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Phase 3B prep > Passmedicine Neurology > Flashcards

Passmedicine Neurology Flashcards

1
Q

Name 2 5-HT3 antagonists

A

Ondansetron, Granisetron, Palonosetron

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2
Q

5-HT3 antagonists side effects?

A

Constipation
Prolonged QT interval

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3
Q

Where is the chemoreceptor trigger zone located?

A

Medulla Oblongata

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4
Q

Where is the lesion causing Wernicke’s aphasia?

A

Superior temporal gyrus

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5
Q

Where is the lesion causing Broca’s aphasia?

A

Inferior frontal gyrus

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6
Q

What supplies the superior temporal gyrus?

A

Inferior division of the left MCA

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7
Q

What supplies the Inferior frontal gyrus?

A

Superior division of the left MCA

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8
Q

What is the similarity & difference between Broca’s and Conduction aphasia?

A

Similarity: Comprehension preserved
Difference: Speech non-fluent in Broca vs fluent in Conduction

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9
Q

What is arnold-chiari malformation?

A

Condition involving downward displacement/herniation of cerebellar tonsils through foramen magnum. May be congenital/acquired through trauma

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10
Q

What are the features of arnold-chiari malformation?

A

non-communicating hydrocephalus may develop as a result of obstruction of cerebrospinal fluid (CSF) outflow
headache
syringomyelia

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11
Q

A lesion where causes peripheral (‘finger-nose ataxia’)?

A

Cerebellar hemisphere lesions

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12
Q

A lesion where causes gait ataxia?

A

Cerebellar vermis lesions

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13
Q

What is autonomic dysreflexia?

A

Autonomic dysreflexia is a condition that emerges after a spinal cord injury, usually when the damage has occurred above the T6 level. Dysregulation of the autonomic nervous system leads to an uncoordinated sympathetic response that may result in a potentially life-threatening hypertensive episode when there is a noxious stimulus below the level of the spinal cord injury

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14
Q

What are the features of autonomic dysreflexia?

A

The result is an unbalanced physiological response, characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke.

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15
Q

What are the common causes of autonomic dysreflexia?

A

The most common triggers for autonomic dysreflexia are faecal impaction and urinary retention

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16
Q

What level does autonomic dysreflexia occur?

A

Autonomic dysreflexia can only occur if the spinal cord injury occurs above the T6 level

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17
Q

What is the management of autonomic dysreflexia?

A

Management of autonomic dysreflexia involves removal/control of the stimulus and treatment of any life-threatening hypertension and/or bradycardia.

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18
Q

What is Bell’s Palsy?

A

Acute, unilateral, idiopathic, facial nerve paralysis.

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19
Q

What causes Bell’s palsy?

A

Unknown, possibly HSV

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20
Q

Epidemiology for Bell’s Palsy?

A

20-40, more common in pregnant women

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21
Q

Features of Bell’s Palsy?

A

lower motor neuron facial nerve palsy → forehead affected
patients may also notice
post-auricular pain (may precede paralysis)
altered taste
dry eyes
hyperacusis

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22
Q

Bell’s Palsy management?

A

there is consensus that all patients should receive oral prednisolone within 72 hours of onset of Bell’s palsy
there is an ongoing debate as to the value of adding in antiviral medications CKS

eye care is important to prevent exposure keratopathy
prescription of artificial tears and eye lubricants should be considered
If they are unable to close the eye at bedtime, they should tape it closed using microporous tape

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23
Q

Criteria for Bell’s Palsy referral?

A

Urgent referral to a specialist dealing with facial nerve paralyses, such as ENT or neurology, is indicated in the following circumstances:
Worsening or new neurological findings
Red flag features of cancer
No sign of improvement after 3 weeks of treatment
Symptoms of aberrant reinnervation 5 months or more after original onset
Unclear diagnosis

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24
Q

Which nerve is responsible for finger flexion, finger extension, finger abduction, finger adduction, thumb abduction?

A

Finger flexion: Median nerve
Finger extension: Radial nerve
Finger abduction: Ulnar nerve
Finger adduction: Ulnar nerve
Thumb abduction: Median nerve

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25
Q

Which nerve is responsible for wrist extension, wrist flexion?

A

Wrist extension: Radial Nerve
Wrist flexion: Median nerve

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26
Q

Which nerve is responsible for elbow extension and flexion?

A

Elbow extension: Radial nerve
Elbow flexion: Radial and musculocutaneous

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27
Q

Which nerve is responsible for shoulder abduction and adduction?

A

Shoulder abduction: Axillary nerve
Shoulder adduction: Thoracodorsal nerve

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28
Q

Klumpke paralysis vs Erb’s palsy?

A

Both involve brachial trunks but Klumpke paralysis involves C8-T1 while Erb’s palsy involves C5-C6

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29
Q

What are the causes of brain absecess?

A

Extension of sepsis from middle ear or sinuses,
Trauma or surgery to the scalp
Penetrating head injuries
Embolic events from endocarditis

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30
Q

What are the features of brain abscess?

A

headache -often dull, persistent
fever -may be absent
focal neurology -e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure
other features consistent with raised intracranial pressure:
nausea
papilloedema
seizures

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31
Q

How to assess brain abscess?

A

CT scan

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32
Q

Brain abscess management?

A

surgery -a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.
IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
intracranial pressure management: e.g. dexamethasone

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33
Q

Which IV abx are used for brain abscess?

A

Cephalosporin and metronidazole

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34
Q

What does a lesion in the parietal lobe cause?

A

Sensory inattention
Apraxias
Astereognosis (tactile agnosia)
Inferior homonymous quadrantanopia
Gerstmann’s syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation

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35
Q

What does a lesion in the occipital lobe cause?

A

Homonymous hemianopia (with macula sparing)
Cortical blindness
Visual agnosia

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36
Q

What does a lesion in the temporal lobe cause?

A

Wernicke’s aphasia
Superior homonymous quadrantanopia
Auditory agnosia
Prosopagnosia (difficulty recognising faces)

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37
Q

What does a lesion in the frontal lobe cause?

A

Expressive (Broca’s) aphasia
Disinhibition
Perseveration
Anosmia
Inability to generate a list

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38
Q

What does a cerebellar lesion cause?

A

midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus

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39
Q

Which tumours spread to the brain?

A

lung (most common)
breast
bowel
skin (namely melanoma)
kidney

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40
Q

Which primary brain tumour is most common?

A

Glioblastoma multiforme

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41
Q

What is the management for GBM?

A

Treatment is surgical with postoperative chemotherapy and/or radiotherapy. Dexamethasone is used to treat the oedema.

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42
Q

What are the features of Brown-Sequard Syndrome?

A

ipsilateral weakness below lesion
ipsilateral loss of proprioception and vibration sensation
contralateral loss of pain and temperature sensation

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43
Q

What are the side effects of carbamazepine?

A

Hyponatraemia secondary to SIADH
SJS
Leucopenia and agranulocytosis
Dizziness
Ataxia

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44
Q

What is cataplexy?

A

Transient loss of muscle tone due to strong emotion. E.g. buckling knees/collapse

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45
Q

Cavernous sinus contents?

A

Oculomotor nerve
Trochlear nerve
Ophthalmic nerve
Maxillary nerve
Internal carotid artery
Abducens nerve

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46
Q

What are the features of cerebellar disease?

A

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia

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47
Q

What is cerebral perfusion pressure?

A

The cerebral perfusion pressure (CPP) is defined as being the net pressure gradient causing blood flow to the brain

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48
Q

What is the Cushing’s triad?

A

Widening pulse pressure, bradycardia and irregular breathing

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49
Q

What is Charcot Marie Tooth?

A

The most common hereditary peripheral neuropathy

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50
Q

Features of CMT?

A

Foot drop
High-arched feet (pes cavus)
Hammer toes
Distal muscle weakness
Distal muscle atrophy
Hyporeflexia
Stork leg deformity

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51
Q

Cluster headache risk factors?

A

Alcohol
Men
Smoking

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52
Q

Features of cluster headache?

A

Intense sharp, stabbing pain around one eye
Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours (Lasts 4-12 weeks)
Accompanied by redness, lacrimation, lid swelling
Nasal stuffiness
Miosis and ptosis in a minority

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53
Q

Cluster headache investigations?

A

Most patients will have neuroimaging - underlying brain lesions are sometimes found even if the clinical symptoms are typical for cluster headache
MRI with gadolinium contrast is the investigation of choice

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54
Q

Cluster headache management?

A

NICE recommend seeking specialist advice from a neurologist if a patient develops cluster headaches
acute
100% oxygen (80% response rate within 15 minutes)
subcutaneous triptan (75% response rate within 15 minutes)

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55
Q

Cluster headache prophylaxis?

A

Verapamil

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56
Q

Common peroneal nerve lesion features?

A

Foot drop
weakness of foot dorsiflexion
weakness of foot eversion
weakness of extensor hallucis longus
sensory loss over the dorsum of the foot and the lower lateral part of the leg
wasting of the anterior tibial and peroneal muscles

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57
Q

What does the sciatic nerve divide into?

A

Tibial nerve and common peroneal nerve

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58
Q

What causes a down and out eye?

A

CN III lesion. It is the result of all but the lateral rectus and superior oblique muscles being paralysed, which then act unopposed to pull the eyeball in this direction.

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59
Q

Which nerve is responsible for corneal reflex?

A

CN V (I)

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60
Q

What is CJD?

A

Creutzfeldt-Jakob disease (CJD) is rapidly progressive neurological condition caused by prion proteins. These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.

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61
Q

What are the features of CJD?

A

Dementia (rapid onset)
Myoclonus

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62
Q

CJD investigations?

A

CSF is usually normal
EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
MRI: hyperintense signals in the basal ganglia and thalamus

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63
Q

What is degenerative cervical myelopathy?

A

Degenerative cervical myelopathy (DCM), also known as cervical spondylotic myelopathy, is a progressive neurological disorder that occurs due to the narrowing of the spinal canal in the cervical (neck) region, resulting in compression and damage to the spinal cord

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64
Q

DCM features?

A

Progressive condition, worsening, deteriorating or new symptoms should be a warning sign.

DCM symptoms can include any combination of [1]:
Pain (affecting the neck, upper or lower limbs)
Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence and/or impotence) - these can occur and do not necessarily suggest cauda equina syndrome in the absence of other hallmarks of that condition
Hoffman’s sign: is a reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.

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65
Q

DCM investigations?

A

An MRI of the cervical spine is the gold standard test where cervical myelopathy is suspected. It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.

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66
Q

DCM management?

A

All patients with degenerative cervical myelopathy should be urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery). This is due to the importance of early treatment. The timing of surgery is important, as any existing spinal cord damage can be permanent. Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery but at present, most patients are presenting too late. In one study, patients averaged over 5 appointments before diagnosis, representing >2 years.

Currently, decompressive surgery is the only effective treatment. It has been shown to prevent disease progression. Close observation is an option for mild stable disease, but anything progressive or more severe requires surgery to prevent further deterioration. Physiotherapy should only be initiated by specialist services, as manipulation can cause more spinal cord damage.

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67
Q

L4,L5,S1 - Where are the dermatome landmarks for these?

A

L4- Knee Caps
L5- Big toe, dorsum of the foot
S1- Lateral foot, small toe

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68
Q

DVLA restrictions for epilepsy?

A

Epilepsy/seizures - all patient must not drive and must inform the DVLA
First unprovoked/isolated seizure: 6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG. If these conditions are not met then this is increased to 12 months
For patients with established epilepsy or those with multiple unprovoked seizures: may qualify for a driving licence if they have been free from any seizure for 12 months
If there have been no seizures for 5 years (with medication if necessary) a ’til 70 licence is usually restored
withdrawawl of epilepsy medication: should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose

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69
Q

DVLA restrictions for TIA?

A

stroke or TIA: 1 month off driving, may not need to inform DVLA if no residual neurological deficit
multiple TIAs over short period of times: 3 months off driving and inform DVLA

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70
Q

DVLA restrictions for syncope?

A

simple faint: no restriction
single episode, explained and treated: 4 weeks off
single episode, unexplained: 6 months off
two or more episodes: 12 months off

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71
Q

Name 2 muscular dystrophies?

A

Duchenne muscular dystrophy & Becker muscular dystrophy

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72
Q

DMD features?

A

progressive proximal muscle weakness from 5 years
calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% of patients have intellectual impairment

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73
Q

BMD features?

A

develops after the age of 10 years
intellectual impairment much less common

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74
Q

Features of encephalitis?

A

fever, headache, psychiatric symptoms, seizures, vomiting
focal features e.g. aphasia
peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis

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75
Q

Encephalitis cause?

A

HSV-1 is responsible for 95% of cases in adults

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76
Q

Encephalitis investigations?

A

cerebrospinal fluid:
lymphocytosis
elevated protein
PCR for HSV, VZV and enteroviruses
neuroimaging:
medial temporal and inferior frontal changes (e.g. petechial haemorrhages)
normal in one-third of patients
MRI is better
EEG: lateralised periodic discharges at 2 Hz

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77
Q

Encephalitis management?

A

intravenous aciclovir should be started in all cases of suspected encephalitis

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78
Q

Epilepsy in children: What are west syndromes?

A

AKA Infantile spasms are characterised by brief spasms of sudden uncontrolled movements including flexion of the head, trunk, limbs, and extension of the arms (Salaam attack).

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79
Q

West syndrome features?

A

key features:
flexion of head, trunk, limbs → extension of arms (Salaam attack); last 1-2 secs, repeat up to 50 times
progressive mental handicap

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80
Q

West syndrome investigations?

A

EEG: hypsarrhythmia (abnormal interictal high amplitude waves and a background of irregular spikes)

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81
Q

West syndrome management?

A

possible treatments include vigabatrin and steroids

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82
Q

Benign rolandic seizures features?

A

most common in childhood, more common in males
features: paraesthesia (e.g. unilateral face), usually on waking up

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83
Q

Lennox-Gastaut syndrome features?

A

onset 1-5 yrs
atypical absences, falls, jerks
90% moderate-severe mental handicap
EEG: slow spike

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84
Q

Lennox-Gastaut syndrome management?

A

treatment: ketogenic diet may help

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85
Q

Juvenile myoclonic epilepsy features?

A

infrequent generalized seizures, often in morning//following sleep deprivation
daytime absences
sudden, shock-like myoclonic seizure (these may develop before seizures)

86
Q

Ictal phase of syncopal episodes vs seizures?

A

Syncopal episodes are associated with a rapid recovery and short post-ictal period. Seizures are associated with a far greater post-ictal period

87
Q

Localising focal seizures: Temporal lobe features?

A

An aura occurs in most patients
typically a rising epigastric sensation
also psychic or experiential phenomena, such as déjà vu, jamais vu
less commonly hallucinations (auditory/gustatory/olfactory)

Seizures typically last around one minute
automatisms (e.g. lip smacking/grabbing/plucking) are common

88
Q

Localising focal seizures: Frontal lobe features?

A

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

89
Q

Localising focal seizures: Parietal lobe features?

A

Paraesthesia

90
Q

Localising focal seizures: Occipital lobe features?

A

Floaters/flashes

91
Q

Epilepsy treatment: Absence seizures?

A

first line: ethosuximide

second line:
male: sodium valproate
female: lamotrigine or levetiracetam
carbamazepine may exacerbate absence seizures

92
Q

Epilepsy treatment: Generalised seizures?

A

males: sodium valproate
females: lamotrigine or levetiracetam

93
Q

Epilepsy treatment: Focal seizures?

A

first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide

94
Q

Epilepsy treatment: Myoclonic seizures?

A

males: sodium valproate
females: levetiracetam

95
Q

Tonic/atonic seizures?

A

males: sodium valproate
females: lamotrigine

96
Q

First presentation seizure management?

A

Following a first seizure, anti-epileptic drug treatment should only be started before specialist review in exceptional circumstances

97
Q

Benign essential tremor inheritance?

A

Autosomal dominant

98
Q

Features of benign essential tremor?

A

postural tremor: worse if arms outstretched
improved by alcohol and rest
most common cause of titubation (head tremor)

99
Q

Benign essential tremor management?

A

Propranolol is first-line
Primidone is sometimes used

100
Q

Where is an extradural bleed usually?

A

The collection is often in the temporal region since the thin skull at the pterion overlies the middle meningeal artery and is therefore vulnerable to injury.

101
Q

What is the imaging of an extradural bleed usually?

A

On imaging, an extradural haematoma appears as a biconvex (or lentiform), hyperdense collection around the surface of the brain. They are limited by the suture lines of the skull.

102
Q

Extradural haematoma management?

A

In patients who have no neurological deficit, cautious clinical and radiological observation is appropriate. The definitive treatment is craniotomy and evacuation of the haematoma.

103
Q

Facial nerve innervates what?

A

face: muscles of facial expression
ear: nerve to stapedius
taste: supplies anterior two-thirds of tongue
tear: parasympathetic fibres to lacrimal glands, also salivary glands

104
Q

Causes of bilateral facial nerve palsy?

A

Sarcoidosis
Guillain-Barre syndrome
Lyme disease
Bilateral acoustic neuromas (as in neurofibromatosis type 2)
as Bell’s palsy is relatively common it accounts for up to 25% of cases f bilateral palsy, but this represents only 1% of total Bell’s palsy cases

105
Q

LMN vs. UMN facial nerve palsy difference?

A

upper motor neuron lesion ‘spares’ upper face i.e. forehead
lower motor neuron lesion affects all facial muscles

106
Q

Which side does a facial nerve palsy lesion affect?

A

If there is a weakness to one side of the face with forehead sparing, this is typically caused by an upper motor neuron lesion of the facial nerve contralateral to the side in which the weakness is found

107
Q

What is the difference between a L5 radiculopathy, sciatic nerve lesion and S1 radiculopathy

A

An L5 lesion would cause web space paraesthesia and weakened dorsiflexion/inversion/eversion.

The sciatic nerve would cause weak dorsiflexion, inversion, and eversion but would also cause weak plantarflexion.

An S1 lesion would cause weakened plantarflexion. It would also cause reduced sensation around the lateral malleolus not the first web-space.

108
Q

4th nerve palsy features?

A

vertical diplopia
classically noticed when reading a book or going downstairs
subjective tilting of objects (torsional diplopia)
the patient may develop a head tilt, which they may or may not be aware of
when looking straight ahead, the affected eye appears to deviate upwards and is rotated outwards

109
Q

GCS: What are the motor scores?

A
  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Abnormal flexion to pain (decorticate posture)
  5. Extending to pain
  6. None
110
Q

GCS: What are the verbal scores?

A
  1. Orientated
  2. Confused
  3. Words
  4. Sounds
  5. None
111
Q

GCS: What are the eye-opening scores?

A
  1. Spontaneous
  2. To speech
  3. To pain
  4. None
112
Q

GCS: What must localising be counted as in movement?

A

To be counted as localising, the arm must be brought above the clavicle, else it should be scored as ‘flexing’

113
Q

What is Guillain Barre syndrome?

A

Guillain-Barre syndrome describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)

114
Q

Millie fisher syndrome features?

A

variant of Guillain-Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first
usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome
anti-GQ1b antibodies are present in 90% of cases

115
Q

GBS features?

A

Initial symptoms
around 65% of patients experience back/leg pain in the initial stages of the illness

The characteristic features of Guillain-Barre syndrome is progressive, symmetrical weakness of all the limbs. The weakness is classically ascending i.e. the legs are affected first
Reflexes are reduced or absent
Sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

Other features
there may be a history of gastroenteritis
respiratory muscle weakness
cranial nerve involvement
diplopia
bilateral facial nerve palsy
oropharyngeal weakness is common
autonomic involvement
urinary retention
diarrhoea

Less common findings
papilloedema: thought to be secondary to reduced CSF resorption

116
Q

GBS investigations?

A

lumbar puncture
rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%

nerve condution studies may be performed
decreased motor nerve conduction velocity (due to demyelination)
prolonged distal motor latency
increased F wave latency

117
Q

GBS management?

A

IV immunoglobulins
Plasma exchange (alternative to IV IG)
Supportive care
VTE prophylaxis (pulmonary embolism is a leading cause of death)
In severe cases with respiratory failure patients may need intubation, ventilation and admission to the intensive care unit.

118
Q

Headache red flags?

A

compromised immunity, caused, for example, by HIV or immunosuppressive drugs
age under 20 years and a history of malignancy
a history of malignancy known to metastasis to the brain
vomiting without other obvious cause
worsening headache with fever
sudden-onset headache reaching maximum intensity within 5 minutes - ‘thunderclap’
new-onset neurological deficit
new-onset cognitive dysfunction
change in personality
impaired level of consciousness
recent (typically within the past 3 months) head trauma
headache triggered by cough, valsalva (trying to breathe out with nose and mouth blocked), sneeze or exercise
orthostatic headache (headache that changes with posture)
symptoms suggestive of giant cell arteritis or acute narrow-angle glaucoma
a substantial change in the characteristics of their headache

119
Q

Herpes Simplex Encephalitis: Features?

A

fever, headache, psychiatric symptoms, seizures, vomiting
focal features e.g. aphasia
peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis

120
Q

Herpes Simplex Encephalitis: Investigations?

A

CSF: lymphocytosis, elevated protein
PCR for HSV
CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
MRI is better
EEG pattern: lateralised periodic discharges at 2 Hz

120
Q

Herpes Simplex Encephalitis: Pathophysiology?

A

HSV-1 is responsible for 95% of cases in adults
typically affects temporal and inferior frontal lobes

121
Q

Herpes Simplex Encephalitis: Management?

A

IV aciclovir

121
Q

CMT inheritance?

A

Autosomal dominant

122
Q

Idiopathic intracranial hypertension: Risk factors?

A

obesity
female sex
pregnancy
drugs
combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium

122
Q

Idiopathic intracranial hypertension: Features?

A

headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present

123
Q

Idiopathic intracranial hypertension: Management?

A

weight loss
whilst diet and exercise are important, medications such as semaglitide and topiramate may be considered by specialists. Topiramate is particularly beneficial as it also inhibits carbonic anhydrase
carbonic anhydrase inhibitors e.g. acetazolamide
topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

123
Q

Internuclear ophthalmoplegia features?

A

impaired adduction of the eye on the same side as the lesion
horizontal nystagmus of the abducting eye on the contralateral side

123
Q

Venous sinus thrombosis?

A

Thrombotic obstruction of the cerebral veins and/or dural sinuses. The thrombus will reduce the venous drainage, increasing the intracranial pressure

123
Q

Venous sinus thrombosis features?

A

headache (may be sudden onset)
nausea & vomiting
reduced consciousness

124
Q

Specific venous sinus thrombosis: Sagittal sinus thrombosis features

A

may present with seizures and hemiplegia
parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
‘empty delta sign’ seen on venography

124
Q

Specific venous sinus thrombosis: Cavernous sinus thrombosis features

A

other causes of cavernous sinus syndrome: local infection (e.g. sinusitis), neoplasia, trauma
periorbital oedema
ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
central retinal vein thrombosis

124
Q

Specific venous sinus thrombosis: Lateral sinus thrombosis features

A

6th and 7th cranial nerve palsies

124
Q

Venous sinus thrombosis investigations?

A

MRI venography is the gold standard
CT venography is an alternative
non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated

125
Q

Venous sinus thrombosis investigations?

A

anticoagulation
typically with low molecular weight heparin acutely
warfarin is still generally used for longer term anticoagulation

125
Q

Lambert eaton syndrome cause?

A

Lambert-Eaton myasthenic syndrome is caused by an antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system

125
Q

LES features?

A

repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
in reality, this is seen in only 50% of patients and following prolonged muscle use muscle strength will eventually decrease
limb-girdle weakness (affects lower limbs first)
hyporeflexia
autonomic symptoms: dry mouth, impotence, difficulty micturating
ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)

125
Q

LES investigations?

A

incremental response to repetitive electrical stimulation

126
Q

LES management?

A

treatment of underlying cancer
immunosuppression, for example with prednisolone and/or azathioprine
3,4-diaminopyridine is currently being trialled
works by blocking potassium channel efflux in the nerve terminal so that the action potential duration is increased. Calcium channels can then be open for a longer time and allow greater acetylcholine release to the stimulate muscle at the end plate
intravenous immunoglobulin therapy and plasma exchange may be beneficial

126
Q

What is lateral medullary syndrome?

A

Lateral medullary syndrome, also known as Wallenberg’s syndrome, occurs following occlusion of the posterior inferior cerebellar artery.

126
Q

Lateral medullary syndrome features?

A

Cerebellar features
ataxia
nystagmus

Brainstem features
ipsilateral: dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss

126
Q

Levodopa overview?

A

usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of L-dopa to dopamine

126
Q

Levodopa S/E?

A

dyskinesia
‘on-off’ effect
postural hypotension
cardiac arrhythmias
nausea & vomiting
psychosis
reddish discolouration of urine upon standing

127
Q

Pattern of damage Median nerve: Wrist

A

e.g. carpal tunnel syndrome
paralysis and wasting of thenar eminence muscles and opponens pollicis (ape hand deformity)
sensory loss to palmar aspect of lateral (radial) 2 ½ fingers

128
Q

Pattern of damage Median nerve: Elbow

A

Same as damage at wrist +

unable to pronate forearm
weak wrist flexion
ulnar deviation of wrist

129
Q

Pattern of damage Median nerve: Anterior interosseous nerve (branch of median nerve)

A

results in loss of pronation of forearm and weakness of long flexors of thumb and index finger

130
Q

Median nerve: Hand motor supply?

A

Motor supply (LOAF)
Lateral 2 lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis

131
Q

Medication headache features?

A

present for 15 days or more per month
developed or worsened whilst taking regular symptomatic medication
patients using opioids and triptans are at most risk
may be psychiatric co-morbidity

132
Q

Medication headache management?

A

simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn

133
Q

Medication headache diagnosis?

A

The first key concept is that patients that have been taking opioid analgesia (codeine or co-codamol in particular) for an extended period, such as this patient, are at risk of MOH. For opioids and triptans, this overuse is defined as ‘using the medication on 10 days or more per month, for 3 months or more’.

The second key concept is that in order to have a definitive diagnosis of MOH, the history of overuse alone is not sufficient - the patient’s symptoms must resolve (or revert back to their original pattern) within 2 months of stopping the causative medication.

134
Q

Meningitis and meningococcal features?

A

headache
fever
nausea/vomiting
photophobia
drowsiness
seizures

neck stiffness
purpuric rash (particularly with invasive meningococcal disease)

135
Q

CSF findings: Bacterial meningitis

A

Appearance: cloudy
Glucose: Low (< 1/2 plasma)
Protein: High (> 1 g/l)
White cells: 10 - 5,000 polymorphs/mm³

136
Q

CSF findings: Viral meningitis

A

Appearance: Clear/cloudy
Glucose: 60-80% of plasma glucose*
Protein: Normal/raised
White cells: 15 - 1,000 lymphocytes/mm³

137
Q

CSF findings: Tuberculous meningitis

A

Appearance: Slight cloudy, fibrin web
Glucose: Low (< 1/2 plasma)
Protein: High (> 1 g/l)
White cells: 10 - 1,000 lymphocytes/mm³

138
Q

Meningitis: Complications

A

Shapes

Sensorineural hearing loss (most common)
Hydrocephalus
Abscess intracerebral
Paralysis
Epilepsy
Seizures

139
Q

Migraine exacerbations?

A

Chocolate
Hangovers
Orgasms
Cheese
Caffeine
The oral contraceptive pill
Lie-ins
Alcohol
Travel
Exercise

140
Q

Migraine features?

A

5 attacks of

Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)
Headache has at least two of the following characteristics:
1. unilateral location
in children, attacks may be shorter-lasting, headache is more commonly bilateral, and gastrointestinal disturbance is more prominent.
2. pulsating quality (i.e., varying with the heartbeat)
3. moderate or severe pain intensity
4. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)

During headache at least one of the following:
1. nausea and/or vomiting*
2. photophobia and phonophobia

Not attributed to another disorder (history and examination do not suggest a secondary headache disorder or, if they do, it is ruled out by appropriate investigations or headache attacks do not occur for the first time in close temporal relation to the other disorder)

141
Q

Hemiplegic migraine?

A

A variant of migraine in which motor weakness is a manifestation of aura in at least some attacks around half of patients have a strong family history
very rare - estimated prevalence is 0.01% (i.e. around only 1 in 1,000 migraine patients), more common in adolescent females

142
Q

Migraine management?

A

acute: triptan + NSAID or triptan + paracetamol
prophylaxis: topiramate or propranolol

143
Q

Migraine: pregnancy, contraception and other hormonal factors -Management plans

A

Migraine during pregnancy
paracetamol 1g is first-line
NSAIDs can be used second-line in the first and second trimester
avoid aspirin and opioids such as codeine during pregnancy

According to the National Institute for Health and Care Excellence (NICE) guidelines, triptans are recommended as second-line treatment when simple analgesics such as paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) have failed.

144
Q

Migraine and COCP

A

if patients have migraine with aura then the COC is absolutely contraindicated due to an increased risk of stroke (relative risk 8.72)

144
Q

MND?

A

Motor neuron disease is a neurological condition of unknown cause which can present with both upper and lower motor neuron signs.

145
Q

MND features?

A

There are a number of clues which point towards a diagnosis of motor neuron disease:
asymmetric limb weakness is the most common presentation of ALS
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
fasciculations
the absence of sensory signs/symptoms
vague sensory symptoms may occur early in the disease (e.g. limb pain) but ‘never’ sensory signs

Other features
doesn’t affect external ocular muscles
no cerebellar signs
abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature

146
Q

MND investigations?

A

The diagnosis of motor neuron disease is clinical, but nerve conduction studies will show normal motor conduction and can help exclude a neuropathy. Electromyography shows a reduced number of action potentials with increased amplitude. MRI is usually performed to exclude the differential diagnosis of cervical cord compression and myelopathy

147
Q

UMN vs. LMN signs?

A

HENS For My Farm House

UMN:
Hyperreflexia
Extensor plantar reflex (AKA. Babinski [when referring to babies])
No muscle wasting
Spastic paralysis/hypertonia

LMN:
Fasiculations
Muscle wasting
Flaccid paralysis/hypotonia
Hyporeflexia

148
Q

What condition is associated with MND?

A

Frontotemporal dementia

149
Q

MND prognosis?

A

poor: 50% of patients die within 3 years

150
Q

MND management?

A

Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months

Respiratory care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months

Nutrition
percutaneous gastrostomy tube (PEG) is the preferred way to support nutrition and has been associated with prolonged survival

151
Q

Which MND type carries the worst prognosis?

A

Progressive bulbar palsy

152
Q

MND types?

A

Amyotrophic lateral sclerosis (50% of patients)
typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

Primary lateral sclerosis
UMN signs only

Progressive muscular atrophy
LMN signs only
affects distal muscles before proximal
carries best prognosis

Progressive bulbar palsy
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

153
Q

Multiple sclerosis?

A

Multiple sclerosis is chronic cell-mediated autoimmune disorder characterised by demyelination in the central nervous system.

154
Q

Multiple sclerosis epidemiology?

A

3 times more common in women
most commonly diagnosed in people aged 20-40 years
much more common at higher latitudes (5 times more common than in tropics)

155
Q

Types of MS?

A

Relapsing-remitting disease
most common form, accounts for around 85% of patients
acute attacks (e.g. last 1-2 months) followed by periods of remission

Secondary progressive disease
describes relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses
around 65% of patients with relapsing-remitting disease go on to develop secondary progressive disease within 15 years of diagnosis
gait and bladder disorders are generally seen

Primary progressive disease
accounts for 10% of patients
progressive deterioration from onset
more common in older people

156
Q

MS features?

A

Visual
optic neuritis: common presenting feature
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia

Sensory
pins/needles
numbness
trigeminal neuralgia
Lhermitte’s syndrome: paraesthesiae in limbs on neck flexion

Motor
spastic weakness: most commonly seen in the legs

Cerebellar
ataxia: more often seen during an acute relapse than as a presenting symptom
tremor

Others
urinary incontinence
sexual dysfunction
intellectual deterioration

157
Q

Diagnosis of MS?

A

Diagnosis can be made on the basis of two or more relapses and either objective clinical evidence of two or more lesions or objective clinical evidence of one lesion together with reasonable historical evidence of a previous relapse

158
Q

What is optic neuritis?

A

Optic neuritis refers to inflammation of the optic nerve, which often presents as visual disturbances such as blurring or loss of vision in one eye, and is frequently accompanied by eye pain.

159
Q

Investigations for MS?

A

MRI
high signal T2 lesions
periventricular plaques
Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum

CSF
oligoclonal bands (and not in serum)
increased intrathecal synthesis of IgG

Visual evoked potentials
delayed, but well preserved waveform

160
Q

Multiple sclerosis management?

A

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

161
Q

Drug options for reducing MS relapse?

A

natalizumab
a recombinant monoclonal antibody that antagonises alpha-4 beta-1-integrin found on the surface of leucocytes
inhibit migration of leucocytes across the endothelium across the blood-brain barrier
generally considered to have the strongest evidence base for preventing relapse of the disease-modifying and hence is often used first-line
given intravenously
ocrelizumab
humanized anti-CD20 monoclonal antibody
like natalizumab, it is considered a high-efficacy drug that is often used first-line
given intravenously
fingolimod
sphingosine 1-phosphate (S1P) receptor modulator
prevents lymphocytes from leaving lymph nodes
oral formulations are available
beta-interferon
not considered to be as effective as alternative disease-modifying drugs
given subcutaneously/intramuscularly
glatiramer acetate
immunomodulating drug - acts as an ‘immune decoy’
given subcutaneously
along with beta-interferon considered an ‘older drug’ with less effectiveness compared to monoclonal antibodies and S1P) receptor modulators

162
Q

Symptom control management for MS?

A

Fatigue
once other problems (e.g. anaemia, thyroid or depression) have been excluded NICE recommend a trial of amantadine
other options include mindfulness training and CBT

Spasticity
baclofen and gabapentin are first-line. Other options include diazepam, dantrolene and tizanidine
physiotherapy is important
cannabis and botox are undergoing evaluation

Bladder dysfunction
may take the form of urgency, incontinence, overflow etc
guidelines stress the importance of getting an ultrasound first to assess bladder emptying - anticholinergics may worsen symptoms in some patients
if significant residual volume → intermittent self-catheterisation
if no significant residual volume → anticholinergics may improve urinary frequency

Oscillopsia (visual fields appear to oscillate)
gabapentin is first-line

163
Q

Patient has neurogenic bladder dysfunction secondary to MS. What is the next appropriate step?

A

The next appropriate step in her management is thus to arrange an ultrasound KUB, to assess her bladder emptying – this will then determine what treatment options are available to her.

xybutynin is an anticholinergic medication, which may be of use in neurogenic bladder dysfunction if there is no significant post-void residual volume. If the patient has a significant post-void residual volume, however, the use of anticholinergic medications will likely precipitate urinary retention. As such, US KUB is required to assess bladder emptying before such drugs are trialled.

164
Q

Multi-system atrophy?

A

rare neurodegenerative disorder that affects multiple systems within the body, including the nervous system. It is characterized by a progressive and relentless deterioration of various functions, leading to a range of symptoms that can significantly impact a person’s quality of life

165
Q

Multi-system atrophy sub-types?

A

1) MSA-P - Predominant Parkinsonian features
2) MSA-C - Predominant Cerebellar features

166
Q

Multi-system atrophy features?

A

Parkinsonism
autonomic disturbance
erectile dysfunction: often an early feature
postural hypotension
atonic bladder
cerebellar signs

167
Q

Myasthenia Gravis?

A

Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors. Antibodies to acetylcholine receptors are seen in 85-90% of cases*. Myasthenia is more common in women (2:1)

168
Q

Myasthenia Gravis features?

A

The key feature is muscle fatigability - muscles become progressively weaker during periods of activity and slowly improve after periods of rest:
extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia

169
Q

Myasthenia Gravis associations

A

thymomas in 15%
autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
thymic hyperplasia in 50-70%

170
Q

Myasthenia Gravis investigations?

A

single fibre electromyography: high sensitivity (92-100%)
CT thorax to exclude thymoma
CK normal
antibodies to acetylcholine receptors
positive in around 85-90% of patients
n the remaining patients, about about 40% are positive for anti-muscle-specific tyrosine kinase antibodies
Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used any more due to the risk of cardiac arrhythmia

171
Q

Myasthenia Gravis management?

A

long-acting acetylcholinesterase inhibitors
pyridostigmine is first-line
immunosuppression is usually not started at diagnosis, but the majority of patients eventually require it in addition to long-acting acetylcholinesterase inhibitors:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy

172
Q

Myasthenic crisis management?

A

plasmapheresis
intravenous immunoglobulins

173
Q

What is a myasthenic crisis?

A

A myasthenic crisis is a state of extreme muscle weakness that can lead to severe respiratory and swallowing difficulties, potentially requiring immediate medical attention. It is considered a medical emergency

174
Q

Rocuronium and suxamethonium in myasthenia gravis

A

Rocuronium and suxamethonium are both neuromuscular blocking drugs (NMBDs), however they act in different ways. Rocuronium is a non-depolarising NMBD, acting as an antagonist the post-synaptic receptor and leaving fewer receptors available for acetylcholine.

Suxamethonium is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Again, due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.

Rocuronium ROCKS Suxamethonium SUCKS

175
Q

Myasthenia Gravis exacerbating drugs?

A

penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

176
Q

Narcolepsy features?

A

typical onset in teenage years
hypersomnolence
cataplexy (sudden loss of muscle tone often triggered by emotion)
sleep paralysis
vivid hallucinations on going to sleep or waking up

177
Q

Narcolepsy investigation?

A

multiple sleep latency EEG

178
Q

Narcolepsy management?

A

daytime stimulants (e.g. modafinil) and nighttime sodium oxybate

179
Q

Neurofibromatosis?

A

There are two types of neurofibromatosis, NF1 and NF2. Both are inherited in an autosomal dominant fashion

NF1 is also known as von Recklinghausen’s syndrome. It is caused by a gene mutation on chromosome 17 which encodes neurofibromin and affects around 1 in 4,000

NF2 is caused by gene mutation on chromosome 22 and affects around 1 in 100,000

180
Q

NF1 vs. NF2?

A

NF1:
Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamatomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas

NF2:
Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas

181
Q

NMS Features?

A

It occurs within hours to days of starting an antipsychotic (antipsychotics are also known as neuroleptics, hence the name) and the typical features are:
pyrexia
muscle rigidity
autonomic lability: typical features include hypertension, tachycardia and tachypnoea
agitated delirium with confusion

182
Q

NMS pathophysiology?

A

The pathophysiology is unknown but one theory is that the dopamine blockade induced by antipsychotics triggers massive glutamate release and subsequent neurotoxicity and muscle damage.

183
Q

NMS biochemical?

A

A raised creatine kinase is present in most cases. Acute kidney injury (secondary to rhabdomyolysis) may develop in severe cases. A leukocytosis may also be seen

184
Q

NMS management?

A

stop antipsychotic
patients should be transferred to a medical ward if they are on a psychiatric ward and often they are nursed in intensive care units
IV fluids to prevent renal failure
dantrolene may be useful in selected cases
thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum
bromocriptine, dopamine agonist, may also be used

185
Q

NMS tetrad?

A

Neuroleptic malignant syndrome tetrad - hyperthermia, muscle rigidity, autonomic instability, altered mental status

186
Q

Neuropathic pain management?

A

NICE updated their guidance on the management of neuropathic pain in 2013:
first-line treatment*: amitriptyline, duloxetine, gabapentin or pregabalin
if the first-line drug treatment does not work try one of the other 3 drugs
in contrast to standard analgesics, drugs for neuropathic pain are typically used as monotherapy, i.e. if not working then drugs should be switched, not added
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems

187
Q

Normal pressure hydrocephalus features?

A

A classical triad of features is seen
urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson’s disease)

188
Q

Normal pressure hydrocephalus investigations

A

Imaging - hydrocephalus with ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement

189
Q

Normal pressure hydrocephalus management?

A

ventriculoperitoneal shunting
around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages

190
Q

Parkinson features?

A

Bradykinesia
poverty of movement also seen, sometimes referred to as hypokinesia
short, shuffling steps with reduced arm swinging
difficulty in initiating movement

Tremor
most marked at rest, 3-5 Hz
worse when stressed or tired, improves with voluntary movement
typically ‘pill-rolling’, i.e. in the thumb and index finger

Rigidity
lead pipe
cogwheel: due to superimposed tremor

Other characteristic features
mask-like facies
flexed posture
micrographia
drooling of saliva
psychiatric features: depression is the most common feature (affects about 40%); dementia, psychosis and sleep disturbances may also occur
impaired olfaction
REM sleep behaviour disorder
fatigue
autonomic dysfunction:
postural hypotension

191
Q

Parkinsons?

A

Parkinson’s disease is a progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra. The reduction in dopaminergic output results in a classical triad of features: bradykinesia, tremor and rigidity. The symptoms of Parkinson’s disease are characteristically asymmetrical.

192
Q

Drug induced parkinsonism features?

A

Drug-induced parkinsonism has slightly different features to Parkinson’s disease:
motor symptoms are generally rapid onset and bilateral
rigidity and rest tremor are uncommon

193
Q

Parkinson’s investigations?

A

Diagnosis is usually clinical. However, if there is difficulty differentiating between essential tremor and Parkinson’s disease NICE recommend considering 123I‑FP‑CIT single photon emission computed tomography (SPECT).

194
Q
A

Phase 3B prep (10 decks)

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