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UKMLA Prep > Neurosciences > Flashcards

Neurosciences Flashcards

Conditions and presentation

1
Q

Chorea

A
  • descibes involuntary, rapid, jerky movements from one part of the body to another.
  • caused by damage to the basal ganglia, especially the caudate nuclues.
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2
Q

What are the causes of Chorea

A

Huntington’s disease, Wilson’s disease, ataxic telangiectasia

Sydenham’s chorea
SLE
anti-phospholipid syndrome
rheumatic fever

drugs
oral contraceptive pill, L-dopa, antipsychotics
neuroacanthocytosi

pregnancy: chorea gravidarum
thyrotoxicosis
polycythaemia rubra vera
carbon monoxide poisoning
cerebrovascular disease

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3
Q

Hemiballism

A

Hemiballism occurs following damage to the subthalamic nucleus.

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

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

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4
Q

When do Hemiballism symptoms reduce?

A

Patients may have reduced symptoms when they are asleep.

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5
Q

Treatment of Haemiballism?

A

Antidopaminergic agents (e.g. Haloperidol)

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6
Q

Huntington’s disease

A

inherited neurodegenerative condition. It is a progressive and incurable condition that typically results in death 20 years after the initial symptoms develop.

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7
Q

Genetics of Huntington’s disease

A

autosomal dominant
* trinucleotide repeat disorder: repeat expansion of CAG
as Huntington’s disease is a trinucleotide repeat disorder, the phenomenon of anticipation may be seen, where the disease is presents at an earlier age in successive generations
results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
due to defect in huntingtin gene on chromosome 4

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8
Q

Features of Huntingtons which develop after 35

A

chorea
personality changes (e.g. irritability, apathy, depression) and intellectual impairment
dystonia
saccadic eye movements

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9
Q

Oculogyric crisis

A

An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions

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10
Q

Features of Oculogyric crisis

A

restlessness, agitation
involuntary upward deviation of the eyes

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11
Q

causes of oculogyric crisis

A

antipsychotics
metoclopramide
postencephalitic Parkinson’s disease

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12
Q

Managment of oculogyric crisis?

A

cessation of causative medication if possible
intravenous antimuscarinic: benztropine or procyclidine

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13
Q

Restless leg syndrome?

A

syndrome of spontaneous, continuous lower limb movements that may be associated with paraesthesia.

It is extremely common, affecting between 2-10% of the general population. Males and females are equally affected and a family history may be present

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14
Q

Clinical features of restless leg syndrome

A

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)

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15
Q

causes and associations of restless leg syndrome

A

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

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16
Q

blood tests and restless leg syndrome

A

Ferritin to rule out anaemia

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17
Q

Managment of restless leg syndrome

A

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

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18
Q

Managment of Tics?

A

clonidine
atypical antipsychotics

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19
Q

Wilson’s disease

A

-Autosomal recessive disorder characterised by excessive copper deposition in the tissues.

-Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.

caused by a defect in the ATP7B gene located on chromosome 13.

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20
Q

incidence of Wilson’s disease?

A

10-25 years
- children will present with liver symptoms first

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21
Q

Signs of Wilson’s disease

A

renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Kayser-Fleischer ring
liver hepatitis and cirrhosis

neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism

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22
Q

Investigations for Wilson’s disease

A

slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene

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23
Q

Managment of Wilson’s disease

A

penicillamine
2nd line is trientine hydrochloride

tetrathiomolybdate is a newer agent that is currently under investigation

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24
Q

when should you refer a child for developmental delay?

A

doesn’t smile at 10 weeks
cannot sit unsupported at 12 months
cannot walk at 18 months
has a hand preference before the age of 12 month

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25
Q

DVLA and CABG

A

4 weeks off driving

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26
Q

DVLA and elective angioplasty

A

1 week off driving

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26
Q

DVLA and hypertension

A

can drive unless treatment causes unacceptable side effects, no need to notify DVLA
if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more

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27
Q

DVLA and ACS

A

4 weeks off driving
1 week if successfully treated by angioplasty

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28
Q

DVLA and angina

A

driving must cease if symptoms occur at rest/at the wheel

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29
Q

DVLA and pacemaker insertion

A

1 week off driving

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30
Q

DVLA and ICD

A

if implanted for sustained ventricular arrhythmia: cease driving for 6 months
if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers

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31
Q

DVLA and successful catheter abalation for arrhythmia

A

2 days off driving

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32
Q

aortic aneurysm of 6cm or more and DVLA

A

notify DVLA. Licensing will be permitted subject to annual review.

an aortic diameter of 6.5 cm or more disqualifies patients from driving

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33
Q

Heart transplant and DVLA

A
  • 6 weeks dont drive
  • Dont need to tell DVLA
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34
Q

DVLA and HGV

A

Patients who have insulin or other hypoglyacemic drugs must meet following criteria to have HGV

-not been any severe hypoglycaemic event in the previous 12 months

the driver has full hypoglycaemic awareness
the driver must show adequate control of the condition by regular blood glucose monitoring,

at least twice daily and at times relevant to driving
the driver must demonstrate an understanding of the risks of hypoglycaemia
here are no other debarring complications of diabetes

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35
Q

VDIAB1I form

A

patients on insulin who want to apply for a Group 2 (HGV) licence

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36
Q

group 1 drivers diabetes

A

if on insulin then patient can drive a car as long as they have hypoglycaemic awareness, not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months and no relevant visual impairment. Drivers are normally contacted by DVLA
if on tablets or exenatide no need to notify DVLA. If tablets may induce hypoglycaemia (e.g. sulfonylureas) then there must not have been more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months
if diet controlled alone then no requirement to inform DVLA

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37
Q

Alcohol missuse and DVLA

A

requires licence revocation or refusal until a minimum 6 month period of controlled drinking or abstinence has been attained

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38
Q

Alcohol dependency and DVLA

A

1 year

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39
Q

Cannabis, amphetamines, ecstasy, LSD and DVLA

A

6 month period free of such use has been attained.

Independent medical assessment and urine screen arranged by DVLA, may be required

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40
Q

Heroin, cocaine, methadone and DVLA

A

1 year no driving
need consultant report when reapplying

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41
Q

DVLA and Epilepsy/seizures

A

MUST report to the DVLA

first unprovoked/isolated seizure: 6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG. If these conditions are not met then this is increased to 12 months

for patients with established epilepsy or those with multiple unprovoked seizures:
may qualify for a driving licence if they have been free from any seizure for 12 months
if there have been no seizures for 5 years (with medication if necessary) a ‘til 70 licence is usually restored
withdrawawl of epilepsy medication: should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose

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42
Q

Syncope and DVLA

A

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

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43
Q

Stoke/ TIA and DVLA

A

1 month off driving

multiple TIAs over short period of times: 3 months off driving and inform DVLA

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44
Q

craniotomy e.g. For meningioma and DVLA

A

1 year off driving

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45
Q

pituitary tumour: craniotomy and DVLA

A

6 months; trans-sphenoidal surgery ‘can drive when there is no debarring residual impairment likely to affect safe driving’

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46
Q

narcolepsy/cataplexy and DVLA

A

cease driving on diagnosis, can restart once ‘satisfactory control of symptoms

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47
Q

chronic neurological disorders e.g. multiple sclerosis, motor neuron disease and the DVLA

A

DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

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48
Q

psychiatric conditions which must stop driving and inform DVLA

A

agitation, behavioural disturbance or suicidal thoughts
Acute psychotic disorder
Hypomania or mania
Severe disability

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49
Q

conditions where people may drive but need to inform the DVLA

A

Pervasive developmental disorders and ADHD
Mild cognitive impairment
Dementia
Mild learning disability
Personality disorder

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50
Q

Monocular vision and DVLA

A

must notify DVLA
may drive if acuity and visual field is normal in the remaining eye

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51
Q

Blepharospasm and DVLA

A

consultant opinion is required

52
Q

visual field defects and DVLA

A
  • Cease driving till requirmenrs are met
53
Q

Differential diagnosis for facial pain

A
  • Trigeminal neuralgia
    -sinusitis
  • dental problems
    -tension-type headaches
  • migraine
    -GCA
54
Q

Trigeminal neuralgia

A

pain syndrome characterised by severe unilateral pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur.

55
Q

e International Headache Society definition of trigeminal neuralgia

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

56
Q

Red flag symptoms of TN

A

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

57
Q

Managment of TN

A

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

58
Q

Down’s syndrome, which neruodegen condition most associated?

A

Alzheimer’s dementia

59
Q

Seizure

A

spontaneous uncontrolled abnormal brain activity

60
Q

Epilepsy

A

a tendency to have seizures. Epilepsy is a symptom, and not a true condition. Epilepsy can be diagnosed after a minimum of 2 seizures.

61
Q

Ictus

A

Can refer to any acute event, in this situation, refers to epilepsy attack itself

62
Q

Prodome

A

a set of not specific symptoms that precede the onset of a disease, in this case, epilepsy

63
Q

Prodome

A

a set of not specific symptoms that precede the onset of a disease, in this case, epilepsy

64
Q

Aura.

A

sensory disturbances that precede an attack, usually just by a few minutes. Can be visual, tactile, olfactory – pretty much any sensation.

65
Q

Triggers for seizures

A

Sleep deprivation
Alcohol (alcohol intake AND alcohol withdrawal)
Drug misuse
Physical/mental exhaustion
Flickering lights –e.g. on TV/video games – cause primary generalised epilepsy only
Infection / metabolic disturbance
Less common:
Loud noises
Hot bath
Reading
Strange shapes
Strange smells
Strange sounds

66
Q

Todd’s paralysis

A

Weakness of the links following a seizing

67
Q

Absent seizures

A

Aka petit mal
childhood onset

Patient unresponsive to stimuli, but still conscious

Patient stares, may go pale
May be some muscle jerking

There is quick recovery after the attack (in petit mal)
They generally last <15s, whereas temporal lobe last >30s.

68
Q

Tonic clinic seizures

A

Aka grand mal
- often aura before presentation

Tonic phase (10-60s)
Rigidity
Epileptic cry
Tongue biting
Incontinence
Hypoxia/cyanosis – no breathing during this phase
Clonic Phase (seconds-minutes)
Convulsions / limb jerking
Eye rolling
Tachycardia
No breathing / random, uncoordinated breaths

69
Q

Tonic phase.

A

Lasts 10-60 seconds
Rigidity
Epileptic cry
Tongue biting
Incontinence
Hypoxia/cyanosis – no breathing during this phase

70
Q

Clonic phase

A

seconds-minutes)
Convulsions / limb jerking
Eye rolling
Tachycardia
No breathing / random, uncoordinated breaths

71
Q

Status epilepticus

A

Seizure that lasts >30minutes
OR
Multiple seizures, inbetween which, consciousness is not recovered, lasting > 30 minutes

72
Q

Status epilepticus

A

Seizure that lasts >30minutes
OR
Multiple seizures, inbetween which, consciousness is not recovered, lasting > 30 minutes

73
Q

What occurs during status epilepticus

A

Electrolyte imbalance as massive energy demands of rapid discharge neurons no longer met
Results in brain swelling and herniation

74
Q

investigations for seizures

A

ECG
Neurological Exam
Serum Clacium
Urine dipstick – diabetes
EEG
CT/MRI – can show focal lesions
PET scan
Bloods
Sugar – hypoglycaemia
U+E’s – renal problems
Calcium – hypoglycaemia
LFT’s
CK – Serum muscle enzymes – raised in true epileptics after clonus and tonic seizures, normal in pseudoseizures
Serum prolactin – to check for pseudoseizures

75
Q

Management of seizures

A

Only start after a minimum of two fits. Only use one drug at a time, and begin with a small dose, and gradually increase it, until control is achieved, toxic affects occur, or the maximum dose is reached.

76
Q

Mechanism of phenobarbital

A

Inhibits sodium channels, thus reducing action potential propagation. Does not lower the seizure threshold.

77
Q

Side effects of phenobarbital

A

Sedation, impairment of motor and cognition systems after long term use, megaloblastic anaemia

78
Q

Phenytoin mechanism

A

Inhibits sodium channels, thus reducing action potential propagation. Acts on voltage dependent channels, and selectively binds when they are in the open state.

79
Q

Side effects Phenytoin

A

Vertigo, nystagmus, headaches, megaloblastic anaemia, hypersensitivity, confusion and cognition problems (high dose). Teratogenic, gum hypertrophy, arrythmias

80
Q

When is Phenytoin used

A

Partial and generalised attacks, but not in absence.
High doses my precipitate attacks

81
Q

What is useful for absent seizures

A

Ethosuximide

82
Q

What is 2nd line for generalised seizures?

A

Lamotrigine

83
Q

1st line for partial seizures

A

Carbamazepine

84
Q

1st line for partial seizures

A

Carbamazepine

85
Q

When is sodium Valporate used as a first line treatment

A

Absence seizures
– Generalised seizures

86
Q

Can Sodium Valporate be used in pregnancy?

A

No
Highly teratogenic

87
Q

What is Wernicke’s aphasia?

A

A type of receptive aphasia due to a lesion of the superior temporal gyrus, characterized by fluent speech, impaired comprehension, and nonsensical sentences.

Typically supplied by the inferior division of the left MCA.

88
Q

What are the main characteristics of Broca’s aphasia?

A

Non-fluent, labored speech with normal comprehension; caused by a lesion of the inferior frontal gyrus.

Typically supplied by the superior division of the left MCA.

89
Q

Define conduction aphasia.

A

A type of aphasia resulting from a stroke affecting the arcuate fasciculus, characterized by fluent speech but poor repetition, with normal comprehension.

Patients are aware of their errors.

90
Q

What is global aphasia?

A

Severe expressive and receptive aphasia due to a large lesion affecting all language areas.

May still communicate using gestures.

91
Q

What is cerebral palsy?

A

A disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain, affecting 2 in 1,000 live births.

It is the most common cause of major motor impairment.

92
Q

List the main causes of cerebral palsy.

A
  • Antenatal (80%): cerebral malformation, congenital infection
  • Intrapartum (10%): birth asphyxia/trauma
  • Postnatal (10%): intraventricular hemorrhage, meningitis, head trauma
93
Q

What are common manifestations of cerebral palsy?

A
  • Abnormal tone in early infancy
  • Delayed motor milestones
  • Abnormal gait
  • Feeding difficulties
94
Q

What percentage of children with cerebral palsy experience learning difficulties?

A

60%

95
Q

What is the classification of cerebral palsy based on muscle tone?

A
  • Spastic (70%)
  • Dyskinetic
  • Ataxic
  • Mixed
96
Q

What is the first-line treatment for essential tremor?

A

Propranolol

97
Q

What defines febrile convulsions?

A

Seizures provoked by fever in otherwise normal children, typically occurring between 6 months and 5 years.

Seen in 3% of children.

98
Q

What are the clinical features of febrile convulsions?

A
  • Occur early in a viral infection
  • Usually brief, lasting less than 5 minutes
  • Most commonly tonic-clonic
99
Q

What is Wernicke’s encephalopathy?

A

A neuropsychiatric disorder caused by thiamine deficiency, often seen in alcoholics, characterized by a classic triad of ophthalmoplegia, ataxia, and encephalopathy.

100
Q

What are the common features of Wernicke’s encephalopathy?

A
  • Oculomotor dysfunction
  • Nystagmus
  • Gait ataxia
  • Encephalopathy
  • Peripheral sensory neuropathy
101
Q

What is a transient ischaemic attack (TIA)?

A

A brief period of neurological deficit due to a vascular cause, typically lasting less than an hour.

102
Q

What are common clinical features of a TIA?

A
  • Unilateral weakness or sensory loss
  • Aphasia or dysarthria
  • Ataxia, vertigo, or loss of balance
  • Visual problems
  • Amaurosis fugax
103
Q

What is the immediate management for suspected TIA?

A

Give aspirin 300 mg immediately unless contraindicated and assess urgently within 24 hours by a stroke specialist clinician.

104
Q

What is the primary goal of lipid modification therapy in TIA management?

A

To reduce non-HDL cholesterol by more than 40%.

105
Q

What are the features of a prolapsed lumbar disc?

A
  • Clear dermatomal leg pain
  • Associated neurological deficits
  • Pain often worse when sitting
106
Q

What is the classical triad of features in Parkinson’s disease?

A
  • Bradykinesia
  • Tremor
  • Rigidity
107
Q

What is the epidemiology of Parkinson’s disease?

A

Around twice as common in men.

108
Q

What is Parkinson’s disease?

A

A progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra.

109
Q

What are the classical triad of features in Parkinson’s disease?

A
  • Bradykinesia
  • Tremor
  • Rigidity
110
Q

What is the mean age of diagnosis for Parkinson’s disease?

A

65 years

111
Q

How does bradykinesia manifest in Parkinson’s disease?

A
  • Poverty of movement (hypokinesia)
  • Short, shuffling steps
  • Reduced arm swinging
  • Difficulty in initiating movement
112
Q

What characterizes the tremor seen in Parkinson’s disease?

A
  • Most marked at rest
  • 3-5 Hz
  • ‘Pill-rolling’ in thumb and index finger
  • Worse when stressed or tired, improves with voluntary movement
113
Q

What types of rigidity are observed in Parkinson’s disease?

A
  • Lead pipe rigidity
  • Cogwheel rigidity (due to superimposed tremor)
114
Q

What are some psychiatric features associated with Parkinson’s disease?

A
  • Depression (most common, affects about 40%)
  • Dementia
  • Psychosis
  • Sleep disturbances
115
Q

True or False: Drug-induced parkinsonism typically has a slower onset compared to Parkinson’s disease.

A

False

116
Q

What diagnostic tool does NICE recommend if differentiating between essential tremor and Parkinson’s disease?

A

123I-FP-CIT single photon emission computed tomography (SPECT)

117
Q

What is the first-line treatment for Parkinson’s disease if motor symptoms affect quality of life?

A

Levodopa

118
Q

What should be considered if motor symptoms of Parkinson’s disease do not affect quality of life?

A

Dopamine agonist (non-ergot derived), levodopa, or monoamine oxidase B (MAO-B) inhibitor

119
Q

What are the common adverse events associated with levodopa?

A
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis
120
Q

Fill in the blank: The phenomenon where motor activity declines towards the end of the dosage interval is called the _______.

A

end-of-dose wearing off

121
Q

What are the risks associated with acute akinesia in Parkinson’s medication management?

A

Risk of neuroleptic malignant syndrome

122
Q

What are the side effects of dopamine receptor agonists?

A
  • Impulse control disorders
  • Excessive daytime somnolence
  • Hallucinations (more likely than levodopa in older patients)
123
Q

What is myasthenia gravis?

A

An autoimmune disorder resulting in insufficient functioning acetylcholine receptors.

124
Q

What is the hallmark feature of myasthenia gravis?

A

Muscle fatigability

125
Q

What is the first-line treatment for myasthenia gravis?

A

Pyridostigmine (long-acting acetylcholinesterase inhibitor)

126
Q

What are common associations with myasthenia gravis?

A
  • Thymomas (15%)
  • Autoimmune disorders: pernicious anemia, autoimmune thyroid disorders, rheumatoid arthritis, SLE
  • Thymic hyperplasia (50-70%)
127
Q

What investigations are useful for diagnosing myasthenia gravis?

A
  • Single fibre electromyography
  • CT thorax
  • Antibodies to acetylcholine receptors
  • Tensilon test (not commonly used)
128
Q

Which drugs may exacerbate myasthenia gravis?

A
  • Penicillamine
  • Quinidine, procainamide
  • Beta-blockers
  • Lithium
  • Phenytoin
  • Antibiotics: gentamicin, macrolides, quinolones, tetracyclines

UKMLA Prep (39 decks)

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