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Phase 3a > Neuro > Flashcards

Neuro Flashcards

1
Q

What information do the ascending tracts carry?

Is the input from the body contralateral or ipsilateral to the side of the brain that receives it?

A

sensory info to the CONTRALATERAL cerebral cortex

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2
Q

How many neurons are the ascending tracts made up of? Where are these neurons found?

A

4
1st order: in dorsal root ganglions
2nd order: spinal cord or brainstem
3rd order: thalamus
4th order: cerebral cortex

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3
Q

What are the 3 key ascending tracts?

A
  1. Dorsal column-medial lemniscus
  2. Spinothalamic
  3. Spinocerebellar
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4
Q

What information does the DCML tract carry?

A

vibration, conscious proprioception, 2-point discrimination, fine touch

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5
Q

There are 2 fascicles that make up the DCML: what are they, where in the spinal column are they found and where do they carry information from?

A
  1. gracilis fascicle > sensation form lower body (medial part of column)
  2. cuneate fascicle > sensation from upper body (lateral part of column)
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6
Q

Where does the DCML tract decussate?

A

dorsal column decussates in the medulla to form the medial lemniscus

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7
Q

What information does the spinothalamic tract carry?

A

crude touch, pain, pressure, temperature

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8
Q

What happens when the spinothalamic tract enters the spinal cord?

A

enters ipsilateral spinal cord > ascends 1-2 segments > decussates at this level to form the anterior and lateral spinothalamic tracts

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9
Q

What information does the anterior spinothalamic tract carry vs the lateral spinothalamic tract?

A

anterior: crude touch and pressure
lateral: pain and temperature

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10
Q

Which receptors detect:
touch/pressure
proprioception
pain
temperature

A

touch/pressure: mechanoreceptors
proprioception: muscle spindles/golgi tendon organs
pain: nociceptors
temperature: thermoreceptors

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11
Q

What information does the spinocerebellar tract carry?

A

unconscious proprioception e.g. stance, flexion of joints
= helps to coordinate movements of muscle in the trunk and limbs

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12
Q

What information do the descending pathways carry?

A

motor information from the brain to the body

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13
Q

What 2 neurons are the descending tracts made up of? Where are they found?

A

UMNs: in cerebral cortex
LMNs: anterior horns of spinal cord > leave spinal cord as peripheral nerves and innervate muscles

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14
Q

What is the difference between direct/pyramidal and indirect/extra-pyramidal descending tracts?

A

pyramidal: control fine, VOLUNTARY muscle movements + originate in the primary motor cortex

extra-pyramidal: innervate larger muscles of balance, posture, muscle tone, coordination + originate in the deep nuclei of the brainstem

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15
Q

What are the 3 key pyramidal descending tracts?

A
  1. Anterior corticospinal tract
  2. Lateral corticospinal tract
  3. Corticobulbar
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16
Q

Which muscles does the anterior corticospinal tract control?

A

controls muscles of the trunk

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17
Q

Where does the anterior corticospinal tract decussate?

A

At desired spinal segment

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18
Q

Which muscles does the lateral corticospinal tract control?

A

controls muscles of the extremities

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19
Q

Where does the lateral corticospinal tract decussate?

A

At the decussation of pyramids in the medulla

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20
Q

Some UMNs of the corticobulbar tract branch into 2 fibres and synapse with the ipsilateral and contralateral CN nuclei. Which CN nuclei receive dual supply?

A

V, XI and part of VII - muscles in upper half of face only

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21
Q

Some UMNs of the corticobulbar tract branch into 2 fibres and synapse with the ipsilateral and contralateral CN nuclei. Why is this important in UMN lesions of the CN VII?

A

Upper half of face receives dual supply from ipsilateral and contralateral UMNS of the corticobulbar tract.

Lower half of the face just receives contralateral supply.

= UMN lesion > forehead sparing

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22
Q

What are the 4 main extra-pyramidal descending tracts?

A
  1. lateral vestibulospinal
  2. reticulospinal
  3. tectospinal
  4. rubrospinal
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23
Q

What 3 parts make up the brainstem?

A
  1. midbrain (incl. red nucleus, crus cerebra)
  2. pons
  3. medulla oblongata
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24
Q

What are UMN lesions caused by?

A

damage to the brain e.g. stroke, infection, tumour
or brainstem, cerebellum, spinal cord

ie above anterior horn level

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25
Q

What are LMN lesions caused by?

A

damage to peripheral nerves, nerve root, anterior horn of spinal cord e.g. poliomyelitis

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26
Q

What signs indicate a UMN lesion?

A

hypertonia
pyramidal weakness (in UL, flexors stronger than extensors and vice versa in LL)
hyperreflexia, +ve Babinski’s
+ve ankle clonus
spastic paralysis

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27
Q

What signs indicate an LMN lesion?

A

hypotonia
weakness
absent/dimished reflexes, -ve Babinski’s
flaccid paralysis
fasciculations
muscle atrophy

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28
Q

What does CN I control?

A

olfactory nerve

sensory info about smell

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29
Q

What may be some causes of anosmia?

A

mucous blockage of nose
head trauma (shearing of CN I)
parkinson’s

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30
Q

What does CN II control?

A

optic nerve

sensory visual info from retina to brain
no motor

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31
Q

What are some key causes of decreased visual acuity?

A

refractive errors
amblyopia (lazy eye)
cataract, corneal scarring
age-related macular degeneration
CN II pathology e.g. optic neuritis

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32
Q

Does papilloedema affect visual acuity?

A

due to optic disc swelling from raised ICP
doesn’t usually affect acuity until late stage

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33
Q

What does CN III, IV and VI control?

A

motor information to extra ocular muscles to control eye movement and eyelid function
+ parasympathetic fibres for pupillary constriction

oculomotor: all extraocular muscles except:
trochlear: superior oblique
abducens: lateral rectus

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34
Q

How does 3rd nerve palsy present?

A

affected eye is down and out (due to unopposed action of LR + SO)
+ ptosis and mydriasis

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35
Q

How does 4th nerve palsy present?

A

up + out position
vertical diplopia when looking down (due to loss of SO pulling eye down) eg walking downstairs
often compensate by tilting head forward and tucking chin in

affected eye elevates more when moved medially
affected iris may be higher than other eye

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36
Q

How does 6th nerve palsy present?

A

convergent squint (due to unopposed adduction of eye)
horizontal diplopia worsened when looking to affected side

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37
Q

What is the action of the superior rectus?

A

elevation

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38
Q

What is the action of the inferior rectus?

A

depression

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39
Q

What is the action of the medial rectus?

A

adduction

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40
Q

What is the action of the lateral rectus?

A

abduction

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41
Q

What is the action of the superior oblique?

A

depresses, abducts and medially rotates

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42
Q

What is the action of the inferior oblique?

A

elevates, abducts and laterally rotates

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43
Q

What does CN V control?

A

trigeminal nerve

sensory info about facial sensation
motor info to muscles of mastication

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44
Q

What are the 3 branches of the trigeminal nerve? What do each of them innervate?

A

V1: ophthalmic > sensation to scalp, forehead, NOSE, cornea of eye

V2: maxillary > sensation to lower eyelid, cheeks, upper lip/teeth/gums

V3: mandibular > sensation to chin, jaw, lower lip/teeth/gums, mouth + motor info to muscles of mastication - masseter, temporalis, pterygoids

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45
Q

What does CN VII control?

A

facial nerve

motor info to the muscles of facial expression and stapedius muscle (regulates hearing)
+ sensation to anterior 2/3rds of tongue = taste

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46
Q

What muscles are affected in facial nerve palsy caused by a LMN lesion? What is the most common cause of this?

A

all ipsilateral muscles of facial expression
most commonly caused by Bell’s palsy

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47
Q

What muscles are affected in facial nerve palsy caused by a UMN lesion? What is the most common cause of this?

A

unilateral facial muscle weakness with forehead sparing (due to bilateral UMN supply)
most commonly caused by stroke

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48
Q

What does CN VIII control?

A

vestibulocochlear nerve

sensory info about sound and balance from inner ear to brain
no motor

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49
Q

What is conductive hearing loss? What can cause it?

A

sound unable to effectively transfer at any point between outer ear and middle ear (ossicles)

excess ear wax, otitis externa or media, perforated tympanic membrane

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50
Q

What is sensorineural hearing loss? What can cause it?

A

dysfunction of the cochlea +/- vestibulocochlear nerve

increasing age, viral infections, excess noise exposure, ototoxic agents e.g. gentamicin

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51
Q

What does CN IX control?

A

glossopharyngeal

motor info to stylopharyngeus (elevates pharynx during swallowing and speech)
sensory info to posterior 1/3rd tongue for taste
+ visceral sensory fibres mediate afferent limb of gag reflex

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52
Q

What does CN X control?

A

vagus

motor info to several muscles of mouth involved in the production of speech
+ efferent limb of gag reflex

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53
Q

Does the uvula deviate away or towards the CN X lesion?

A

away from

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54
Q

What does CN XI control?

A

accessory

motor info to sternocleidomastoid and trapezius
no sensory

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55
Q

What does CN XII control?

A

hypoglossal

motor info to extrinsic muscles of the tongue (except for palatoglossus = CN X)
no sensory

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56
Q

How does hypoglossal palsy present?

A

atrophy of ipsilateral tongue
deviation of tongue towards side of lesion

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57
Q

What are the 3 primary headaches?

A

migraine
tension headache
cluster headache

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58
Q

Define a migraine

A

episodic but continuous throbbing headache often preceded by an aura

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59
Q

What are the RFs for a migraine?

A

FHx
female
age - 1st likely to be in adolescence

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60
Q

What are the common triggers of a migraine?

A

CHOCOLATE:
Chocolate/cheese
Hangover
OCP
Caffeine
orgasm
lie in
alcohOL
Travel/tumult
Exercise

+ smoking, periods, hunger, sensory

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61
Q

What is the usual pattern of onset of a migraine?

A

long duration (>4hrs) with recurrent acute attacks

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62
Q

What is the usual severity of a migraine?

A

moderate-severe, increase in severity more rapidly than a tension headache

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63
Q

POUND describes the main sx of a migraine - what does it stand for?

A

Pulsating
Onset 4-72hrs
Unilateral
Nausea
Disabling

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64
Q

What are the key sx of a migraine?

A

unilateral and frontal pulsating headache
worse on head movements/physical activity
N&V
photo/phonophobia
with or without an aura

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65
Q

How does a migraine with aura present?

A

Aura precedes attack by minutes
Usually visual > flashes, lines/dots/zigzags (fortification spectra), scotoma, hemianopia
May get pins and needles spreading from fingers to phase, dysphasia

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66
Q

How is a suspected primary headache investigated?

A

mainly clinical diagnosis

exclude other causes e.g. ESR/CRP, BP, papilloedema, examine head/neck

CT/MRI + LP later may be indicated if e.g. thunderclap headache, abnormal neuro exam

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67
Q

What is the acute management of a migraine?

A

triptans e.g. sumatriptan + NSAIDs
+/- anti-emetic

Do not offer ergots or opioids

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68
Q

What is the prophylactic management of a migraine?

A

reduce triggers e.g. dietary factors
stop COCP if have aura

1st line = propanolol
2nd line = topiramate (anticonvulsant) = CI in pregnancy/child-bearing age women
3rd line = amitriptyline

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69
Q

A migraine with aura whilst a pt is on the COCP is a RF for what?

A

ischaemic stroke

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70
Q

What is there a risk of causing when treating migraines?

A

medication overuse headache

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71
Q

Define a tension headache

A

bilateral tight band around head

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72
Q

What are the common triggers of a tension headache?

A

stress, anxiety
sleep deprivation
eyestrain
noise

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73
Q

How long do tension headaches last?

A

Usually long duration - can last from 30 mins to 7 days
Fluctuating severity

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74
Q

What is the severity of a tension headache?

A

mild-mod

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75
Q

What are the key sx of a tension headache?

A

bilateral
pressing/tight band-like sensation, non-pulsatile

+/- scalp tenderness, pressure behind eyes, photo/phonophobia

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76
Q

What sx differentiate a tension headache from a migraine?

A

does not worsen with physical activity/head movement
no N&V
bilateral
non-pulsatile

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77
Q

What is the management of a tension headache?

A

Reassurance + lifestyle advice e.g. regular exercise
Avoidance of triggers+ stress relief e.g. acupuncture, ADs

Symptomatic treatment - aspirin, NSAIDs, paracetamol
Limit to no more than 6 days/mo

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78
Q

Which analgesics increase the risk of a medication overuse headache?

A

opioids
mixed analgesics e.g. paracetamol + codeine

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79
Q

Define a cluster headache

A

Excruciating unilateral episodic headaches with autonomic symptoms

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80
Q

What are the RFs for a cluster headache?

A

smoking
male
genetics - AD gene

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81
Q

What can trigger a cluster headache?

A

alcohol

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82
Q

What is the pattern of onset of a cluster headache?

A

usually short duration (<4hrs), lasts 15-60mins once/twice per day
usually at the same time, often nocturnal/early morning and wakes from sleep

episodic: clusters of a few weeks and then pain-free periods of months-yrs
or can be chronic

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83
Q

How severe are cluster headaches?

A

severe-very severe

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84
Q

What are the key sx of a cluster headache?

A

rapid abrupt onset of excruciating UNILATERAL pain around eye/temple/forehead, usually affects same side

with ipsilateral autonomic features - bloodshot eye with lid swelling, miosis, ptosis, lacrimation, facial flushing, rhinorrhea

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85
Q

What is the acute management of a cluster headache?

A

100% oxygen for 15 mins via non-rebreathable mask
+ SC sumatriptan

analgesics unhelpful

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86
Q

What is the preventative management for cluster headaches?

A

Ca2+ channel blocker - verapamil = 1st line

Avoid alcohol
Corticosteroids eg prednisone may help during

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87
Q

How does trigeminal neuralgia typically present?

A

paroxysmal sharp severe stabbing pain
lasts seconds - 2 mins
unilateral in distribution of trigeminal nerve branches, face screws up with pain
triggered by cutaneous stimuli e.g. light, touch, shaving, washing area, eating, talking

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88
Q

What is the most common cause of trigeminal neuralgia?

A

compression of CN V by loop of vein/artery
can be 2ndary due to aneurysm/tumour

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89
Q

How is trigeminal neuralgia managed?

A

anticonvulsants - carbamazepine
surgical options available

analgesics/opioids do not work

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90
Q

What are the most common causes of acute headaches?

A

infection: meningitis, encephalitis
brain haemorrhage
sinusitis headache
venous sinus thrombosis
post-dural puncture headache after LP/epidural
acute glaucoma
hydrocephalus

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91
Q

What are the most common causes of a chronic headache?

A

raised ICP e.g. SOL, idiopathic intracranial HTN
medication overuse headache
primary headaches
GCA
trigeminal neuralgia

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92
Q

Define epilepsy.

A

The recurrent tendency to have spontaneous, abnormal electrical activity in part of the brain, causing sudden attacks of altered behaviour, consciousness, sensation or autonomic function, manifesting in seizures.

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93
Q

What are the RFs for the development of epilepsy?

A

FHx
lesions/scarring of the brain e.g. stroke, tumour, infection, trauma > focal seizures
in children: premature, prenatal injury, febrile seizures
developmental disorders e.g. autism
alzheimer’s

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94
Q

What are the common triggers for seizures in a pt with epilepsy?

A

flashing lights
recreational drugs, alcohol, alcohol withdrawal
sleep deprivation

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95
Q

What is the most common cause for epilepsy?

A

2/3rds idiopathic - can be brain injury, SOL, infection, alcohol etc

often familial

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96
Q

Using the following headings, how is syncope differentiated from a seizure?

timing
prodrome
duration
tonic-clonic movement?
colour change
injury
incontinence
recovery

A

timing:
seizure: anytime, commonly during activity
syncope: day, usually standing, often after prolonged standing

prodrome:
seizure: brief - twitching, hallucinations
syncope: longer, light-headed, dizzy, confusion, tunnel vision, vertigo, n&v, headache, palpitations

duration:
seizure: variable
syncope: <5mins

tonic-clonic movement:
seizure: common with tongue biting, head turning
syncope: none

colour change
seizure: may be cyanosed
syncope: pallor

injury:
seizure: common
syncope: rare

incontinence:
seizure: common
syncope: rare

recovery:
seizure: post-octal sx - drowsiness, confusion, headache, myalgia, sore tongue
syncope: quick

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97
Q

How does a non-epileptic attack present?

A

normal colour
eyes closed with active resistance to opening
retained consciousness, combative
pelvic thrust, arching back, erratic movements

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98
Q

What factors should make you think a seizure is due to NEAD not epilepsy?

A

lots of other unexplained medical/psych problems
no known epilepsy

things that won’t happen in epilepsy:
pt may be able respond to you
may have continuous convulsions
more likely to have normal vital signs
won’t respond to medications

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99
Q

When can NEAD be fatal?

A

if mistreated with excess medication, can cause respiratory depression

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100
Q

How is an NEAD seizure managed?

A

correct diagnosis vital - don’t give epileptic medication

reassure pt, wait for it to pass, no medication needed - just time needed to feel better

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101
Q

What are the key differential diagnoses of epilepsy?

A

cardiac syncope, postural hypotension, vertigo
NEAD
TIA
migraine
hypoglycaemia
dystonia

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102
Q

What are the 4 elements of a seizure?

A
  1. prodrome - changes of mood/behaviours, precedes seizure
  2. aura - part of seizure where pt is aware, manifestations like deja vu, lights, strange feeling in gut (implies focal)
  3. ictus - attack itself, +ve sx e.g. jerking
  4. post-ictal - after seizure, -ve sx e.g. weakness, drowsy, headache, confusion, myalgia, sore tongue
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103
Q

What are the 2 categories of epileptic seizure? What is the difference between their presentations?

A
  1. primary generalised
    - onset of electrical discharge throughout the whole cortex, no localising features
    - bilateral symmetrical motor manifestations
    - always associated with loss of consciousness
  2. partial/focal
    - features restricted to limited part of cortex of one hemisphere
    - often have hx of cerebral injury e.g. stroke
    - may remain conscious
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104
Q

A partial/focal seizure may later become generalised, what is this called?

A

secondary generalised seizure

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105
Q

How long does an epileptic seizure usually last?

A

30 secs - 2 mins

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106
Q

What are the 4 key types of primary generalised seizure?

A
  1. generalised tonic-clonic (grand mal)
  2. absence (petit mal)
  3. myoclonic
  4. atonic
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107
Q

Describe a generalised tonic-clonic seizure

A

epileptic cry at onset
sudden rigid stiff limbs (tonic) followed by bilateral rhythmic muscle jerking
+/- tongue biting, frothing, eyes remain open, incontinence
lose consciousness

postnatal drowsiness and confusion, headache common
often no aura, flashing lights can trigger

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108
Q

Describe an absence seizure

A

sudden cessation of motor activity/speech > blank stare, blinking, still, pales for few seconds then continue e.g. might stop talking mid sentence then carry on where they left off and not realise

no aura, lasts <30 secs, no post-ictal
may have a few muscle jerks

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109
Q

Who do absence seizures usually affect? What might they develop into?

A

disorder of childhood
tend to develop into generalised tonic-clonic seizures as an adult

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110
Q

Describe a myoclonic seizure

A

repetitive but brief isolated shock-like symmetrical jerks of a limb/face/trunk

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111
Q

Describe an atonic seizure?

A

sudden loss of muscle tone > ‘drop attack’
usually conscious

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112
Q

What is the difference between a simple and complex partial seizure?

A

simple - consciousness preserved, asynchronous tonic or clonic movements, no post-octal sx +/- aura

complex - impaired consciousness at some point, automatisms common after LoC +/- aura, usually from temporal lobe

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113
Q

What is the most common headache?

A

tension headache

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114
Q

How does a focal seizure from the temporal lobe present?

A

aura (80%) - deja-vu, auditory hallucinations, smells, fear, vertigo
anxiety/out of body experience

automatisms - lip smacking, chewing, fiddling

post-octal confusion/headache/dysphasia

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115
Q

What is the main cause of temporal lobe epilepsy?

A

hippocampal sclerosis

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116
Q

How does a focal seizure from the frontal lobe present?

A

motor features > posturing, peddling movements

Jacksonian march: motor seizure spreads from hand/foot/face to other areas on ipsilateral side

post-ictal Todd’s palsy: paralysis of limbs involved in seizure for several hrs
more rapid recovery as no post-ictal confusion

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117
Q

How does a focal seizure from the parietal lobe present?

A

sensory disturbances e.g. tingling/numbness, feeling skin crawl, odd noises

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118
Q

How does a focal seizure from the occipital lobe present?

A

visual phenomena e.g. spots, lines, flashes

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119
Q

How many seizures need to occur for a diagnosis of epilepsy?

A

at least 2 unprovoked seizures occurring >24hrs apart

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120
Q

What is the investigation process for suspected epilepsy?

A
  1. make diagnosis: clinically, eyewitness important, other causes of LoC ruled out
  2. determine seizure type: EEG - almost always abnormal during a seizure (cortical spike focus, generalised spike activity)
  3. identify underlying cause (esp if pt has focal signs): MRI for localised lesions e.g. hippocampal sclerosis, tumour, stroke
  4. bloods: screen for alternative causes - FBC, U&Es, LFTS, glucose
    12-lead ECG
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121
Q

How is an epileptic seizure treated in an emergency? When is a seizure an emergency?

A

3min+ seizure
ABCDEF(fluids)G(glucose) assessment
1st line: rectal/IV diazepam/lorazepam - repeat x2 until it stops
2nd line: IV phenytoin if still fitting

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122
Q

When is long-term management started after an epileptic seizure?

A

started after 2nd seizure
or after 1st if high risk of recurrence - neurological defect, +ve EEG, structural abnormality

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123
Q

What is the 1st line management for primary generalised seizures?

A

men: sodium valproate
women: lamotrigine/levetiracetam

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124
Q

What is the 1st line management for partial/focal seizures?

A

1st line: lamotrigine/levetiracetam
2nd line: carbamazepine

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125
Q

What non-pharmacological advice should be given to epileptic pts?

A

must inform DVLA - cannot drive until free of daytime seizures for >1yr

avoid swimming/dangerous sports alone
leave door open when taking a bath

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126
Q

What is the aim with pharmacological treatment for epilepsy?

A

start on 1 anti-epileptic drug, dose increased until seizure control achieved

aim = MONOTHERAPY, try not to use multiple
1/3rd of pts resistant to treatment

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127
Q

What are the surgical options for epilepsy if medication isn’t working?

A

if cause identified e.g. tumour > surgical resection, hemispherectomy, non-dom lobectomy

vagal nerve stimulation - less effective

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128
Q

What is status epilepticus?

A

continuous seizures (>30 mins or 2+ seizures without recovery of consciousness)
tend to occur for 2-3 mins > rest period > more convulsions

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129
Q

What can cause status epileptics in pts with known epilepsy?

A

most common = poor adherence to medication

infections, worsening of primary cause e.g. tumour, alcohol

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130
Q

What can cause status epileptics in pts with SE as a 1st presentation of epilepsy?

A

most common = alcohol abuse

acute brain problem: stroke, trauma, infection, hypoglycaemia

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131
Q

In status epilepticus, where should the seizure stop and when does brain injury occur?

A

T0 = when seizure starts
10 mins/T1 = when seizure should stop
30 mins/T2 = when brain injury occurs

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132
Q

How is status epileptics investigated?

A

EEG
bloods - FBC, LFTs, U&Es, glucose, BCs if pyrexic

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133
Q

How is status epileptics managed?

A

Benzos - 2 doses
then AEDs e.g. IV valproate or phenytoin

Find an treat underlying cause
- alcohol related > thiamine
- medication not working > think non-epileptic
can be stopped with anaesthetics = very dangerous

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134
Q

What is the prognosis of status epilepticus?

A

10% mortality
long-term morbidity e.g. if hypoxic brainn injury occurs
risk of cardio resp failure

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135
Q

Define MS

A

Chronic inflammatory disorder of the CNS in which there is demyelination within the CNS giving rise of a multitude of different sx

136
Q

Who does MS usually affect?

A

females > males
presentation typically between 20-40yrs
white people, live far from the equator - low vitamin D?

137
Q

What are the potential causes of MS?

A

not well understood - combination of inherited genetic susceptibility + a trigger e.g.
- exposure to epstein-barr virus
- low vit D levels

138
Q

What is the pathophysiology behind MS?

A

T-cell mediated immune response > demyelinated plaques in the CNS

Myelin sheath regenerates but is less efficient (why remissions occur) > multiple areas of sclerosis form along neurones > slows/blocks conductions of signals > impairs movement/sensation

139
Q

What part of the nervous system does MS affect? And therefore which cells?

A

CNS
targets oligodendrocytes not the Schwann cells of the PNS

140
Q

What are the 3 key types of MS?

A
  1. relapsing + remitting (80%) - gets worse with each episode, usually partial/complete recovery between attacks, episode must last >48hrs
  2. primary progressive: gradually worsens from onset without relapses or remissions
  3. secondary progressive: follows on from relapsing + remitting, late stage with gradually worsening symptoms and fewer remissions
141
Q

What is a singular attack of MS like sx/signs called? Does it always progress to MS?

A

clinical isolated syndrome

must last >24hrs
about half progress to MS especially if MRI signs are found

142
Q

What are the visual sx of MS?

A

OPTIC NEURITIS = often 1st sign - unilateral eye pain on movement, loss of central vision (due to demyelination of optic nerve)

Uhtoff’s phenomenon: worsening of visual sx when body temp in increased eg hot bath
RAPD
Internuclear ophthalmoplegia - decreased adduction of IL eye + nystagmus on abduction of CL eye

143
Q

What are the sensory sx of MS?

A

Numbness, tingling
Trigeminal neuralgia
Lhermitte’s sign: electric shock-like sensation (from neck down spine to limbs) on neck flexion

144
Q

What are the motor sx of MS?

A

Spastic weakness
UMN signs - brisk reflexes, hypertonia, pyramidal weakness

145
Q

What are the cerebellar signs of MS?

A

Ataxia
Diplopia, nystagmus
Intention tremor
Vertigo

146
Q

What are the other/spinal cord sx of MS?

A

Fatigue
Urinary incontinence
Sexual dysfunction
Intellectual deterioration

147
Q

What are the 2 named signs seen in MS?

A

Uhtoff’s phenomenon: worsening of visual sx when body temp in increased eg hot bath

Lhermitte’s sign: electric shock-like sensation (from neck down spine to limbs) on neck flexion

148
Q

What diagnostic criteria is used in MS? What are it’s key requirements for a diagnosis?

A

MCDONALD CRITERIA

  • Evidence of relapses (that last >24hrs) and clinical evidence of lesions
  • DISSEMINATED IN TIME (>1mo apart) AND SPACE (clinically or on MRI)

And no alternative neurological disease which might explain it

149
Q

What investigations are done for suspected MS?

A

Exclude differentials with FBC, inflammatory markers, U&Es, LFTs, TFTs, glucose, HIV serology, autoantibodies, Ca2+, vitamin B12

  1. MRI - DIAGNOSTIC (if history fits) = see demyelinated plaques disseminated in space
  2. LP > oligoclonal IgG bands (unique to the CSF compared to serum = shows inflammatory process)
150
Q

What kind of MRI scan does MS demyelination show up on best?

A

FLAIR scan - bright white areas

151
Q

Where are areas of demyelination in MS most likely to occur?

A

periventricular areas = most common

juxtacortical lesions, perivenular (causes Dawson’s fingers - projections that follow the vein), brainstem, temporal lobe (quite unique to MS)

152
Q

How is an acute relapse of MS treated?

A

high dose methylprednisolone for 5 days

aim to use

153
Q

How is MS treated in the long-term?

A

DMARDs - don’t alter disease progression

  1. SC beta-interferon - reduces relapses, reduces lesions on MRI

Others used - glatiramer acetate, dimethyl fumarate, fingolimod
MABs used but more dangerous due to SE profiles e.g. alemtuzumab

154
Q

What non-pharmacological interventions can be used to manage MS?

A

encourage stress-free lifestyle
reduce other RFs e.g. smoking, obesity
if poor diet/sun exposure - give vitamin D

155
Q

Give some examples of key debilitating sx and symptomatic relief that can be given to patients with MS?

A

spasticity > physiology, baclofen or botulinum injection into affected muscle
fatigue > physio, exercise
bowel/bladder dysfunction > self-catheterisation, laxatives, anticholinergics for incontinence e.g. doxazosin
depression > psychotherapy, consider SSRI
neuropathic pain > gabapentin, amitriptylline
physio/OT input for CI and mobility issues

156
Q

What are the most common causes of death in MS?

A

aspiration pneumonia due to dysphagia
complications of immobility e.g. UTI

PPS/older age of onset > poor prognosis

157
Q

What does the grey matter of the spinal cord contain?

A

dorsal horns > cell bodies of sensory neurons
central canal > contains CSF
ventral/anterior horns > cell bodies of motor neurons

158
Q

What does the white matter of the spinal cord contain?

A

axons of neurons organised into tracts

159
Q

What is the blood supply of the spinal cord?

A

largely anterior spinal artery - supplies anterior 2/3rds = occlusion is a big risk!

160
Q

Name some key causes of spinal cord disorders?

A

trauma
degenerative disc disease - spondylosis, canal stenosis
inflammatory - MS, transverse myelitis
neoplastic
infective - HIV, abscess, empyema
vascular - anterior spinal cord artery occlusion, spinal dural fistula

161
Q

When sx indicate a spinal cord emergency?

A

acute onset
bladder/bowel dysfunction, saddle paraesthesia, bilateral leg weakness, significant back pain radiating to legs
constant sensory deficit - large segment

> acute imaging of spine to rule out cord compression

162
Q

What are some red flag signs that would indicate a patient has an anterior horn disorder (e.g. MND) and not a radiculopathy?

A
  1. progressive
  2. sounds like a nerve root problem but absence of radiating limb pattern pain
  3. absence of dermatomal sensory loss
  4. more than one apparent nerve root involved
163
Q

Is ALS a motor or sensory disorder?

A

purely motor = no sensory/cognitive sx, bowel and bladder function spared

164
Q

What are the signs usually seen in ALS?

A

primarily affects anterior horn neutrons > LMN signs e.g. symmetric flaccid paralysis, atrophy, hyporeflexia, fasciculations

affects motor neurons of corticospinal + corticobulbar path too > UMN signs

mixed UMN and LMN signs = pathognomonic

165
Q

What sx are usually seen in ALS?

A

inability to manipulate small items
frequent falls
corticobulbar tract involved > pseudo bulbar palsy = head and neck weakness, dysarthria, dysphagia
can progress to breathing muscles > resp failure/death

166
Q

What is the 1st line tx for ALS?

A

riluzole (Na+ channel blocker)

167
Q

What can cause spinal cord infarction?

A

Occlusion of the anterior spinal artery

iatrogenic - during surgery
complication of trauma, aortic dissection, thrombosis/embolism, vasculitis, severe hypotension

168
Q

What is the area of the spinal cord most susceptible to ischaemia?

A

below T8 > only supplied by a artery of adamkiewucz (from the aorta) - vulnerable to damage

above T8 > supplied by branches of the vertebral arteries

169
Q

What are the signs of anterior spinal artery occlusion?

A

bilateral LMN signs (anterior 2/3rds of spinal cord affected > LMNs in anterior horn at level of lesion damaged)
bilateral UMN signs below lesion (no signal from corticospinal tract below lesion )
bilateral loss of pain and temp below lesion (spinothalamic)

dorsal columns unaffected

170
Q

What is syringomelia?

A

expansion of the central canal of the spinal cord

171
Q

What is the main cause of syringomelia?

A

congenital disorder - chiari malformation (when the cerebellar tonsils slips into the foramen magnum)

other causes - anything that blocks flow of CSF e.g. trauma, tumour, abscess

172
Q

What is the hallmark sx of syringomelia?

A

hydrocephalus

cerebellum blocks normal flow of CSF into the SA space and spinal cord > fluid backs up in spinal cord > widens = syringomelia

173
Q

What conditions can cause damage to the dorsal columns?

A

neurosyphilis
vit B12 deficiency

174
Q

What is caudal equine syndrome?

A

damage to peripheral nerves protruding from bottom of spinal cord (caudal equina) = medical emergency

175
Q

How many spinal vertebrae are there?

A

33
7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused to form sacral bone), 4 coccygeal (fused to form coccyx)
each separated by an intervertebral disc (apart from C1 and C2)

176
Q

Where does the spinal cord end?

A

L2 - forms the conus medullaris

177
Q

How many pairs of spinal nerves are there? How do they form the cauda equina?

A

31
each nerve leaves spinal canal through corresponding intervertebral foramen
spinal canal longer than the cord > the lumbar, sacral and coccygeal nerves travel down the spinal canal to their openings forming a nerve bundle = cauda equina

178
Q

What does the cauda equina innervate?

A

motor innervation to genitals, internal + external anal sphincter, detrusor muscle, muscles of leg
knee and ankle reflexes
sensation of leg and pelvis

179
Q

What are the most common causes of cauda equina?

A

most common: lumbar disc herniation

spinal stenosis > narrowing of the vertebral foramen (congenital or degenerative e.g. ankylosing spondylitis)
spondylolisthesis > vertebra displaced by trauma, surgery, degenerative spinal disease
trauma > nerve damage, compression directly or by haematoma
growths in spinal canal > tumour, cyst, abscess

180
Q

How does lumbar canal stenosis present?

A

pain all the way down legs in distribution of nerves
weakness occurs on standing and is improved on sitting or bending over

whereas vascular claudication will be just pain in the calves

181
Q

How will lumbar disc herniation without cauda equina present?

A

shooting pain down legs

182
Q

What are the key sx of cauda equina?

A

bowel and bladder (often the 1st sign noticed by pt) dysfunction
saddle paraesthesia - feels strange sitting down/wiping
bilateral leg weakness/paraplegia/loss of reflexes
back pain that radiates down the leg
sexual dysfunction

183
Q

How is cauda equina diagnosed?

A

clinical hx and confirmed by MRI = gold standard

potentially PR to examine sphincter tone
screening blood tests - FBC, ESR, B12, LFT, U&Es, syphilis

184
Q

How is cauda equina treated?

A

depends on cause

disc herniation, trauma, tumours or abscess = acute onset > surgical decompression asap + abx if abscess
degenerative disease = slow onset > anti-inflammatories + corticosteroids
confirm if malignancy present?

185
Q

What is radiculopathy?

A

nerve root pinching due to disc prolapse/osteophyte formation etc

186
Q

Where in the spine does radiculopathy usually occur?

A

cervical and lumbar
thoracic rare

187
Q

How does radiculopathy typically present?

A

RADIATING LIMB pain - ask them to identify the furthest it has radiated to = indicate dermatome
sharp, shooting pins and needles pain
weakness more unusual

188
Q

What are the common cervical radiculopathies and their presentations?

A

cervical - shooting pain below elbow

C6: pain radiates to base of thumb, can affect biceps (6 letters) muscle (wasting/weakness)
C7: radiates to middle finger, can affect triceps (7 letters) - elbow extension

189
Q

What are the common lumbar radiculopathies and their presentations?

A

L5 - numbness and radiation to top of foot, big toe, may affect dorsiflexion
> foot drop/has to lift other foot higher, scuffing shoes, slaps foot down

S1 - numbness and radiation to small toe, side of foot, sole of foot = S + back of ankle, may affect plantar flexion
> can’t go on tip toes, struggles with pedals in car

190
Q

What is myelopathy?

A

injury to the spinal cord

191
Q

What are the s&s of myelopathy?

A

affects descending tracts > fine movements go first
then dampen down spinal reflexes = UMN signs - hypertonia, babinski’s, clonus etc
> shoelaces, coins, phone, buttons difficult
> ground doesn’t feel hard, stiff
e.g. cervical = clumsy hands and tingling

192
Q

What are the common causes of myelopathy?

A

disc osteophyte OA cord compression
acute myelopathy - abscess, mets etc

193
Q

How is myelopathy managed?

A

surgery - won’t improve condition but stops them progressing so needs to be done asap

194
Q

What are some peripheral nerve causes of weakness?

A

polyneuropathy (peripheral neuropathy)
mononeuropathy
mononeuritis multiplex

Causes: DIABETES, IDIOPATHIC, B12 deficiency, alcohol/toxins/drugs, paraneoplastic syndromes, metabolic abnormalities eg uraemia, thyroid
GBS!

195
Q

What nerves are affected in polyneuropathy vs mononeuropathy vs mononeuritis complex?

A

Poly: lots of nerves affected all over the body
Mono: just one nerve affected eg carpal tunnel syndrome
Mononeuritis: lots of nerves affected all over randomly

196
Q

How does peripheral neuropathy classically present?

A

GLOVE + STOCKING DSITRBUTION, usually symmetrical
chronic, slowly progressive
starts in legs and longer nerves (furthest from heart affected first)
sensory, motor or both

patient’s often don’t know they have it - may feel unsteady/can’t feel ground when they walk

197
Q

What signs are usually seen in peripheral neuropathy?

A

discordance between pinprick and vibration sense loss - vibration lost up to mid shin but pinprick usually normal/just lost in foot
trophic changes - dry, scaly, thinned, shiny, pigmented skin with collosities/ulcers/deformed nails in feet

198
Q

Both arms and legs are weak/numb. Where is the lesion?

A

cervical spine - would expect neck pain, UMN bladder/bowel sx, clumsy hands, stiff legs/gait

peripheral nerves

brainstem - would expect CN palsy (ask about vision loss/double vision, smell, facial muscle strength, sensation on face, bulbar palsy - swallow, speech)
cerebellum - would expect ataxia, vertigo, nystagmus, balance, tremor

199
Q

What could be the cause of peripheral neuropathy?

A

diabetes
charcot-marie-tooth disease

200
Q

Where do mononeuropathies most often occur?

A

mostly upper limb nerves at compression points

201
Q

How does mononeuritis multiplex present?

A

individual nerves picked off randomly eg wrist drop, leg numbness, foot drop
subacute presentation (months)

202
Q

How would a UMN bladder problem present?

A

urgency - sometimes incontinence but usually know they will they need to go
urinary frequency

203
Q

How would a LMN bladder problem present? Give an example of an LMN bladder problem.

A

back pain
numbness over buttock area
don’t get sense of needing a wee/feeling of urination > incontinence

cauda equina

204
Q

What is painless urinary retention a serious red flag for?

A

cauda equina

205
Q

What is mononeuritis complex caused by?

A

inflammatory: inflammation of the vasa nervorum can block off blood supply
immune mediated: vasculitis (wegner’s, PAN, RA), sarcoidosis

206
Q

How is neuropathy generally investigated?

A

Neuropathy screen if symmetrical presentation - FBC, ESR, U&Es, glucose, TFTs, B12, folate

Vasculitic screen is asymmetrical - FBC, U&Es, CRP + ESR, ANA, ANCA, anti-dsDNA, RhF, complement

EMG, nerve conduction studies
CSF sample if MS suspected
Nerve biopsy

207
Q

How is neuropathy treated?

A

Often idiopathic - no tx except sx relief: neuropathic analgesia eg gabapentin, pregabalin, amitriptyline
Treat underlying cause eg DM

Inflammatory neuropathies - prednisolone + steroid sparing agent eg azathioprine
Vasculitis neuropathy - treat quickly with prednisolone + cyclophosphamide to avoid irreversible damage

208
Q

What is the most common mononeuropathy?

A

median nerve - carpal tunnel syndrome?

209
Q

What are the nerve roots, sensory supply and motor supply of the median nerve?

A

C5-T1
sensory: lateral 3.5 digits on palm and their fingertips
motor: flexors + pronators in forearm, thenar muscles + lateral 2 lumbricals

210
Q

How does median nerve palsy present?

A

pain/pins and needles/numbness in thumb, index finger and middle finger
palm usually spared in CTS
wakes people from sleep in morning
can’t open jars due to weakness of thenar eminence

211
Q

What are the signs of CTS?

A

often none

Wasting of thenar eminence
+ve Phalen’s test, Tinel’s test
Hand of benediction - tries to make fist but only little and index fingers flex

212
Q

Why might you get CTS?

A

Sleep in curled up foetal position
Pinched as people get older and flexors in wrist thicken
Lots of RFs e.g. diabetes, pregnancy

213
Q

What are the nerve roots, sensory supply and motor supply of the ulnar nerve?

A

C8-T1
sensory: medial 1.5 digits plus associated palm
motor: majority of intrinsic muscles of the hand
flexor carpi ulnari and flexor digitorum profundus in the forearm

214
Q

How does ulnar nerve palsy present?

A

usually factorial, resolves over time

tingling/numbness/impaired movement of the ring and little finger and forearm

215
Q

What are the signs of ulnar nerve palsy?

A

froment’s sign
can’t grip paper placed between fingers
wasting of hypothenar eminence

216
Q

Why might you get ulnar nerve palsy?

A

entrapment at elbow due to fracture/arthritis

217
Q

How does axillary nerve palsy present? When can it happen?

A

tingling/numbness at the shoulder
weak shoulder abduction/deltoid movement

can occur on relocation of a dislocated shoulder

218
Q

What are the nerve roots, sensory supply and motor supply of the radial nerve?

A

C5-T1
sensory: most of posterior forearm, lateral dorsal of hand, dorsal surface of lateral 3.5 digits
motor: triceps brachii, extensor muscles of forearm

219
Q

What is the classic key sign of radial nerve palsy?

A

can’t extend fingers, wrist or forearm > wrist drop (unopposed flexion)

220
Q

When can radial nerve palsy occur?

A

at the axilla - dislocation of shoulder/fracture of proximal humerus
falls in the elderly - spiral fracture of humerus
sitting/sleeping with arm rested on chair/behind someone

221
Q

What is the classic sign of common peroneal nerve palsy?

A

foot drop

222
Q

What is guillian-barre syndrome?

A

demyelinating disease of the PNS

223
Q

What is the pathophysiology behind GBS?

A

demyelination in patches along the axon
infective organisms share molecular patterns with an antigen in the PNS tissue > auto-antibody mediated nerve cell damage

initially Schwann cells make new myelin > over time can’t keep up > irreversible damage > nerve impulses become slower

224
Q

What is GBS similar to?

A

MS but in the PNS not the CNS

225
Q

What can cause GBS?

A

Unknown but usually triggered by an infection
most commonly: campylobacter jejuni or viral - cytomegalovirus, EPV

226
Q

What are is the presentation of GBS?

A

depends on nerves affected

progressive onset limb weakness/paralysis + peripheral neuropathy
ascending = starts distally and spreads proximally
usually symmetrical >
- sensory: paraesthesia
and motor: weakness + absence of reflexes (ankles first then knees, arms) i.e. LMN signs

CNs can also be involved - diplopia, difficulty speaking, facial muscles (bulbar palsy)
autonomic nerves - constipation, urinary incontinence, orthostatic hypotension

227
Q

What is the most serious possible complication of GBS?

A

involves resp muscles > respiratory failure/death

228
Q

How is GBS diagnosed?

A

clinical diagnosis

LP - CSF shows increase in protein/albumin without raised white cells, normal glucose
Nerve conduction tests and electromyographic studies - shows slowing of motor conduction
= can all be normal in early stages

pulmonary function tests

229
Q

What needs to be monitored serially in a pt with GBS?

A

monitor FVC with spirometry - GBS can cause resp depression

230
Q

What are the differential diagnoses of GBS?

A

other causes of neuromuscular paralysis e.g. hypokalaemia, polymyositis
do MRI spine to exclude transverse myelitis/cord compression if suspected

231
Q

How is GBS treated?

A

aimed at reducing sx

Supportive therapy - heparin to prevent DVT, physio, NG/PEG feeding for swallow problems

Immunosuppressants: IV IG - reduces duration and severity of paralysis
Plasmapheresis (plasma filtered to eliminate bad antibodies)

232
Q

What is the prognosis of a pt with GBS?

A

slowly recovers over weeks/months usually

can die from resp failure
20% have long-term neurological damage/disability

233
Q

What is Miller-Fisher syndrome?

A

variant of GBS that affects the CNS and eye muscles

characterised by ophthalmoplegia (paralysis of eye muscles) + ataxia

234
Q

Where is the bleeding in a subarachnoid haemorrhage?

A

into the subarachnoid space - between the arachnoid and pia mater

235
Q

Who are SAHs more likely to occur in?

A

black pts
females
age 45-70

236
Q

What are the RFs for a SAH?

A

HTN
smoking
excess alcohol, cocaine use
FHx

237
Q

What conditions are associated with an increased of SAH?

A

ADPKD!
sickle cell anaemia
connective tissue disorders e.g. Marfan, Ehler’s danlos

238
Q

What are the 2 main causes of a SAH?

A
  1. rupture of berry aneurysm = most common
  2. arteriovenous malformation (10%)

some are idiopathic

239
Q

What are the 3 main differential diagnoses for a sudden onset headache?

A

SAH
migraine
venous thrombosis

240
Q

Other than meningitis, what other condition can cause neck stiffness and other meningeal signs?

A

SAH

241
Q

What signs associated with neck stiffness are usually positive in a pt with a SAH?

A

kernig’s and brudzinski’s

242
Q

How does a pt with a SAH present?

A

worst ever sudden onset thunderclap occipital headache

neck stiffness
photophobia
N&V
vision loss/diplopia
other neuro sx e.g. speech changes, weakness, seizures, LoC

243
Q

How is a suspected SAH investigated?

A
  1. immediate CT head
  2. LP 12hrs after onset of sx if CT does not confirm

CT angio once confirmed to locate source of bleeding

244
Q

What does the LP of a pt with a SAH show?

A

12hrs later > xanthochromia (yellow CSF) due to bilirubin, the breakdown of haem + raised RCC

before 12hrs would just be blood stained

245
Q

What does the CT scan of a pt with SAH show?

A

hyperdense (white) blood in SA space
sometimes seen as star lesion due to blood filling the sulci
also look for hydrocephalus

246
Q

What is the immediate management of a SAH?

A

Refer to neurology

ABCDE management
- pts with reduced consciousness may require intubation/ventilation
- rapid aggressive BP lowering - aim for 130-140 and maintain (needs to be high enough to perfuse brain)
- monitor GCS

Reversal of anticoagulant treatment with beriplex + IV vitamin K

247
Q

What is the surgical management of a SAH?

A

to prevent rebleeding
1st line - coiling if aneurysm confirmed (coil fitted inside aneurysm)
or clip (seal aneurysm off with a clip)

248
Q

What are the 5 key complications of an SAH and what tx is given for each to prevent them?

A
  1. rebleeding > tx: surgical management with clip/coil
  2. vasospasm > tx: nimodipine (Ca2+ channel blocker) as can lead to ischaemia + hydration
  3. seizures > tx: anti epileptics e.g. keppra
  4. hydrocephalus > tx if occurs: LP or shunt
  5. cerebral salt wasting > tx: give salts and water back with fluids
249
Q

Where is the bleeding in a subdural haemorrhage?

A

in the subdural space between the arachnoid and dura mater

250
Q

What are the RFs for intracranial bleeds (SDH + EDH)?

A

head injury
HTN
aneurysms
ischaemic stroke
tumours
anticoagulants

251
Q

Which pts are more likely to have a SDH?

A

pts with lots of brain atrophy e.g. elderly/dementia, alcoholics, childhood abuse
= makes vessels more vulnerable to rupture
pts with comorbidities that make them more vulnerable to falls

252
Q

Who do EDHs classically occur in?

A

young males

253
Q

What is the most common cause of an SDH?

A

traumatic head injury - often deceleration injuries, can be minor/from a long time ago and therefore forgotten about
often temporal side of head

254
Q

A SDH causes rupture of which vessels? What does this lead to?

A

rupture and bleeding of bridging veins between the dura and arachnoid mater

causes raised ICP > can lead to shift in midline structures

255
Q

How does the presentation of an acute SDH differ from a chronic one?

A

acute - presents similarly to extradural
chronic - gradual, fluctuating conscious level, less dramatic raised ICP features

256
Q

What are the typical sx of an SDH?

A

fluctuating consciousness physical/intellectual slowing
confusion, drowsiness
signs of raised ICP > headache, N&V, seizures

poor balance, weakness, parasthesia i.e. focal neurology occurs later

257
Q

What is the interval between the injury and sx in a SDH?

A

can be days to months
develop much slower in elderly

258
Q

What is seen on CT with a SDH? How can it change in repeat scans?

A

hyperdense CRESCENT SHAPED blood in 1 hemisphere, can cross over cranial sutures
may see shift of midline structures

become more isodense as clot ages, eventually becomes hypodense

259
Q

How is a suspected SDH investigated?

A
  1. immediate CT

bloods - FBC, U&Es, LFTs, coag, G&S
monitor GCS
MRI may be used to identify underlying causes e.g. malignancy, stroke but not in acute setting

260
Q

How is a SDH managed?

A

ABCDE management
+ reverse anticoagulants
+ consider anticonvulsants meds
+ consider mannitol to reduce ICP

surgical:
conservative if small
acute: craniotomy if significant mass effect or decompressive craniotomy if large with cerebral oedema
chronic: burr hole craniotomy

261
Q

Where does the bleeding occur in an EDH?

A

between dura mater and skull bone

262
Q

What usually causes an EDH?

A

traumatic head injury - skull trauma to temporoparietal region e.g. falls, assault, sports injury
majority associated with skull#

263
Q

Where is the most vulnerable part of the skull to fractures?

A

pterion - where parietal, frontal, sphenoid and temporal bones fuse

264
Q

Which artery is usually lacerated and causes the bleeding in an EDH?

A

middle meningeal

265
Q

If the ICP continues increasing in an EDH, what might happen?

A

midline shift + tentorial herniation > BRAINSTEM DEATH eventually

266
Q

What might you see o/e of a pt with an EDH?

A

signs of brainstem compression!
tenderness of skull
reduced GCS
CN deficits - CN III palsy (fixed dilation of IL pupil)
Motor/sensory loss of U/LL
Hyperreflexia, spasticity, Babinski +ve
Cushing’s triad

267
Q

What is Cushing’s triad?

A

response to raised ICP

bradycardia + HTN + deep irregular breathing

268
Q

What are the typical sx of an EDH?

A

head injury followed by brief LoC/drowsiness, then a lucid period for hrs/days, then rapid decline in consciousness as haematoma compresses other structures

raised ICP > seizures, headache, N&V, confusion

269
Q

How is a suspected EDH investigated?

A
  1. immediate CT head

skull XR not routine but all suspected fractures must have urgent CT if they are done
MRI/cerebral angio later for underlying cause

blood glucose - rule out hypoglycaemia as cause of reduced GCS
ECG
bloods

270
Q

What does an EDH look like on CT?

A

hyper dense biconvex/lemon shaped blood adjacent to the skull
look for midline shift + brainstem herniation = needs early surgical intervention

271
Q

How is an EDH managed initially?

A

ABCDE management -
maintain airway via intubation/ventilation in unconscious
+ reversal of anticoagulants
+ consider abx in open skull#
+ consider anticonvulsants
+ IV mannitol for increased ICP

regular obs, prevent secondary insults e.g. oedema, ischaemia. ICP monitoring, repeat CT.

272
Q

What is the surgical management for an EDH?

A

conservative if small
acute: burr hole craniotomy/trauma craniotomy if significant mass effect
decompressive craniotomy if large and with cerebral oedema

273
Q

What are the possible complications of an EDH?

A

compression of local structures + rise in ICP > cerebellar herniation > brainstem death

infection due to skull#
cerebral ischaemia
seizures
hydrocephalus due to obstruction of ventricles

274
Q

What is an intracerebral haemorrhage? How does it present?

A

bleeding into the brain tissue

presents similarly to ischaemic stroke with sudden onset focal neurological defect
+ rapid LoC, features of raised ICP

275
Q

Where can intracerebral haemorrhages occur in the brain?

A

lobar, deep, intraventricular, cerebellum
most common = basal ganglia (arteries branch off MCA)

276
Q

How would an intracerebral haemorrhage show up on CT?

A

hyper dense, irregularly shaped area in brain parenchyma

277
Q

Define stroke

A

sudden focal neurological defecit

278
Q

What are the key RFs for ischaemic stroke?

A

increasing age, male
CVS RF’s: HTN!!, smoking, DM, hypercholesterolaemia
alcohol
obesity

past TIA/stroke
AF!!
carotid stenosis
CVS disease - valvular, angina, MI, PVD

polycythaemia, vaculitis
COCP

279
Q

How can AF lead to stroke?

A

stasis of blood in poorly contracting atria > thrombus formation

280
Q

What are the 4 types of ischaemic stroke?

A
  1. thrombotic - local arterial obstruction
  2. embolic - vessel blocked by embolism elsewhere in the body usually from a thrombus or from the heart
  3. hypoxic - systemic hypo perfusion e.g. septic shock, MI, in birth, drowning
  4. cerebral venous sinus thrombosis - clots in veins that drain the brain > venous congestion and tissue hypoxia
281
Q

What is the key condition to rule out as a cause of sudden onset neurological defect? What are some stroke mimics?

A

EXCLUDE HYPOGLYCAEMIA

stroke mimics:
complicated migraine - preceding aura, headache, previous hx
seizures - postictal periods can cause weakness on one side (Todd’s paralysis)
tumours - gradual progression of sx, sometimes seizures
MS

282
Q

Are sx on the CL or IL of the lesion in a stroke?

A

CL side
except in brainstem strokes = bilateral

283
Q

What type of motor sx are seen in an ischaemic stroke?

A

flaccid paralysis initially then spastic paralysis and hyperreflexia later

284
Q

What type of sensory sx are seen in an ischaemic stroke?

A

numbness
reduced pain and vibration sense

285
Q

How is a suspected stroke investigated?

A

use FAST outside hospital, exclude hypoglycaemia

  1. immediate non-enhanced CT to rule out haemorrhage (probably won’t confirm infarct)

If thrombectomy might be indicated > CTA after CT

Non-urgent:
bloods to establish cause
Carotid doppler - look for carotid stenosis
MRI later if CT shows no infarct and still suspect
ECG - look for AF
Consider echo

286
Q

What might a haemorrhage or ishcaemic stroke look like on CT?

A

haemorrhage = white
infarct = hyperdense/dark

early signs of stroke won’t be an infarct - often shows nothing or hypodense MCA/blockage of other artery

287
Q

What is the immediate management pathway for an ischaemic stroke?

A
  1. admit everyone with suspected stroke to ward, seen by specialist within 24hrs
  2. thrombolysis with alteplase if present within 4.5hrs of onset of sx + haemorrhage has been excluded
  3. consider for thrombectomy within 6 hrs
  4. start on 300mg aspirin for 2 weeks or until discharge (may need a PPI too)
  5. BP control if have hypertensive emergency - small fall can compromise cerebral perfusion, keep >210/100

O2 therapy if indicated, maintain BG

288
Q

What is the long-term management after an ischaemic stroke?

A

Swallow assessment - NBM/NG? Screen nutrition - MUST score. Manage hydration, mobilise ASAP. Consider IPCD for pts with reduced mobility.
(this is the same for haemorrhagic strokes)

  1. Clopidrogel 75mg (or aspirin + dipyridamole) after the 2wks of aspirin
  2. 80mg atorvastatin
  3. Carotid endarterectomy or stenting within 2 weeks for pts with internal carotid stenosis
  4. treat modifiable RFs:
    - for AF do CHADSVASC and HASBLED, weigh up and consider anticoagulation 2 wks after e.g. warfarin
    - BP control - ACEi
    - diabetes control
    - smoking/alcohol cessation, exercise, weight loss, diet
    - stop HRT it on it
  5. rehabilitation with MDT - physio, OT, SALT
289
Q

How long do you have to stop driving after having a stroke/TIA?

A

1 month
unless sx are ongoing

290
Q

What are the components of the CHADSVASc score?

A

Risk of stroke for pts with AF
CHF = 1
HTN = 1
Age 75+ = 2
Diabetes = 1
Previous stroke/TIA/VTE = 2
Vascular disease = 1
Age 65-74 = 1
Sex Category female = 1

consider anticoagulation in pts with any RFs other than their sex
1st line = DOACs e.g. apixaban

291
Q

What are the components of the HASBLED score?

A

HTN = 1
Abnormal renal or liver function = 1 each
Stroke = 1
Bleeding (prior/tendency) = 1
Labile INR = 1
Elderly (>65) = 1
Drugs (e.g. NSAIDs, anti platelets) or alcohol = 1 each

292
Q

What are the potential complications of an ischaemic stroke?

A

Long term significant disability/mortality
aspiration pneumonia
DVT
raised ICP due to cerebral oedema/haemorrhage > midline shift > possible coning
pressure sores, depression, delirium, CI, seizures

293
Q

What are the 2 main causes of a haemorrhagic stroke? What is the difference between a haemorrhage and haemorrhagic stroke?

A
  1. intracerebral haemorrhage (due to HTN)
  2. SAH (due to ruptured aneurysm)
    Increased risk when on anticoagulation/had thrombolysis !!!
    Carotid/vertebral artery dissection

They count as a stroke because they are predisposed by disease of the vessels e.g. aneurysm, HTN. Other bleeds e.g. extradural are caused by non-vascular factors e.g. trauma.

294
Q

What drugs significantly increase risk of a haemorrhagic stroke?

A

anticoagulants
post-thrombolysis

295
Q

What are the signs of increased ICP? How is it treated?

A

headache
N&V
papilloedema
cushing’s triad (response to raised ICP) - HTN + bradycardia + irregular deep breathing

tx with mannitol - osmotic diuretic

296
Q

How is a haemorrhagic stroke treated long-term?

A

MRI/CT done 4-8 wks later - look for vascular malformations, brain tumour
rigorous HTN control
cholesterol/diabetes control
exercise, quit smoking, diet

297
Q

What are the 2 main risks of thrombolysis treatment? What is done to monitor these risks?

A
  1. haemorrhage
  2. reaction

2nd CT head done within 24hrs to check if they’ve had a bleed

298
Q

What are the contraindications for thrombolysis?

A

on anticoagulants (can if on warfarin and below 1.7)
haemorrhagic stroke
>6hrs after onset of sx
recent surgery or GI bleed
active cancer
HTN - cut off is 185/110

299
Q

Why might a thrombectomy be offered to a stroke pt instead of thrombolysis?

A

better treatment just less accessible
often used in conjunction with thrombolysis if possible

longer time frame to be effective (6hrs or more)
can be used on pts who are on anticoagulants

300
Q

What happens to BP in an ischaemic stroke?

A

cerebral auto regulation occurs in ischaemic areas > brain increases BP to increase tissue perfusion

balanced by stopping it going too high which might cause reperfusion haemorrhage
needs to be <185/110 for rtPA

301
Q

What is a TIA?

A

transient neurological dysfunction due to ischaemia without infarction
sx usually last <24hrs

302
Q

What are the S&S of a TIA?

A

sudden loss of function for a few mins to 24hrs with complete recovery

until recovery it’s impossible to differentiate one from a stroke

303
Q

How is a suspected TIA investigated?

A

CT not offered unless suspicious of alternative diagnosis
Carotid doppler - look for stenosis
72hr ECG - AF. Consider echo/CTA.
Consider MRI after specialist assessment

304
Q

How is a TIA managed?

A

no immediate management

seen by specialist within 24 hrs
long-term management same as ischaemic stroke - aspirin then clopidogrel + secondary presentation of CVS disease
physio

305
Q

What is the ABCD2 score? What are it’s components?

A

risk of stroke after suspected TIA

Age 60+ = 1
BP 140/90+ = 1
Clinical features:
- unilateral weakness = 2
- speech disturbance without weakness = 1
Duration of sx:
- 10-59 mins = 1
- 60+ mins = 2
Diabetes = 1

306
Q

What ABCD2 scores indicate what management?

A

0-3 = low risk
4-5 = moderate risk > assessment from specialist within 24hrs
6-7 = high risk > strongly predicts stroke - refer to specialist immediately

high risk if in AF, >1 TIA in 1wk, TIA whilst on anticoagulants

307
Q

What is a crescendo TIA?

A

2+ TIAs within a wk
high risk of developing a stroke

308
Q

What arteries are involved in an anterior circulation stroke?

A

internal carotid artery so the ACA and MCA

309
Q

How can an ACA and MCA occlusion be differentiated? What areas of the brain do they supply?

A

ACA > frontal lobe
MCA > frontal, superior tempora, parietal lobes

ACA:
- hemiparesis and sensory loss of legs
- disinhibition, executive dysfunction, emotional disturbance - apathy, reduced concentration etc
- sometimes akinetic mutism (drowsy + reduced spontaneous speech)

MCA: most common stroke
- hemiparesis + sensory loss of hands, arm and face (facial droop)
- legs often spared
- homonymous hemianopia
- language centres if dominant hemisphere affected (brook’s + wernicke’s) > dysphasia, aphasia

310
Q

What vessels are involved in a posterior circulation stroke?

A

basilar and vertebral arteries

311
Q

What ares of the brain are affected in a posterior circulation stroke?

A

cerebellum, brainstem, occipital lobes, hippocampus etc
i.e. more catastrophic

312
Q

How does a posterior circulation stroke present?

A

depends on location:

LoC
occipital lobe > CL homonymous hemianopia, cortical blindness
cerebellum > gait and limb ataxia, nystagmus, N&V, dysarthria
brainstem > CN palsies causing diplopia, facial sensory loss/weakness, dysphagia etc

313
Q

How does a brainstem stroke present?

A

drowsiness
crossed sensory + motor findings
CN palsies (LMNs in brainstem)

locked in syndrome (upper brainstem) - all voluntary muscles paralysed except eye movement
pseudobulbar palsy - lower brainstem

314
Q

What are lacunar strokes?

A

Small strokes due to blockages in small arteries supplying deep brain structures eg thalamus, pons

315
Q

How might a lacunar stroke present?

A

cortical function preserved

depends on location , can be:
Purely motor – weakness in contralateral arm, leg, face
Purely sensory – sudden paraesthesia in contralateral arm, leg, face
Or sensorimotor
Ataxia, dysarthria, clumsy hands

316
Q

What is the Bamford classification criteria for a TACS/PACS?

A

For TOTAL ACS (TACS): all 3 required

Unilateral weakness +/- sensory deficit of face, arm, leg
Homonymous hemianopia
Higher cerebral dysfunction eg dysphasia, visuospatial disorder

Only 2 required for PARTIAL ACS (PACS)

317
Q

What is the Bamford classification criteria for a POCS?

A

1 of the following required:

Cerebellar (eg vertigo, nystagmus, ataxia) or brainstem syndromes
LoC
Isolated homonymous hemianopia

318
Q

What is the Bamford classification criteria for a lacunar stroke?

A

No loss of higher cerebral functions

1 of the following required:

Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three
Pure sensory stroke
Ataxic hemiparesis

319
Q

What can cause an intracerebral haemorrhage?

A

HTN!! > rupture of microvasculature

can occur spontaneously or due to bleeding into an ischaemic infarct, tumour, rupture of aneurysm

320
Q

What is the main tx for an inctracerebral haemorrhage?

A

clot evacuation

321
Q

Infarcts in which lobes cause which types of homonymous quadrantopias?

A

PITS

parietal = inferior
temporal = superior
on the contralateral side

322
Q

What is an incongruous versus congruous visual field defect? Where are the lesions that cause each?

A

incongruous = different in each eye > optic tract lesions

congruous = same in both eyes > optic radiation lesion, occipital cortex

323
Q

Homonymous hemianopia with macula sparing is caused by what lesion?

A

occipital cortex lesion

324
Q

Which type of dementia is a/w MND?

A

FTD

325
Q

What is the traid for normal pressure hydrocephalus?

A

incontinence
gait apraxia
dementia

326
Q

Name 2 parkinson’s plus syndromes? What are their symptoms?

A

corticobasal degeneration - alien hand syndrome (limbs move on their own), apraxia, aphasia, parkinson sx

progressive supranuclear palsy - supranuclear opthalmoplegia (can’t look down, progresses to inability to look left and right), pseudobulbar palsy (inability to control facial movements), neck dystonia, balance issues > falls, behavioural and cognitive impairment, Parkinsonism.

327
Q

What is the parkinson’s tx pathway?

A

GS = co-careldopa (L-dopa + carbidopa (peripheral decarboxylase inhibitor to prevent breakdown of dopamine)
- wears off over time so reserved for when other meds can’t control sx
- SE: dyskinesia

delay use of L-dopa then used in combo to reduce dose of L-dopa needed:
- dopamine agonist: mimic dopamine
ergot derived eg bromocriptine, cabergoline = more SEs, used if non-ergot don’t work
non-ergot derived eg ropinirole, pramipexole, rotigitine
SE = pulmonary fibrosis
OR
- MAO-Bi - MAO-B breaks down dopamine = inhibit eg selegiline, rasagiline

3rd line: COMTi eg entacapone - add to co-carel to slow breakdown of dopamine + prolong effectiveness of L-dopa

328
Q

What is multi-system atrophy?

A

parkinsonism + autonomic sx eg bladder disturbance, postural hypotension, erectile dysfunction

329
Q

How to differentiate idiopathic and drug-induced parkinsons?

A

idiopathic = asymmetrical
drug-induced = symmetrical sx

330
Q

What drugs cause parkinsons?

A

anything that blocks dopamine
eg neuroleptics

331
Q

How is an absence seizure treated?

A

1st: ethosuximide
males 2nd: SV
females 2nd: lam/lev

332
Q

How is a myoclonic seizure treated?

A

males: SV
females: lev

333
Q

How is an atonic seizure treated?

A

males: SV
females: lam

334
Q

Which anti-epileptic can exacerbate absence seizures?

A

carbamazepine

335
Q

How does a cerebral abscess present?

A

headahce
fever
focal neurology

336
Q

What are the possible complications of acute sinusitis?

A

cerebral abscess - focal neurology
cavernous sinus thrombosis - CN palsy, ophthalmoplegia
meningitis
orbital cellulitis - painful ophthalmoplegia, proptosis, eye swelling

337
Q

How should neuropathic pain relief be prescribed?

A

as monotherapy - switch do not add

Phase 3a (11 decks)

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