely cause of the rupture?

Answer 250

Subarachnoid haemorrhage - Aneurysm

Question 251

How does an intracerebral haemorrhage differ from a subarachnoid haemorrhage + what is the most common cause?

Answer 251

- Intracerebral haemorrhage is more focal - involves smaller branches within the brain - presentation depends on area od brain affected - caused by an aneurysm (same as subarachnoid haem)

Question 252

Venous drainage of the brain - a closer look

Answer 252

- cerebral veins drain into venous sinuses within the dura mater - cerebral veins cross the subarachnoid space . - the dural venous sinus in the image is the superior sagittal sinus

Question 253

Subdural haemorrhage - is this arterial or venous haemorrhage + risk factors

Answer 253

- risk factors --> weaker veins ...

Question 254

Which of these is a subdural haemorrhage + why is a subdural haemorrhage less life-threatening than the other hemorrhages of the brain?

Answer 254

Answer = B - subdural haemorrhage is a venous bleed - slow increase in pressure - arterial pressure --> quick increase in pressure --> more dangerous

Question 255

Table comparison of haemorrhages of the brain

Answer 255

- Sub arachnoid - pt can experience a bad headache a few days before a catastrophic bleed

Question 256

Label this diagram

Answer 256

Question 257

Where is CSF produced and secreted from?

Answer 257

Choroid plexus - produces and secretes CSF in response to hormone, CSF pressure, and blood pressure stimuli

Question 258

What is CSF reabsorbed by and where is it drained into?

Answer 258

- Reabosrbed by arachnoid ghranulations - Drained into venous system

Question 259

Main functions of CSF?

Answer 259

- Glucose-rich - Provides buoyancy to the brain - protects - Homeostasis - carries lots of electrolytes - Waste disposal system - carries unwanted stuff into the lymphatic system/venous drainage system

Question 260

What is hydrocephalus?

Answer 260

Excessive CSF present due to overproduction or lack of drainage

Question 261

If there is leakage of CSF, where would it leak through and into + what is the test for this?

Answer 261

CSF leaks through ethmoid bone into nasal cavity - persistently runny nose - positive glucose test on this fluid indicates likely CSF leak (remember CSF is glucose-rich)

Question 262

Headache red flags

Answer 262

- New severe or unexpected headache - Thunderclap headache --> reaching maximal intensity within 5 mins of onset may indicate subarachnoid haemorrhage - Progressive or persistent headache - Headache with fever, nausea/vomiting, neck stiffness, or reduced level of consciousness - Focal neuro symptoms/signs - neuro deficit, change in personality, cognitive impairment - Visual disturbance - can be associated with migraine, but also with serious causes such as angle-closure glaucoma and temporal arteritis - Older age - Following trauma

Question 263

Case: 45yr old woman presents with a sudden onset of a very severe headache, initially at the back of the head, becoming generalised within a few minutes, associated with vomiting O/E: she was alert, afebrile, photophobic, and had moderate neck stiffness, fundoscopy shows blood at back of eye, abnormal ocular movements + ptosis - what is your main differential and what investigations would you do?

Answer 263

Subarachnoid haemorrhage - symptoms (thunderclap headache, photophobia and neck stiffness, vomiting ...) + 3rd nerve palsy --> SAH - CT if acute, LP if after 12hrs

Question 264

Ptosis can indicate a 3rd nerve palsy or Horner's syndrome - symptoms + what is the difference in ptosis?

Answer 264

- Horner's syndrome involves triad of ptosis, miosis, and anhydrosis (+/- enopthalmos) - 3rd nerve (oculomotor) palsy causes ptosis, dilated non-reactive pupil, and divergent strabismus ("down and out") - 3rd nerve palsy typically has more pronounced ptosis compared to Horner's due to the complete paralysis of the levator palpebrae superiors muscle

Question 265

Which muscle causes a ptosis in a 3rd nerve palsy due to being paralysed?

Answer 265

- levator palpebrae superioris muscle - main muscle responsible for elevating the eyelid

Question 266

Neurysm of which artery in the brain can cause a 3rd nerve palsy?

Answer 266

- Posterior Communicating Artery (PCOM) aneurysm is a classic caused of 3rd nerve palsy - the aneurysm (bulging of arterial wall) can compress the oculomotor nerve as it exits the brainstem

Question 267

Case: 50 yr old man who was playing squash developed a sudden pain in left front-orbital region and transient loss of vision in the left eye O/E: left ptosis and small left pupil and there was mild tenderness on the left side of the neck - What is your main differential and why is this not a cluster headache? - what is the management of your main differential?

Answer 267

Carotid artery dissection - sudden-onset pain - front-orbital region - transient vision loss (amaurosis fugax - caused by embolisation from the dissection affecting the retinal artery) - left ptosis and small pupil (miosis) - signs of Horner's syndrome - neck tenderness - suggests local irritation of the vessel wall at the site of dissection - Precipitating event - playing squash involves rapid neck movements --> can traumatise the carotid artery . Management focuses on prevention of stroke and managing symptoms: - antiplatelet therapy (eg. 300mg aspirin) - for symptoms - analgesia + avoid strenuous activities, Valsalva maneuvers, and neck manipulation

Question 268

Case: 75yr old woman complained of a constant right-sided headache for the past 8 weeks. She had felt vaguely unwell and had lost her appetite during this period. On further questioning she admitted to about 3kg weight loss and pains in her legs. In the last week before seeing her GP she had had a few episodes of 'black spots' in front of her eyes. - What is your main differential - What initial investigation would you do + what is the management

Answer 268

Giant cell arteritis (aka. temporal arteritis) - symptoms suggest GCA - jaw claudication (cramping pain when chewing) is also a common symptom - 'Black spots' in front of the eyes - likely amaurosis fugax (transient vision loss), indicating involvement of the ophthalmic artery - Initial investigation - raised ESR + temporal artery biopsy (definitive diagnostic test) - Management - immediate high-dose corticosteroids (prednisolone 40-60mg OD) (if visual symptoms are present (amaurosis fugax), then initiate IV methylprednisolone to prevent permanent vision loss)

Question 269

What rheumatological condition is giant cell arteritis (GCA) associated with?

Answer 269

Polymyalgia rheumatica (PMR)

Question 270

Case: 25yr old woman presents with 6 weeks of persistent generalised headaches worse with coughing and straining. Intermittently she experiences fleeting episodes of visual loss in her right eye. She has been on the OCP (oral contraceptive pill) for the past 3 months, but takes no other medications O/E: fundoscopy shows papilloedema - What is your main differential - What is your management

Answer 270

Idiopathic Intracranial Hypertension (IIH) - Generalised headache - persistent and worse with coughing/straining --> classic for raised ICP - Visual symptoms - transient episodes of visual loss occur due to papilloedema compressing the optic nerve - Papilloedema on fundoscopy - confirms raised ICP - Risk factors - young woman on OCP (associated with fluid retention and hormonal factors that may contribute to IIH) (note: tumour still in differentials --> MRI to assess) Treatment - treat underlying cause - Acetazolamide is first-line (topiramate is alternative + causes weight loss in pts) - Refractory cases - loop diuretics, repeated LPs for temporary management - Analgesia - to manage pain - Surgical potions (if vision at risk) - optic nerve sheath fenestration (to protect optic nerve and preserve vision) +/- CSF shunting (reduce CSF pressure)

Question 271

35yr old woman complains of tingling sensation in her left face and arm which feels heavy. Over 5 minutes it spread to her leg and persisted for around 40 minutes. Her speech was slurred and difficult. Afterwards she felt muzzy headed and tired. - Diagnosis?

Answer 271

- Migraine - not a stroke as symptoms are over minutes (stroke would be sudden and maximal) - Also, in 95% of ppl, the speech areas (Broca's and Wernicke's) are in the left hemisphere of the brain so this speech presentation doesn't make sense

Question 272

52 yr old man complains of several episodes of pins and needles in his left hand and face. Each episode feels identical like water running up his leg and down his arm over 5 seconds. - Diagnosis?

Answer 272

- Seizures - still important and serious - tumour or metastasis? (sitting on sensory cortex)

Question 273

76 yr old man. Hypertensive, smoker, complains of sudden painless loss of strength and sensation from the waist down. No movement in either leg but vibration sense and proprioception preserved. - Diagnosis?

Answer 273

Spinal stroke (anterior) - risk factors for vascular disease - "waist down" - spinal problem - symptoms suggest anterior spinal stroke

Question 274

82 yr old woman with two episodes of sudden monocular loss of vision has been having aching shoulders for months, headaches and jaw pain for weeks. - Diagnosis?

Answer 274

Ophthalmic TIA due to GCA - amaurosis fugax - also worried about carotid artery disease/stenosis (surgery?)

Question 275

Todd's paresis

Answer 275

- refers to temporary (mins to hrs) weakness or paralysis in a part of the body following a seizure - usually affects contralateral side to the area of the brain that was involved in the seizure - stroke mimic - neuroimaging to assess

Question 276

Virchow's triad

Answer 276

Set of 3 key factors that contribute to the development of venous thromboembolism (VTE) - eg. DVT, PE: - Stasis of blood flow - eg. AF - Endothelial/vessel wall injury - eg. atherosclerosis - Hypercoagulability - lots of conditions (eg. sickle cell, DIC, polycythemia vera, TTP), pregnancy

Question 277

What symptoms of a migraine would make you suspect a stroke?

Answer 277

- prolonged/frequent aura - > 60 mins --> MRI - if presents with neurological deficit - rare for migraines to have hemiparesis

Question 278

What medication should be avoided in pts with migraines over 60 yrs?

Answer 278

Triptans - can increase risk of an ischaemic attack (stroke)

Question 279

Case: 18 yr old female. PMH: migraine only 1 week left sided headache and eye pain, 2-minute episode of muddled speech yesterday, woke up this morning - R hand feels clumsy and numb. She looks like this (image) - Diagnosis?

Answer 279

Horner's syndrome - worried about carotid dissection

Question 280

Case: 28 yr old man, no known PMH, presents with right-sided weakness and severe aphasia. Systolic murmur and skin rash. - Diagnosis? - Treatment?

Answer 280

Infective endocarditis - part of vegetations have come off and embolised to the brain - Blood cultures --> antibiotics

Question 281

Case: 27 yr old female, 5 days post-partum - uncomplicated. PMH: migraine Progressive headache 24hrs Sudden onset visual loss --> Left and ataxia - Diagnosis

Answer 281

PRES (Posterior reversible encephalopathy syndrome) - young woman, post partum, progressive headache - MRI shows posterior changes to the brain - PRES mainly affects posterior areas

Question 282

MELAS (Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes) - classic set of symptoms - how does it affect the brain - CSF?

Answer 282

- Short diabetes, deafness, cardiomyopathy, epilepsy - non-vascular territory strokes - imaging doesn't fit with a standard stroke - CSF raised lactate

Question 283

CADASIL - genetic condition and is a rare genetic smooth muscle vasculopathy that primarily affects the brain leading to recurrent ischaemic strokes and progressive neurological decline, what inheritance pattern does CADASIL have and what mutation?

Answer 283

Autosomal dominant - mutations in the NOTCH3 gene

Question 284

Fabry's disease - what symptoms - what inheritance pattern does it have - deficiency of α-galactosidase A leads to an accumulation of what?

Answer 284

- symptoms - neuro pain, angiokeratomas (shown in image), renal failure, cardiomyopathy, and stroke - X-linked - only males affected - accumulation of Gb3 - toxic to smooth muscle

Question 285

Case

Answer 285

Antiphospholipid syndrome - cause of stroke (sticky blood) - image shows livedo reticularis

Question 286

What are the 2 components to consciousness?

Answer 286

- Arousal (alertness/being awake) - dependent on the reticular activating system (RAS) and diencephalon - Awareness (ability to know what's going on) - mediated by cerebral cortex

Question 287

What GCS score requires intubation to protect the airway?

Answer 287

GCS ≤ 8

Question 288

Cheyne-Stokes breathing

Answer 288

Reflects instability in the control of ventilation - gradual increase in depth and rate of breathing (hyperventilation), followed by a gradual decrease in breathing until a temporary apnoea

Question 289

Name some causes of coma: - Vascular - Infections - Metabolic - Autoimmune - Abnormal electrical activity

Answer 289

Vascular: - Ischaemic stroke - Intracranial haemorrhage - extradural, subdural, SAH, intracerebral - CVST . Infections: - Sepsis - Meningitis - meningoencephalitis . Metabolic: - DKA - hx of T1DM - Hypoglycaemia - eg. fasting - Hepatic encephalopathy - ammonia accumulation in liver failure - Uremic encephalopathy - toxins accumulation due to renal failure - Myxedema coma . Autoimmune: - Limbic encephalitis . Abnormal electrical activity: - Seicure

Question 290

Bacterial meningitis VS Viral meningitis (CSF analysis)

Answer 290

- Bacterial meningitis - raised polymorphonuclear neutrophils + low glucose + high protein - Viral meningitis - raised lymphocytes + normal glucose/protein

Question 291

Epilepsy definition + epileptic seizure definition

Answer 291

- Epilepsy = a condition characterized by an increased susceptibility to spontaneous epileptic seizures (caused by excessive excititation or insufficient inhibition) - Epileptic seizure = a transient epidose of abnormal neurological function caused by sudden excessive or hypersynchronous cortical neuronal activity

Question 292

Excitation and inhibition of nerve pathways - What is meant by each of these terms - Which ions are involved in each + name some neurotransmitters for each

Answer 292

Excitation = occurs when a neuron is stimulated and depolarised to generate an action potential (nerve impulse), which propagates along the axon to excite downstream neurons or effector tissues - Occurs when the neuron's membrane potential becomes less negative (depolaristaion) - influx of positive ions (Na+ and Ca2+ channels opening) - Glutamate and aspartate - major excitatory neurotransmitter in the brain - Acetylcholine - another excitatory neurotransmitter Inhibition = reduces or prevents the likelihood of generating an action potential - inhibitory signals hyperpolarise the neuronal membrane, making it more negative occurs by increasing negative ion influx (Cl-) or positive ion efflux (K+) - GABA - main inhibitory neurotransmitter in the CNS

Question 293

What are the two main types of seizures?

Answer 293

Focal and generalised

Question 294

Focal seizures: - what is meant by this term - what are the 2 types of focal seizure - symptoms (motor, sensory, autonomic, cognitive)

Answer 294

Focal seizures occur in one specific area of the brain (localised region), the effects depend on the area of the brain affected (frontal, temporal, parietal, occipital): Two types: 1. Focal seizures without impaired consciousness (simple partial) - person remains conscious during seizure 2. Focal seizures with impaired consciousness (complex partial) - pt experiences altered consciousness (confused), may include automatisms (eg. lip-smacking, repetitive movements), staring, and a lack of awareness Symptoms: - Motor - jerking, twitching, or stiffening of a part of the body - Sensory - tingling, numbness - Autonomic - sweating, HR changes, or nausea - Cognitive - impaired speech, confusion, or memory disturbances

Question 295

Generalised seizures: - what is meant by this term - types of generalised seizures

Answer 295

Generalised seizures involve abnormal electrical activity in both hemispheres of the brain, usually leading to a loss of consciousness and widespread symptoms Types: - Tonic-Clonic seziures (grand mal) - Absence seziures (petit mal) - Myoclonic seizures - Atonic seizures - Tonic seizures

Question 296

Myoclonic seizures, Atonic seizures, and Tonic seizures - symptoms

Answer 296

- Myoclonic - brief, sudden muscle jerks or twitches, consciousness usually retained, may be precipitated by alcohol withdrawal and sleep deprivation - Atonic - sudden loss of muscle tone, consciousness usually impaired, lasts few seconds, leading to falls or head drops - Tonic - sudden muscle stiffness/contraction, consciousness usually impaired, common during sleep, can lead to sudden forceful falls

Question 296

Tonic-Clonic seizures (grand mal) - describe the tonic and clonic phase

Answer 296

- Tonic phase - sudden muscle stiffening and loss of consciousness - Clonic phase - rhythmic jerking movements of the body (typically lasts 1-3 mins)

Question 297

Absence seizures - symptoms

Answer 297

- Characterised by brief episodes of staring or "zoning out" lasting seconds - no convulsive activity, and the person may not be aware of the seizure

Question 298

Focal seizures VS Generalised seizures table

Answer 298

Question 299

What is post-ictal confusion ?

Answer 299

a temporary state of confusion and other symptoms that can occur after a seizure

Question 300

Absence VS Complex partial seizure differences

Answer 300

Question 301

Causes of epileptic seizures

Answer 301

Question 302

Childhood absence epilepsy (CAE)

Answer 302

- Onset usually between 4-10 yrs, more common in girls - Frequent absence seizures (up to 100/day) - Characteristic EEG - generalised 3Hz spike and wave discharges --> often triggered by hyperventilation - +ve family hx of epilepsy - Usually remits at puberty - Treatment - Ethosuximide or Sodium Valproate

Question 303

Juvenile myoclonic epilepsy

Answer 303

- Onset typically in adolescence - Characterised by myoclonic jerks (typically within 1hr of awakening - Circadian distribution), may also have generalised tonic-clonic seizures, and less commonly absence seizures - Triggers include sleep deprivation, stress, and alcohol - EEG findings - irregular 3-6Hz spike/polyspike and slow wave discharges - Prognosis - lifelong (different to CAE which remits at puberty), seizures well-controlled with medication - Management - Lifestyle advice, sodium valproate or clonazepam, OR in young women of child-bearing age Levetiracetam)

Question 304

What medications should be avoided in juvenile myoclonic epilepsy due to risk of exacerbation of myoclonus

Answer 304

vigabatrin, tiagabine, carbamazepine

Question 305

Temporal lobe epilepsy due to mesial temporal sclerosis

Answer 305

- Focal epilepsy accounts for 70% of all epilepsies - temporal lobe epilepsy is the most common form of focal epilepsy in adults due to its vulnerable cortical architecture - Often associated with a hx of febrile seizures in childhood - involves scarring and neuronal loss in the hippocampus and other mesial temporal structures - Clinical features - focal seizure often with impaired awareness, deja vu, epigastric rising sensation (abdominal aura), fear, olfactory or gustatory hallucinations, and automatism (lip-smacking, hand movements) - MRI - hippocampal atrophy and increased T2 signal on MRI, consistent with sclerosis - Management - often resistant to medical therapy - can do surgery (anterior temporal lobectomy) which can be curative in drug-resistant cases - first-line - carbamazepine or lamotrigine

Question 306

In simple terms how fo anti-epileptic drugs work?

Answer 306

- Block excitatory pathways or enhance inhibitory pathways (GABA)

Question 307

Which AED for an absence seizure?

Answer 307

1. Ethosuximide 2. Sodium valproate 3. Lamotrigine

Question 308

Which AED for focal seizures and generalised tonic-clonic seizures?

Answer 308

1. Focal - Lamotrigine, carbamazepine 2. Generalised - Sodium valproate, lamotrigine (in practice, levetiracetam often used first choice)

Question 309

Which AED for myoclonic seizures/jerks + what should be avoided?

Answer 309

1. Sodium valproate 2. Levetiracetam (AVOID carbamazepine, gabapentin, oxcarazepine, pregabalin, vigabatrin, tiagabine)

Question 310

Which AED for atonic and tonic seizures?

Answer 310

1. Sodium valproate 2. Lamotrigine 3. Topiramate

Question 311

What is SUDEP

Answer 311

Main cause of excess mortality in chronic epilepsy - risk factors - young, GTCS, uncontrolled epilepsy, learning disability, seizures during sleep

Question 312

Antidepressants used in treating depression in epilepsy

Answer 312

- SSRI - citalopram, sertraline - SNRI - venlafaxine - Mirtazapine

Question 313

How does surgery work in simple terms to treat epilepsy

Answer 313

basically just take out the part of the brain which is causing the seizures - only suitable in 10-20% of pts with medically refractory epilepsy

Question 314

Vagal nerve stimulation (VNS) in epilepsy

Answer 314

- implantable device (like a pacemaker for the brain) - device delivers mild, preprogrammed intermittent electrical pulses to the let vagus nerve (vagus nerve sends 80% of sensory signals to the brain) - has an anti-epileptic effect

Question 315

Lacrimal drainage anatomy

Answer 315

Question 316

Function of eyelids

Answer 316

- lubrication of the ocular surface - protection from infection

Question 317

Microbial keratitis - results of long-term dryness of eye (lack of lubrication)

Answer 317

- irritation - stinging - burning - red sticky eye in morning --> can lead to loss of vision

Question 318

What is lagophthalmos?

Answer 318

Incomplete eye lid closure

Question 319

Blepharitis - anterior lid margin vs posterior lid margin

Answer 319

- anterior lid margin - more common in younger pts - posterior lid margin - more common in elderly pts

Question 320

Chalazia

Answer 320

often associated with blepharitis

Question 321

Entropion

Answer 321

Inward turning of the eyelid - Treatment - lubricants, taping, botox, surgery (lateral canthal sling)

Question 322

Ectropion

Answer 322

outward turning of the eyelid - main cause is lid laxity due to ageing - treatment - lubrication, surgery

Question 323

Cicatricial ectropion

Answer 323

condtiion where the anterior lamella of the eyelid shortens - causing the eyelid margin to pull away from the eye

Question 324

2 main causes of acute ptosis

Answer 324

- Horner's syndrome - 3rd nerve palsy

Question 325

dermatochalasis

Answer 325

excess skin and muscle in the eyelids - also known as "baggy eyes"

Question 326

benign vs malignant lid lesions

Answer 326

- Benign - long hx, gradual change, asymptomatic, may be tender - malignant - recent onset, rapid growth, bleeding, pigmented

Question 327

Examples of benign lesions

Answer 327

note: xanthelasma is another benign lid lesion

Question 328

Premalignant lid lesions

Answer 328

note - keratoacanthoma - similar to SCC so need to excise and biopsy

Question 329

Malignant lid (periocular) lesions

Answer 329

treatment - excision or radiotherapy (Merkel cell responds well to this)

Question 330

Treatment of periocular BCCs

Answer 330

- Excision - conventional or Mohs - +/- reconstruction by an ophthalmologist trained in oculoplastic surgery

Question 331

What will the pt experience if the lacrimal gland is partially (or fully) excised during a surgery?

Answer 331

Dry eyes - lack of lacrimation - pt will need lifelong lubrication

Question 332

Dacryocystitis

Answer 332

Infection/abscess of the lacrimal sac - usually caused by a blockage in the nasolacrimal duct - blood stained tears (red flag sign) - lacrimal sac tumour - treatment - antibx

Question 333

Dacroadenitis

Answer 333

inflammation of the lacrimal glands

Question 334

Orbital disease

Answer 334

pressure on optic nerve

Question 335

Orbital cellulitis

Answer 335

Question 336

Most common cause of proptosis

Answer 336

Thyroid eye disease

Question 336

What common cause of red eye is this + treatment?

Answer 336

Herpes simplex eye - treatment - topical acyclovir

Question 337

Common in children (umbilicated)

Answer 337

Molluscum contagiosum (Pox virus) - Treatment - prompt curettage to stop spread

Question 337

What is shown here + treatment ?

Answer 337

Blepharitis - anterior lid - younger pt - posterior lid - elderly pt - Treatment - good lid hygiene, if inflammation --> oral doxycycline + steroid drops

Question 337

What is shown here (serious condition)?

Answer 337

Herpes Zoster ophthalmicus (aka. ophthalmic shingles) - serious condition (can lose sight!) - viral infection that affects the eye and is caused by reactivation of varicella-zoster virus - Treatment - oral acyclovir 1 week + topical steroids if inflamed

Question 337

This condition is usually caused by blepharitis - note the ulceration of the corneal edge

Answer 337

Marginal keratitis - inflammation of the cornea - treatment - topical steroids + antibx + treat blepharitis

Question 338

What is shown here + treatment

Answer 338

Conjunctivitis - treatment - topical antibx + good lid hygiene + prevent spread

Question 339

Causative pathogen of adult chlamydial keratoconjunctivits + treatment

Answer 339

- chlamydia trachomatis - treatment - topical tetracycline and oral tetracycline or macrolide

Question 340

Answer 340

Pterygium

Question 341

Left and right - what is shown

Answer 341

Subconjunctival haemorrhage - can be due to trauma or spontaneous (heavy straining) - shown on the right is hyphema (medical emergency)

Question 342

Scleriitis - what is it + potential progression + treatment

Answer 342

Scleritis = serious inflammatory disease that affects the sclera (can be autoimmune or result of an infection) - can lead to avascular patches and scleral necrosis - treatment - oral steroids + immunosuppressive agents

Question 343

Pt who went swimming with contact lenses in

Answer 343

Acanthamoeba keratitis

Question 344

Answer 344

Corneal foreign body

Question 345

Answer 345

- white dots on left image --> keratic precipitates on corneal endothelium - right image shows perilimbal congestion

Question 346

Case: - sudden onset painful red eye - severe pain +/- vomiting - decreased visual acuity due to corneal oedema - may see rainbow halos round lights - semi-dilated oval pupil - stony hard eyeball

Answer 346

EMERGENCY - acute angle closure glaucoma - trabecular meshwork blocked

Question 347

Treatment of acute angle closure glaucoma

Answer 347

- lie pt supine - acetazolamide 500mg IV - pilocarpine 2% to both eyes - topical pressure-lowering drops - topical steroids - for inflammation - Definitive - laser peripheral iridotomy

Question 348

Glaucoma definition

Answer 348

A progressive optic neuropathy associated with characteristic structural damage to the optic nerve and associated visual dysfunction

Question 349

Label this diagram

Answer 349

Question 350

Label this diagram

Answer 350

Question 351

Basic pathology of glaucoma - damage/death of ? cells

Answer 351

Damage/death to the retinal ganglion cells

Question 352

Fundoscopy (optic disc) - Normal VS Glaucoma

Answer 352

Question 353

Visual field loss in glaucoma

Answer 353

- Arcuate scotoma - arc-shaped defect extending from blind spot in peripheral nasal field corresponding to the reinal nerve fibre layer (RNFL) - Paracentral scotomas - small defects near fixation (close to central visual field) - Peripheral vision progressively diminishes --> creating a "tunnel vision" effect - central macular fibres are usually spared until very late disease

Question 354

Image showing "tunnel vision" in glaucoma

Answer 354

Question 355

Main risk factor for glaucoma

Answer 355

Raised IOP (intraocular pressure)

Question 356

Open VS Closed angle glaucoma

Answer 356

Open-angle: - chronic, progressive optic neuropathy - open anterior chamber angle but imapired aqueous humor drainage --> leads to gradual increased IOP - treatment is topical medications to lower IOP Closed angle: - characterised by a sudden rise in IOP due to obstruction of the trabecular meshwork by the iris - preventing aqueous humor reaching the meshwork for drainage - Treatment - laser (to open angle or create an alternative outflow pathway) + IOP-lowering medications

Question 357

Acute Primary Angle Closure - Management

Answer 357

- Acetazolamide 500mg IV - Pilocarpine 2% drops to both eyes - Mannitol IV - Dexamethasone drops - lie pt supine - Laser peripheral iridotomy

Question 358

Are thicker or thinner corneas associated with a greater risk of glaucoma progression?

Answer 358

Thinner

Question 359

Machine used to assess visual fields

Answer 359

Question 360

Visual fields results interp.

Answer 360

- top left - accuracy - black on the graph shows visual field defect / bind spot

Question 361

What is the most common type of eye drop to give in management of glaucoma?

Answer 361

Prostaglandin analogue

Question 362

What is trabeculectomy?

Answer 362

A surgical procedure to treaet glaucoma by creating a new pathway for fluid to drain from the eye

Question 363

Glaucoma - DVLA driving standards for group 1 (cars, motorcycles) and group 2 (HGVs, lorries, buses) drivers

Answer 363

Question 364

Maculopathy

Answer 364

maculopathy = retinopathy within the macular

Question 365

What is a characteristic feature/'Hallmark' of early AMD (age-related macular degeneration)?

Answer 365

Drusen deposits - glycoprotein collections - note: Drusen characteristics correlated with progression to wet AMD

Question 366

Dry AMD vs Wet AMD

Answer 366

AMD is a leading cause of central vision loss in older adults - it primarily affects the macula, the central part of the retina responsible for sharp, detailed vision Dry AMD (non-exudative): - Drusen deposits (yellow deposits) under retina + RPE degeneration + geogrpaical atrophy (well-demarcated areas of complete photoreceptor and RPE loss) - Treatment - lifestyle changes + monitor with Amsler grid for early detection of wet AMD Wet AMD (exudative): - choroidal neovascularization + leakage/haemorrhage of fragile new vessels + fibrosis - Treatment - Anti-VEGF therapy (intravitreal injections)

Question 367

What is the arrow pointing to - seen in end-stage AMD (age-related macular degeneration)

Answer 367

Question 368

What is amaourosis fugax?

Answer 368

- Transient and sudden mononuclear blindness - often described as a shade or curtain that obscures vision in one eye - usually last < 10 mins and are painless - carotid or cardiac emboli should be suspected

Question 369

most common cause of retinal artery occlusion

Answer 369

embolus

Question 370

Central retinal artery occlusion fundoscopy findings

Answer 370

Cherry red spot and retinal whitening

Question 371

Central retinal artery occlusion VS Branch retinal artery occlusion

Answer 371

Central retinal artery occlusion: - causes diffuse ischaemia of the entire retina complete vision loss - fundoscopy - cherry red spot and retinal whitening - increased risk of stroke/TIA Branch retinal artery occlusion: - occlusion of a branch of the central retinal artery (only part of retina affected) - localised retinal ischaemia - partial vision loss - fundoscopy - retinal whitening in distribution of the affected branch

Question 372

Management of central retinal artery occlusion

Answer 372

Urgent referral to ophthalmology (+ elderly pts should be screened for GCA!) 1. ocular massage - dislodges embolus and restores blood flow 2. anterior chamber paracentesis (only if visual loss has been present > 24 hrs) 3. Hyperbaric oxygen (HBO) therapy may be beneficial if initiated within 2-12 hrs of symptom onset 4. IOP-lowering medications - acetazolamide + mannitol IV

Question 373

Non-proliferative Diabetic Retinopathy - fundoscopy findings

Answer 373

Question 374

Retinal argon laser - used to treat macular oedema "threatening" the fovea and leading to loss of acuity

Answer 374

Question 375

Intravitreal injection of anti-VEGF

Answer 375

Question 376

Answer 376

photocoagulation on fundoscopy

Question 377

Proliferative diabetic retinopathy (PDR)

Answer 377

PDR is a more advanced stage of diabetic retinopathy characterized by the growth of new blood vessels (neovascularization) in the retina due to chronic retinal ischemia. These new vessels are fragile and prone to leakage, which can lead to vitreous hemorrhage and retinal detachment, both of which can cause significant vision loss if untreated

Question 378

Hypertensive retinopathy fundoscopy signs

Answer 378

Question 379

If pt has a painful eye, what can you give them in order to examine the eye?

Answer 379

Anaesthetic eye drops - tetracaine

Question 380

Which type of conjunctivitis is an emergency?

Answer 380

Gonococcal conjunctivitis - caused by Neisseria gonorrhoea

Question 381

Answer 381

Corneal laceration - clean out + suture (note: if pupil is misshaped (right image) then indicates that there is 'more' going on

Question 382

Which one is caused by acid and which by alkali + which is worse + management of chemical eye injuries

Answer 382

- Left is acid, right is alkali - basically everything is damaged (if limbus damaged then no new epithelial growth factors --> BAD!) - Alkali is worse than acid . Management: 1. wash eyes (irrigate) with plenty of saline + remove debris if any 2. check pH of tear film + obtain info ab the chemical 3. Refer ! (beware the 'white' eye --> end stage)

Question 383

Acute angle closure diagram

Answer 383

- aq still being produced, but has nowhere to go

Question 384

Laser treatment of acute angle closure glaucoma - Peripheral Iridotomy

Answer 384

Creates a small hole in the iris - allows drainage of fluid - note: only used as a last resort - medications tried first

Question 385

Retinal tear and detachment

Answer 385

- Retinal tear = rip in the retina, caused by the vitreous pulling on the retina (eg. PVD) - Retinal detachment = occurs when the neurosensory layer of the retina separates from the underlying retinal pigment epithelium (RPE) - subretinal fluid can accumulate between neurosensory retina and RPE

Question 386

Jaw claudication is a characteristic symptom of giant cell arteritis (GCA), this is due to ischaemia of ? muscle

Answer 386

masseter

Question 386

Answer 386

- Left image shows BRAO - Right image shows CRAO - "cherry red" spot

Question 387

What is hypopyon?

Answer 387

Hypopyon = a collection of white blood cells that pools in the front part of the eye (anterior chamber), usually as a result of inflammation in the middle layers of the eye

Question 388

What is the most common cause of dementia?

Answer 388

Alzheimer's disease (note: Alzheimer's is a condition itself and not all people with Alzheimer's have dementia, but it is common)

Question 389

Is there impairment in consciousness in dementia?

Answer 389

NO, there is impiarment in multiple cognitive domains, but consciousness is not impaired (eg. drunk, concussed, delirious)

Question 390

An approach to cognitive impairment...

Answer 390

- note the delirium screen and ruling out other causes (eg. meningitis, encephalitis - LP/CT)

Question 391

What type of memory loss occurs in Alzheimer's disease?

Answer 391

Progressive episodic memory loss - not just "short-term memory loss"

Question 392

MRI scans of vascular dementia

Answer 392

Question 393

How is a diagnosis of dementia made?

Answer 393

Mainly clinical - imaging has a role in confirming diagnosis, ruling out other causes, and refining the diagnosis, but clinical is the main bit - note: imaging can often be normal in dementia - but if clinically you think they have dementia then they have dementia

Question 394

What causes dementia?

Answer 394

Proteins are laid down in an abnormal way - leads to death of neurons

Question 395

What proteins are affected in Alzheimer's disease?

Answer 395

Amyloid + Tau

Question 396

What proteins are affected in Frontotemporal dementia (FTD)?

Answer 396

Tau + TDP-43

Question 397

What protein is affected in Motor neuron disease +/- FTD?

Answer 397

TDP-43

Question 398

What protein is affected in Parkinson’s/Dementia with Lewy Bodies/Multisystems Atrophy?

Answer 398

Alpha Synclein

Question 399

Cognitive and neuroanatomical profiles of some major dementia syndromes

Answer 399

Question 400

What cognitive disoder do the following examples describe? - Can't find the chair --> - Doesn’t know what a chair is --> - Falls getting out of the chair --> - Slow and shakey --> - Stuck to the floor --> - Fast and wriggly --> - Bed-bound and twitchy -->

Answer 400

- Can't find the chair --> Visuospatial – Posterior Cortical Atrophy - Alzheimer's - Doesn’t know what a chair is --> Semantic Dementia (TDP-43) - Falls getting out of the chair --> Progressive Supranuclear Palsy (Tau) - Slow and shakey --> Parkinson’s / Dementia with Lewy Bodies - Stuck to the floor --> Vascular Dementia /Normal Pressure Hydrocephalus - Fast and wriggly --> Huntington’s Disease - Bed bound and twitchy --> CJD

Question 401

What lobes are affected in semantic dementia?

Answer 401

Atrophy of the temporal lobes

Question 402

What condition is 'split hand' a characteristic symptom of?

Answer 402

ALS (Amyotrophic Lateral Sclerosis) - a type of MND

Question 403

Which muscle is most affected in Benign cramp fasciculation syndrome?

Answer 403

Calf muscles - commonly in middle-aged men

Question 404

what condition presents with 'scalloping arms'?

Answer 404

Inclusion body myositis

Question 405

What conditions is 'Gower's sign' seen in?

Answer 405

Duchenne muscular dystrophy (DMD), Becker's muscular dystrophy

Question 406

Muscle pain and raised CK - what is the difference (in terms of duration of movement/exercise in which pain onsets) between a glucose problem and a fatty acid problem?

Answer 406

- Glucose problem - immediate onset as soon as start exercise/movement - Fatty acid problem - delayed onset (20 mins) after exercise/movement

Question 407

What is shown here?

Answer 407

Lissencephaly - smooth brain

Question 408

MRC power scale

Answer 408

Question 409

Measuring power in the upper body

Answer 409

Question 410

Measuring power in the lower body

Answer 410

Question 411

What is shown in this diagram?

Answer 411

Gower's sign

Question 412

Reflexes - root level

Answer 412

Question 413

Reflexes - grades

Answer 413

Question 414

Examination findings - UMN VS LMN

Answer 414

Question 415

What is myotonia?

Answer 415

- a symptom of neuromuscular disorders that causes muscles to have delayed relaxation after contraction or stimulation - it can manifest as stiffness, cramping, or locking of the muscles

Question 416

In the majority of patients with Myasthenia Gravis, what does the initial presentation involve?

Answer 416

onset involves extraocular muscles - diplopia and/or bulbar involvement

Question 417

Which usbtype of IgG are the autoantibodies in AChR-MG and MuSK-MG?

Answer 417

- AChR-MG: IgG 1, 2, and 3 - MuSK-MG: IgG 4

Question 418

Role of the thymus

Answer 418

promotes the normal development of T lymphocytes

Question 419

Central pattern generators (CPGs)

Answer 419

a neural circuit in the spinal cord that produces rhythmic motor patterns, such as walking, breathing, and swimming - CPGs are self-organizing and can produce these patterns without sensory input

Question 420

Primary motor cortex - corticospinal tract and corticobulbar tract

Answer 420

1. Corticospinal tract: carries movement-related signals to the spinal cord to cause movements of the body 2. Corticobulbar tract: carries signals to the brainstem to cause movements of the head, neck, and face

Question 421

Non-primary motor cortex

Answer 421

Question 422

Corticospinal tract anatomy

Answer 422

Question 423

Basal ganglia - anatomy video (Dr Matt and Dr Mike)

Answer 423

https://www.youtube.com/watch?v=5psr91yrAto

Question 424

Basal ganglia and cerebellum - basic function

Answer 424

- Basal ganglia - smoothes out movements - Cerebellum - fine tunes error/minimises movement error (muscle tone, coordination, balance/posture)

Question 425

Cerebellum anatomy video (Dr Matt and Dr Mike)

Answer 425

https://www.youtube.com/watch?v=-Y2_JrSCQtc

Question 426

Question: A 32-year-old basketball player mentally rehearses free throw shots while lying in bed. Which option best describes the area of the brain that is involved in generating a motor image of this action in the absence of actual movement? - Basal Ganglia - Cerebellum - Limbic System - Premotor Cortex - Primary Motor Cortex

Answer 426

Premotor Cortex - The premotor cortex generates nerve signals for complex patterns of movements rather than discrete patterns generated by the primary motor cortex. The most anterior part of the premotor area first develops a motor image of the total muscle movement that is to be performed. Next, the successive pattern of muscle activity required to achieve the image excites neurones in the posterior premotor cortex; from here signals are sent directly to the primary motor cortex to excite specific muscles or by way of the basal ganglia and thalamus and then to the primary motor cortex

Question 427

Question: All of the following structures are part of the basal ganglia EXCEPT one. Which one is the exception? - Caudate nucleus - Red nucleus - Substantia nigra - Putamen

Answer 427

Red nucleus - The basal ganglia are located on either side of the brain mainly lateral to and surrounding the thalamus; they consist of the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. The red nucleus is located in the rostral midbrain

Question 428

Question: A 77-year-old man visits his GP because of a tremor in his hands, trouble sleeping, constipation, and dizziness. Physical examination shows a resting tremor, rigidity, and bradykinesia. The man is alert, engaging and optimistic. Which of the following is most likely to be decreased in this man? - Serotonin neurons in the raphe nuclei - GABA neurons in the caudate nucleus and putamen - Dopamine neurons in the substantia nigra - Acetylcholine neurons in the magnocellular forebrain nucleus

Answer 428

Dopamine neurons in the substantia nigra - This man with Parkinson Disease has a loss of pigmented dopaminergic neurons of the substantia nigra pars compacta that send dopamine-secreting nerve fibres to the caudate nucleus and putamen - The causes of abnormal motor movements are poorly understood; however, dopamine is an inhibitory transmitter in the caudate nucleus and putamen. It is therefore possible the overactivity of the caudate nucleus and putamen could result from the decrease dopamine levels in this patient with Parkinson disease; these brain structures are largely responsible for voluntary movement

Question 429

Question: As the axons of motor neurons leave the spinal cord and course peripherally to the skeletal muscle, they must pass through which structure? - Posterior column - Posterior root - Ventral white commissure - Posterior horn - Anterior horn

Answer 429

Anterior horn - Axons of the motor neurons on the anterior horn exit the spinal cord through the anterior root. The posterior root serves the entry point for sensory fibres coming into the spinal cord -The posterior column and the ventral white commissure are fibre tracts located solely within the spinal cord

Question 430

Hypokinetic VS Hyperkinetic movement disorders

Answer 430

Hypokinetic: - Parkinsonism / Akinetic rigid syndrome . Hyperkinetic: - Tremor - Tics - Chorea - Myoclonus - Dystonia

Question 431

Parkinsonism VS Parkinson's disease

Answer 431

- Parkinsonism is an umbrella term that refers to a group of movement disorders sharing similar symptoms, such as tremors, bradykinesia (slowness of movement), rigidity, and postural instability. It encompasses Parkinson's disease (PD) but also includes other conditions with similar features. - Parkinson's disease, on the other hand, is a specific neurodegenerative disorder that is the most common cause of parkinsonism. It is primarily due to the progressive loss of dopamine-producing neurons in the substantia nigra of the brain.

Question 432

Types of tremor

Answer 432

- Resting remor (eg. Parkinson's disease) - Action trmeor (eg. cerevellar tremor / essential tremor) - Postural tremor (eg. Essential tremor) - Kinetic tremor (on movement)

Question 433

Parkinsonims features

Answer 433

- Akinesia (fundamental feature): bradykinesia/slowness/poverty of movement + fatiguing and decrement in size and speed of repetitive movement - Rigidity - Tremor - Postural and gait disturbances

Question 434

Parkinson's disease VS Essential tremor table

Answer 434

Question 435

Causes of Parkinsonism

Answer 435

Degenerative: - Parkinson's disease (PD) - Lewy body dementia (LBD) - Progressive supranuclear palsy (PSP) - Multiple system atrophy (MSA) - Corticobasal degeneration (CBD) . Secondary: - Drugs (eg. antidopaminergics) - Toxins - Cerebrovascular disease - Post-encephalitic - Anoxic brain injury -Traumatic brain injury

Question 436

Typical clinical features for Parkinson's disease (UK Brain Bank criteria)

Answer 436

Question 437

Where in brain does Parkinson's disease affect? + diagram

Answer 437

Substantia nigra - nigrostriatal pathway degenerates

Question 438

Substantia nigra - pathology in Parkinson's and Lewy body dementia

Answer 438

Question 439

Parkinson's disease - symptoms

Answer 439

Question 439

Which antibodies are involved in myasthenia gravis?

Answer 439

- Acetylcholine receptor (AChR) - 80% of all cases - Muscle-specific kinase (MuSK) - Seronegative MG

Question 440

What is the main drug treatment in Parkinson's disease?

Answer 440

Levodopa (replacing the dopamine)

Question 441

Clinical features of myasthenia gravis

Answer 441

Question 442

Clinical subtypes of AChR-MG

Answer 442

Question 443

What triggers acetylcholine (ACh) release at the neuromuscular junction (NMJ)?

Answer 443

Action potentials cause calcium influx, which triggers ACh release into the synaptic cleft

Question 444

What happens when ACh binds to acetylcholine receptors (AChRs) on the postsynaptic membrane?

Answer 444

Sodium influx occurs, leading to muscle fibre depolarisation and contraction if the endplate potential reaches the threshold

Question 445

What is MuSK, and what is its role in AChR clustering?

Answer 445

MuSK (Muscle-Specific Kinase) is a key regulator activated by the agrin-LRP4 interaction, essential for clustering AChRs at the NMJ.

Question 446

What is the role of agrin and LRP4 in the AChR clustering pathway?

Answer 446

Agrin binds to LRP4 on the muscle membrane, initiating the clustering process.

Question 447

How does rapsyn contribute to AChR clustering?

Answer 447

Rapsyn anchors and stabilises AChRs on the postsynaptic membrane, ensuring efficient NMJ transmission.

Question 448

What is myasthenia gravis (MG)?

Answer 448

An autoimmune disorder where antibodies disrupt NMJ transmission, leading to fatigable muscle weakness.

Question 449

What do anti-AChR antibodies do in myasthenia gravis?

Answer 449

Block ACh binding: - Accelerate AChR degradation. - Activate complement, damaging the postsynaptic membrane.

Question 450

How do anti-MuSK antibodies contribute to MG?

Answer 450

They impair MuSK signalling, disrupting AChR clustering at the NMJ.

Question 451

What effect do anti-LRP4 antibodies have in MG?

Answer 451

They prevent the agrin-LRP4 interaction, impairing AChR clustering

Question 452

What is the main result of disrupted AChR clustering in MG?

Answer 452

Reduced functional AChRs lead to weakened synaptic transmission and muscle fibre depolarisation failure

Question 453

What are the key clinical features of myasthenia gravis?

Answer 453

Fatigable muscle weakness, often affecting ocular, bulbar, and limb muscles.

Question 454

How does complement activation contribute to MG pathology?

Answer 454

It damages the postsynaptic membrane, worsening the AChR deficit and impairing NMJ transmission

Question 455

What causes synaptic instability in MG?

Answer 455

Loss of AChR clustering and complement-mediated damage to the postsynaptic membrane.

Question 456

Which types of IgG subclasses are autoantibodies in AChR-MG and MuSK-MG?

Answer 456

- AChR-MG: IgG1, 2, and 3 - MuSK-MG: IgG4

Question 457

Myasthenia gravis - diagram of pathogenic mechanisms in AChR-MG

Answer 457

Question 458

Myasthenia gravis VS Lambert-Eaton myasthenic syndrome: - Location of pathology (presynaptic or postsynpatic) - clinical features

Answer 458

- Location of pathology: MG is post-synaptic membrane, Lamber Eaton is presynaptic membrane - Clinical features: MG worse with exercise/movement, Lamber Eaton myasthenic syndrome better with exercise/movement

Question 459

What is used for atnibody detection in myasthenia gravis (MG) ?

Answer 459

Radioimmunoprecipitation assay (RIA) is gold standard - high sensitivity and specificity for both AChR and MuSK-MG

Question 460

Myasthenia gravis - Principles of treatment

Answer 460

Note: steroids are titrated up - MuSK-MG responds well to Rituximab (CD20 depletion treatment)

Question 461

How does the brain plan movements? (need to edit this)

Answer 461

frontal cortex, primary frontal cortex (direct communication), corticospinal tracts, extrapyrimdal..., cerebellum, + issues with each part of the process CNS or PNS? cerebellum, basal gnalgia, NMJ, muscle itself

Question 462

A patient presents with early falls with no LOC

Answer 462

PSP (progressive supranuclear palsy) - midbrain problem - not Parkinson's!

Question 463

A patient presents with severe postural hypotension (autonomic problems), urinary dysfunction, and stridor

Answer 463

MSA (multi-systems atrophy) - Parkinsonian disorder with stridor --> think MSA (separate q?)

Question 463

A patient presents with asymmetric, apraxia, alien limb, cortical sensory loss

Answer 463

CBD (corticobasal degeneration)

Question 464

Huntington's - genetics

Answer 464

- CAG repeat expansion on chromosome 4 - autosomal dominant, shows anticipation

Question 465

Most common initial presentation of myasthenia gravis

Answer 465

Double vision and bilateral ptosis (then you get the proximal muscle weakness)

Question 466

cancer associated with lambert eaton syndrome

Answer 466

small cell lung cancer