Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MRCP > Neurology > Flashcards

Neurology Flashcards

1
Q

what medication is contraindicated in absence seizures?

A

Carbamazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when should anti-epileptics be started following a first seizure?

A

he 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the treatment for generalised tonic-clonic seizures?

A

males: sodium valproate
females: lamotrigine or levetiracetam
girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the treatment of focal seizures?

A

first line: lamotrigine or levetiracetam

second line: carbamazepine, oxcarbazepine or zonisamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the treatment of absence seizures?

A

first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam

** carbamazepine may exacerbate absence seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the treatment for myoclonic seizures?

A

males: sodium valproate
females: levetiracetam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the treatment for tonic or atonic seizures?

A

males: sodium valproate
females: lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the symptoms of MS?

A

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

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

Motor
spastic weakness: most commonly seen in the legs

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

Others
urinary incontinence
sexual dysfunction
intellectual deterioration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is vestibular neuronitis?

A

Vestibular neuronitis is a cause of vertigo that often develops following a viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the features of vestibular neuronitis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the differentials for vestibular neuronitis?

A

viral labyrinthitis
posterior circulation stroke: the HiNTs exam can be used to distinguish vestibular neuronitis from posterior circulation stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can you manage vestibular neuronitits?

A

buccal or intramuscular prochlorperazine is often used to provide rapid relief for severe cases

a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine) may be used to alleviate less severe cases

vestibular rehabilitation exercises are the preferred treatment for patients who experience chronic symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the laws around seizure and driving?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the rules around syncope and driving?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how long do you need off driving with stroke or TIA?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how is motor neurone disease managed?

A

MND - both upper and lower motor neurone disease

Riluzole - prevents stimulation of glutamate receptors, used mainly in ALS, prolongs life by 3 months

Respiratory care - NIV, usually BIPAP is used at night - survival benefit of around 7 months

Nutrition - PEG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what characterised Meziere’s disease?

A

Meniere’s disease is characterized by unilateral sensorineural hearing loss, in which case sound lateralizes towards the contralateral normal ear during the Weber test.

Tinnitus
Aural Fullness
vertigo attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is otosclerosis?

A

Otosclerosis describes the replacement of normal bone by vascular spongy bone. It causes a progressive conductive deafness due to fixation of the stapes at the oval window. Otosclerosis is autosomal dominant and typically affects young adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the characteristics of otosclerosis?

A

Onset is usually at 20-40 years - features include:
conductive deafness
tinnitus
tympanic membrane
the majority of patients will have a normal tympanic membrane
10% of patients may have a ‘flamingo tinge’, caused by hyperaemia
positive family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

when is Rinnes test positive?

A

Rinnes test is positive when air conduction is better than bone conduction. This is seen in normal examinations or when patients have sensorineural hearing loss. A negative test signifies conductive hearing loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Guillain Barre syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the pathogenesis of Guillain Barre Syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Miller Fisher Syndrome?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the features of Guillan-Barre Syndrome?

A

progressive, symmetrical weakness of all the limbs.
the weakness is classically ascending i.e. the legs are affected first
reflexes are reduced or absent
sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are the investigations of Guillain Barre syndrome?

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is Guillain Barre syndrome managed?

A

IVIG or plasma exchange (IVIG is first line)

FVC regular to monitor respiratory function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

at what time should a lumbar puncture be done when suspecting a subarachnoid haemorrhage?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the causes of SAH?

A

intracranial aneurysm (saccular ‘berry’ aneurysms)
accounts for around 85% of cases
conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta

arteriovenous malformation

pituitary apoplexy

mycotic (infective) aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the clinical presentation of SAH?

A

headache - usually of sudden-onset (‘thunderclap’ or ‘hit with a baseball bat’), severe (‘worst of my life’), occipital
typically peaking in intensity within 1 to 5 minutes, there may be a history of a less-severe ‘sentinel’ headache in the weeks prior to presentation
nausea and vomiting
meningism (photophobia, neck stiffness)
coma
seizures
ECG changes including ST elevation may be seen
this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the investigations for SAH?

A

non-contrast CT - acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

If CT head is done within 6 hours of onset and is normal new guidelines suggest not doing a LP, consider alternative diagnosis

If CT head is done > 6 hours after onset and is normal then LP should be done, at least 12 hours following onset

LP - xanthochromia,

If SAH confirmed - CT intracranial angiogram +/- digital subtraction angiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is SAH managed?

A

supportive
bed rest
analgesia
venous thromboembolism prophylaxis
discontinuation of antithrombotics (reversal of anticoagulation if present)

vasospasm is prevented using a course of oral nimodipine

intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the complications of aneurysmal SAH ?

A

re-bleeding - happens in around 10% of cases and most common in the first 12 hours, if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged, associated with a high mortality (up to 70%)

hydrocephalus - hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt

vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
ensure euvolaemia (normal blood volume)
consider treatment with a vasopressor if symptoms persist

hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are common side effects of MAO-B inhibitors?

A

fatigue, constipation and a dry mouth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the treatment for Parkinson’s ?

A

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

If a patient continues to have symptoms despite optimal levodopa treatment or has developed dyskinesia then NICE recommend the addition of a dopamine agonist, MAO-B inhibitor or catechol-O-methyl transferase (COMT) inhibitor as an adjunct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what can happen if Parkinson’s medication is not taken/absorbed?

A

risk of acute akinesia or neuroleptic malignant syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

when is impulse control disorder more common in Parkinson’s medication?

A

dopamine agonist therapy
a history of previous impulsive behaviours
a history of alcohol consumption and/or smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what medication can be used in orthostatic hypotension in parkinsons?

A

midodrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what medication can be used to manage drooling of saliva in patients with parkinsons

A

glycopyronium bromide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

why is levodopa prescribed with a decarboxylase inhibitor?

A

e.g. carbidopa or benserazide
this prevents the peripheral metabolism of levodopa to dopamine outside of the brain and hence can reduce side effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the common adverse effects of levodopa?

A

dry mouth
anorexia
palpitations
postural hypotension
psychosis

some adverse effects are due to the difficulty in achieving a steady dose of levodopa
end-of-dose wearing off: symptoms often worsen towards the end of dosage interval. This results in a decline of motor activity
‘on-off’ phenomenon: large variations in motor performance, with normal function during the ‘on’ period, and weakness and restricted mobility during the ‘off’ period
dyskinesias at peak dose: dystonia, chorea and athetosis (involuntary writhing movements)
these effects may worsen over time with - clinicians therefore may limit doses until necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are examples of dopamine receptor agonists?

A

bromocriptine, ropinirole, cabergoline, apomorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the adverse effects of dopamine receptor agonists?

A

ergot-derived dopamine receptor agonists (bromocriptine, cabergoline) have been associated with pulmonary, retroperitoneal and cardiac fibrosis. The Committee on Safety of Medicines advice that an echocardiogram, ESR, creatinine and chest x-ray should be obtained prior to treatment and patients should be closely monitored

more likely than levodopa to cause hallucinations in older patients. Nasal congestion and postural hypotension are also seen in some patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are MAO-B inhibitors?

A

MAO-B (Monoamine Oxidase-B) inhibitors
e.g. selegiline
inhibits the breakdown of dopamine secreted by the dopaminergic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the mechanism of action of amantadine and what are the side effects?

A

mechanism is not fully understood, probably increases dopamine release and inhibits its uptake at dopaminergic synapses
side-effects include ataxia, slurred speech, confusion, dizziness and livedo reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are COMT inhibitors ?

A

Catechol-O-Methyl Transferase inhibitors
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

when are antimuscarinics and when are they used?

A

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)

47
Q

what is syringomyelia?

A

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

Syringobulbia is a similar phenomenon in which there is a fluid-filled cavity within the medulla of the brainstem. This is often an extension of the syringomyelia but in rare cases can be an isolated finding.

48
Q

what are the causes of Syringomyelia?

A

a Chiari malformation: strong association
trauma
tumours
idiopathic

49
Q

what are the features of Syringomyelia?

A

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

50
Q

What are the investigations and treatment for Syringomyelia?

A

Investigations
full spine MRI with contrast to exclude a tumour or tethered cord
a brain MRI is also needed to exclude a Chiari malformation

Treatment will be directed at treating the cause of the syrinx. In patients with a persistent or symptomatic syrinx, a shunt into the syrinx can be placed.

51
Q

what is internuclear ophthalmoplegia?

A

a cause of horizontal disconjugate eye movement
due to a 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

52
Q

what are the features of internuclear ophthalmoplegia?

A

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

53
Q

what are the causes of internuclear ophthalmoplegia?

A

multiple sclerosis
vascular disease

54
Q

where would the lesion be leading to the left homonymous hemianopia?

A

lesion of the right optic tract

55
Q

where would the lesion be for homonymous quadrantopias?

A

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

56
Q

when would you see incongruous visual field defects vs congruous visual field defects?

A

incongruous defects = optic tract lesion; congruous defects = optic radiation lesion or occipital cortex

A congruous defect simply means complete or symmetrical visual field loss and conversely an incongruous defect is incomplete or asymmetric.

57
Q

what would cause homonymous hemianopia?

A

incongruous defects: lesion of optic tract
congruous defects: lesion of optic radiation or occipital cortex
macula sparing: lesion of occipital cortex

58
Q

What would cause a homonymous quadrantanopias?

A

superior: lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)
inferior: lesion of the superior optic radiations in the parietal lobe
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

59
Q

what would cause a bitemporal hemianopia?

A

lesion of optic chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

60
Q

what are the adverse effects of Levodopa?

A

Usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of L-dopa to dopamine
reduced effectiveness with time (usually by 2 years)
no use in neuroleptic induced parkinsonism

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

61
Q

where would the stoke be if there is Contralateral hemiparesis and sensory loss, lower extremity > upper

A

Anterior cerebral artery

62
Q

where would the stroke be if there was Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

A

middle cerebral artery

63
Q

what symptoms would you have if you had a posterior cerebral artery stroke?

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia

64
Q

what is weber’s syndrome?

A

a stoke to the branches of the posterior cerebral artery that supply the midbrain

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

65
Q

what symptoms would you get if there was a posterior inferior cerebellar artery stroke?

A

lateral medullary syndrome, Wallenberg syndrome

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

66
Q

What symptoms would you get if you had an anterior inferior cerebellar artery ?

A

lateral pontine syndrome

Symptoms are similar to Wallenberg’s, but:
Ipsilateral: facial paralysis and deafness

67
Q

what symptoms would you get if you had a retinal/ophthalmic artery stroke?

A

Amaurosis fugax

68
Q

what symptoms would you get with a basilar artery stroke?

A

locked in syndrome

69
Q

How does lacunar stroke present?

A

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

70
Q

what does the dorsal column-medial lemniscal pathway carry?

A

the sensory modalities of fine touch, vibration and proprioception
In the spinal cord, information travels via the dorsal (posterior) columns. In the brainstem it is transmitted through the medial lemniscus

the fibres decussate (cross to the other side of the CNS in the medulla oblongata)

71
Q

what does the anterior lateral system carry ?

A

Anterior spinothalamic tract – carries the sensory modalities of crude touch and pressure.

Lateral spinothalamic tract – carries the sensory modalities of pain and temperature.

they enter the spinal cord asked 1-2 vertebral levels and synapse at the tip of the dorsal horn - an area known as the substantial gelatinous. These fibres decussate within the spinal cord and then form two distinct tracts:

Crude touch and pressure fibres – enter the anterior spinothalamic tract.
Pain and temperature fibres – enter the lateral spinothalamic tract.

72
Q

what are the spinal tracts that carry unconscious proprioceptive information?

A

The tracts that carry unconscious proprioceptive information are collectively known as the spinocerebellar tracts.

Posterior spinocerebellar tract – Carries proprioceptive information from the lower limbs to the ipsilateral cerebellum.
Cuneocerebellar tract – Carries proprioceptive information from the upper limbs to the ipsilateral cerebellum.
Anterior spinocerebellar tract – Carries proprioceptive information from the lower limbs. The fibres decussate twice – and so terminate in the ipsilateral cerebellum.
Rostral spinocerebellar tract – Carries proprioceptive information from the upper limbs to the ipsilateral cerebellum.

73
Q

what is subacute combined degeneration of the spinal cord?

A

Subacute combined degeneration of the spinal cord is due to vitamin B12 deficiency resulting in impairment of the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts..

Recreational nitrous oxide inhalation may also result in vitamin B12 deficiency → subacute combined degeneration of the spinal cord.

74
Q

What are the features of subacute combined degeneration of the spinal cord?

A

dorsal column involvement
distal tingling/burning/sensory loss is symmetrical and tends to affect the legs more than the arms
impaired proprioception and vibration sense
lateral corticospinal tract involvement
muscle weakness, hyperreflexia, and spasticity
upper motor neuron signs typically develop in the legs first
brisk knee reflexes
absent ankle jerks
extensor plantars
spinocerebellar tract involvement
sensory ataxia → gait abnormalities
positive Romberg’s sign

75
Q

what are the features of autonomic neuropathy?

A

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

76
Q

what are the causes of autonomic neuropathy?

A

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

77
Q

what can cause brain abscess?

A

Brain abscesses may result from a number of causes including, extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis

78
Q

how will brain abscess present?

A

symptoms will depend on site of access

headache
fever
focal neurology - e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised intracranial pressure

other features associated with raised intracranial pressure - nausea, papilloedema, seizures

79
Q

how do you manage a brain access?

A

surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.

IV antibiotics: IV 3rd-generation cephalosporin + metronidazole

intracranial pressure management: e.g. dexamethasone

80
Q

what features indicate a diagnosis of MND?

A

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

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

81
Q

how is an acute ischaemic stroke managed?

A

CBGs, hydration, sats and temp should be maintained within normal limits
Blood pressure should not be lowered in the acute phase unless there are complications e.g. hypertensive encephalopathy or are they being considered for thrombolysis - blood pressure control should be considered for patients who present with an acute ischaemic stroke, if they present within 6 hours and have systolic blood pressure > 150mmHg.

Aspirin 300mg as soon as hemorrhagic stroke has been excluded

Anticoagulants should not be started until 14 days have passed from the onset of an ischaemic stroke

if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation

Thrombolysis

Thrombectomy

82
Q

what is the criteria for thrombolysis for acute ischaemic stroke?

A

it is administered within 4.5 hours of onset of stroke symptoms
haemorrhage has been definitively excluded (i.e. Imaging has been performed)

The 2023 National Clinical Guideline for Stroke broadened the potential inclusion criteria:
patients with an acute ischaemic stroke, regardless of age or stroke severity, who were last known to be well more than 4.5 hours earlier, should be considered for thrombolysis with alteplase if:
treatment can be started between 4.5 and 9 hours of known onset, or within 9 hours of the midpoint of sleep when they have woken with symptoms, AND
they have evidence from CT/MR perfusion (core-perfusion mismatch) or MRI (DWI-FLAIR mismatch) of the potential to salvage brain tissue
this should be irrespective of whether they have a large artery occlusion and require mechanical thrombectomy.
there are specific criteria in the guidelines that determine the imagine criteria that determine whether thrombolysis should be performed

Blood pressure should be lowered to 185/110 mmHg before thrombolysis.

83
Q

What are the contraindicaitions to thrombolysis?

A

Absolute
- Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke or traumatic brain injury in preceding 3 months
- Lumbar puncture in preceding 7 days
- Gastrointestinal haemorrhage in preceding 3 weeks
- Active bleeding
- Oesophageal varices
- Uncontrolled hypertension >200/120mmHg

Relative
- Pregnancy
- Concurrent anticoagulation (INR >1.7)
- Haemorrhagic diathesis
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery / trauma in the preceding 2 weeks

84
Q

What is thrombectomy?

A

Mechanical thrombectomy is an exciting new treatment option for patients with an acute ischaemic stroke. NICE incorporated recommendations into their 2019 guidelines. It is important to remember the significant resources and senior personnel to provide such a service 24 hours a day. NICE recommend that all decisions about thrombectomy take into account a patient’s overall clinical status:

NICE recommend a pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

85
Q

When should thrombectomy offered?

A

Offer thrombectomy as soon as possible and within 6 hours of symptom onset, together with intravenous thrombolysis (if within 4.5 hours), to people who have:
acute ischaemic stroke and
confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA

Offer thrombectomy as soon as possible to people who were last known to be well between 6 hours and 24 hours previously (including wake-up strokes):
confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
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

Consider thrombectomy together with intravenous thrombolysis (if within 4.5 hours) as soon as possible for people last known to be well up to 24 hours previously (including wake-up strokes):
who have acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (that is, basilar or posterior cerebral artery) demonstrated by CTA or MRA and
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

86
Q

what is the secondary prevention in ischaemic stroke?

A

clopidogrel plus MR dipyridamole in people who have had an ischaemic stroke

Carotid endarterectomy is recommend if the patient has suffered a stroke or TIA in the carotid territory and is not severely disabled
should only be considered if the stenosis > 50%
It should be performed asap - within 7 days

87
Q

What would a lesion in the parietal lobe cause?

A

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

88
Q

What would a lesion in the occipital lobe cause?

A

homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia

89
Q

What would a lesion in the temporal lobe cause?

A

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)

90
Q

What would a lesion in the frontal lobe cause?

A

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
anosmia
inability to generate a list

91
Q

What would a lesion in the cerebellum cause?

A

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

92
Q

What is Acalculia?

A

Acalculia refers to an acquired impairment in numerical and calculation abilities. It is most commonly associated with lesions in the parietal lobe, particularly on the dominant (usually left) side. The parietal lobe plays a crucial role in processing numerical information and performing calculations. Thus, a glioma in this area would likely disrupt these functions, leading to acalculia.

93
Q

what is the mechanism of action of pyridostigmine?

A

Pyridostigmine is a long-acting acetylcholinesterase inhibitor that reduces the breakdown of acetylcholine in the neuromuscular junction, temporarily improving symptoms of myasthenia gravis

94
Q

what is neuroleptic malignant syndrome?

A

Neuroleptic malignant syndrome is a rare but dangerous condition seen in patients taking antipsychotic medication. It carries a mortality of up to 10% and can also occur with atypical antipsychotics. It may also occur with dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced.

95
Q

what are the features of Neuroleptic malignant syndrome?

A

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

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

96
Q

How is Neuroleptic malignant syndrome managed?

A

stop antipsychotic

patients should be transferred to a medical ward if they are on a psychiatric ward and often they are nursed in intensive care units

IV fluids to prevent renal failure

dantrolene may be useful in selected cases
thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum

bromocriptine, dopamine agonist, may also be used

97
Q

what is the mechanism of action on lamotrigine and what are the adverse effects?

A

Mechanism of action
sodium channel blocker

Adverse effects
Stevens-Johnson syndrome

98
Q

What is the diagnostic criteria of a migraine?

A

The International Headache Society has produced the following diagnostic criteria for migraine without aura:

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

  1. aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
    D During headache at least one of the following:
  2. nausea and/or vomiting*
  3. 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)

Migraine with aura (seen in around 25% of migraine patients) tends to be easier to diagnose with a typical aura being progressive in nature and may occur hours prior to the headache. Typical aura include a transient hemianopic disturbance or a spreading scintillating scotoma (‘jagged crescent’). Sensory symptoms may also occur

99
Q

what migraine symptoms are atypical and may prompt further investigation?

A

motor weakness
double vision
visual symptoms affecting only one eye
poor balance
decreased level of consciousness.

100
Q

what is Ramsay hunt syndrome?

A

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.

101
Q

what are the symptoms of Ramsay hunt syndrome?

A

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

102
Q

what is the management of Ramsay Hunt syndrome?

A

oral aciclovir and corticosteroids are usually given

103
Q

what is Hoffmans sign?

A

To elicit it, the examiner should flick the patients distal phalanx (usually of the middle finger) to cause momentary flexion. A positive sign is exaggerated flexion of the thumb.

A positive Hoffmans sign is a sign of upper motor neuron dysfunction and points to a disease of the central nervous system

104
Q

What is degenerative cervical myelopathy?

A

Degenerative cervical myelopathy (DCM) is caused by compression (pinching) of the spinal cord in the neck.

105
Q

How does degenerative cervical myelopathy present?

A

Early symptoms are often subtle and can vary in severity day to day, making the disease difficult to detect initially. However as a progressive condition, worsening, deteriorating or new symptoms should be a warning sign.

DCM symptoms can include any combination of :
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.

106
Q

how would you investigate for degenerative cervical myelopathy?

A

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

107
Q

How is degenerative cervical myelopathy managed?

A

urgent referral for assessment by spinal services.
Importance of early treatment

Any existing spinal cord damage can be permanent. Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery

Currently, decompressive surgery is the only effective treatment.

108
Q

What is an essential tremor?

A

Essential tremor (previously called benign essential tremor) is an autosomal dominant condition which usually affects both upper limbs

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

109
Q

what is the management of an essential tremor?

A

propranolol is first-line
primidone is sometimes used

110
Q

What are the adverse effects of sodium valproate?

A

teratogenic
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

111
Q

what kind of drug is ondasatron?
Where does it act?

A

5-HT3 antagonists are antiemetics used mainly in the management of chemotherapy-related nausea. They mainly act in the chemoreceptor trigger zone area of the medulla oblongata.

112
Q

What are the teratogenic effects of epilepsy medications?
sodium valproate
carbamazepine
Phenytoin
lamotrigine

A

Sodium valproate: associated with neural tube defects
carbamazepine: often considered the least teratogenic of the older antiepileptics
phenytoin: associated with cleft palate
lamotrigine: studies to date suggest the rate of congenital malformations may be low. The dose of lamotrigine may need to be increased in pregnancy

It is advised that pregnant women taking phenytoin are given vitamin K in the last month of pregnancy to prevent clotting disorders in the newborn

113
Q

which anti-epileptic medications can be taken when breast feeding?

A

Breast feeding is generally considered safe for mothers taking antiepileptics with the possible exception of the barbiturates

MRCP (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions