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3a > Neuro > Flashcards

Neuro Flashcards

1
Q

How quickly do you need to give thrombolysis?

A

Within 4.5 hours of onset of symptoms

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2
Q

Give 5 contraindications to thrombolysis:

A
  1. Seizure at onset of stoke
  2. Symptoms suggestive of SAH (thunderclap headache)
  3. Stroke or serious head injury in the preceding three months
  4. Current anticoagulation (INR>1.7)
  5. Significant bleeding
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3
Q

What is a thrombectomy?

A

Mechanical retrieval of a clot if seen in the proximal anterior circulation

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4
Q

Give 10 investigations you might do on a patient admitted with a possible stroke:

A
  1. Routine obs
  2. Neuro exam
  3. Bloods (FBC, U&E, LFT, CRP, lipids, coagulation factors)
  4. NIH Scale
  5. ECG
  6. CT Head
  7. MRI Head
  8. Angiography
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5
Q

Following thrombolysis, a patient’s GCS drops to 7 and their condition is worsening. What might be happening?

A

Haemorrhagic transformation and/or raised ICP

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6
Q

Give 5 possible long term stroke complications:

A
  1. Aspiration pneumonia
  2. Pressure sores
  3. Depression
  4. Cognitive impairment
  5. Seizures (often caused by termporal lobe haemorrhagic strokes)
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7
Q

Define stroke:

A

A clinical syndrome consisting of rapid onset neurological deficit which is the result of a vascular lesion and is associated with infarction of central nervous tissue

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8
Q

What are the two types of stroke?

A
  1. Ischaemic e.g. embolism, thrombosis (87%)

2. Haemorrhagic (13%)

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9
Q

Give 6 risk factors for stroke:

A
  1. HTN
  2. Diabetes Mellitus
  3. Smoking
  4. Hyperlipidaemia
  5. Obesity
  6. Alcohol
  7. AF
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10
Q

Give 4 signs of raised ICP:

A
  1. Decreasing GCS
  2. Papilloedema
  3. Midline shift or herniation on imaging
  4. Vomiting
  5. Severe headache
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11
Q

Two types of haemorrhagic stroke:

A
  1. Intracerebral (75%)

2. Subarachnoid (25%)

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12
Q

Give 3 signs of meningism:

A
  1. Neck stiffness
  2. Photophobia
  3. Positive Kernig’s sign
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13
Q

What is a positive kernig’s sign?

A

Severe stiffness causing an inability to straighten the leg when the hip is flexed to 90 degrees

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14
Q

Give 2 causes of an SAH:

A
  1. Berry aneurysm
  2. Clotting disorder e.g. warfarin
  3. Traumatic and infectious aneurysms
  4. Dural Ateriovenous Malformation (AVM)
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15
Q

Give 6 classic symptoms of an SAH:

A
  1. New severe headache (NB: 30% of SAH occur during sleep)
  2. N&V
  3. Prodromal sentinel headache (occaisonally)
  4. Confusion
  5. Visual changes (loss/diplopia)
  6. Sudden, often transient, LOC at onset
  7. Thunderclap headache (25%)
  8. Orbital pain
  9. Photophobia
  10. Onset during sex
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16
Q

Give 6 classic signs of an SAH:

A
  1. Altered GCS
  2. Meningism
  3. Hyperpyrexia
  4. Sensory motor deficits
  5. Cardiac arrhythmias
  6. Seizures
  7. Rentinal haemorrhages (Terson’s syndrome)
  8. CN palsies
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17
Q

What is Terson’s syndrome?

A

Occurs in 8-19% of SAH. Intraocular/vitreous haemorrage of the eye.

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18
Q

A patient comes in with a suspected SAH. CT Head confirms the diagnosis, what is the next step?

A
  1. Start nimodipine
  2. CT angiogram
  3. Possible neurosurgical clipping or endovascular coiling of aneurysm depending on site, clinical condition and comorbidity
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19
Q

What type of drug is nimodipine?

A

A calcium channel blocker

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20
Q

A patient with a confirmed SAH needs to be started on Nimodipine, what dose/frequency/route should you give? How long should they continue this treatment?

A

If systolic BP>100, give 60mg 4-hourly

If systolic BP<100, give 30mg 2-hourly

Given PO/NG

Continue for 21 days

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21
Q

What is the prognosis for SAH?

A

30% die, usually out of hospital
30% recover completely
30% recover with some disability

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22
Q

When might you do an LP in a patient with a suspected SAH?

A

If the CT head is negative, but there is still a high suspicion of SAH (provided there are no contraindications on the CT).
The LP should ideally take place over 12 hours after the onset of the headaches.

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23
Q

What might an LP in a patient with an SAH show?

A

Xanthochromia (yellow discolouration)

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24
Q

What might a CT head in a patient with an SAH show?

A

Hyperdense (bright) areas of acute blood in the basal cisterns and sulci. Looks like a star shaped pattern.

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25
Q

Why do you give nimodipine in SAH?

A

To prevent vasospasm

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26
Q

What supportive treatment do you give after thrombolysis? (6)

A
  1. Cautious BP control
  2. Oxygen
  3. Glucose control
  4. IV fluids
  5. TEDs
  6. NGT if swallow impaired (BUT! Do not insert for 24 hours following, risk of bleeding)
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27
Q

24 hours after thrombolysis you need to start your patient on aspirin - what must you make sure has been done first?

A

A follow up head CT to confirm no haemorrhagic changes post-thrombolysis

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28
Q

A patient with an ischaemic stroke is NOT suitable for thrombolysis. What is the next alternative step in their treatment?

A

Consider thrombectomy.

If not suitable for thrombectomy, start 300mg aspirin PO for 2 weeks then 75mg daily.

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29
Q

Following an iscaehmic stroke, what dose/frequency/duration of aspirin do you give?

A

300mg for 2 weeks then lifelong clopidogrel

NB: always give PPI cover!

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30
Q

What is CHA2DS2-VASc?

A

Determines the 1 year risk of a thromboembolic event in a non-anticoagulated patient with non-valvular AF

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31
Q

Components of CHA2DS2-VASc:

A
  1. Age (<65, 65-74, >75)
  2. Sex (F=1, M=0)
  3. Congestive HF (1)
  4. HTN (1)
  5. Previous stroke/TIA/TE (2)
  6. Vascular disease (e.g. MI, PAD) (1)
  7. Diabetes (1)
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32
Q

Give 2 groups at increased risk of subdural haematoma:

A
  1. Eldery
  2. Alcoholics

Due to cerebral atrophy (and weakened/stretched bridging veins from the cortex to one of the draining venous sinuses)

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33
Q

Give 3 symptoms of subdural haematoma:

A
  1. Headache
  2. Drowsiness
  3. Alternating consciousness
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34
Q

What might you see on a head CT of a patient with a subdural haematoma?

A

Crescent shape haemorrhage

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35
Q

What causes an extradural haematoma?

A

Trauma to the temporal bone damaging the middle meningeal artery

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36
Q

How is consciousness level affected by an acute extradural haematoma?

A

Rapid deterioration in conscious level, associated with focal neurological signs

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37
Q

How do you treat a extradural haematoma?

A

Immediate surgical drainage

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38
Q

What score is used to calculate the risk of a stroke in a patient who has had a TIA?

A

ABCD2

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39
Q

What are the components of ABCD2?

A 
Age >60 (1)
BP > 140/90 (1)
Unilateral weakness (2)
Speech disturbance without weakness (1)
Duration <10 mins (0)
Duration 10-59 mins (1)
Duration >60 mins (2)
Diabetes (1)
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40
Q

Give 3 causes of optic neuritis

A

Inflammation of the optic nerve, can be caused by:

  1. MS
  2. Infection e.g. Lyme, syphilis, HIV
  3. B12 deficiency
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41
Q

Give 5 features of optic neuritis:

A
  1. Pain on eye movement
  2. Poor visual acuity
  3. Relative afferent pupillary defect (RAPD)
  4. Dyschromatopsia (deficiency in perception of colours)
  5. Usually resolves in ~6 weeks

NB: Give steroids to reduce pain and increase speed of recovery

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42
Q

Name 3 patterns of MS:

A
  1. Relapsing and remitting (stepwise progression of disability, or increases then decreases)
  2. Secondary progressive (starts as R&R, then changes to linear increase in disability)
  3. Primary progressive (increasingly disabled from first onset)
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43
Q

Described the pathophysiology of MS:

A

A cell mediated autoimmune condition
Repeated episodes of inflammation of the nervous tissue in the brain and spinal cord
Leads to loss of the myelin sheath

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44
Q

What is internuclear ophthalmoplegia?

A

An ocular movement disorder.
Seen as:
- Impaired adduction in one eye
- Nystagmus in the other eye

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45
Q

What is internuclear ophthalmoplegia a common sign of?

A

Multiple sclerosis

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46
Q

What lesion results in internuclear ophthalmoplegia?

A

A lesion in the medial longitudinal fasciculus

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47
Q

Give 5 signs of MS:

A
  1. UMN signs
  2. Optic neuritis
  3. Internuclear opthalmoplegia
  4. Lhermitte’s sign (electric shock feeling)
  5. Uhtoff’s sign (increasing body temp further slows nerve conduction and worsens symptoms)
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48
Q

What is the difference between Clinically Isolated Symptoms (CIS) and Mutliple Sclerosis (MS)?

A

CIS: First episode of symptoms due to acute inflammatory demyelination

MS: Multiple lesions differing in both space and time

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49
Q

How would you manage a relapse episode in a patient with MS?

A
  1. IV methylprednisolone 500mg/day given over four hours (PO medication also available)
  2. Give gastric protection - ranitidine 150mg BD or omeprazole 20mg OD
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50
Q

Name two precautions to be aware of when giving steroids in an MS relapse:

A
  1. Give gastric protection (omeprazole 20mg OD or ranitidine 150mg BD)
  2. Avoid use of steroids on more than 3 occaisons per year or for longer than 3 weeks on any one occaison
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51
Q

Name 3 DMARDs used in MS:

A
  1. Beta interferon
  2. Ocrelizumab
  3. Alemtuzumab
  4. Fingolimod
  5. Stem cell transplants
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52
Q

Give 4 signs of Giant Cell Arteritis:

A
  1. Jaw claudication
  2. Scalp tenderness
  3. Anorexia
  4. Anaemia
  5. Fatigue
  6. Age > 70
  7. Elevated ESR & CRP
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53
Q

How long does a migraine typically last?

A

6-8 hours

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54
Q

Give 5 signs of a migraine:

A
  1. Aura
  2. Photophobia
  3. Phonophobia
  4. N&V
  5. Gradual onset over 45-60mins
  6. Associated with a trigger (varies from person to person)
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55
Q

How do you manage an acute migraine?

A

High dose aspirin (900mg dispersable)

Triptans - tablets, nasal spray or injection (most powerful)

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56
Q

What is the mechanism of action of a triptan?

A

5HT-1-receptor agonists

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57
Q

Give 3 contraindications for triptans:

A
  1. Uncontrolled HTN
  2. Coronary heart disease or cerebrovascular disease
  3. Coronary vasospasm
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58
Q

How do you manage chronic migraines?

A
  1. Address any triggers
  2. Prophylaxis:
    - Propranolol 80-160mg daily in divided doses, OR;
    - Topiramate, OR;
    - Amitriptyline (at night)
  3. Botulinum injections (if very severe)
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59
Q

Give 3 features of a cluster headache:

A
  1. Unilateral pain behind the eye
  2. High severity pain
  3. Sudden onset (‘clockwork’ headache, always the same time everyday)
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60
Q

Why are they called cluster headaches?

A

They occur in ‘clusters’ i.e. Lots of attacks in a week, then remission for a period of time

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61
Q

Acute management of a cluster headache: (2)

A
  1. Oxygen

2. Triptan (SC or nasal)

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62
Q

Prophylaxis of cluster headaches:

A

Verapamil (calcium channel blocker)

240-960 mg daily, in 3-4 divided doses

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63
Q

3 features of a tension headache:

A
  1. Tight band around forehead
  2. Often related to stress
  3. More gradual onset, more variable in duration, more constant in quality and less severe than migraine
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64
Q

Management of tension headache: (3)

A
  1. Simple analgesics (ibuprofen)
  2. Amitriptyline (SE dry mouth, start at night)
  3. Lifestyle modification
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65
Q

How does trigeminal neuralgia present?

A

2 seconds of stabbing pain in unilateral trigeminal nerve distribution
Face screws up with pain

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66
Q

What is glaucoma?

A

Drainage of the aqueous humour of the eye suddenly becomes occluded, leading to increased ocular pressure.

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67
Q

Give 5 signs of glaucoma:

A
  1. Unilateral vision loss
  2. Pain
  3. Red eye
  4. N&V
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68
Q

An acute headache can be an emergency, what 3 conditions should be careful to rule out?

A
  1. Meningism
  2. GCA/temporal arteritis
  3. Glaucoma
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69
Q

Give 2 groups at a higher risk of developing Bell’s Palsy:

A
  1. Diabetics

2. Pregnant women

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70
Q

Which cranial nerve is affected in Bell’s Palsy?

A

Facial Nerve (VII)

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71
Q

What is the function of the facial nerve? (3)

A
  1. Control of muscles of facial expression
  2. Control of hearing via stapedius muscle
  3. Taste sensation to the anterior two-thirds of the tongue
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72
Q

A 49 year old woman presents to A&E with a drooping face on the right side. She says she noticed it when she looked in the mirror this morning and she also feels like everything is sounding louder. What is the likely diagnosis?

A

Bell’s Palsy - a lower motor neuron lesion of the ipsilateral (R) facial nerve (VII).

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73
Q

Give 3 symptoms of Bell’s Palsy:

A
  1. Acute unilateral facial drooping
  2. Hyperacusis (everything sounds louder)
  3. Disturbance in taste to the anterior two-thirds of the tongue
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74
Q

Is the forehead involved in Bell’s Palsy? Why/why not?

A

Yes the forehead is affected. In a LMN lesion the forehead is affected, in UMN lesions the forehead/upper face is spared.

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75
Q

Prognosis of Bell’s Palsy:

A

Most recover fully within 3-4 months.

Around 15% have permanent moderate to severe weakness.

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76
Q

How do you manage Bell’s Palsy? (3)

A
  1. Oral prednisolone within 72 hours of onset
  2. Advise about eye care & prescription of artificial tears/eye lubricants
  3. Advice to return if no improvement in 3 weeks (then refer to ENT)
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77
Q

Give four key features of Parkinson’s disease:

A
  1. Bradykinesia (gradual slowing of movement)
  2. Rigidity (cog wheel)
  3. Tremor (in 70% of pts)
  4. Postural instability

Other features include:

  1. Depression
  2. Autonomic dysfunction (constipation, urinary freq)
  3. Anosmia
  4. Dementia
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78
Q

Describe the pathophysiology of Parkinson’s: (4)

A
  • Insufficient dopamine
  • Depigmentation of the substantia nigra
  • Relative overactivity of ACh
  • Presence of lewy bodies
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79
Q

Name the three types of drug used in the management of motor symptoms & an example of each:

A
  1. Levodopa - e.g. Co-beneldopa, entacapone
  2. Dopamine agonists e.g. Apomorphine
  3. MAO-B inhibitors e.g. Selegiline
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80
Q

How does Levodopa work to improve symptoms in Parkinson’s?

A

Levodopa is a dopamine pre-cursor which is decarboxylated to form dopamine in the brain, this makes up for the lack of endogenous dopamine and stimulates dopaminergic receptors.

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81
Q

What type of medication is Entacapone?

A

A COMT inhibitor - slows the breakdown of levodopa in the brain and periphery

82
Q

What neurological emergency must you look out for in a patient taking an MAO-B inhibitor and an SSRI?

A

Serotonin syndrome: pyrexia, agitation, tremor, sweating, diarrhoea

83
Q

How does carbamazepine work? What is it used to treat?

A

Binds to sodium channels increasing their refractory period. Epilepsy.

84
Q

What is expressive dysphagia?

What type of lesion would cause expressive dysphasia?

A

Reduced ability to produce language, laboured speech, non-fluent.
A lesion of Broca’s area, located in the (left) inferior posterior frontal lobe.

85
Q

What is receptive dysphasia?

What type of lesion would cause receptive dysphasia?

A

A lack of comprehension and understanding of language.

A lesion of Wernicke’s area, located in the (left) temporal lobe.

86
Q

Vertical diplopia indicates a palsy/lesion of which cranial nerve? (double vision going down the stairs)

A

Trochlear nerve (IV) - supplies the superior oblique muscle responsible for intorsion/depression

87
Q

A ‘down and out’ eye position indicates a palsy of which cranial nerve?

A

Oculomotor nerve (III) - supplies almost all the extraocular muscles

88
Q

A constantly adducted eye indicates a palsy of which cranial nerve?

A

Abducens (VI) - supplies the lateral rectus muscle responsible for abduction

89
Q

What is Horner’s syndrome? (3 features)

A
  1. Ptosis
  2. Miosis (pupil constriction)
  3. Anhidrosis (absence of sweating on the ipsilateral side of face)
90
Q

Give 3 causes of Horner’s syndrome:

A
  1. A central lesion e.g. in a stroke or MS
  2. A pre-ganglionic lesion e.g. trauma or tumour
  3. A post-ganglionic lesion e.g. carotid aneurysm
91
Q

What bacteria is the most common cause of meningitis in adults?

A

Strep. pneumoniae

92
Q

What is an epileptic seizure?

A

A clinical manifestation of disordered electrical activity in the brain (paroxysmal discharge of cerebral neurons)

93
Q

Give 3 differentials for a blackout episode:

A
  1. Syncope
  2. Epilepsy
  3. Non-epileptic attacks
94
Q

Give 3 causes of syncope:

A
  1. Vasovagal
  2. Orthostatic (primary or secondary)
  3. Cardiac (e.g. arrythmia, valvular disease)
95
Q

Give 3 possible triggers of an epileptic seizure:

A
  1. Sleep deprivation
  2. Flashing lights
  3. Menstruation
  4. Alcohol and alcohol withdrawal
96
Q

Give 4 features of a non-epileptic attack:

A
  1. Waxing and waning course
  2. Pelvic thrusting
  3. Eyes closed
  4. Arms flexing and extending
97
Q

How does the recovery period after syncope, an epileptic seizure and a non-epileptic attack differ?

A

Syncope: little/no confusion, quick

Seizure: confusion/headache, possible amnesia, may take several hours, needs sleep

NEA: atypically quick recovery

98
Q

What is the first-line drug used in an acute epileptic seizure?

A

Benzodiazepines e.g. Lorazepam - 4mg IV bolus, repeat after 10-20 minutes if seizure continues

99
Q

Give 5 causes of epilepsy:

A
  1. Head injury
  2. CNS infection (meningitis, encephalitis)
  3. Brain neoplasm
  4. Neurodegenerative disease e.g. Alzheimer’s
  5. Genetic diseases/syndromes
  6. Drugs e.g. alcohol withdrawal
  7. Metabolic disorders e.g. hyponatremia
100
Q

What AED might you give to a 25 year old woman with recurrent epileptic seizures?

A

Iamotrigine
Levetiracetam
(if not tolerated and/or pregnancy prevention is definitely in place then you might give sodium valproate)

101
Q

What is diaphoresis?

A

Excessive sweating

102
Q

What area of the brain does the posterior cerebral artery supply?

A

Medial and lateral parts of the posterior cerebrum. Such as: the occipital lobe, the inferomedial surface of the temporal lobe, midbrain, thalamus and the choroid plexus of the 3rd and lateral ventricles

103
Q

What area of the brain does the anterior cerebral artery supply?

A

Anteromedial portions of the cerebrum. Such as portions of the primary motor and somatosensory cortices responsible for the leg, foot and trunk.

104
Q

What area of the brain does the middle cerebral artery supply?

A

The majority of the lateral part of the brain. Such as: the majority of the primary motor and somatosensory cortices.

105
Q

Give 3 associated effects of a lesion in the anterior cerebral artery:

A
  1. Contralateral hemiparesis
  2. Contralateral sensory loss
  3. Affects lower extremities more than upper (trunk, leg, foot)
106
Q

Give 5 associated effects of a lesion in the middle cerebral artery:

A
  1. Contralateral hemiparesis
  2. Contralateral sensory loss
  3. Affects upper extremities more than lower
  4. Contralateral homonymous hemianopia
  5. Aphasia
107
Q

What is homonymous hemianopia?

A

Vision loss on the same side of the visual field in both eyes. E.g. you can’t see the left half of your visual field in both eyes

108
Q

Give 2 associated affects of a lesion in the posterior cerebral artery:

A
  1. Contralateral homonymous hemianopia with macular sparing

2. Visual agnosia

109
Q

What is visual agnosia?

A

A disorder of recognition in which a person cannot arrive at the meaning of some or all categories of previously known non-verbal visual stimuli.

110
Q

What is amaurosis fugax? Give two examples of conditions that can cause it:

A

A sudden curtain descends across the visual field. Caused by:

  1. Giant cell arteritis/temporal arteritis
  2. Stroke with a lesion in the retinal/opthamic artery
111
Q

What is Weber’s syndrome?

A

A stroke affecting the branches of the posterior cerebral artery that supply the medial portion of the midbrain e.g. parts of the substantia nigra, corticospinal fibers, corticobulbar tract and oculomotor fibers.

112
Q

Give 2 features of Weber’s syndrome:

A
  1. Ipsilateral CN III palsy

2. Contralateral weakness of upper and lower extremities

113
Q

What causes Wallenberg’s syndrome?

A

Also known as Lateral Medullary Syndrome, occurs following an occlusion of the posterior inferior cerebellar artery.

114
Q

Give 2 cerebellar and 2 brainstem features of Wallenberg’s syndrome:

A 
Cerebellar:
1. Ataxia
2. Nystagmus
Brainstem:
1. Ipsilateral: dysphagia, facial numbness, CN palsy
2. Contralateral limb sensory loss
115
Q

Give 3 common signs of motor neuron disease:

A
  1. Mixed UMN and LMN signs
  2. Fasciculations
  3. Foot drop
  4. Absence of sensory signs/symptoms
  5. Wasting of the small hand muscles/tibialis anterior
116
Q

What are bulbar symptoms in MND?

A

Speech and swallowing difficulties - resulting in increased risk of aspiration and therefore pneumonia

117
Q

Give 3 features of MND that might help you differentiate it from an alternative diagnosis:

A
  1. Does not affect external ocular muscles
  2. No cerebellar signs
  3. Abdominla reflexes are usually preserved, if present sphincter dysfunction is a late feature
118
Q

Name the only drug proven to have disease-modifying efficacy in MND:

A

Riluzole - a neuroprotective glutamate-release inhibitor

119
Q

What is ‘the phenomenon of anticipation’ in Huntington’s disease?

A

Huntinton’s is a trinucleotide repeat disorder (CAG), because of this the disease may present at an earlier age in successive generations

120
Q

When do features of Huntington’s typically start to present? Give 4 typical features of Huntington’s disease:

A

After 35 years of age.

  1. Chorea
  2. Personality changes (irritability, apathy, depression) and intellectual impairment
  3. Dystonia
  4. Saccadic eye movements (rapid intermittenet eye movement when attempting to move from fixing on one point to another)
121
Q

What is dystonia?

A

Involuntary muscle contraction of the large trunk and limb muscles causing repetitive or twisting movements.
Results in prolonged abnormal posture, e.g. sustained head retraction or foot inversion.

122
Q

Give 3 signs of chorea:

A
  1. Movements move from one area of the body to another
  2. Milkmaid sign: ‘squeeze my finger at a constant pressure’ - patient squeezes intermittently, can’t maintain pressure
  3. Darting tongue sign: patient cannot stick out tongue and hold it there still
123
Q

Give 2 examples of dystonic movements:

A
  1. Spasmodic torticollis (AKA wry neck) - unilateral deviation of the neck
  2. Writer’s cramp - muscles of the hand and forearm tighten on attempting to write and pain might occur
124
Q

What is chorea?

A

Involuntary movements that are rapid, brief, irregular and repetitive. Typically affect the mouth, face, limbs and trunk.

125
Q

What is Creutzfeldt-Jakob disease? Give 4 key features:

A

A neurodegenerative illness. It can be sporadic, hereditary, iatrogenic (neurosurgery), or caused by eating infected meat (mad cow disease).

  1. Progressive ataxia
  2. Dementia
  3. Choreiform movements
  4. Dystonic movement
126
Q

What is progressive supranuclear palsy?

A

The most common atypical Parkinsonian syndrome. Strongly associated with tau pathology. Affects eye movements, cognition and posture.

127
Q

Give 4 characteristics of progressive supranuclear palsy:

A
  1. Postural instability
  2. Akinesia
  3. Cognitive dysfunction
  4. Occular motor dysfunction (vertical gaze dysfunction!!)
128
Q

What are glial cells in the brain? What are their roles?

A

Supporting cells of the CNS, they provide nutrition, insulation and help with signal transmission. Includes astrocytes, oligodendrocytes and ependymal cells.

129
Q

What is the most common type of primary brain tumour?

A

Glioma

130
Q

How are brain tumours managed? (4)

A
  1. Resect tumour where possible
  2. Treat hydrocephalus for symptom relief
  3. External beam radiotherapy
  4. Chemo that can cross the BBB e.g. temozolomide
131
Q

What spinal level is the cauda equina?

A

~L2

132
Q

4 causes of cauda equina:

A
  1. Trauma
  2. Infection
  3. Tumour
  4. Herniation of a lumbar disc
133
Q

5 features of cauda equina:

A
  1. Bilateral sciatica
  2. Bowel and/or bladder dysfunction
  3. Sexual dysfunction
  4. Low back pain
  5. Lower limb motor weakness and sensory deficit
134
Q

How might spinal compression present? (4 features)

A
  1. Progressive weakness of the legs with UMN pattern and eventual paralysis
  2. Onset in hours to days (fast)
  3. Arms only affected if the lesion is above the thoracic spine
  4. Sensory loss below the lesion
135
Q

What is carpal tunnel syndrome?

A

Entrapment of the median nerve against the carpal tunnel.

136
Q

Give 5 features of carpal tunnel:

A
  1. Pain and paraesthesia in the hand
  2. Worse at night
  3. Loss of sensation along the distribution of the median nerve
  4. Tinel’s sign
  5. Phalen’s sign
137
Q

What is tinel’s sign:

A

Lightly percuss over the median nerve at the wrist to produce pain or paraesthesia in the median nerve distribution

138
Q

What is phalen’s sign:

A

Flex wrist for 60 seconds to produce pain in the median nerve distribution

139
Q

Where is the median nerve distribution in the hand?

A

Anterior: Almost all of the palm excluding the little finger and half of the fourth finger.
Posterior: fingertips of the thumb, index and half the fourth finger.

140
Q

Give 3 groups at increased risk of carpal tunnel:

A
  1. Diabetics
  2. People with hypothyroidism
  3. Pregnant people
141
Q

What is Brown-Sequard syndrome?

A

A lesion in one half of the spinal cord. Seen in trauma, neoplasia, MS, spinal cord herniation or vascular events.

142
Q

3 features of Brown-Sequard syndrome:

A
  1. Ipsilateral UMN weakness below the lesion = severed corticospinal tract
  2. Ipisilateral loss of proprioception and vibration = severed dorsal column
  3. Contralateral loss of pain and temperature sensation = severed spinothalamic tract
143
Q

What is Guillain-Barre syndrome? Give 3 triggers/causes:

A

An acute inflammatory demyelinating polyneuropathy.

  1. Campylobacter jejuni
  2. CMV
  3. Other preceding infection
  4. No cause is found in 40%
144
Q

Give 4 features of Guillain-Barre syndrome:

A
  1. Progressive ascending limb weakness that peaks at 4 weeks
  2. Autonomic dysfunction (sweating, bp changes, raised pulse, arrhythmias)
  3. Reflexes usually lost
  4. Pain
145
Q

How do you manage Guillain-Barre syndrome? (3)

A
  1. IV immunoglobulin
  2. Monitor FVC for respiratory muscle involvement - ventillate if needed
  3. Plasma exchange possible if needed
146
Q

Give 6 contrasting UMN and LMN signs:

A

UMN:

  1. Spastic paralysis
  2. Hyperreflexia
  3. Hypertonic
  4. Disuse atrophy
  5. NO fasiculations
  6. Positive babinski sign

LMN:

  1. Flaccis paralysis
  2. Hyporeflexia
  3. Hypotonic
  4. Wasting atrophy
  5. No babinski sign
147
Q

What is Myasthenia Gravis?

A

An autoimmune disease mediated by antibodies to nicotinic acetylcholine receptors on the postsynaptic side of the NM. Involves both B and T cells.

148
Q

Give 3 classic signs of myasthenia gravis:

A
  1. Ptosis
  2. Diplopia
  3. Myasthenic snarl/smiling
  4. Normal tendon reflexes
149
Q

How might myasthenia gravis present?

A

Increasing and relapsing muslce fatigue.
Muslce groups affected in order: extraocular, bulbar, face, neck, limb girdle, trunk.
Other classic signs: ptsosis, snarl, diplopia

150
Q

Give 3 features of managing myasthenia gravis:

A
  1. Anticholinesterase drug e.g. pyridostigmine
  2. Immunosuppression e.g. prednisolone
  3. Thyrectomy (beneficial in younger patients)
151
Q

Explain the pathogenesis of Huntington’s disease: (inheritance and how the brain is affected)

A

An autosomal dominant condition.
Expansion of a CAG repeat on chromosome 4.
Presence of mutant Huntingtin protein.
Leads to loss of neurons in the caudate nuclear and putamen.
Causes depletion of ACh and GABA.
Dopamine is spared!

152
Q

How do you manage Giant Cell Arteritis? (4)

A
  1. Prednisolone PO immediately, OR;
  2. IV methylprednisolone if visual loss
  3. Urgent temporal artery biopsy within 2 weeks of starting steroids
  4. Continue steroids for 2 years
153
Q

5 key features of giant cell arteritis:

A
  1. Age > 50 years
  2. New onset or new type of headache
  3. Tender temporal artery/Scalp tender (combing hair hurts)
  4. Elevated ESR
  5. +/- Amaurosis fugax (emergency!!)
154
Q

What is Giant cell arteritis?

A

A systemic immmune mediated vasculitis affecting medium and large sized arteries

155
Q

Give 4 non-motor symptoms of Parkinson’s disease:

A
  1. Depression
  2. Autonomic dysfunction (constipation, urinary freq, postural hypotension)
  3. Anosmia
  4. Dementia
  5. Psychosis
  6. Sleep disturbance
156
Q

What is encephalitis? Give 3 typical causes:

A

Inflammation of the brain parenchyma.

  1. Viral e.g. HSV, EBV, varicella zoster virus
  2. TB
  3. Listeria
157
Q

Give 4 features of encephalitis:

A
  1. Preceding flu-like illness
  2. Decreasing GCS or coma
  3. Fever
  4. Altered behaviour/confusion
  5. Headache
  6. Memory loss
158
Q

Give 4 possible investigations for encephalitis:

A
  1. LP (with PCR test for HSV, VZV and enteroviruses)
  2. FBC and blood film
  3. Other bloods: cultures, U&E, creatinine, LFTs, glucose, ESR and CRP
  4. MRI/CT
  5. EEG
159
Q

What drug might you give for encephalitis in a patient with EBV?

A

Acyclovir

160
Q

What is meningitis, what is the most common cause?

A

Inflammation of the meninges, most commonly caused by a virus e.g. enterovirus, HSV, VZV

161
Q

5 key signs/symptoms of meningitis:

A
  1. Fever
  2. Headache
  3. Stiff neck
  4. Photophobia
  5. Kernig’s sign
  6. Back rigidity
162
Q

3 categories of symptoms seen in dementia:

A
  1. Cognitive impairment
  2. Psychiatric disturbances
  3. Difficulties with ADLs
163
Q

What is Lewy Body dementia? How might you differentiate it from other types of dementia clinically (3 signs)?

A

Dementia caused by the deposition of abnormal protein within neurons in the brainstem and neocortex.
An early hallmark sign is visual hallucinations. Patients also experience fluctuating levels of awareness and attention. There are also signs of mild Parkinsonism.

164
Q

What is Alzheimer’s disease? Give 3 pathological features seen in the brain:

A

The most common cause of dementia, involved progressive degeneration of the cerebral cortex.

  1. Amyloid plaques
  2. Neurofibrillary tangles
  3. Less ACh
165
Q

Investigations for dementia: (4)

A
  1. Cognitive assessment (MoCA)
  2. MRI/CT to exclude other pathologies (e.g. tumour)
  3. Bloods to exclude other causes
  4. SPECT to differentiate type of dementia
166
Q

Pharmacological management of dementia

A
  1. AChE inhibitors e.g. donepezil
  2. NMDA antagonist e.g. Memantine
  3. Managment of other symptoms e.g. antidepressants (avoid TCAs as worsen cognition
167
Q

What 3 types of cell are damaged by hyperglycaemia in diabetes mellitus?

A
  1. Retinal endothelium
  2. Mesangial cells in the glomeruli
  3. Schwann cells in peripheral nerves (excessive oxidation causes damage)
168
Q

Give 3 possible causes of a chronic peripheral neuropathy;

A
  1. Diabetes mellitus
  2. Coeliac disease
  3. Alcohol abuse
  4. CKD
169
Q

What drug might you give to manage pain in a patient with peripheral neuropathy?

A

Amitriptyline

Gabapentin

170
Q

What is the most common cause of bacterial meningitis is adults?

A

Strep. pneumoniae

171
Q

What is hemiballismus? What causes it?

A

Uncontrollable thrashing movements associated ith lesions of the subthalamic nucleus e.g. in a stroke

172
Q

Guillian-Barre syndrome is classically triggered by an infection with what bug? How might this present? (3)

A

Campylobacter jejuni

  1. Back pain
  2. GI symptoms (diarrhoea)
  3. Ascending weakness
173
Q

Inferior homonymous quadrantanopia results from a lesion in which lobe of the brain?

A

Parietal lobe

PITS: parietal = inferior, temporal = superior

174
Q

Superior homonymous quadrantanopia is caused by a lesion in which lobe of the brain?

A

Temporal lobe

PITS: parietal = inferior, temporal = superior

175
Q

What is thoracic outlet syndrome?

A

A disorder involving compression of the brachial plexus, subclavain artery or subclavian vein at the site of the thoracic outlet.

176
Q

Who is the typical patient you might meet with thoracic outlet syndrome (age, gender, physical features) and what causes it?

A

Patients are typically young thing women with long necks and drooping shoulders.
It’s caused by trauma in anatomically predisposed people. It can be vascular or neurogenic.

177
Q

2 signs/symptoms of neurogenic thoracic outlet syndrome:

A
  1. Painless muscle wasting of the hand

2. Sensory symptoms e.g. numbness, tingling

178
Q

2 signs/symptoms of vascular thoracic outlet sydrome:

A

Painful diffuse arm swelling with distended veins (if subclavian vein compressed)
Painful claudication leading to ulceration and gangrene (if subclavian artery compressed)

179
Q

What do the dorsal columns conduct?

A

Light touch
Vibration
Proprioception

180
Q

What does the lateral corticospinal tract conduct?

A

Limb motor information

181
Q

What does the ventral corticospinal tract conduct?

A

Axial muscle information

182
Q

What dose the lateral spinothalamic tract conduct?

A

Pain

Temperature sensation

183
Q

What does the anterior spinothalamic tract conduct?

A

Crude touch

184
Q

What is Erb-Duchenne paralysis? What causes it?

A

An injury to the brachial plexus, commonly affecting the union of C5 and C6, occurs during breech delivery. Affects the suprascaular nerve, musculocutaneous nerve and axillary nerve.

185
Q

What classic sign will Erb-Duchenna paralysis present with?

A

Waiter’s tip:
Affected arm is held by the side and rotated medially. Elbow is extended with a pronated forearm and flexed wrist on the affected side.

186
Q

Elhers-Danlos syndrome is a risk factor for which type of brain haemorrhage?

A

Sub-arachnoid

187
Q

What does relative afferent pupillary defect indicate?

A

An optic nerve lesion or severe retinal disease

188
Q

How long are you not allowed to drive (a car or motorcycle) for following a one-off seizure that was found to have no underlying structural or EEG abnormalities?

A

6 months

189
Q

A patient with epilepsy wants to know if they can apply for a driving licence - how long will they have to have been seizure free for in order to qualify?

A

12 months

190
Q

A patient with long standing epilepsy is trying to conceive, they are still taking their AED, what medication changes need to be advised?

A

Add 5mg of folic acid

191
Q

5 features associated with narcolepsy:

A
  1. Onset in teenage years
  2. Hypersomnolence
  3. Cataplexy (sudden loss of muscle tone often triggered by emotion)
  4. Sleep paralysis
  5. Vivid hallucinations on going to sleep or waking
192
Q

What is the gold standard investigation for narcolepsy?

A

Multiple sleep latency EEG

193
Q

How do you manage narcolepsy?

A

Daytime stimulant: modafinil

Nightime: sodium oxybate

194
Q

What are 5-HT3 antagonists? Where in the brain do they act?

A

Antiemetics used in the management of chemo related nausea

Act on the medulla oblongata

195
Q

Lip smacking and post-ictal dysphagia are localising features of a seizure in which lobe of the brain?
Give two other common features of seizures of this type:

A

temporal lobe

hallucinations
amnesia/deja-vu sensations

196
Q

What is autonomic dysreflexia?

A

A clinical syndrome that occurs in patients who have had a spinal injury at or above T6

197
Q

Features of autonomic dysreflexia: (4)

A
  1. Extreme hypertension
  2. Flushing and sweating above level of cord lesion
  3. Agitation
  4. Haemorrhagic stroke if untreated
198
Q

Triggers for autonomic dysreflexia:

A

Faecal impaction or urinary retention

199
Q

What drug might be useful in managing tremor in drug-induced parkinsonism?

A

Procyclidine

200
Q

Cabergoline has been associated with which condition?

A

pulmonary fibrosis

3a (8 decks)

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