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Flashcards in Neuro Deck (50)
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1
Q

5 parts of basal ganglia

A

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

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.

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

4
Q

Define a TIA

A

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

5
Q

4 causes of TIA

A

Atherothromboembolism, hyperviscosity, cardiac thrombus, postural hypotension

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’

7
Q

4 signs and symptoms of a TIA

A

Hemiparesis, aphasia, ataxia, hemisensory loss, amaurosis fugax

8
Q

What is the timeframe for symptoms of a TIA?

A
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

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)
11
Q

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

A

Rigidity, bradykinesia/hypokinesia and tremor

12
Q

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

A

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

13
Q

At what age does Parkinson’s typically present?

A

65

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

15
Q

What are Lewy bodies?

A

Intracytoplasmic rounded eosinophilic inclusions containing aggregates of α-synuclein

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

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

18
Q

What is epilepsy?

A

A recurrent tendency to spontaneous and intermittent seizures

19
Q

When is epilepsy most likely to present?

A

Before the age of 20 or after 60

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.

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 ?

A

Lorazepam

24
Q

What is myasthenia gravis?

A

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

25
Q

At what age is myasthenia gravis most common?

A

50 for men

26
Q

How will myasthenia gravis present?

A

muscle weakness - face/eye/swallowing, ptosis, ocular palsies, slurred speech, myasthenic snarl on smiling, tendon reflexes normal diplopia

27
Q

Which antibodies are present in myasthenia gravis?

A

Anti-acetylcholine receptor (AChR) antibody - present in 90% of cases, diagnostic

28
Q

How is myasthenia gravis treated?

A

Symptom control, pyridostigmine - reduces rate of degradation of acetylcholine in neuromuscular junction by inhibiting cholinesterase

29
Q

What is Guillain Barré syndrome?

A

Acute inflammatory demyelinating neuropathy (most common acute polyneuropathy)

30
Q

How does Guillain Barré syndrome present?

A

Typically a few weeks post infection with ascending symmetrical weakness. Progresses quickly, affecting all limbs at once, proximal muscles more affected, pain common.

31
Q

What investigations would be carried out in Guillain Barré syndrome and what are their likely results?

A

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
Q

How would Guillain Barré syndrome be managed?

A

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
Q

What is encephalitis?

A

Acute inflammation on the brain parenchyma (viral in 90%)

34
Q

List some signs and symptoms of encephalitis

A

Odd behaviour, personality changes, decreased consciousness, seizures, speech disturbances, fever, headache,

35
Q

What would investigations in encephalitis show?

A

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
Q

How is encephalitis treated?

A

Aciclovir ideally within 30 minutes of the patient arriving. Supportive treatement eg Phenytoin for seizures

37
Q

How would giant cell arteritis present?

A

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
Q

How is giant cell arteritis treated?

A

Prompt steroids to avoid permanent vision loss- prednisolone

39
Q

Who are cluster headaches most common in?

A

Men 40-60

40
Q

How do cluster headaches present?

A

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
Q

How are cluster headaches treated?

A

Sumatriptan s/c, 100% O2

42
Q

Who does trigeminal neuralgia most commonly present in?

A

60-70 year olds, more common in males

43
Q

What causes trigeminal neuralgia?

A

Compression of trigeminal root - tumour, inflammation, aneurysm. Pain stimulated by cold, washing, shaving.

44
Q

How is trigeminal neuralgia treated?

A

MRI needed to exclude any other causes, then carbamazepine

45
Q

What is Huntingdons disease?

A

Incurable progressive neurodegenerative disorder.

46
Q

What pattern of inheritance does Huntingdons follow?

A

Autosomal dominant with full penetrance

47
Q

Explain the pathology of Huntingdons

A

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
Q

How would a patient with Huntingdons present?

A

Early –> late - decreased personal hygiene, change in personality, fidgeting, tics, disarthria, chorea

49
Q

What is multiple sclerosis?

A

Chronic autoimmune T cell mediated inflammatory disorber

50
Q

Who does MS most commonly affect?

A

Women twice as much as men, 20-40yrs