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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Define epilepsy

A

neurological disorder that can cause someone to experience recurrent seizures (sudden, uncontrolled, disorganised electrical activity in the brain)

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2
Q

Define seizure

A

(sudden, uncontrolled, disorganised electrical activity in the brain)

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3
Q

What’s the difference between focal and generalised seizures?

A

Focal = in a specific area, on one side of the brain

Generalised = involves networks on both sides of the brain

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4
Q

Name four types of focal seizures

A

Temporal - aura (hallucinations, experiential phenomena, rising epigastric sensation), automatisms
Frontal - head/ leg movements, posturing, post-ictal weakness, Jacksonian march
Parietal - paraesthesia
Occipital - floaters/ flashes

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5
Q

Presentation of temporal seizure

A

aura (hallucinations, experiential phenomena, rising epigastric sensation)

automatisms (lip-smacking)

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6
Q

Presentation of frontal lobe seizure

A

head/ leg movements

Posturing

Post-ictal weakness

Jacksonian march - seizure begins with tingling/ twitching in finger/ toe/ corner of mouth, spreads to larger area of body (licking limbs, head turning, eye movements)

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7
Q

Presentation of parietal seizure

A

Paraesthesia

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8
Q

Presentation of occiptal seizure

A

floaters/ flashes

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9
Q

Types of generalised seizure

A

Tonic - tensing, clenching, tongue biting, incontinence
Atonic - complete loss of tone, collapse
Myoclonic - jerking limb, eye rolling, convulsions
Grand mal - aura + tonic (10-60s) + clonic (seconds - minutes)
Absence (petit mal) - patient unresponsive but conscious, stares, many attacks in one day

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10
Q

Features of a tonic seizure

A

Tensing
Clenching
Tongue biting
Incontinence

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11
Q

Features of atonic seizure

A

Complete loss of tone, collapse

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12
Q

Features of myoclonic seizure

A

Jerking limbs
Eye rolling
COnvulsions

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13
Q

Features of grand mal seizure

A

Aura + tonic seizure (10-60s) + clonic seizure (seconds- minutes)

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14
Q

Features of petit mal seizure

A

patient unresponsive but conscious, stares, many attacks in one day

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15
Q

Preventative management of focal seizures

A

Levetiracetam/ lamotrigine (men + women)

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16
Q

Management of generalised tonic-clonic

A

Men - sodium valproate
Women - Levetiracetam/ lamotrigine

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17
Q

Management of myoclonic seizures

A

Men - sodium valproate
Women - Levetiracetam

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18
Q

Management of tonic-clonic seizures

A

Men - sodium valproate
Women - Lamotrigine

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19
Q

Management of absence seizures

A

Ethosuximide (men + women)

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20
Q

What medication would you definitely not use for women of childbearing age who have epilepsy?

A

maternal use of sodium valproate is associated with a significant risk of neurodevelopmental delay in children. Guidance is now clear that sodium valproate should not be used during pregnancy and in women of childbearing age unless clearly necessary.

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21
Q

DVLA + epilepsy

A

Patient must inform the DVLA (or Doctor if the patient refuses). Can’t drive - seizure in the last 12 months/ changed medication in the last 6 months.

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22
Q

Define status epilepticus

A

Single seizure > 5 mins, 2 + seizures within a 5 minute period

Mx:
A to E
PR dizaepam/ buccal midazolam (pre-hospital), IV lorazepam (in hospital)
2nd dose of BDZs if unresolved after 5-10 minutes
IV phenytoin (or levetiracetam, sodium valproate)
Refractory status - induce general anaesthesia

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23
Q

Management of status epilepticus

A

Single seizure > 5 mins, 2 + seizures within a 5 minute period

Mx:
A to E
PR dizaepam/ buccal midazolam (pre-hospital), IV lorazepam (in hospital)
2nd dose of BDZs if unresolved after 5-10 minutes
IV phenytoin (or levetiracetam, sodium valproate)
Refractory status - induce general anaesthesia

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24
Q

What is Non-epileptic attack disorder?

A

type of seizure which looks similar to an epileptic seizure but it is not caused by abnormal electrical discharges or blood pressure

Occur when brain can’t handle particular emotion/ thoughts/ memories/ sensations

Patients may have a Hx of mental health problems or personality disorder

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25
Q

What is narcolepsy?

A

brain unable to regulate sleep-wake cycle, characterised by excessive daytime sleepiness (EDS) + REM abnormalities for > 3 months

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26
Q

Clinical presentation of narcolepsy

A

Onset in teenage years: EDS, hypnagogic (falling asleep)/ hypnopompic (waking) hallucinations, sleep paralysis, sleep attacks, catoplexy (conscious collapse)

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27
Q

Define catoplexy

A

sudden loss of muscle tone while patient is conscious (conscious collapse), triggered by loud noise or emotion e.g. laughter/ surprise.

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28
Q

Management of narcolepsy

A

Sleep hygiene + lifestyle modifications (e.g. forced naps)
Stimulants e.g. Modafinil
Antidepressants e.g. SSRIs

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29
Q

What is shingles?

A

acute unilateral pain blistering caused by reactivation of VSV (lie dormant in dorsal root/ cranial nerve ganglia), most commonly affects dermatomes T1-L2

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30
Q

Most common dermatomes affected by shingles

A

T1-L2

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31
Q

Clinical presentation of shingles

A

Prodrome (burning pain over dermatome for 2-3 days, fever, headache, lethargy) →

Erythematous macular rash (does not cross midline)

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32
Q

Diagnosis of shingles

A

Clinical

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33
Q

Management of shingles

A

Advice (avoid high-risk groups e.g. pregnant women/ immunocompromised)

Analgesia (paracetamol + NSAIDs → amitriptyline → oral corticosteroids if immunocompetent)

Antivirals - acyclovir, famciclovir, valacyclovir
Avoid if <50YO w/ mild rash + mild pain + no underlying RFs

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34
Q

Where does VSV lie dormant before reactivating and causing shingles?

A

Dorsal root/ cranial nerve ganglia

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35
Q

Most common complication of shingles

A

post-herpetic neuralgia (lasting pain in area of shingles, most resolve within 6 months)

36
Q

Complications of shingles

A

Most common = post-herpetic neuralgia (lasting pain in area of shingles, most resolve within 6 months)

Others - herpes zoster ophthalmicus (ocular complications), herpes zoster oticus (ear lesions/ facial paralysis)

37
Q

What is Wernicke-Korsakoff syndrome?

A

Thiamine (Vitamin B1) deficiency most commonly caused by excess alcohol consumption.

If Wernicke’s encephalopathy is left untreated, Korsakoff syndrome will develop

38
Q

Triad of Wernicke’s encephalopathy

A

Encephalopathy: confusion, disorientation, indifference, inattentiveness

Occulomotor disturbance (nystagmus, opthalmoplegia)

Ataxia

39
Q

Clinical features of Korsakoff’s syndrome

A

Memory impairment (antero + retrograde)

Confabulation

Behavioural change

40
Q

Management of Wernicke-Korsakoff syndrome

A

Requires urgent thiamine supplementation + abstinence from alcohol

((Wernicke’s encephalopathy = medical emergency with high mortality if untreated, Korsakoff syndrome = generally irreversible))

41
Q

What is Huntington’s?

A

inherited (autosomal dominant) neurodegenerative disorder that causes progressive neurological dysfunction, starts from 30-50YO

42
Q

Pathophysiology of Huntington’s

A

Trinucleotide repeat disorder (repeat expansion of CAG) causes defect in huntington gene on chromosome 4 → degeneration of cholinergic + GABAnergic neurons in the striation of the basal ganglia

Exhibits genetic anticipation - successive generations have more repeats in gene → earlier age of onset + increased severity

43
Q

Inheritance pattern of Huntington’s disease

A

Autosomal dominant

44
Q

What is genetic anticipation? which disease is it associated with?

A

Trinucleotide repeat disorder –> successive generations have more repeats in gene → earlier age of onset + increased severity

Huntington’s

45
Q

Genetic defect that causes Huntington’s disease

A

Trinucleotide repeat disorder (repeat expansion of CAG) causes defect in huntington gene on chromosome 4 → degeneration of cholinergic + GABAnergic neurons in the striation of the basal ganglia

46
Q

Clinical presentation of Huntington’s

A

30-50YO.

Cognitive/ psychiatric/ mood problems → movement disorder (chorea, dystonia, rigidity, eye movement disorders, dysarthria, dysphagia)

47
Q

Management of Huntington’s

A

Supportive (no options to slow/ stop progression)
Tetrabenazine - chorea
SSRIs - depression
Physiotherapy
Speech and language therapy
Genetic counselling for relatives/ children

48
Q

Medical management of Chorea in Huntington’s disease

A

Tetrabenazine

49
Q

What is Parkinson’s disease?

A

progressive neurodegenerative disorder caused by degeneration of dopaminergic neurons in the substantia nigra → classic triad (bradykinesia, tremor, rigidity) of features that present asymmetrically

50
Q

Clinical presentation of Parkinson’s disease

A

Asymmetrical

Triad: bradykinesia (short, shuffling gait w/ reduced arm swing), tremor (pin-rolling), rigidity (cogwheel)

Other: mask-like face, psychiatric symptoms (depression, dementia, psychosis, sleep disturbance), impaired olfaction

51
Q

Parkinson’s vs. benign essential tremor

A

BET = symmetrical, 6-12Hz, improves at rest/ worse on voluntary movement
Parkinson’s = asymmetrical, 4-8Hz, worse at rest/ improves on voluntary movement

52
Q

Management of Parkinson’s

A

Motor symptoms affecting QOL = levodopa
Usually combined with carbidopa to reduce side effects (dry mouth, anorexia, palpitations, postural hypotension, psychosis)

Motor symptoms not affecting QOL = dopamine agonist, MAO-B inhibitor (e.g. selegiline) or levodopa

((Ease symptoms but don’t slow progression))

53
Q

Management of Parkinson’s - motor symptoms affecting QOL

A

levodopa

Usually combined with carbidopa to reduce side effects (dry mouth, anorexia, palpitations, postural hypotension, psychosis)

54
Q

Management of Parkinson’s - motor symptoms not affecting QOL

A

dopamine agonist, MAO-B inhibitor (e.g. selegiline) or levodopa

55
Q

Why is levodopa usually combined with carbidopa?

A

To reduce side effects: dry mouth, anorexia, postural hypotension, psychosis, palpitations

56
Q

What is dementia?

A

Syndrome characterised by progressive, irreversible global cognitive deficits. Memory impairment is often the first symptom with progression to other symptoms.

57
Q

What is the most common cause of Dementia in the UK?

A

Alzheimer’s disease

58
Q

Pathophysiology of Alzheimer’s Disease

A

amyloid plaques + neurofibrillary tangles (tau protein) accumulate → decreased information transmission → widespread cerebral atrophy involving the cortex + hippocampus

59
Q

Clinical presentation of Alzheimer’s Disease

A

60yrs +, progressive memory loss over time

60
Q

Management of Alzheimer’s disease

A

acetylcholinesterase inhibitor (e.g. donepezil, rivastigmine, galantamine) + memantine

61
Q

What is vascular dementia?

A

Second most common cause of dementia in the UK. Cognitive impairment caused by vascular damage + impaired blood supply to the brain.

62
Q

Clinical presentation of Vascular Dementia

A

several months/ years of a sudden/ stepwise deterioration of cognitive function. Difficulty w/ attention/ concentration, seizures, memory/ gait/ speech/ emotional disturbance.

63
Q

RFs for Vascular dementia

A

Hx of CVA (or family Hx), AF, HTN, DM, hyperlipidaemia, smoking, obesity

64
Q

What type of dementia is associated with a stepwise progression?

A

Vascular dementia

65
Q

What is Lewy Body dementia?

A

Type of dementia associated with Parkinson’s.

Charcaterised by the presence of Lewy bodies in the substantia nigra/ paralimbic + neocortical areas.

66
Q

Where can Lewy bodies be found in Lewy body dementia?

A

the substantia nigra/ paralimbic + neocortical areas.

67
Q

What type of dementia can be characterised by fluctuation in cognition + parkinsonism + psychiatric features?

A

Lewy body dementia

68
Q

Clinical presentation of Lewy Body dementia

A

progressive cognitive impairment (FLUCTUATES) affecting executive functioning + attention > memory. Parkinsonism. Psychiatric features (hallucinations + delusions)

69
Q

Management of Lewy Body Dementia

A

Acetylcholinesterase + memantine.

AVOID NEUROLEPTICS - high percentage of DLB patients exhibit worsening parkinsonism, sedation, immobility, or even neuroleptic malignant syndrome (NMS) after exposure to antipsychotics

70
Q

Why should antipsychotics be avoided in patients with Lewy Body dementia?

A

high percentage of DLB patients exhibit worsening parkinsonism, sedation, immobility, or even neuroleptic malignant syndrome (NMS) after exposure to antipsychotics

71
Q

What is fronto-temporal dementia?

A

Degeneration of frontal + temporal lobes of brain –> personality change + impaired social conduct. Starts at a younger age

72
Q

Behavioural presentation of fronto-temporal dementia

A

altered emotional responsiveness, decreased interpersonal skis, change in preferences

73
Q

What type of dementia more commonly affects 40-60YOs?

A

Frontal-temporal dementia

74
Q

Semantic presentation of Fronto-temporal dementia

A

reduced understanding of words, name retrieval difficult, inability to recognise objects/ family faces

75
Q

Non-fluent presentation of fronto-temporal dementia

A

speech takes effort, breakdown in output of language, speech apraxia

76
Q

The types of presentation seen in patients with fronto-temporal dementia

A

Behavioural - altered emotional responsiveness, decreased interpersonal skis, change in preferences

Semantic - reduced understanding of words, name retrieval difficult, inability to recognise objects/ family faces

Non-fluent - speech takes effort, breakdown in output of language, speech apraxia

77
Q

Methods to assess dementia

A

AMTS - 6-8/10 = dementia
MMSE - 24/30 = dementia
MoCA - 26/30 = dementia
Addenbrookes - 82-88/100 = dementia

78
Q

What are the five domains tested in the Addenbrookes assessment of Dementia?

A

Attention

Memory

Language

Visuospatial functioning

Verbal functioning

79
Q

What is normal pressure hydrocephalus?

A

Abnormal build up of CSF in brain’s ventricles –> dilatation of centricles + pressure on the brain. Typically caused by head injury/ SAH/ meningitis.

80
Q

Pathophysiology of normal pressure hydrocephalus

A

Normal flow of CSF blocked (decreased CSF absorption at arachnoid villi) → build up of fluid in ventricles → ventricles enlarge and put pressure on the brain

81
Q

Clinical presentation of normal pressure hydrocephalus

A

Triad: urinary incontinence + dementia/ bradyphrenia + gait abnormality

Symptoms develop over a few months

82
Q

What condition typically presents with: urinary incontinence + dementia/ bradyphrenia + gait abnormality?

A

Normal pressure hydrocephaus

83
Q

Investigation of normal pressure hydrocephalus?

A

Non-contrast CT - visualise hydrocephalus + dilatation of ventricles

84
Q

Management of normal pressure hydrocephalus

A

Ventriculoperitoneal shunting (complication = seizures, infections, intracerebral haemorrhage)

85
Q
A

Phase 3a (5 decks)

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