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Year 6 > Neurology > Flashcards

Neurology Flashcards

1
Q

What are first line treatments for neuropathic pain? (incl. drug class)

A

amitriptyline - TCA
duloxetine - SNRI
gabapentin - antiepileptic (blocks Ca2+ channels to inhibit release of glutamate from pain nerve endings)
pregabalin - antiepileptic (-II-)

(monotherapy!)

PAGD - don’t want to get PAGeD about neuropathic pain

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2
Q

What is neuropathic pain?

A

pain which arises following disruption or damage of the nervous system

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3
Q

what are some causes of neuropathic pain?

A

diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disk

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4
Q

Defective downward gaze and vertical diplopia - which cranial nerve is affected?

A

CN IV

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5
Q

Between which layers is the bleed in a subdural haemorrhage?

A

damage to the bridging veins between the cortex and the venous sinuses

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6
Q

Name a diuretic that can cause gynaecomastia and explain how

A

Spironolactone (spironoLACTone)

It competitively inhibits the binding of dihydrotestosterone (DHT) to androgen receptors

-> leading to a decrease in testosterone levels and an increase in estrogen levels

-> This hormonal imbalance results in the development of breast tissue enlargement in men.

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7
Q

Characteristic presentation of clostridium botulinum infection

A

IVDU/eating contaminated (canned) food with descending paralysis, diplopia and bulbar palsy

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8
Q

Spreading of reflexes

A
  • this is an abnormal sign that can be seen on neurological examination
  • when you elicit a reflex, a different muscle twitches too
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9
Q

Sx of MND

A

Presentation:
- onset usually age 50-70
- asymmetric weakness in hands/feet
- onset tends to be focal, distal and asymmetrical; progresses in a segmental fashion from one limb to the other.
- initial presentation is highly variable
- atypical/non-specific symptoms at presentation: subtle vocal changes

Life-threatening sx as the condition progresses:

  • respiratory impairment
  • dysphagia
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10
Q

Age of onset of MND + gender

A

50-70

more common in males (2:1)

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11
Q

Other names for MND

A

Amyotrophic lateral sclerosis (ALS) is often used synonymously (although you could also say that ALS is a subtype of MND)

Lou Gehrig’s disease

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12
Q

what does ALS stand for?

A

amyotrophic lateral sclerosis

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13
Q

prognosis of MND

A

Most patients die within 3-5 years

30% have a chance of living longer

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14
Q

How is MND diagnosed?

A

MND is a clinical diagnosis -> hx and clinical examination showing UMN and LMN signs

there is constant disease progression

there may be an element of cognitive impairment

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15
Q

What is the split hand sign and what condition is it seen with?

A

wasting pattern of the hands in which the muscles of the thenar eminence atrophy due to degeneration of the lateral portion of the anterior horn of the spinal cord.
Muscles of the hypothenar eminence are spared.

-> associated with MND (relatively specific)
-> can also be a lesion of the ulnar nerve (exclude this first)

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16
Q

What form of dementia is associated with MND/ALS?

A

frontotemporal dementia

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17
Q

Ix in ?MND

A
  • MRI brain and spinal cord to exclude other causes
  • EMG supports the diagnosis (shows presence of denervation) - can also see EMG changes of the tongue
  • nerve conduction studies are usually normal but can show a reduction in motor nerve conduction amplitudes)
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18
Q

Management of MND

A
  • supportive (there is no cure)
  • see in MND specialist clinic
  • MDT: includes PT/OT, Psychology, SALT, neurologist - may need noninvasive respiratory support, symptom management (e.g. cramps, spasticity, pain), walking aids, feeding tubes etc.
  • consider the carer(s)

Medicines:
- Rilouzole - glutamate receptor antagonist in the CNS, prolongs survival and slows functional decline by about 3 months (-> rilouzole rilly helps Lou Gehrig’s) - check liver enzymes

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19
Q

What is the first line treatment of ocular myasthenia gravis?

A

long acting ACh esterase inhibitor

e.g. pyridostigmine

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20
Q

What are Broca’s and Wernicke’s areas for? What happens in Broca’s and wernicke’s aphasia?

A

Broca’s: Producing speech
-> B’s aphasia: Cannot speak fluently, is very effortful and halting; understands speech and can read;
->classically caused by lesions affecting the frontal lobe (think: what you say makes up who you are -> frontal lobe)

Wernicke’s: Understanding & processing speech
-> W Aphasia: speaks, however the content is non-sensical. issues with reading and repeating what was said.
-> Associated with lesions in the posterior superior temporal gyrus

B= broken speech
W= what? struggles understanding

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21
Q

Pyridostigmine MoA and indications

A

long-acting ACh esterase inhibitor

Used in:
- myasthenia gravis

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22
Q

what is myasthenia gravis?

A

an autoimmune condition affecting the NMJ

most commonly with antibodies against the ACh R
(but can be other postsynaptic antibodies)

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23
Q

signs and symptoms of myasthenia gravis

A
  • diplopia
  • muscle weakness
  • ptosis
  • blurred vision
  • sx worsening after repetition of movements / worse in evening
  • difficulty standing from chair/brushing hair/climbing stairs.
  • bulbar muscle involvement: difficulty chewing, swallowing, dyspnoea
  • often eye muscle movement issues initially, then involvement of larger muscles.
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24
Q

What is a myasthenic crisis and how is it treated?

A

worsening of muscle weakness resulting in respiratory failure needing intubation and ventilation.

treated with plasmapharesis and IVIG

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25
Q

pathophys of myasthenia gravis

A

myoid cells in the thymus express AChR -> autoreactive targeting by T-cells -> production of AChR antibodies

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26
Q

How is Myasthenia gravis diagnosed?

A

Clinically you see:
- weakness (limb weakness is symmetrical)
- eye signs of MG (diplopia, ptosis, blurry vision)
- FATIGUABILITY

Can do the following ix to aid the diagnosis:
- antibody testing for anti-AChR (however a minority of patients can be seronegative)
- EMG
- tensilon test (after injection sx should improve; not used commonly anymore because of risk of cardiac arrythmias;)
- CT chest to screen for thymoma

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27
Q

how is Myasthenia gravis managed?

A

Medical:
- Pyridostigmine (long acting ACh esterase inhibitor)
- Immunosuppression (initially prednisolone, can also use azathioprine, cyclosporine, MMF)

Surgical:
- thymectomy if the patient has a thymoma

+ CT chest to screen for thymoma

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28
Q

What is classically associated with a pancoast tumour?

A

Horners syndrome

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29
Q

What is Bell’s palsy?

A

An idiopathic, unilateral, acute facial nerve (CNVII) paresis/paralysis.

(there are other (secondary) causes of a facial nerve palsy e.g. trauma, infections, brainstem stroke, tumours and metabolic d/o but these are then not called Bell’s.

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30
Q

Signs and symptoms of Bell’s palsy

A
  • decreased or absent movement in the facial muscles
  • hyperacusis
  • altered taste
  • dry eyes and mouth
  • decreased lacrimation
  • lagophthalmos (inability to close eyes completely)
  • sensory disturbances: painful sensation around or behind the ear, impairment of taste in the anterior tongue, hyperacusis.
  • can get bell’s phenomenon (eye sign)
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31
Q

Aetiology of Bell’s palsy

A

idiopathic

?links to HSV infection

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32
Q

Management of Bell’s palsy

A
  • give prednisolone within 72h of onset of palsy (?25 mg BD for 10/7 or 6mg daily for 5/7 followed by 10mg/day for 5/7 more and total 10/7 -> pred increases the chance of complete recovery to 82%
  • there is an ongoing debate about the addition of antivirals
  • Eye care: advise to make sure eye is closed for sleep and prescribe artificial tears/lubricants; consider taping eye over night.

F/U

  • follow up after 3 w
  • if not improved after 3 weeks, refer urgently to ENT
  • can refer to plastics in long-standing weakness (several months)
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33
Q

Prognosis of Bell’s palsy

A
  • most people make a full recovery after 3-4 months.
  • if untreated, around 15% people have permanent moderate to severe weakness.
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34
Q

Metoclopramide MoA

A

Dopamine antagonist with 5HT3A antagonist activity

-> antiemetic

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35
Q

Why does a CN III palsy cause ptosis?

A

Due to the impairment of the innervation of the levator palpaebrae superioris?

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36
Q

albumino-cytologic dissociation - what does this mean and what condition is it seen in?

A

CSF has high protein but normal WCC

seen in Guillian Barre syndrome

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37
Q

What is Ramsay Hunt Syndrome?

A

Herpes Zoster infection of the facial nerve (CN VII)

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38
Q

What is optic neuritis?

A

inflammation of the optic nerve

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39
Q

causes of optic neuritis

A

Most common cause is MS

Can also be due to Infection (TB, syphilis, lyme disease, viral infection)

Toxic: ethambutol/methanol poisoning

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40
Q

sx of optic neuritis

A
  • blurry vision
  • sudden vision loss
  • colour blindness
  • visual field defects (e.g. central scotoma)
  • mild pain on eye movement (=retrobulbar pain)
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41
Q

ix findings for optic neuritis

A
  • clinical examination: relative afferent pupillary defect
  • neurological examination showing the signs listed above
  • ophthalmoscopy: retrobulbar neuritis -> normal findings on ophthalmoscopy usually; papillitis: poorly defined papilla, hyperemia, haemorrhage at the border of the papilla.
  • VEP (Visual evoked potential)
  • MRI head
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42
Q

management of optic neuritis

A

steroids!

also manage MS if this is the cause

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43
Q

prognosis of optic neuritis

A
  • visual improvement usually starts after 2/52
  • visual acuity is usually good after 1 year
  • frequent persistence of deficits in color vision and contrast sensitivity
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44
Q

Definition and aetiology of Wernicke’s

A

Definition:
An acute reversible presentation caused by thiamine deficiency. Patients present with at least one of 1. confusion, 2, ophthalmoplegia, 3. ataxic gait.

Aetiology:
Due to thiamine deficiency, most commonly in chronic heavy alcohol use.
Thiamine is needed for glucose metabolism. Deficiency causes symmetrical loss of brain function.

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45
Q

Signs, sx and ix in Wernicke’s

A

Signs/Symptoms:
- Confusion
- Ataxic gait (small steps, wide-based steps), +ve Romberg’s
- Oculomotor dysfunction (diplopia, nystagmus, conjugate gaze palsy

Examination:
- fluctuating mental state/confusion
- Ataxic gait (small steps, wide-based steps), +ve Romberg’
- Oculomotor dysfunction (diplopia, nystagmus, conjugate gaze palsy
- there may be signs of chronic liver disease

Investigations:
- clinical diagnosis!
- thiamine levels in the blood can be used in rare cases where clinical findings alone are insufficient for the diagnosis.
- tests to consider/rule out other diganoses (bloods, urine dip, head imaging)

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46
Q

Management of Wernicke’s

A

Give Thiamine!!

if the patient also needs glucose:
thiamine should be given before glucose or concurrently.
Do not give glucose before thiamine as this can worsen the symptoms (thiamine is needed for glucose metabolism)

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47
Q

Prognosis of Wernicke’s

A

Prognosis:
depends on how fast you give thiamine
partial recovery within the day followed by full recovery within weeks is possible if thiamine is started rapidly.

If untreated:
20% mortality rate if untreated
other survivors develop psychosis and Wernicke-korsakoff syndrome which is irreversible.

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48
Q

Acronym for Wernicke’s

A

Wernicke’s COAT

C - confusion
O - ophthalmoplegia
A - ataxia
T - give THIAMINE

49
Q

Cerebellar signs of stroke

A

DANISH

dysdiadokinesia
ataxia
nystagmus
intention tremor
slurred speech
hypotonia

50
Q

what is nimodipine used for in aneurysmal SAH?

A

reduce the risk of vasospasm

?vasospasm can lead to stroke?

51
Q

How long do cluster headaches typically last?

A

15 min - 3h

52
Q

Investigations for cluster headache

A

MRI head with gadolinium contrast

(-> sometimes underlying brain lesions are found even if the clinical sx are typical for a cluster headache)

53
Q

cluster headache management

A

100% FiO2 Oxygen

Triptans (subcut triptan in acute episodes)

Prophylaxis:
- verapamil
- tapering dose of prednisolone could be used

seek expert advice from a neurologist if pt develops CH

54
Q

cluster headache prognosis and complications

A

Prognosis:
- 25% have a single episode only
- thought to be a lifelong disorder, but there may be less frequent bouts and longer periods of remission between bouts with increasing age

Complications:
- impact QoL
- associated with depression and anxiety

55
Q

cluster headache - summarise the durations

A

These headaches last 15 min - 3h, occur 1-2x /day

they occur in ‘clusters’ lasting several weeks (4-12)

clusters occur typically once a year

56
Q

cluster headache - signs and symtpoms

A
  • unilateral headache (always on the same side) - intense, sharp, stabbing
  • headache affecting the periorbital region and forehead (trigeminal innervation area)
  • agitation and restlessness during attack

Ipsilateral autonomic sx:
- lacrimation
- rhinorrhoea
- conjunctival injection
- partial Horner’s syndrome

57
Q

RFs for cluster headache

A
  • smoking
  • male gender (3:1)
58
Q

define cluster headache

A

A primary headache disorder causing agonising unilateral headaches with symptoms of increased cranial autonomic activity affecting mainly young men in an episodic pattern.

59
Q

verapamil drug class

A

CCB

60
Q

RoA of triptans I acute cluster headache presentation

A

sc

61
Q

What is the standard anticoagulation regimen given post stroke?

A

aspirin 300mg for 2 weeks

followed by 75 mg clopidogrel OD long term

62
Q

clopidogrel drug class

A

antiplatelet medication

63
Q

What is the most appropriate treatments for migraine

A

propranolol (1st line)
other drug starting with ?T
amitriptyline
candesartan

acupuncture

64
Q

opening pressure and LP results in bacterial meningiits

A

high opening pressure (>25 cmCSF)

raised neutrophils
raised protein
reduced glucose

65
Q

Temporal lobe seizure presentation

A

palpitations
rising sensation in abdomen
loss of sensation
writhering movement of ?arm

66
Q

how common are cerebellar seizures?

A

very rare

67
Q

frontal lobe seizures signs

A

screaming
abnormal behaviour
some moevments

68
Q

ocipital lobe onset seizurecommon prodrome

A

visual symptoms at onset

69
Q

Vestibular neuritis - aetiology, sx, and how is it different to labyrinthitis

A

idiopathic inflammation of the vestibular nerve

aetiology unclear, but commonly occurs after upper airway infections

sx: acute vestibular syndrome with persistent, acute onset vertigo, N&V, gait instability in otherwise healthy patients

when hearing loss is present it is sometimes referred to as labyrinthitis

70
Q

BPPV timings

A

recurrent
usually lasts for seconds

dizziness or spinning sensation with a particular positions (e.g turning head or turning in bed)

71
Q

What does fast phase to one side in nysstagmus suggest?

A

fast phase to one side suggests peripheral rather than central cause of nystagmus

72
Q

vestibular migraine timings

A

comes and goes
duration?

73
Q

Management of vestibular neuritis

A
  • buccal or intramuscular prochlorperazine is often used to provide rapid relief for severe cases
  • a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine) may be used to alleviate less severe cases
  • vestibular rehabilitation exercises are the preferred treatment for patients who experience chronic symptoms
74
Q

How do lacunar strokes present?

A
  • unilateral motor disturbance affecting the face, arm or leg or all 3
  • complete one-sided sensory loss
  • ataxia hemiparesis

involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

75
Q

What first-line drugs are available for migraine prophylaxis?

A

propranolol (b-blocker)
Topiramate (ideally not in females of childbearing age)

76
Q

What is amaurosis fugax?

A

it is a ‘‘stroke’’ of the retinal/ophthalmic artery (which stems from the internal carotid artery)

It causes a painless, transient monocular vision loss. The vision loss is vertical, often described as a curtain closing.

caused by microemboli.

77
Q

What is an RAPD?

A

relative afferent pupillary defect

= there is a defect in th pupil that affects the afferent (=sensory) pathway

on swinging light test, you get no constriction (or even paradoxical dilatation) of the pupils when shining light into one eye.

= impaired pupillary constriction due to an afferent defect in the pupillary reflex pathway

78
Q

in what conditions can you see a RAPD?

A

MS
optic neuritis
retinal detachment
retinal ischaemia
….

79
Q

What is bulbar palsy?

A
80
Q

Bulbar Palsy vs parabulbar palsy

A
81
Q

Timing of LP in ?SAH

A

To detect a subarachnoid haemorrhage the LP should be done at least 12 hours after the start of the headache

82
Q

What is the best long term anti-thrombotic for carotid artery stenosis?

a. warfarin
b. clopidogrel
c. aspirin
d. apixaban
e. LMWH

A

Clopidogrel 75 mg long term

initially can use aspirin 300mg in acute setting.

if pt had AF you would use apixaban (because it would be a cardiembolic cause)

83
Q

% stenosis considered to be significant and require carotid endartecotmy

A

> 70 %

(in MDT discussion can consider 50-70%)

84
Q

What prophylactic medication in pt with carotid artery stenosis and AF to prevent stroke?

A

DOAC

e.g. apixaban

85
Q

pharmacological management of stroke/TIA

A

14 days aspirin 300mg OD

then clopidogrel 75mg OD

86
Q

List the different causes of stroke

A

Atherosclerosis
- carotid and vertebral stenosis
- intracranial stenosis
- aortic arch atheroma
- small vessel disease

Cardioembolic
- AF
- cardiac thrombus

Arterial dissection

Inflammatory vascular disorders
- GCA
- vasculitis

Genetic
- CADASIL
- MELAS

87
Q

Cerebellum stroke - side of signs

A

ipsilateral signs

  • dysdiadokinesia and tremor on the right
  • fast phase of nystagmus to the side of the lesion
88
Q

Brainstem stroke: side of signs

A

Cross signs:

?lesion would be on the side where the facial signs are?

89
Q

Stroke management

A

EMERGENCY
- put out a thrombolysis /stroke call

thrombolysis within 4.5h

thrombectomy:
- needs a large vessel occlusion (=needs imaging)
- 6h timeframe (but sometimes can be extended up to 24h, depending on some imaging modalities)

90
Q

Causes of SAH

A
  • aneurysm
  • traumatic
  • AVM
  • infectious
  • IE -> mycotic aneurysms
  • abnormal clotting e.g. warfarin
91
Q

1st line ix in thunderclap headache

A

CT head

(if SAH, 98% positive)
if -ve and high suspicion -> LP

92
Q

LP timeframe for SAH

A

12 h from onset

93
Q

Mx of stroke >4.5h

A
94
Q

Do you give thrombolysis and aspirin in stroke?

A

No

not at the same time

if the stroke team give thrombolysis, the aspirin would not be started until the next day.

95
Q

What is the initial management of status epilepticus?

A

IV lorazepam is pharmacological mx

  • protect airway
  • give oxygen
  • time
  • DEFG - check glucose!
  • check if they are on antiepileptics
  • contact ITU if no response

(can also give buccal midazolam or rectal diazepam)

96
Q

What is the definition of status epilepticus?

A
97
Q

What is the difference between a seizure and epilepsy?

A

epilepsy = continuing tendency to have seizures

seizure = area of paradoxical discharge of electrical activity, the episode itself

98
Q

safety advice for pts with epilepsy

A
  • inform DVLA
  • showers > baths
99
Q

is cauda equina a LMN or UMN lesion?

A

LMN

100
Q

What is syringomyelia

A

A condition where an abnormal, flui-filled cavity develops within the central canal of the spinal cord. The syrinx is a result of disrupted CSF drainage from the central canal, commonly caused by a chiari malformation or previous trauma to the cervical or thoracic spine/

sx include sensory loss in a cape-like distribution.

MRI is used to diagnose.

Mx: supportive therapy like PT, psychotherapy, beclofen for spasticity, analgesia.
Surgical treatment: decompression/removal of tumour if present.

101
Q

What are causes of both UMN and LMN signs?

A
  • MND
  • can also have multiple lesions (MRI brain, nerve conduction studies - to make sure you exclude other causes that can mimic MND)
102
Q

Ix for GBS

A
  • bloods
  • LP (raised protein)
  • EMG/NCS
  • spirometry (measure FVC as a measure of respiratory muscle function. may need ITU and intubation)

may self resolve, may need IVIG or plasmapheresis

103
Q

What is a neuropathy?

A
104
Q

What are the different types of neuropathies?

A

Predominantly sensory
- diabetes
- thiamine deficiency
- malignancy
- leprosy
- hereditary sensory neuropathies
- amyloid
- uraemia

Predominantly motor
- Guillian Barre syndrome
- porphyria
- diphtheria
- botulism
- lead
- charcot marie tooth

105
Q

What L-DOPA side effects can patients get?

A
106
Q

MS - location and time

A

lesions are disseminated in space and time

107
Q

What part of the tongue does the facial nerve innervate?

A

anterior 2/3

the Chorda tympani

108
Q

Which nerves innervate the taste in the tongue?

A

facial N: anterior 2/3

glossopharyngeal (XI): posterior 1/3

109
Q

How can you differentiate acute and chronic subdural haematoma on CT head?

A

There is a crescent shaped bleed in both

in acute: bleed is hyperdense (bright)

in chronic: bleed in hypodense (dark)

110
Q

What is the key diagnostic test in Guillian Barre syndrome?

A

LP

shows raised protein with a normal WCC

111
Q

What are watershed strokes?

A

Watershed strokes have been described previously as ischemic strokes located in vulnerable border zones between brain tissue supplied by the anterior, posterior, and middle cerebral arteries in the distal junction between two non-anastomotic arterial territories.

112
Q

Uhthoff phenomenon

A

temporary, short lived and stereotyped worsening of neurological function among multiple sclerosis patients in response to increases in body core temperature

e.g. due to fever e.g. from UTI, exercising, saunas, hot tubs etc.

113
Q

Management of acure relapse in MS

A

high dose steroids (e.g. oral or IV methylprednisolone) may be given for 5 days to shorten the length of an acute relapse

-> shorten the duration but do not alter the degree of recovery i.e. whether the patient returns to their baseline function

114
Q

features of normal pressure hydrocephalus

A

dementia
urinary incontinence
gait abnormality

115
Q

Description of a chronic subdural haematoma on CT

A

hypodense (dark)
crescenteric collection around the convexity of the brain
not limited to suture lines

116
Q

contrast or non-contrast MRI for ?MS

A

contrast MRI of brain and spine

can show acute demyelination

varying degrees of contrast enhancement can also indicate recent vs active demyelination

117
Q

presentation of HD

A

middle aged
personality changes
involuntary movements
cognitive decline

118
Q

Huntington’s disease underlying pathology

A

CAG repeats (trinucelotide repeat d/o -> anticipation phenomenon may be seen = the more repeats, the earlier onset and more severe the condition )

autosomal dominant

Year 6 (37 decks)

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