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Phase 2A > Neuro > Flashcards

Neuro Flashcards

1
Q

5 parts of basal ganglia

A

Lentiform nucleus, Globus pallidus, Caudate nucleus, Substantia nigra, Subthalamic nucleus

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2
Q

Where is Broca’s area located and what is it responsible for?

A

Frontal lobe of dominant hemisphere superior to lateral fissure (supplied by middle cerebral artery). Production of speech.

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3
Q

Where is Wernicke’s area and what is it responsible for?

A

Superior temporal gyrus of dominant hemisphere (supplied by middle cerebral artery). Comprehension and understanding of speech

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4
Q

Define a TIA

A

Sudden onset of focal CNS phenomena brought about by a temporary occlusion of cerebral circulation

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5
Q

4 causes of TIA

A

Atherothromboembolism, hyperviscosity, cardiac thrombus, postural hypotension

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6
Q

What is amaurosis fugax?

A

Progressive painless vision loss due to embolus in retinal artery ‘like a curtain dropping down over the eye’

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7
Q

4 signs and symptoms of a TIA

A

Hemiparesis, aphasia, ataxia, hemisensory loss, amaurosis fugax

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8
Q

What is the timeframe for symptoms of a TIA?

A
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9
Q

How would you treat a TIA?

A

Control cardiac risk factors (BP etc), clopidogrel +/- aspirin, warfarin if cardiac emboli confirmed, carotid endarterectomy if >70% stenosis, avoid driving for 1 month

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10
Q

What scoring system is used to evaluate the risk of stroke after TIA?

A 
ABCDD
Age >60 (1)
Blood pressure >140/90 (1)
Clinical features (unilateral weakness=2, speech=1)
Duration of symptoms (1hr=2)
Diabetes (1)
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11
Q

What is the classic triad of presentations of Parkinson’s?

A

Rigidity, bradykinesia/hypokinesia and tremor

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12
Q

What other symptoms might a patient with Parkinson’s experience?

A

Characteristic pill rolling of thumbs, anosmia, depression, postural weakness, dementia, hallucinations

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13
Q

At what age does Parkinson’s typically present?

A

65

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14
Q

Explain the pathology of Parkinson’s

A

Progressive loss of dopaminergic neurones from pars compacta of substantia nigra, surviving neurones have Lewy bodies. Loss of these neurones causes a deficiency of dopamine

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15
Q

What are Lewy bodies?

A

Intracytoplasmic rounded eosinophilic inclusions containing aggregates of α-synuclein

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16
Q

How would you treat Parkinson’s disease?

A

Assess disability and cognition regularly, decide when is best to start Levodopa - will eventually stop working + possibility of dopamine induced dyskinesias. Dopamine agonists (ropinirole) can delay starting levodopa. Can combine levodopa with dopa decarboxylate inhibitor to reduce side effects

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17
Q

What is an epileptic seizure?

A

A sudden synchronous discharge of neurons causing symptoms that are apparent to either the patient or an onlooker

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18
Q

What is epilepsy?

A

A recurrent tendency to spontaneous and intermittent seizures

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19
Q

When is epilepsy most likely to present?

A

Before the age of 20 or after 60

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20
Q

How are seziures classified?

A

Partial - either simple (awareness unimpaired) or complex (loss of awareness, post ictal symptoms).
Generalized - absence, tonic clonic or myoclonic.

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21
Q

Describe the difference between a tonic clonic seizure and a myoclonic seizure

A

Tonic clonic - Limbs stiffen then jerk, loss of consciousness, post ictal symptoms - drowsiness, confusion
Myoclonic - Sudden jerking of a limb, face or trunk

22
Q

What is the medical treatment for the different types of seizures?

A

TC - sodium valproate/lamotrigine
Absence - sodium valproate/lamotrigine/ethosuximide
Partial - Carbamazepine

23
Q

What drug would be given first in a case of status epilepticus ?

24
Q

What is myasthenia gravis?

A

Autoimmune disease mediated by antibodies to nicotinic acetylcholine receptors interfering with neuromuscular transmission

25
At what age is myasthenia gravis most common?
50 for men
26
How will myasthenia gravis present?
muscle weakness - face/eye/swallowing, ptosis, ocular palsies, slurred speech, myasthenic snarl on smiling, tendon reflexes normal diplopia
27
Which antibodies are present in myasthenia gravis?
Anti-acetylcholine receptor (AChR) antibody - present in 90% of cases, diagnostic
28
How is myasthenia gravis treated?
Symptom control, pyridostigmine - reduces rate of degradation of acetylcholine in neuromuscular junction by inhibiting cholinesterase
29
What is Guillain Barré syndrome?
Acute inflammatory demyelinating neuropathy (most common acute polyneuropathy)
30
How does Guillain Barré syndrome present?
Typically a few weeks post infection with ascending symmetrical weakness. Progresses quickly, affecting all limbs at once, proximal muscles more affected, pain common.
31
What investigations would be carried out in Guillain Barré syndrome and what are their likely results?
CSF would show increased protein and a normal WCC, FVC 4 hourly to check for respiratory involvement. Nerve conduction studies would show slow conduction.
32
How would Guillain Barré syndrome be managed?
Resolves in 4 weeks usually, respiratory involvement is the big danger - check FVC and ventilate sooner rather than later if needed. IV immunoglobulin for 5 days. Steroids are no help. 85% make full recovery.
33
What is encephalitis?
Acute inflammation on the brain parenchyma (viral in 90%)
34
List some signs and symptoms of encephalitis
Odd behaviour, personality changes, decreased consciousness, seizures, speech disturbances, fever, headache,
35
What would investigations in encephalitis show?
Contrast CT showing focal bilateral temporal lobe involvement is suggestive of HSV. Blood cultures. LP - moderately raised CSF protein and lymphocytes, decreased glucose. EEG showing diffuse abnormalities can be diagnostic but cant show a cause.
36
How is encephalitis treated?
Aciclovir ideally within 30 minutes of the patient arriving. Supportive treatement eg Phenytoin for seizures
37
How would giant cell arteritis present?
Tender scalp 'painful to comb hair', jaw claudication 'trouble chewing food', difficulty protruding tongue, tender thickened pulseless temporal arteries. ESR would be greatly elevated
38
How is giant cell arteritis treated?
Prompt steroids to avoid permanent vision loss- prednisolone
39
Who are cluster headaches most common in?
Men 40-60
40
How do cluster headaches present?
Sudden onset acute pain behind one eye 'worst pain ever felt', also known as suicide headaches. Attacks last around an hour and may happen once or twice a day for 4-12 weeks before going away for often years before reccuring
41
How are cluster headaches treated?
Sumatriptan s/c, 100% O2
42
Who does trigeminal neuralgia most commonly present in?
60-70 year olds, more common in males
43
What causes trigeminal neuralgia?
Compression of trigeminal root - tumour, inflammation, aneurysm. Pain stimulated by cold, washing, shaving.
44
How is trigeminal neuralgia treated?
MRI needed to exclude any other causes, then carbamazepine
45
What is Huntingdons disease?
Incurable progressive neurodegenerative disorder.
46
What pattern of inheritance does Huntingdons follow?
Autosomal dominant with full penetrance
47
Explain the pathology of Huntingdons
Increased CAG repeats on chromosome 4. >27 abnormal, >40 almost certainly get symptoms. Basal ganglia die, decreased striatal volume = increased size of lateral horns of ventricles. Increased dopamine and expression of dopamine receptors reduced.
48
How would a patient with Huntingdons present?
Early --> late - decreased personal hygiene, change in personality, fidgeting, tics, disarthria, chorea
49
What is multiple sclerosis?
Chronic autoimmune T cell mediated inflammatory disorber
50
Who does MS most commonly affect?
Women twice as much as men, 20-40yrs

Phase 2A (9 decks)

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