General

Question 1

Examples of 5HT3 antagonists and their mechanism?

Answer 1

Ondansetron and palonsetron
5HT3 receptor antagonist - centrally acting in medulla oblongata in chemoreceptor trigger zone

Question 2

Side effects of 5HT3 antagonists?

Answer 2

Constipation
QT prolongation

Question 3

Advantage of palonsetron vs ondansetron?

Answer 3

Second generation 5HT3 antagonist
Less QT prolongation

Question 4

Who do absence seizures mostly affect?

Answer 4

onset of 3-10 years old and girls are affected twice as commonly as boys

Question 5

Features of absence seizures?

Answer 5

absences last a few seconds and are associated with a quick recovery
seizures may be provoked by hyperventilation or stress
the child is usually unaware of the seizure
they may occur many times a day
EEG: bilateral, symmetrical 3Hz spike and wave pattern

Question 6

EEG: bilateral, symmetrical 3Hz spike and wave pattern, suggestive of?

Answer 6

Absence seizure

Question 7

Management of absence seizures?

Answer 7

sodium valproate and ethosuximide are first-line treatment
good prognosis - 90-95% become seizure free in adolescence

Question 8

Cause of absent plantar reflexes + extensor planters

Answer 8

subacute combined degeneration of the cord
motor neuron disease
Friedreich’s ataxia
syringomyelia
taboparesis (syphilis)
conus medullaris lesion

Question 9

Where is the lesion if plantar reflexes + extensor planters

Answer 9

lesion producing both upper motor neuron (extensor plantars) and lower motor neuron (absent ankle jerk) signs

Question 10

What is acute disseminated encephalomyelitis?

Answer 10

autoimmune demyelinating disease of the central nervous system
post-infectious encephalomyelitis

Question 11

Some causes of acute disseminated encephalomyelitis?

Answer 11

Common infections include measles, mumps, rubella and varicella and more

Question 12

Clinical course of acute disseminated encephalomyelitis ?

Answer 12

Lag time, followed by acute onset multifocal neurological symptoms with rapid deterioration
Nonspecific features: Fever, nausea. vomiting, oculomotor effects
MRI imaging may show areas of supra and infra-tentorial demyelination
No biomarkers

Question 13

Treatment of disseminated encephalomyelitis?

Answer 13

intravenous glucocorticoids and the consideration of IVIG

Question 14

What is anti NMDA encephalitis?

Answer 14

Anti-NMDA receptor encephalitis is a paraneoplastic syndrome, presenting as prominent psychiatric features

Question 15

Features of anti-NMDA encephalitis ?

Answer 15

agitation, hallucinations, delusions and disordered thinking; seizures, insomnia, dyskinesias and autonomic instability

Question 16

Associated findings with anti-NMDA receptor encephalitis?

Answer 16

Ovarian teratomas are detected in up to half of all female adult patients

Question 17

CSF finding in anti-NMDA receptor encephalitis ?

Answer 17

Pleocytosis
If not normal

Question 18

Management of anti-NMDA receptor encephalitis?

Answer 18

based of immunosuppression with intravenous steroids, immunoglobulins, rituximab, cyclophosphamide or plasma exchange, alone or in combination. Resection of teratoma is also therapeutic.

Question 19

What antibodies are associated in anti-NMDA receptor encephalitis?

Answer 19

Anti-GM1
Anti-MuSK

Question 20

Important points about wernicke’s area

Answer 20

lesion of the superior temporal gyrus
Blood supply: Inferior division left MCA
Area ‘forms’ the speech before ‘sending it’ to Broca’s area.

Question 21

Features of wernicke’s aphasia (receptive aphasia) ?

Answer 21

Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent - ‘word salad’

Comprehension impaired

Question 22

Important points about Broca’s area (expressive aphasia)?

Answer 22

Due to a lesion of the inferior frontal gyrus. It is typically supplied by the superior division of the left MCA

Question 23

Features of Broca’s aphasia?

Answer 23

Speech is non-fluent, laboured, and halting. Repetition is impaired

Comprehension is normal

Question 24

Features of conductive aphasia ?

Answer 24

Speech is fluent but repetition is poor. Aware of the errors they are making

Comprehension is normal

Question 25

What causes a conductive aphasia?

Answer 25

Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area

Question 26

Features of global aphasia

Answer 26

Large lesion affecting all 3 of the above (Brocas, wernickes and arcuate fasiculus) resulting in severe expressive and receptive aphasia

May still be able to communicate using gestures

Question 27

What is an Arnold chiari malformation ?

Answer 27

Arnold-Chiari malformation describes the downward displacement, or herniation, of the cerebellar tonsils through the foramen magnum.

Malformations may be congenital or acquired through trauma.

Question 28

Features of Arnold chair malformation?

Answer 28

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

Question 29

In ataxia telectangesia, what is the genetic mutation and its impact?

Answer 29

Defect in the ATM gene which encodes for DNA repair enzymes.
It is one of the inherited combined immunodeficiency disorders.

Question 30

Features of ataxia telengectasia?

Answer 30

Autosomal recessive
cerebellar ataxia
telangiectasia (spider angiomas)
IgA deficiency resulting in recurrent chest infections
10% risk of developing malignancy, lymphoma or leukaemia, but also non-lymphoid tumours

Question 31

Differences between Fredrick’s ataxia and ataxia telengectasia?

Answer 31

Question 32

Features of autonomic neuropathy?

Answer 32

impotence, inability to sweat, postural hypotension
postural hypotension e.g. drop of 30/15 mmHg
loss of decrease in heart rate following deep breathing
pupils: dilates following adrenaline instillation

Question 33

Causes of autonomic neuropathy?

Answer 33

diabetes
Guillain-Barre syndrome
multisystem atrophy (MSA), Shy-Drager syndrome
Parkinson’s
infections: HIV, Chagas’ disease, neurosyphilis
drugs: antihypertensives, tricyclics
craniopharyngioma

Question 34

Mechanism of baclofen and its use?

Answer 34

agonist of GABA receptors
acts in the central nervous system (brain and spinal cord)

Used to treat spasticity

Question 35

What is Bell’s palsy?

Answer 35

acute, unilateral, idiopathic, facial nerve paralysis.
Possible associated herpes simplex virus
Peak incidence 20-40 yrs

Question 36

In lower motor neurological facial palsy, is forehead affected?

Answer 36

Yes

Question 37

Features of Bell’s palsy?

Answer 37

lower motor neuron facial nerve palsy - forehead affected
in contrast, an upper motor neuron lesion ‘spares’ the upper face
patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis

Question 38

Management in Bell’s palsy?

Answer 38

oral prednisolone within 72 hours of onset of Bell’s palsy
eye care is important to prevent exposure keratopathy
- prescribe tears and tape

Question 39

Features of BPPV?

Answer 39

Vertigo with change of head position

vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
may be associated with nausea
each episode typically lasts 10-20 seconds
positive Dix-Hallpike manoeuvre, indicated by:
patient experiences vertigo
rotatory nystagmus

Question 40

Treatment for BPPV and how successful is it?

Answer 40

Epley manoeuvre (successful in around 80% of cases)
teaching the patient exercises they can do themselves at home, termed vestibular rehabilitation, for example Brandt-Daroff exercises

Question 41

Benign rolandic epilepsy features?

Answer 41

seizures characteristically occur at night
seizures are typically partial (e.g. paraesthesia affecting face) but secondary generalisation may occur (i.e. parents may only report tonic-clonic movements)
child is otherwise normal

Normally resolves by adolescence

Question 42

Erbs palsy?

Answer 42

damage to C5,6 roots
winged scapula
may be caused by a breech presentation
Waiter’s tip

Question 43

Klumpkes palsy?

Answer 43

damage to T1
loss of intrinsic hand muscles
due to traction
Claw hand

Question 44

How do brain abscesses occur?

Answer 44

extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis

Question 45

Features of brain asbcess?

Answer 45

headache
- often dull, persistent
fever
- may be absent and usually not the swinging pyrexia seen with abscesses at other sites
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

Question 46

Management of brain abscess?

Answer 46

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

Question 47

Features of lesions in the parietal lobe?

Answer 47

sensory inattention
apraxias
astereognosis (tactile agnosia)
inferior homonymous quadrantanopia
Gerstmann’s syndrome (lesion of dominant parietal): alexia, acalculia, finger agnosia and right-left disorientation

Question 48

Occipital lobe lesion?

Answer 48

homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia

Question 49

Temporal lobe lesion?

Answer 49

Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)

Question 50

Frontal lobe lesion?

Answer 50

expressive (Broca’s) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting
disinhibition
perseveration - repeating particular phrase
anosmia
inability to generate a list

Question 51

Cerebellum lesion ?

Answer 51

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

Question 52

Area affected in Wernicke and Korsakoff syndrome

Answer 52

Medial thalamus and mammillary bodies of the hypothalamus

Question 53

Area affected in hemiballisus

Answer 53

Subthalamic nucleus of the basal ganglia

Question 54

Area affected by Huntington’s chorea?

Answer 54

Striatum (caudate nucleus) of the basal ganglia

Question 55

Area affected by Kluver-Bucy syndrome (hypersexuality, hyperorality, hyperphagia, visual agnosia

Answer 55

Amygddala

Question 56

Features of brown sequared syndrome?

Answer 56

Lateral hemisection of the cord

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

Question 57

What is CADASIL?

Answer 57

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)
rare cause of multi-infarct dementia
patients often present with migraine

Question 58

What is CADASIL?

Answer 58

Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)
rare cause of multi-infarct dementia
patients often present with migraine

Question 59

Uses of carbsmazepine?

Answer 59

Trigeminal neuralgia
Bipolar
Epilepsy

Question 60

Adverse side effects of carebmazepine ?

Answer 60

P450 enzyme inducer
dizziness and ataxia
drowsiness
headache
visual disturbances (especially diplopia)
Steven-Johnson syndrome
leucopenia and agranulocytosis
hyponatraemia secondary to syndrome of inappropriate ADH secretion

Question 61

Why may patients see new seizures after start carbamazepine ?

Answer 61

exhibit autoinduction,
Induces the enzyme that metabolisies it
hence when patients start carbamazepine they may see a return of seizures after 3-4 weeks of treatment.

Question 62

What is cataplexy?

Answer 62

sudden and transient loss of muscular tone caused by strong emotion (e.g. laughter, being frightened). Around two-thirds of patients with narcolepsy have cataplexy.

Question 63

Unilateral cerebellar lesions affects ipsilateral or contralateral side?

Answer 63

Ipsilateral

Question 64

Features of cerebellar syndrome?

Answer 64

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

Question 65

Causes of cerebellar syndrome

Answer 65

Friedreich’s ataxia, ataxic telangiectasia
neoplastic: cerebellar haemangioma
stroke
alcohol
multiple sclerosis
hypothyroidism
drugs: phenytoin, lead poisoning
paraneoplastic e.g. secondary to lung cancer

Question 66

Normal values for cerebrospinal fluid?

Answer 66

Normal values of cerebrospinal fluid (CSF) are as follows:
pressure = 60-150 mm (patient recumbent)
protein = 0.2-0.4 g/l
glucose = > 2/3 blood glucose
cells: red cells = 0, white cells < 5/mm³

Question 67

Associatied with high lymphocytes in CSF?

Answer 67

viral meningitis/encephalitis
TB meningitis
partially treated bacterial meningitis
Lyme disease
Behcet’s, SLE
lymphoma, leukaemia

Question 68

What is the mechanism behind chorea?

Answer 68

Chorea is caused by damage to the basal ganglia, especially the caudate nucleus.

Question 69

What is chorea?

Answer 69

Chorea describes involuntary, rapid, jerky movements which often move from one part of the body to another.

Question 70

Causes of chorea?

Answer 70

Huntington’s disease, Wilson’s disease, ataxic telangiectasia
SLE, anti-phospholipid syndrome
rheumatic fever: Sydenham’s chorea
drugs: oral contraceptive pill, L-dopa, antipsychotics
neuroacanthocytosis
pregnancy: chorea gravidarum
thyrotoxicosis
polycythaemia rubra vera
carbon monoxide poisoning
cerebrovascular disease

Question 71

What is athetosis?

Answer 71

Sinuous movement of the limbs is termed athetosis

Question 72

Features of cluster headache?

Answer 72

pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
clusters typically last 4-12 weeks
intense sharp, stabbing pain around one eye (recurrent attacks ‘always’ affect same side)
the patient is restless and agitated during an attack
accompanied by redness, lacrimation, lid swelling
nasal stuffiness
miosis and ptosis in a minority

Question 73

Management of cluster headache?

Answer 73

acute: 100% oxygen (80% response rate within 15 minutes), subcutaneous triptan (75% response rate within 15 minutes)
prophylaxis: verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone
NICE recommend seeking specialist advice from a neurologist if a patient develops cluster headaches with respect to neuroimaging

Question 74

What are the autonomic cephalgia?

Answer 74

cluster headache, paroxysmal hemicrania and short-lived unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT)

Question 75

What does the sciatic nerve divide into?

Answer 75

The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula

Question 76

Common pudenal nerve injury?

Answer 76

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

Question 77

Types of chronic regional pain syndrome?

Answer 77

type I (most common): there is no demonstrable lesion to a major nerve
type II: there is a lesion to a major nerve

Question 78

Features of chronic regional pain syndrome ?

Answer 78

progressive, disproportionate symptoms to the original injury/surgery
allodynia
temperature and skin colour changes
oedema and sweating
motor dysfunction
the Budapest Diagnostic Criteria are commonly used in the UK

Question 79

Management of chronic regional pain syndrome?

Answer 79

early physiotherapy is important
neuropathic analgesia in-line with NICE guidelines
specialist management (e.g. Pain team) is required

Question 80

Mechanism in CJD?

Answer 80

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.

Question 81

Features of CJD?

Answer 81

Myoclonus
Dementia rapid onset

Question 82

Investigation summary in CJD?

Answer 82

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

Question 83

Types of CJD?

Answer 83

Sporadic
New variant

Question 84

Features of new variant CJD?

Answer 84

psychological symptoms such as anxiety, withdrawal and dysphonia are the most common presenting features

Question 85

Prion protein is new variant CJD is encoded by what chromosome?

Answer 85

Chromosome 20

Question 86

Risk factor for developing new variant CJD?

Answer 86

methionine homozygosity at codon 129 chromosome 20

Question 87

Risk factor for developing new variant CJD?

Answer 87

methionine homozygosity at codon 129 chromosome 20

Question 88

Other forms of prion diseases?

Answer 88

kuru
fatal familial insomnia
Gerstmann Straussler-Scheinker disease

Question 89

Presentation of degenerative cervical myelopathy?

Answer 89

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.

Question 90

What are risk factors of degenerative cervical myelopathy?

Answer 90

Occupation
Smoking
Genetics

Question 91

Signed used to test for degenerative cervical myelopathy?

Answer 91

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.

Question 92

Best imaging for degenerative cervical cord myelopathy?

Answer 92

MRI

Question 93

Treatment of cervical myelopathy?

Answer 93

Decompressive surgery
Urgent referral - should be seen / treated within 6 months of diagonosis
Prevents further damage

Question 94

Drugs that cause peripheral neuropathy?

Answer 94

amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole

Question 95

Driving advice: Once off seizure + No structural brain damage?

Answer 95

6 months

Question 96

Driving advice: Once off seizure + structural brain damage?

Answer 96

12 months

Question 97

Seizure free for 12 months?

Answer 97

Can apply for driving liscence

Question 98

No seizure for 5 years - driving?

Answer 98

Can apply for a until 70 driving licence

Question 99

Driving advice after one episode of syncope?

Answer 99

4 weeks once treated and explained

Question 100

Driving advice for syncope when unexplained?

Answer 100

6 months off

Question 101

Two or more episodes of syncope?

Answer 101

12 months off

Question 102

Time off driving from stroke or TIA?

Answer 102

1 month

Question 103

Driving advice: Multiple TIAs ?

Answer 103

3 months

Question 104

Driving advice after craniotomy? Including transpheoidal surgery

Answer 104

If well - consider after 6 months
If not 1 year

Question 105

Narcolepsy / cataplexy - driving?

Answer 105

Once symptoms satisfactorially under control

Question 106

What is the function of dystrophin?

Answer 106

large membrane associated protein in muscle which connects the muscle membrane to actin, part of the muscle cytoskeleton

Question 107

Inheritence of the muscular dystrophies?

Answer 107

X linked

Question 108

Genetic mutation in duchene muscular dystrophy?

Answer 108

frameshift mutation resulting in one or both of the binding sites ( of the protein) are lost leading to a severe form

Question 109

Genetic mutation in becker’s muscular dystrophy?

Answer 109

non-frameshift insertion in the dystrophin gene resulting in both binding sites being preserved leading to a milder form

Question 110

Features of duchene muscular dystrophy?

Answer 110

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

Question 111

Features of becker muscular dystrophy?

Answer 111

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

Question 112

Features of infantile spasms? (West syndrome)

Answer 112

Brief spasms beginning in the first few months of life

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

usually secondary to serious neurological abnormality (e.g. tuberous sclerosis, encephalitis, birth asphyxia) or may be idiopathic

Question 113

Treatment of west syndrome?

Answer 113

possible treatments include vigabatrin and steroids
has a poor prognosis

Question 114

Features of petit Mal seizure? Absence seizures?

Answer 114

onset 4-8 yrs
duration few-30 secs; no warning, quick recovery; often many per day
EEG: 3Hz generalized, symmetrical

good prognosis: 90-95% become seizure free in adolescence

Question 115

Treatment of absence seizures?

Answer 115

sodium valproate, ethosuximide

Question 116

Features of Lennox- gas taut syndrome?

Answer 116

may be an extension of infantile spasms
onset 1-5 yrs
features:
atypical absences, falls, jerks
90% moderate-severe mental handicap
EEG: slow spike

Question 117

Treatment of Lennox-gas taut syndrome?

Answer 117

treatment: ketogenic diet may help

Question 118

Features of benign rolandic epilepsy?

Answer 118

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

Question 119

Features of juvenile myoclonic epilepsy? Jana syndrome

Answer 119

typical onset is in the teenage years, more common in girls
features:
infrequent generalized seizures, often in morning//following sleep deprivation
daytime
s
sudden, shock-like myoclonic seizure (these may develop before seizures)
treatment: usually good response to sodium valproate

Question 120

What is a focal seizure ?

Answer 120

previously termed partial seizures
these start in a specific area, on one side of the brain
awareness depends on area affected

Question 121

How can focal seizures be classified?

Answer 121

focal seizures can be classified as being motor (e.g. Jacksonian march), non-motor (e.g. déjà vu, jamais vu; ) or having other features such as aura

Must classify by awareness: focal aware vs focal impaired awareness

Question 122

Features of generalised seizures?

Answer 122

engage or involve networks on both sides of the brain at the onset
consciousness lost immediately.

Question 123

How can generalised seizure be divided?

Answer 123

Motor: tonic clonic
Non-motor: absence

Question 124

Localising feature of temporal lobe epilepsy?

Answer 124

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)

Question 125

Localising feature of frontal lobe epilepsy?

Answer 125

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

Question 126

Localising features of partial lobe epilepsy?

Answer 126

Paraesthesia

Question 127

Localising features of occipital lobe epilepsy?

Answer 127

Floaters/flashes

Question 128

What should women with epilepsy do before becoming pregnant?

Answer 128

Folic acid 5mg

Question 129

How much does taking anti-epileptics during pregnant increase risk of neural tube defect?

Answer 129

1-2% normal patients
3-4 in epilepsy

Question 130

How should you aim to manage patients with epilepsy wishing to become pregnant?

Answer 130

Aim for mono therapy
Should not need to monitor medication levels

Question 131

Congenital defect associated with sodium valporate?

Answer 131

Neural tube defect
Neurodevelopmental delay

Women of child bearing age should not be put on this drug if possible

Question 132

Which anti-epileptic is considered to have the least teratogenic effect?

Answer 132

carbamazepine

Question 133

Congenital defect associated with phenytoin?

Answer 133

cleft pallet

Question 134

Is breast feeding safe?

Answer 134

Yes
Providing not on barbiturate

Question 135

When should anti-epileptics be started?

Answer 135

Generally after second seizure

Question 136

When should anti-epileptics be started after first seizure?

Answer 136

• The patient has a neurological deficit
• Brain imaging shows a structural abnormality
• The EEG shows unequivocal epileptic activity
• The patient or their family or carers consider the risk of having a further seizure unacceptable

Question 137

Treatment of generalised tonic clonic seizure?

Answer 137

Male: sodium valproate
Female: Lamotrigene

Question 138

Treatment of focal seizures?

Answer 138

1. Lamotrigene, leveiteracetam
2. carbamazepine, oxcarbazepine or zonisamide

Question 139

Myoclonic seizure treatment?

Answer 139

males: sodium valproate
females: levetiracetam

Question 140

Treatment of absence seizure?

Answer 140

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

Question 141

Treatment of tonic and atonic seizures?

Answer 141

males: sodium valproate
females: lamotrigine

Question 142

Inheritance of essential tremor?

Answer 142

Autosomal dominant

Question 143

Features of essential tremor?

Answer 143

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

Question 144

Treatment of essential tremor?

Answer 144

propranolol is first-line
primidone is sometimes used

Question 145

Mechanism of ethosuximide?

Answer 145

blocks T-type calcium channels in thalamic neurons

Question 146

What is the afferent and efferent function of the facial nerve?

Answer 146

It is a mostly efferent nerve
Afferent: Taste (genicular ganglion)
Efferent: muscles of facial expression, digastric muscle and glands

Supply - ‘face, ear, taste, tear’
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

Question 147

Causes of bilateral facial palsy?

Answer 147

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 bilateral is only 1% of total Bell’s palsy cases

Question 148

Causes of lower motor neurone facial nerve palsy?

Answer 148

Lower motor neuron
Bell’s palsy
Ramsay-Hunt syndrome (due to herpes zoster)
acoustic neuroma
parotid tumours
HIV
multiple sclerosis*
diabetes mellitus

Question 149

Cause of upper motor neurone facial nerve?

Answer 149

Stroke

Question 150

How do you determine a LMN vs a UMN facial palsy?

Answer 150

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

Question 151

Where are the sensory and motor nuclei of the facial nerve?

Answer 151

Motor: Pons
Sensory: Nervus intermedius

petrous temporal bone into the internal auditory meatus with the vestibulocochlear nerve. Here they combine to become the facial nerve.

Question 152

What is facioscapulohumeral dystrophy?

Answer 152

Autosomal dominant dystrophy

facial muscles are involved first - difficulty closing eyes, smiling, blowing etc
weakness of the shoulder and upper arm muscles
abnormal prominence of the borders of the shoulder blades - ‘winging’
lower limb: hip girdle weakness, foot drop

Question 153

Causes of foot drop?

Answer 153

Occurs due to weakness in foot dorsiflexors

common peroneal nerve lesion - the most common cause
L5 radiculopathy
sciatic nerve lesion
superficial or deep peroneal nerve lesion
other possible includes central nerve lesions (e.g. stroke) but other features are usually present

Question 154

Features of an isolated peroneal nerve neuropathy?

Answer 154

if the patient has an isolated peroneal neuropathy there will be weakness of foot dorsiflexion and eversion. Reflexes will be normal
weakness of hip abduction is suggestive of a L5 radiculopathy

Question 155

CN IV palsy?

Answer 155

supplies superior oblique (depresses eye, moves inward)

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

Question 156

Genetic mechanism behind Fredrick’s ataxia?

Answer 156

Autosomal recessive, trinucleotide repeat disorder characterised by a GAA repeat in the X25 gene on chromosome 9 (frataxin).
Does not demonstrate anticipation

Question 157

Fredrick’s ataxia phenotype?

Answer 157

Gait ataxia and kyphoscoliosis are the most common presenting features.

Neurological features
absent ankle jerks/extensor plantars
cerebellar ataxia
optic atrophy
spinocerebellar tract degeneration

Other features:
hypertrophic obstructive cardiomyopathy (90%, most common cause of death)
diabetes mellitus (10-20%)
high-arched palate

Question 158

Causes of gingival hyperplasia?

Answer 158

Drug causes of gingival hyperplasia
phenytoin
ciclosporin
calcium channel blockers (especially nifedipine)

Other causes of gingival hyperplasia include
acute myeloid leukaemia (myelomonocytic and monocytic types)

Question 159

What triggers Guillain barre syndrome?

Answer 159

Triggered by an infection (classically Campylobacter jejuni)

Question 160

Pathogenesis of Guillain barre syndrome?

Answer 160

cross-reaction of antibodies with gangliosides in the peripheral nervous system
correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated
anti-GM1 antibodies in 25% of patients

Question 161

What is Miller Fischer Syndrome?

Answer 161

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

Question 162

Features of Guillain barre syndrome?

Answer 162

Initial symptom: Backpain
Guillain-Barre syndrome is progressive, symmetrical weakness of all the limbs.
Weakness is typically ascending
Reduced / absent reflexes

Other features
- There may be a history of gastroenteritis
- Respiratory muscle weakness
- Cranial nerve involvement
1.diplopia
2.bilateral facial nerve palsy
3.oropharyngeal weakness is common
- Autonomic involvement
urinary retention
diarrhoea

Question 163

Investigations in Guillain barre syndrome?

Answer 163

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

Question 164

Management of Guillain barre?

Answer 164

1. Intravenous immunoglobulin
2. REGULAR MONITORING OF RESPIRATORY FUNCTION
3. Plasma exchange

Question 165

Poor prognostic factors for Guillain barre?

Answer 165

age > 40 years
poor upper extremity muscle strength
previous history of a diarrhoeal illness (specifically Campylobacter jejuni)
high anti-GM1 antibody titre
need for ventilatory support

Question 166

Factors indicating a head CT within 1 hour?

Answer 166

GCS < 13 on initial assessment
GCS < 15 at 2 hours post-injury
suspected open or depressed skull fracture
any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
post-traumatic seizure.
focal neurological deficit.
more than 1 episode of vomiting

Question 167

Factors indicating a head CT within 8 hours?

Answer 167

age 65 years or older
any history of bleeding or clotting disorders including anticogulants
dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
more than 30 minutes’ retrograde amnesia of events immediately before the head injury

warfarin who have sustained a head injury with no other indications for a CT head scan, perform a CT head scan within 8 hours of the injury.

Question 168

What is a primary brain injury?

Answer 168

focal (contusion/haematoma) or diffuse (diffuse axonal injury)
diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and tearing of axons

Question 169

Headinjury: Haematoma vs contusion?

Answer 169

haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact

Question 170

What is a secondary brain injury?

Answer 170

occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma rendering the brain more susceptible to blood flow changes and hypoxia

Question 171

What is Cushing’s reflex?

Answer 171

hypertension and bradycardia) often occurs late and is usually a pre terminal event

Question 172

Where is the bleed in a extradural bleed?

Answer 172

Bleeding into the space between the dura mater and the skull
Bleed from middle meningeal artery
Exhibit a lucid interval –> crash
Features: Raised intracranial pressure

Question 173

Where is the bleed in a subdural haematoma?

Answer 173

Bleeding into the outermost meningeal layer. Most commonly occur around the frontal and parietal lobes.

Risk factors include old age, alcoholism and anticoagulation.

Slower onset of symptoms than a epidural haematoma. There may be fluctuating confusion/consciousness

Question 174

Features of migraine?

Answer 174

Severe headache which is usually unilateral and throbbing in nature
May be be associated with aura, nausea and photosensitivity
Aggravated by, or causes avoidance of, routine activities of daily living. Patients often describe ‘going to bed’.
In women may be associated with menstruation

Question 175

Features of tension headache?

Answer 175

Recurrent, non-disabling, bilateral headache, often described as a ‘tight-band’
Not aggravated by routine activities of daily living

Question 176

Cluster headache features?

Answer 176

Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours with clusters typically lasting 4-12 weeks
Intense pain around one eye (recurrent attacks ‘always’ affect same side)
Patient is restless during an attack
Accompanied by redness, lacrimation, lid swelling
More common in men and smokers

Question 177

Temporal arteritis?

Answer 177

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%) - tiredness of muscles of mastication
Tender, palpable temporal artery
Raised ESR

Question 178

Medical overuse headache?

Answer 178

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

Question 179

Causes of acute headache?

Answer 179

meningitis
encephalitis
subarachnoid haemorrhage
head injury
sinusitis
glaucoma (acute closed-angle)
tropical illness e.g. Malaria

Question 180

Causes of chronic headache?

Answer 180

chronically raised ICP
Paget’s disease
psychological

Question 181

Damage to what causes hemiballism?

Answer 181

Subthalamic nucleus

Question 182

What is hemiballism?

Answer 182

involuntary, sudden, jerking movements which occur contralateral to the side of the lesion.

ballisic movements primarily affect the proximal limb musculature whilst the distal muscles may display more choreiform-like movements

Question 183

Treatment of hemiballism?

Answer 183

Anti-dopamine
Halloperidol

Question 184

What lobes of the brain does herpes simplex encephalitis typically affect?

Answer 184

Temporal lobes most
Can affect inferior frontal

Question 185

Features of herpes simplex encephalitis?

Answer 185

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

Question 186

What virus is implicated in hopers simplex encephalitis?

Answer 186

HSV1

Question 187

Investigation finding in herpes simplex encephalitis?

Answer 187

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

Question 188

Investigation in herpex simplex encephalitis?

Answer 188

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

Question 189

Treatment of herpes simplex encephalitis?

Answer 189

Intravenous acyclovir

Question 190

What is charco-marie tooth called now?

Answer 190

Hereditary sensorimotor neuropathy

Question 191

What are the two types of HSMN?

Answer 191

HSMN type I: primarily due to demyelinating pathology
HSMN type II: primarily due to axonal pathology

Question 192

Features of HSMN type 1 ?

Answer 192

autosomal dominant
due to defect in PMP-22 gene (which codes for myelin)
features often start at puberty
motor symptoms predominate
distal muscle wasting, pes cavus, clawed toes
foot drop, leg weakness often first features

Question 193

Features of Huntington disease?

Answer 193

Features typical develop after 35 years of age
chorea
personality changes (e.g. irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movements

Question 194

Genetics behind Huntington’s disease?

Answer 194

autosomal dominant
trinucleotide repeat disorder: repeat expansion of CAG
- anticipation occurs
results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
due to defect in huntingtin gene on chromosome 4

Question 195

Risk factors of idiopathic intracranial hypertension?

Answer 195

obesity
female sex
pregnancy
drugs*

combined oral contraceptive pill
steroids
tetracyclines
vitamin A
lithium

Question 196

Features of idiopathic intracranial hypertension

Answer 196

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

Question 197

Management of idiopathic intracranial hypertension

Answer 197

weight loss
diuretics e.g. acetazolamide
topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture
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

Question 198

Where is the lesion in internuclear ophthalmoplegia ?

Answer 198

Lesion in the medial longitudinal fasciculus (MLF)
controls horizontal eye movements by interconnecting the IIIrd, IVth and VIth cranial nuclei
located in the paramedian area of the midbrain and pons

Question 199

Features of internuclear ophthalmoplegia?

Answer 199

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

Question 200

Causes of internuclear ophthalmoplegia?

Answer 200

MS
Vascular disease

Question 201

Features of intracranial venous thrombosis?

Answer 201

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

Question 202

Investigations for intracranial venous thrombosis?

Answer 202

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

Question 203

Specific syndrome associated with intracranial venous thrombosis ?

Answer 203

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

Cavernous sinus thrombosis
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

Question 204

Management of intracranial venous thrombosis?

Answer 204

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

Question 205

Features of saggital sinus syndrome?

Answer 205

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

Question 206

Features of cavernous sinus thrombosis?

Answer 206

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

Question 207

Features of lateral sinus thrombosis?

Answer 207

6th and 7th cranial nerve palsies

Question 208

Pathophysiology behind Lambert eaton syndrome?

Answer 208

antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.

Question 209

Features of Lambert eaton syndrome?

Answer 209

repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
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)

Question 210

Findings on EMG in Lambert eaton syndrome?

Answer 210

incremental response to repetitive electrical stimulation

Question 211

Management of Lambert eaton syndrome?

Answer 211

treatment of underlying cancer
immunosuppression, for example with prednisolone and/or azathioprine
3,4-diaminopyridine is currently being trialled
IVIG
Plasma exchange

Question 212

Adverse effect of lamotrigine?

Answer 212

Steven Johnson syndrome

Question 213

Mechanism of lamotrigine?

Answer 213

Sodium channel blocker

Question 214

What is lateral medullary syndrome also known as?

Answer 214

Wallenburg syndrome

Question 215

Pathophysiology behind lateral medullary syndrome?

Answer 215

Occlusion of posterior inferior cerebellar artery

Question 216

Features of lateral medullary syndrome?

Answer 216

Cerebellar features + brainstorm features

Cerebellar features:
1. Ataxia
2. Nystagmus

Brainstem features:
1. ipsilateral: dysphagia, facial numbness, cranial nerve 2. palsy e.g. Horner’s
3. contralateral: limb sensory loss

Question 217

Adverse effect of levodopa?

Answer 217

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

Question 218

Why is levodopa used with a decarboxylase inhibitor?

Answer 218

Prevents peripheral metabolism of levodopa to dopamine

Question 219

Cause of macroglossia?

Answer 219

hypothyroidism
acromegaly
amyloidosis
Duchenne muscular dystrophy
mucopolysaccharidosis (e.g. Hurler syndrome)

Down syndrome has apparent marcoglossia due to face hypoplasia

Question 220

Features of Ménière’s disease?

Answer 220

Unknown cause - path ins endolymph system dilation

recurrent episodes of vertigo, tinnitus and hearing loss (sensorineural). Vertigo is usually the prominent symptom
a sensation of aural fullness or pressure is now recognised as being common
other features include nystagmus and a positive Romberg test
episodes last minutes to hours
typically symptoms are unilateral but bilateral symptoms may develop after a number of years

Question 221

What is Romberg’s test?

Answer 221

determines if your balance issues are related to the function of your dorsal column by removing the visual and vestibular components that contribute to maintaining balance

Feet together - close eyes

Question 222

Management of Meniere’s?

Answer 222

ENT assessment
Must tell DVLA

Acute attacks: buccal or intramuscular prochlorperazine. Admission is sometimes required
prevention: betahistine and vestibular rehabilitation exercises may be of benefit

Question 223

Meningitis complications?

Answer 223

Neurological sequalae:
- sensorineural hearing loss (most common)
- seizures
- focal neurological deficit

Pressure
- brain herniation
- hydrocephalus

Question 224

What is the risk with mengineal meningitis?

Answer 224

Waterhouse-Friderichsen syndrome (adrenal insufficiency secondary to adrenal haemorrhage).

Question 225

Diagnostic criteria for migraine?

Answer 225

A At least 5 attacks fulfilling criteria B-D

B Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)

C Headache has at least two of the following characteristics:
1. unilateral location*
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)

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

E 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)

Question 226

Migraine mangement

Answer 226

Acute:
1. Triptan and Paracetamol or NSAID
2. Young people consider nasal triptan
3. Then consider non-oral antiemetics, triptan, NSAID

Prophylaxis:
Give if experience > 2 episodes per month
1. Topiramte or Propanolol
- Give propanolol in women - topiramate is teratogenic
2. Riboflavin may reduced frequency of attacks

Question 227

Treatment of menstrual migraine prophylaxis?

Answer 227

recommend either frovatriptan (2.5 mg twice a day) or zolmitriptan (2.5 mg twice or three times a day) as a type of ‘mini-prophylaxis’

Question 228

Other prophylaxis options for migraine, not on NICE guidance?

Answer 228

Candesartan
monoclonal antibodies directed against the calcitonin gene-related peptide (CGRP) receptor: examples include erenumab

Question 229

How to treat acute migraine in a pregnant woman?

Answer 229

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

Question 230

Acute treatment of migraine with pregnancy?

Answer 230

mefanamic acid or a combination of aspirin, paracetamol and caffeine. Triptans are also recommended in the acute situation

Question 231

Causes of miosis?

Answer 231

Causes of miosis (small pupil)
Horner’s syndrome
Argyll-Robertson pupil
senile miosis
pontine haemorrhage
congenital

Drugs causes
opiates
parasympathomimetics: pilocarpine
organophosphate toxicity

Question 232

Features of motor neurone disease?

Answer 232

fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common

Question 233

Things MND does not do?

Answer 233

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

Question 234

Treatment of motor neurone disease?

Answer 234

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

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

Question 235

MND types?

Answer 235

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

Question 236

Pathophysiology of MS?

Answer 236

Type 4 hypersensitivity
Central demyelination

Question 237

Risk factors for MS?

Answer 237

High latitude
Women
Genetics ( monozygotic twins 30%)

Question 238

Trajectories / subtypes of MS?

Answer 238

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

Question 239

Visual symptoms in MS?

Answer 239

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

Question 240

Sensory features in MS?

Answer 240

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

urinary incontinence
sexual dysfunction
intellectual deterioration

Question 241

Motor features in MS?

Answer 241

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

Question 242

Investigations in MS?

Answer 242

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

Question 243

CSF analysis in MS?

Answer 243

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

Question 244

Acute management of MS?

Answer 244

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

Question 245

Indication for initiating long term treatment in MS?

Answer 245

Typical indications for disease-modifying drugs include:
relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided

secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)

Question 246

Mechanism of natalizumab?

Answer 246

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

Question 247

Mechanism of ocrelizumab?

Answer 247

humanized anti-CD20 monoclonal antibody
like natalizumab, it is considered a high-efficacy drug that is often used first-line
given intravenously

Question 248

Mechanism of fingolimod?

Answer 248

sphingosine 1-phosphate (S1P) receptor modulator
prevents lymphocytes from leaving lymph nodes
oral formulations are available

Question 249

Mechanism of glatiramer?

Answer 249

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

Question 250

DMARD drugs in MS?

Answer 250

Natalizumab
Ocrelizumab
Fingolimod
Beta interferon
glatiramer acetate

Question 251

Treatment of spasticity in MS?

Answer 251

baclofen and gabapentin are first-line. Other options include diazepam, dantrolene and tizanidine

Question 252

Treatment of bladder dysfunction in MS?

Answer 252

if significant residual volume → intermittent self-catheterisation
if no significant residual volume → anticholinergics may improve urinary frequency

Question 253

What is Oscillopsia? How should it be managed in MS?

Answer 253

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

Question 254

Prognostic features of MS?

Answer 254

Good prognosis features
female sex
age: young age of onset (i.e. 20s or 30s)
relapsing-remitting disease
sensory symptoms only
long interval between first two relapses
complete recovery between relapses

Question 255

What are the types of multisystem atrophy?

Answer 255

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

Question 256

What are the features of mutlisystem atrophy?

Answer 256

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

Question 257

What is the mechanism behind myasthenia gravis?

Answer 257

Antibodies to acetylcholine receptors

Question 258

Features of myasthenia gravis?

Answer 258

muscles become progressively weaker
extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia

Question 259

Associations with myasthenia gravis?

Answer 259

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

Question 260

Investigations in myasthenia ?

Answer 260

Single fibre electromyography: high sensitivity (92-100%)
CT thorax to exclude thymoma
CK normal
antibodies to acetylcholine receptors

Question 261

Management of myasthenia?;

Answer 261

long-acting acetylcholinesterase inhibitors - pyridostigmine is first-line
Immunosuppression note started at diagnosis - eventually needed:
- prednisolone initially
- azathioprine, cyclosporine, mycophenolate mofetil may also be used

Management of myasthenic crisis
plasmapheresis
intravenous immunoglobulins

Question 262

Myasthenia gravis exacerbating factors?

Answer 262

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

Question 263

Genetics behind myotonic dystrophy?

Answer 263

autosomal dominant
a trinucleotide repeat disorder
DM1 is caused by a CTG repeat at the end of the DMPK (Dystrophia Myotonica-Protein Kinase) gene on chromosome 19
DM2 is caused by a repeat expansion of the ZNF9 gene on chromosome 3

Question 264

Features of DM1 mutation myotonic dystrophy ?

Answer 264

• DMPK gene on chromosome 19
• Distal weakness more prominent

Question 265

Features of DM2 mutation myotonic dystrophy ?

Answer 265

• ZNF9 gene on chromosome 3
• Proximal weakness more prominent
• Severe congenital form not seen

Question 266

What are the features of myotonic dystrophy?

Answer 266

General:
myotonic facies (long, ‘haggard’ appearance)
frontal balding
bilateral ptosis
cataracts
dysarthria

Other features:
myotonia (tonic spasm of muscle)
weakness of arms and legs (distal initially)
mild mental impairment
diabetes mellitus
testicular atrophy
cardiac involvement: heart block, cardiomyopathy
dysphagia

Question 267

Features of narcolepsy?

Answer 267

early onset of REM sleep
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

Question 268

What is the HLA association of narcolepsy?

Answer 268

associated with HLA-DR2

Question 269

Investigation of narcolepsy?

Answer 269

multiple sleep latency EEG
associated with low levels of orexin (hypocretin),

Question 270

Management of narcolepsy?

Answer 270

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

Question 271

Features of lymphoma?

Answer 271

Rubbery, painless lymphadenopathy
The phenomenon of pain whilst drinking alcohol is very uncommon
There may be associated night sweats and splenomegaly

Question 272

Features of thyroglossal cyst?

Answer 272

More common in patients < 20 years old
Usually midline, between the isthmus of the thyroid and the hyoid bone
Moves upwards with protrusion of the tongue
May be painful if infected

Question 273

Features of thyroid swelling?

Answer 273

May be hypo-, eu- or hyperthyroid symptomatically
Moves upwards on swallowing

Question 274

Features of pharyngeal pouch?

Answer 274

More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough

Question 275

Features of cystic hygroma?

Answer 275

A congenital lymphatic lesion (lymphangioma) typically found in the neck, classically on the left side
Most are evident at birth, around 90% present before 2 years of age

Question 276

Features of branchial cyst?

Answer 276

An oval, mobile cystic mass that develops between the sternocleidomastoid muscle and the pharynx
Develop due to failure of obliteration of the second branchial cleft in embryonic development
Usually present in early adulthood

Question 277

Features of cervical rib?

Answer 277

More common in adult females
Around 10% develop thoracic outlet syndrome

Question 278

Features of carotid aneurysm?

Answer 278

Pulsatile lateral neck mass which doesn’t move on swallowing

Question 279

How does a nerve conduction study demonstrate axonal pathology?

Answer 279

Axonal
normal conduction velocity
reduced amplitude

Question 280

How does a nerve conduction study demonstrate demyelinating pathology?

Answer 280

Demyelinating
reduced conduction velocity
normal amplitude

Question 281

Features of neurofibromatosis 1?

Answer 281

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

Question 282

Features of neurofibromatosis 2?

Answer 282

Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas

Question 283

Difference between neurofibromatosis and tuberous sclerosis

Answer 283

Question 284

Features of neuroleptic malignant syndrome?

Answer 284

Taken antipsychotic
pyrexia
muscle rigidity
autonomic lability: typical features include hypertension, tachycardia and tachypnoea
agitated delirium with confusion
Rhabdomyolysis

Question 285

Mechanism of neuroleptic malignant syndrome?

Answer 285

dopamine blockade induced by antipsychotics triggers massive glutamate release and subsequent neurotoxicity and muscle damage.

Question 286

Treatment of neuroleptic malignant syndrome?

Answer 286

stop antipsychotic
IVF
Dantrolene
- 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

Question 287

Mechanism of dantrolene?

Answer 287

• decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum

Question 288

Features of Neuromyelitis optica?

Answer 288

Diagnosis requires bilateral optic neuritis, myelitis and 2 of the following 3 criteria:
1. Spinal cord lesion involving 3 or more spinal levels
2. Initially normal MRI brain
3. Aquaporin 4 positive serum antibody (NMO IgG)

Question 289

What is neurmyelitis optica?

Answer 289

Neuromyelitis optica (NMO) is a monophasic or relapsing-remitting demyelinating CNS disorder
involves the optic nerves and cervical spine, with imaging of the brain frequently normal. Vomiting is also a common presenting complaint.

Question 290

Treatment of neuromyelitis optica?

Answer 290

immunosuppressant e.g. with anti-CD20 agent rituximab)

Question 291

Causes of neuropathic pain?

Answer 291

diabetic neuropathy
post-herpetic neuralgia
trigeminal neuralgia
prolapsed intervertebral disc

Question 292

Treatment of neuropathic pain?

Answer 292

amitriptyline, duloxetine, gabapentin or pregabalin
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)

Question 293

Features of normal pressure hydrocephalus?

Answer 293

urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson’s disease)

Question 294

Mechanism behind normal pressure hydrocephalus?

Answer 294

reversible cause of dementia
secondary to reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.

Question 295

Imaging in normal pressure hydrocephalus?

Answer 295

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

Question 296

Management of normal pressure hydrocephalus?

Answer 296

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

Question 297

Lesions that cause an upbeat nystagmus location?

Answer 297

Upbeat nystagmus
cerebellar vermis lesions

Question 298

Lesions that cause an downbeat nystagmus location?

Answer 298

Arnold-Chiari malformation

Question 299

What is osteosclerosis?

Answer 299

Autosomal dominant condition
replacement of normal bone by vascular spongy bone
progressive conductive deafness due to fixation of the stapes at the oval window

Question 300

Features of osteosclerosois

Answer 300

Onset is usually at 20-40 years - features include:
conductive deafness
tinnitus
normal tympanic membrane*
positive family history

Question 301

What is Lambert eaton syndrome associated with?

Answer 301

Small cell lung cancer
antibody directed against pre-synaptic voltage gated calcium channel in the peripheral nervous system
can also occur independently as autoimmune disorder

Question 302

What is anti-Hu antibody associated with?

Answer 302

associated with small cell lung carcinoma and neuroblastomas
sensory neuropathy - may be painful
cerebellar syndrome
encephalomyelitis

Question 303

What is anti-Yo associated with?

Answer 303

associated with ovarian and breast cancer
cerebellar syndrome

Question 304

What is anti- GAD antibody associated with?

Answer 304

associated with breast, colorectal and small cell lung carcinoma
stiff person’s syndrome or diffuse hypertonia

Question 305

What is anti-Ri associated with?

Answer 305

associated with breast and small cell lung carcinoma
ocular opsoclonus-myoclonus

Question 306

What is Purkinje cell antibody associated with?

Answer 306

• peripheral neuropathy in breast cancer

Question 307

What is the classic triad of Parkinson’s disease?

Answer 307

Classic triad of features: bradykinesia, tremor and rigidity.

Question 308

Pathophysiology in Parkinson’s?

Answer 308

degeneration of dopaminergic neurons in the substantia nigra

Question 309

Features of bradykinesia?

Answer 309

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

Question 310

Tremor associated in Parkinson’s disease?

Answer 310

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

Question 311

Features or rigidity in Parkinson’s ?

Answer 311

lead pipe
cogwheel: due to superimposed tremor

Question 312

Other than classic features, what else is seen in Parkinson’s?

Answer 312

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

Question 313

Features that are different in drug induced Parkinson’s?

Answer 313

motor symptoms are generally rapid onset and bilateral
rigidity and rest tremor are uncommon

Question 314

Treatment in Parkinson’s disease?

Answer 314

if the motor symptoms are affecting the patient’s quality of life: levodopa

if the motor symptoms are not affecting the patient’s quality of life: dopamine agonist (non-ergot derived), levodopa or monoamine oxidase B (MAO‑B) inhibitor

Question 315

In the case that levodopa does not work, what else can be added in Parkinson treatment?

Answer 315

dopamine agonist, MAO‑B inhibitor or catechol‑O‑methyl transferase (COMT) inhibitor as an adjunct

Question 316

What are Parkinson patients at risk of if they don’t take their medication?

Answer 316

Acute akinesia
Neuroleptic malignant syndrome

Question 317

Management of hyper salivation in Parkinson’s?

Answer 317

Glycoperoneum

Question 318

Side effects of levodopa?

Answer 318

dry mouth
anorexia
palpitations
postural hypotension
psychosis

Question 319

When do patients with Parkinson’s get dyskinesia?

Answer 319

At peak dose
dystonia, chorea and athetosis

Question 320

Examples of dopamine receptor agonists?

Answer 320

bromocriptine, ropinirole, cabergoline, apomorphine

Question 321

Adverse effects of dopamine receptor agonists?

Answer 321

pulmonary, retroperitoneal and cardiac fibrosis
impulse control disorders and excessive daytime somnolence

Question 322

What MAO-B is used in parsons and what is it mechanism?

Answer 322

e.g. selegiline
inhibits the breakdown of dopamine secreted by the dopaminergic neurons

Question 323

Mechanism of amantadine?

Answer 323

mechanism is not fully understood, probably increases dopamine release and inhibits its uptake at dopaminergic synapses

Question 324

Side effects of amantadine?

Answer 324

side-effects include ataxia, slurred speech, confusion, dizziness and livedo reticularis

Question 325

Mechanism of COMT inhibitors in Parkinson’s?

Answer 325

e.g. entacapone, tolcapone
COMT is an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy
used in conjunction with levodopa in patients with established PD

Question 326

Treatment in drug induced Parkinson’s?

Answer 326

block cholinergic receptors
now used more to treat drug-induced parkinsonism rather than idiopathic Parkinson’s disease
help tremor and rigidity
e.g. procyclidine, benzotropine, trihexyphenidyl (benzhexol)

Question 327

Causes of Parkinsonism?

Answer 327

Parkinson’s disease
drug-induced e.g. antipsychotics, metoclopramide*
progressive supranuclear palsy
multiple system atrophy
Wilson’s disease
post-encephalitis
dementia pugilistica (secondary to chronic head trauma e.g. boxing)
toxins: carbon monoxide, MPTP

Question 328

Causes of motor peripheral neuropathy ?

Answer 328

Guillain-Barre syndrome
porphyria
lead poisoning
hereditary sensorimotor neuropathies (HSMN) - Charcot-Marie-Tooth
chronic inflammatory demyelinating polyneuropathy (CIDP)
diphtheria

Question 329

Causes of sensory peripheral neuropathy?

Answer 329

diabetes
uraemia
leprosy
alcoholism
vitamin B12 deficiency
amyloidosis

Question 330

Demyelinating peripheral neuropathy causes?

Answer 330

Guillain-Barre syndrome
chronic inflammatory demyelinating polyneuropathy (CIDP)
amiodarone
hereditary sensorimotor neuropathies (HSMN) type I
paraprotein neuropathy

Question 331

Axonal peripheral neuropathy causes?

Answer 331

alcohol
diabetes mellitus*
vasculitis
vitamin B12 deficiency*
hereditary sensorimotor neuropathies (HSMN) type II

Question 332

Mechanism of phenytoin?

Answer 332

Mechanism of action
binds to sodium channels increasing their refractory period

Question 333

Adverse effects of phenytoin?>

Answer 333

Acute
initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures

Chronic
common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

Idiosyncratic
fever
rashes, including severe reactions such as toxic epidermal necrolysis
hepatitis
Dupuytren’s contracture*
aplastic anaemia
drug-induced lupus

Teratogenic
associated with cleft palate and congenital heart disease

Question 334

How should phenytoin be monitored?

Answer 334

Trough immediately before next dose

Question 335

What is pituitary apoplexy?

Answer 335

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

Question 336

Precipitating causes of pituitary apoplexy?

Answer 336

Precipitating factors
hypertension
pregnancy
trauma
anticoagulation

Question 337

Features of pituitary apoplexy?

Answer 337

sudden onset headache similar to that seen in subarachnoid haemorrhage
vomiting
neck stiffness
visual field defects: classically bitemporal superior quadrantic defect
extraocular nerve palsies
features of pituitary insufficiency
e.g. hypotension/hyponatraemia secondary to hypoadrenalism

Question 338

Management of pituitary apoplexy?

Answer 338

urgent steroid replacement due to loss of ACTH
careful fluid balance
surgery

Question 339

How long does post LP headache last?

Answer 339

Up to a couple of days

Typical features
usually develops within 24-48 hours following LP but may occur up to one week later
may last several days
worsens with upright position
improves with recumbent position

Question 340

Management of post LP headache?

Answer 340

supportive initially (analgesia, rest)
if pain continues for more than 72 hours then specific treatment is indicated, to prevent subdural haematoma
treatment options include: blood patch, epidural saline and intravenous caffeine

Question 341

Features of progressive supra nuclear palsy?

Answer 341

postural instability and falls
patients tend to have a stiff, broad-based gait
impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
parkinsonism
bradykinesia is prominent
cognitive impairment
primarily frontal lobe dysfunction

Question 342

What is Ramsay hunt syndrome ?

Answer 342

Ramsay Hunt syndrome (herpes zoster oticus) is caused by the reactivation of the varicella zoster virus in the geniculate ganglion of the seventh cranial nerve.

Question 343

Features of Ramsay hunt syndrome?

Answer 343

auricular pain is often the first feature
facial nerve palsy
vesicular rash around the ear
other features include vertigo and tinnitus

Question 344

Management of Ramsay hunt syndrome?

Answer 344

oral aciclovir and corticosteroids are usually given

Question 345

Clincial features of restless legs syndrome?

Answer 345

uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest
paraesthesias e.g. ‘crawling’ or ‘throbbing’ sensations
movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)

Question 346

Associations of restless legs syndrome?

Answer 346

there is a positive family history in 50% of patients with idiopathic RLS
iron deficiency anaemia
uraemia
diabetes mellitus
pregnancy

Question 347

What investigation should be done for restless legs syndrome?

Answer 347

Ferritin

Question 348

Management of restless legs syndrome

Answer 348

simple measures: walking, stretching, massaging affected limbs
treat any iron deficiency
dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
benzodiazepines
gabapentin

Question 349

What is Reyes syndrome?

Answer 349

Reye’s syndrome is a severe, progressive encephalopathy affecting children that is accompanied by fatty infiltration of the liver, kidneys and pancreas

Question 350

Management of Reyes syndrome?

Answer 350

The peak incidence is 2 years of age, features include:
there may be a history of preceding viral illness
encephalopathy: confusion, seizures, cerebral oedema, coma
fatty infiltration of the liver, kidneys and pancreas
hypoglycaemia

Question 351

Mechanism of sodium valproate?

Answer 351

Increases GABA activity

Question 352

Adverse effects of sodium valproate

Answer 352

P450 inhibitor
gastrointestinal: nausea
increased appetite and weight gain
alopecia: regrowth may be curly
ataxia
tremor
hepatotoxicity
pancreatitis
thrombocytopaenia
hyponatraemia
hyperammonemic encephalopathy: L-carnitine may be used as treatment if this develops

Question 353

Causes of spastic paresis?

Answer 353

describes a upper motor neuron pattern of weakness in the lower limbs

demyelination e.g. multiple sclerosis
cord compression: trauma, tumour
parasagittal meningioma
tropical spastic paraparesis
transverse myelitis e.g. HIV
syringomyelia
hereditary spastic paraplegia
osteoarthritis of the cervical spine

Question 354

Describe the spinal cord tract?

Answer 354

Question 355

Definition of status epileptics ?

Answer 355

Status epilepticus is defined as:
a single seizure lasting >5 minutes, or
>= 2 seizures within a 5-minute period without the person returning to normal between them

Question 356

Treatment of status epileptics?

Answer 356

First-line drugs are IV benzodiazepines such as diazepam or lorazepam
in the prehospital setting PR diazepam or buccal midazolam may be given
in hospital IV lorazepam is generally used. This may be repeated once after 10-20 minutes

Question 357

Features of stroke in the anterior cerebral artery?

Answer 357

Contralateral hemiparesis and sensory loss, lower extremity > upper

Question 358

Features of stroke in the middle cerebral artery?

Answer 358

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

Question 359

Features of stroke in the posterior cerebral artery?

Answer 359

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

Question 360

stroke to toe basilar artery?

Answer 360

locked in syndrome

Question 361

Features of weber syndrome?

Answer 361

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

branches of the posterior cerebral artery that supply the midbrain)

Question 362

Features of Lacunar stroke?

Answer 362

present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule

Question 363

When should anti-hypertensive be used in stroke?

Answer 363

post ischaemic stroke if there is a hypertensive emergency with one or more of the following serious concomitant medical issues (according to the NICE guidelines):
Hypertensive encephalopathy
Hypertensive nephropathy
Hypertensive cardiac failure/myocardial infarction
Aortic dissection
Pre-eclampsia/eclampsia

Or if thrombolysis has been carried out

Question 364

Management of blood pressure in stroke?

Answer 364

UptoDate suggest using intravenous labetalol, nicardipine and clevidipine as first-line agents, due to the possibility for rapid and safe titration to control blood pressure

Question 365

Post thrombolysis what is the blood pressure target post stroke?

Answer 365

However, in patients who are candidates for thrombolytic therapy for acute stroke, blood pressure should be reduced to 185/110mmHg or lower
Elevated BP can affect thrombolytic eligibility and delay treatment
Timely management of elevated BP is crucial when patients are otherwise eligible for intravenous thrombolysis
After thrombolytic therapy, UptoDate recommend ensuring that the blood pressure is stabilised and maintained at or below 180/105mmHg for at least 24 hours after treatment

Question 366

First line imaging for suspected stroke?

Answer 366

Non contrast CT

Question 367

Features of a stroke?

Answer 367

The following criteria should be assessed:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

Question 368

Diagnostic criteria for total anterior circulation stroke?

Answer 368

involves middle and anterior cerebral arteries

All 3 criteria must be present:

The following criteria should be assessed:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

Question 369

Diagnostic criteria for a partial anterior circulation stroke?

Answer 369

involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery

2 criteria of below must be satisfied:

The following criteria should be assessed:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

Question 370

Diagnostic criteria for lacunar infarcts?

Answer 370

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

Question 371

Diagnostic criteria of posterior circulation infarction?

Answer 371

Posterior circulation infarcts (POCI, c. 25%)
involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia

Question 372

What causes subacute degeneration of the spinal cord?

Answer 372

due to vitamin B12 deficiency
dorsal columns + lateral corticospinal tracts are affected

Question 373

Features of subacute degeneration of the spinal cord?

Answer 373

dorsal columns + lateral corticospinal tracts are affected
joint position and vibration sense lost first then distal paraesthesia
upper motor neuron signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks
if untreated stiffness and weakness persist

Question 374

Most common type of subarachnoid haemorrhage?

Answer 374

Traumatic subarachnoid haemorrhage

Question 375

Causes of spontaneous subarachnoid haemorrhage?

Answer 375

Causes of spontaneous SAH include:
Intracranial aneurysm* (saccular ‘berry’ aneurysms): this accounts for around 85% of cases. Conditions associated with berry aneurysms include adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
Arteriovenous malformation
Pituitary apoplexy
Arterial dissection
Mycotic (infective) aneurysms
Perimesencephalic (an idiopathic venous bleed)

Question 376

Features of subarachnoid haemorrhage?

Answer 376

Classical presenting features include:
Headache: typically sudden-onset (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’) and occipital
Nausea and vomiting
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
ECG changes including ST elevation may be seen

Question 377

How should subarachnoid haemorrhage be confirmed?

Answer 377

1. Computed tomography (CT) head
   - Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.
   - CT is negative for SAH (no blood seen) in 7% of cases.
2. Lumbar puncture (LP)
   - Used to confirm SAH if CT is negative.
   - LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown).
   - Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure).
   - As well as xanthochromia, CSF findings consistent with subarachnoid haemorrhage include a normal or raised opening pressure

Question 378

Once SAH confirmed, what test needs to be completed?

Answer 378

CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
+/- digital subtraction angiogram (catheter angiogram)

Question 379

Complications post aneurysmal SAH?

Answer 379

Re-bleeding
Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
Seizures
Hydrocephalus
Death

Question 380

How is vasospasm prevented in SAH?

Answer 380

nimodipine (a calcium channel inhibitor targeting the brain vasculature)

Question 381

Predictive factors in SAH?

Answer 381

conscious level on admission
age
amount of blood visible on CT head

Question 382

How can subdural haemorrhages be classified?

Answer 382

Subdural haematomas can be classified in terms of their age:
Acute
Subacute
Chronic

Question 383

How does an acute subdural haemorrhage look?

Answer 383

subdural space and is most commonly caused by high-impact trauma
associated with high-impact injuries, there is often other brain underlying brain injuries.
hey will appear hyperdense (bright) in comparison to the brain. Large acute subdural haematomas will push on the brain (‘mass effect’) and cause midline shift or herniation.

Question 384

Where is the bleed in a chronic subdural haemorrhage?

Answer 384

Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding.

Question 385

How do chronic subdural appear differential to acute subdural?

Answer 385

In contrast to acute subdurals, chronic subdurals are hypodense (dark) compared to the substance of the brain.

Question 386

What is Syriangomyelia? Or a syrinx?

Answer 386

Syringomyelia (‘syrinx’ for short) describes a collection of cerebrospinal fluid within the spinal cord.

Question 387

Causes of a syrinx?

Answer 387

Causes include:
a Chiari malformation: strong association
trauma
tumours
idiopathic

Question 388

Features of a syrinx?

Answer 388

A ‘cape-like’ (neck, shoulders and arms)
Loss of sensation to temperature but the preservation of light touch, proprioception and vibration
classic examples are of patients who accidentally burn their hands without realising

• this is due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected

spastic weakness (predominantly of the lower limbs)
neuropathic pain
upgoing plantars

autonomic features:
Horner’s syndrome due to compression of the sympathetic chain, but this is rare
bowel and bladder dysfunction
scoliosis will occur over a matter of years if the syrinx is not treated

Question 389

What is the best imaging modality for a syrinx?

Answer 389

MRI

Question 390

Features of a third nerve palsy?

Answer 390

eye is deviated ‘down and out’
ptosis
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

Question 391

Causes of a third nerve palsy?

Answer 391

diabetes mellitus
vasculitis e.g. temporal arteritis, SLE
false localizing sign* due to uncal herniation through tentorium if raised ICP
posterior communicating artery aneurysm
- pupil dilated
- often associated pain
cavernous sinus thrombosis
Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain strokes
other possible causes: amyloid, multiple sclerosis

Question 392

Features of a thyroglossal cyst?

Answer 392

Features
usually midline, between the isthmus of the thyroid and the hyoid bone
moves upwards with protrusion of the tongue
may be painful if infected

Question 393

If a patient has sudden onset senorsineural hearing loss, waht should be considered?

Answer 393

Acoustic neuroma

Question 394

Drugs that cause tinnitus?

Answer 394

Aspirin/NSAIDs
Aminoglycosides
Loop diuretics
Quinine

Question 395

If a patient has pulsatile tinnitus, what should be completed?

Answer 395

Imaging for a possible aneurysm
MRI best choice

Question 396

What is the mechanism of topiramate ?

Answer 396

blocks voltage-gated Na+ channels
increases GABA action
carbonic anhydrase inhibition: this results in a decrease in urinary citrate excretion and formation of alkaline urine that favours the creation of calcium phosphate stone

Question 397

What are adverse effects of topiramate?

Answer 397

reduced appetite and weight loss
dizziness
paraesthesia
lethargy and poor concentration
rare but important: acute myopia and secondary angle-closure glaucoma

Enzyme inducer - may affect taking contraception

Question 398

Features of transient global amnesia?

Answer 398

acute onset of anterograde amnesia (the inability to form new memories)

Features
patients may appear anxious and repeatedly ask the same question
episodes are self-limited and resolve within 24 hours

Question 399

Definition of a TIA?

Answer 399

a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

Question 400

Features of a TIA?

Answer 400

Features typically resolve within 1 hour:

unilateral weakness or sensory loss.
aphasia or dysarthria
ataxia, vertigo, or loss of balance
visual problems
- sudden transient loss of vision in one eye (amaurosis fugax)
- diplopia
- homonymous hemianopia

Question 401

Management of TIA?

Answer 401

Immediate antithrombotic therapy:
give aspirin 300 mg immediately,

UNLESS

1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
3. Aspirin is contraindicated: discuss management urgently with the specialist team

Question 402

What score can be used to determine if a patient has had a stroke?

Answer 402

Rosier score

Rosier Scale
Has there been LOC or syncope?
Has there been seizure activity?
NEW ACUTE onset (or on awakening from sleep)?
Asymmetric facial weakness Asymmetric arm weakness Asymmetric leg weakness Speech disturbance Visual field defect
TOTAL SCORE
Stroke is likely if total scores are >= 1.
Scores <1 have a low possibility of stroke but are not completely excluded

Question 403

What is a crescendo TIA?

Answer 403

patient has had more than 1 TIA (‘crescendo TIA’)

Question 404

When is a specialist review required for TIA?

Answer 404

1. if the patient has had more than 1 TIA (‘crescendo TIA’) or has a suspected cardioembolic source or severe carotid stenosis:
2. If the patient has had a suspected TIA in the last 7 days: arrange urgent assessment (within 24 hours) by a specialist stroke physician
3. if the patient has had a suspected TIA which occurred more than a week previously: refer for specialist assessment as soon as possible within 7 days

Advise not to drive until seen by specialist*

Question 405

What imaging is require for TIA?

Answer 405

CT not required unless other diagnosis suspected
MRI best to determine area of ischaemia
Carotid imaging - assessment for atheoscleorsis and embolic events

Question 406

Management of TIA?

Answer 406

clopidogrel is recommended first-line (as for patients who’ve had a stroke)

Question 407

Causes of transverse myelitis?

Answer 407

Causes of transverse myelitis
viral infections: varicella-zoster, herpes simplex, cytomegalovirus, Epstein-Barr, influenza, echovirus, human immunodeficiency virus
bacterial infections: syphilis, Lyme disease
post-infectious (immune mediated)
first symptom of multiple sclerosis (MS) or neuromyelitis optica (NMO)

Question 408

What are the features of transverse myelitis?

Answer 408

s include weakness and numbness of the limbs, deficits in sensation and motor skills, dysfunctional urethral and anal sphincter activities, and dysfunction of the autonomic nervous system
often a “sensory level” at the spinal ganglion of the segmental spinal nerve, below which sensation to pain or light touch is impaired. Motor weakness occurs due to involvement of the pyramidal tracts and mainly affects the muscles that flex the legs and extend the arms.[1]

Question 409

Features of trigeminal neuralgia?

Answer 409

a unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve
the pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously
small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)
the pains usually remit for variable periods

Question 410

Red flags with trigeminal neuralgia?

Answer 410

Sensory changes
Deafness or other ear problems
History of skin or oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years

Question 411

Management of trigeminal neuralgia?

Answer 411

carbamazepine is first-line
failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

Question 412

Mechanism of triptans?

Answer 412

Triptans are specific 5-HT1B and 5-HT1D agonists used in the acute treatment of migraine.

Question 413

Genetic inheritance of tuberous sclerosis?

Answer 413

Autosomal dominant

Question 414

Features of tuberous sclerosis ?

Answer 414

Cutaneous features
depigmented ‘ash-leaf’ spots which fluoresce under UV light
roughened patches of skin over lumbar spine (Shagreen patches)
adenoma sebaceum (angiofibromas): butterfly distribution over nose
fibromata beneath nails (subungual fibromata)
café-au-lait spots* may be seen

Neurological features
developmental delay
epilepsy (infantile spasms or partial)
intellectual impairment

Also
retinal hamartomas: dense white areas on retina (phakomata)
rhabdomyomas of the heart
gliomatous changes can occur in the brain lesions
polycystic kidneys, renal angiomyolipomata
lymphangioleiomyomatosis: multiple lung cysts

Question 415

Features of viral labrynthitis?

Answer 415

Recent viral infection
Sudden onset
Nausea and vomiting
Hearing may be affected

Question 416

Features of vestibular neuronitis?

Answer 416

recurrent vertigo attacks lasting hours or days
nausea and vomiting may be present
horizontal nystagmus is usually present
no hearing loss or tinnituss

Question 417

Features of BPV?

Answer 417

Gradual onset
Triggered by change in head position
Each episode lasts 10-20 seconds

Question 418

Features of Vertebrobasilar ischaemia?

Answer 418

Elderly patient
Dizziness on extension of neck

Question 419

Features of acoustic neuroma?

Answer 419

Hearing loss, vertigo, tinnitus
Absent corneal reflex is important sign (blinking)
Associated with neurofibromatosis type 2

Question 420

Management of vestibular neuritis?

Answer 420

1. buccal or intramuscular prochlorperazine
2. Short course of oral prochlorperazine
3. Vestibular rehab

Question 421

What is vigabatrin?

Answer 421

Antiepileptic. Inhibitors GABA transaminase - potentiates GABA

Question 422

Adverse effects of vigabatrin?

Answer 422

40% of patients develop visual field defects, which may be irreversible
visual fields should be checked every 6 months

Question 423

What is von hipel Linda syndrome?

Answer 423

autosomal dominant condition predisposing to neoplasia. It is due to an abnormality in the VHL gene located on short arm of chromosome 3

Question 424

Features of von hippel lindau syndrome?

Answer 424

cerebellar haemangiomas: these can cause subarachnoid haemorrhages
retinal haemangiomas: vitreous haemorrhage
renal cysts (premalignant)
phaeochromocytoma
extra-renal cysts: epididymal, pancreatic, hepatic
endolymphatic sac tumours
clear-cell renal cell carcinoma

Question 425

What is the cause of werincke’s encephalopathy?

Answer 425

Thiamine deficiency
A classic triad of ophthalmoplegia/nystagmus, ataxia and encephalopathy may occur.

Question 426

Fetures of wernicke’s encephalopathy?

Answer 426

Features
oculomotor dysfunction
nystagmus (the most common ocular sign)
ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy
gait ataxia
encephalopathy: confusion, disorientation, indifference, and inattentiveness
peripheral sensory neuropathy

REMEMBER CAN OPEN
Confusion
Ataxia
Nystagmus
Ophthamoplegia
PEripheral
Neuropathy

Question 427

Investigations of wernicke’s encephalopathy?

Answer 427

MRI
Red cell transketolase deficiency

Question 428

If wernicke’s is untreated, what can it become?

Answer 428

Korsakoff syndrome
Amnesia
Confabulation

Question 429

Bitemporal hemianopia: upper quadrant defect > lower quadrant defect = ?

Answer 429

inferior chiasmal compression, commonly a pituitary tumour

Question 430

Bitemporal hemianopia: lower quadrant defect > upper quadrant defect = ?

Answer 430

superior chiasmal compression, commonly a craniopharyngioma

Question 431

In neuropathic pain, how should medications be added?

Answer 431

Medications should be removed, then new one started. Do not add drugs

Question 432

When should mechanical thrombectomy be considered?

Answer 432

6-24 hours
if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

Question 433

Palatal myoclonus - where is the lesion?

Answer 433

Olivary nucleus

Question 434

Fluctuating consciousness ?

Answer 434

Consider subdural haematoma

Question 435

Sited of action of 5HT3 inhibitors?

Answer 435

Medulal oblongata

Question 436

Headache + CN III palsy

Answer 436

Increased ICP
Uncle herniation

Question 437

Migainres: Why get pro kinetics + paracetamol?

Answer 437

There is delayed gastric emptying

Question 438

painful cn iii palsy?

Answer 438

posterior communicating artery aneurysm

Question 439

lobe affected for change in behaviour?

Answer 439

Temporal

Question 440

What is Parinaud syndrome ?

Answer 440

a lesion at the dorsal midbrain
Upward gaze palsy, often manifesting as diplopia
Pupillary light-near dissociation (Pseudo-Argyll Robertson pupils)
Convergence-retraction nystagmus

Question 441

What controls vertical gaze?

Answer 441

Rostral interstitial nucleus of medial longitudinal fasciculus lies at the dorsal midbrain and control vertical gaze. They project to the vestibular nuclei.

Question 442

Causes of parinaud syndrome?

Answer 442

Brain tumours in the midbrain or pineal gland (pinealoma)
Multiple sclerosis
Midbrain stroke

Question 443

Treatment of absence seizures?

Answer 443

1. Sodium v alporate / ethosuxiadmie
2. Lamotigrene

Question 444

What medications makes absence seizures worse?

Answer 444

Carbamazepine

Question 445

What type of drugs is ropinirole for restless legs?

Answer 445

Dopamine antagonist

Question 446

Trinucledotide repeat GAA?

Answer 446

Friedrick ataxia

Question 447

Trinucleotide repeat CGG?

Answer 447

fragile X syndrome

Question 448

Trinucleotide repeat CTG

Answer 448

myotonic dystrophy

Question 449

Temporal lobe epilepsy localising features?

Answer 449

Lip smacking + post-ictal dysphasia

Question 450

Acalcula - which lobe?

Answer 450

Parietal

Question 451

Acalcula - which lobe?

Answer 451

Parietal

Question 452

what is the time interval for thrombolysis?

Answer 452

4.5 hours

Question 453

In Guillain barre how is respiratory function monitored?

Answer 453

FVC - forced vital capacity

Question 454

Essential tremor prophylaxis when asthmatic?

Answer 454

Primidone

Question 455

What can topiramate do to eyes?

Answer 455

Acute angle closure glaucoma

Question 456

Ergot-derived dopamine agonist?

Answer 456

bromoCRIPTINE / dihydroergoCRTPTINE
lisuRIDE
pergoLIDE
cabergoline

Question 457

Non-ergot dopamine agonist not associated with fibrosis?

Answer 457

Ropinirole

Question 458

Drugs used in relapsing remitting MS?

Answer 458

glatiramer acetate
beta-interferon
fingolimod
ocrelizumab
natalizumab

Question 459

What is Shy Drager syndrome?

Answer 459

Form of multi system atrophy

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

Question 460

Demyelinating pathology?

Answer 460

Guillain-Barre syndrome
chronic inflammatory demyelinating polyneuropathy (CIDP)
amiodarone
hereditary sensorimotor neuropathies (HSMN) type I
paraprotein neuropathy

Question 461

Axonal pathology?

Answer 461

alcohol
diabetes mellitus*
vasculitis
vitamin B12 deficiency*
hereditary sensorimotor neuropathies (HSMN) type II

Question 462

What is a Jacksonian march?

Answer 462

characteristically starts by affecting a peripheral body part such as a toe, finger or section of the lip and then spreads quickly ‘marches’ over the respective foot, hand or face.

Question 462

What is a Jacksonian march?

Answer 462

characteristically starts by affecting a peripheral body part such as a toe, finger or section of the lip and then spreads quickly ‘marches’ over the respective foot, hand or face.

Question 463

Parts of the cord involved in subacute degernation?

Answer 463

Dorsal + Lateral

Question 464

What are triptans contraindicated in?

Answer 464

Ischaemic heart disease

Question 465

What anti-emetic is likely to give extrapyramidal signs

Answer 465

Metoclopramide

Question 466

Foster Kennedy syndrome?

Answer 466

frontal lobe tumour - usually a meningioma in this age group - leading to ipsilateral optic atrophy and papilloedema

Question 467

Features of von hippie Lindau?

Answer 467

Von - Vitreous haemorrhages
Hippel - Haemangiomas (cerebellar + retinal)
Lindau - Lots of cysts (renal + extrarenal)
Syndrome- sadly, cancers (renal clear cell + endolymphatic sac)

Question 468

Homonymous hemianopia?

Answer 468

homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)

Question 469

congruous defects?

Answer 469

congruous defects= optic radiation lesion or occipital cortex

Question 470

Difference in kidney lesions in tuberous sclerosis vs von hippie Linda?

Answer 470

Angiomyolipoma = Tuberous sclerosis
Angiomatosis = Von Hippel Lindau syndrome

Question 471

What stroke syndrome can be caused by PICA strokes?

Answer 471

Lateral medullary syndrome

Question 472

Neurofibromatosis chromosome ?

Answer 472

Chromosome 17 - Type 1
Chromsone 22 - Type 2

Question 473

VHL chromosome?

Answer 473

Chromosome 3p

Question 474

Most common ECG changes in myotonic dystrophy?

Answer 474

PR lengthening

Question 475

What is Alexia, and where is the lesion ?

Answer 475

inability to read out writing
Corpus collosum

Question 476

Hockey stick sign ?

Answer 476

CJD

Question 477

If cannot tolerate clopidogrel for secondary prevention?

Answer 477

Aspirin + dipyridamole lifelong

Question 478

Anterior spinal cord syndrome?

Answer 478

Bilateral spastic paresis and loss of pain and temperature sensation - anterior spinal artery occlusion

Question 479

areflexia, ataxia, ophthalmoplegia

Answer 479

Miller Fischer syndrome (bad guillaine barre)

Question 480

Side effects of natalizumab?

Answer 480

Natalizumab can cause reactivation of the JC virus causing progressive multifocal leukoencephalopathy (PML)

Question 481

facial weakness (e.g. difficulty closing eyes, smiling, blowing), winged scapula and weakness of the shoulderm upper arm and hip girdle muscles

Answer 481

facioscapulohumeral dystrophy

Question 482

How does phenytoin cause bleeding?

Answer 482

Phenytoin induces vitamin K metabolism, which can cause a relative vitamin K deficiency, creating the potential for heamorrhagic disease of the newborn

Question 483

tachycardia + hyporeflexia + flacid paralysis?

Answer 483

guillaiin barre

Question 484

How does subacute cord degeneration present?

Answer 484

Loss of proprioception, vibration sense and hyperreflexia

Question 485

Damage craniopharyngoma removal causes weight gain? why?

Answer 485

ventromedial area of the hypothalamus is often invaded by craniopharyngiomas. This area of the thalamus controls the satiety center and it is removed during surgery, the patient can have uninhibited hunger leading to significant weight gain.

Question 486

What part of the hypothalamus is responsible for ADH?

Answer 486

supraoptic nucleus of the hypothalamus is responsible for the synthesis of antidiuretic hormone and oxytocin, which are transported to the posterior hypothalamus for storage and release.

Question 487

Unicentric castleman disease?

Answer 487

lymphoproliferative disorder associated in a subset of cases with HIV and HHV-8.

follicles with atrophic and hyalinized germinal centres surrounded by prominent mantle zones containing small lymphocytes

Question 488

Treatment for spasticity in MS?

Answer 488

Baclofen
Gabapentin

Question 489

What type of drug is procyclidine?

Answer 489

Anti-muscarinic

Question 490

Loss of corneal reflex?

Answer 490

Think acoustic neuroma

Question 491

What type of drug is pyridostigmine?

Answer 491

long acting acetylcholinesterase inhibitor

Question 492

Features of progressive supra nuclear palsy?

Answer 492

postural instability and falls
patients tend to have a stiff, broad-based gait
impairment of vertical gaze (down gaze worse than up gaze - patients may complain of difficultly reading or descending stairs)
parkinsonism
bradykinesia is prominent
cognitive impairment
primarily frontal lobe dysfunction

Poor response to leva dopa

Question 493

Trigger for cluster headaches?

Answer 493

Alcohol

Question 494

Features of transient global amnesia?

Answer 494

Transient global amnesia is characterized by the acute onset of anterograde amnesia (the inability to form new memories). The aetiology is unknown, thought to be due to transient ischaemia to the thalamus (in particular the amygdala and hippocampus).

Features
patients may appear anxious and repeatedly ask the same question
episodes are self-limited and resolve within 24 hours

Question 495

Type of peripheral neuropathy in uraemia?

Answer 495

Sensory peripheral neuropathy?

Question 496

. It is found on T2-weighted MRI imaging which reveals poorly-defined hyperintensities in the subcortical white matter.

Answer 496

acute disseminated encephalomyelitis

Question 497

IV phenytoin causes?

Answer 497

hypotension

Question 498

Chronic subdural haematoma?

Answer 498

chronic subdural haematoma will appear as a hypodense (dark), crescentic collection around the convexity of the brain