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Phase 3a medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Cluster headache pain/symptoms

A

Unilateral excruciating pain centred over one eye lasting a few minutes, ptosis/miosis/runny nose/vomiting

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2
Q

What is Temporal Arteritis?

A

Granulomatous inflammation of the temporal arteries

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3
Q

Temporal Arteritis pain/symptoms

A

Scalp pain, jaw and tongue claudication

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4
Q

Tension headache pain/symptoms

A

Constant band-like pressure

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5
Q

Causes of Tension headache

A

Stress, fumes, depression, sleep deprivation, medication overdose

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6
Q

Cluster headache treatment

A

Triptans, high flow oxygen, sodium valproate, beta-blocker prophylaxis, avoid alcohol

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7
Q

Temporal Arteritis treatment

A

Prednisolone 60mg, temporal artery biopsy, raise ESR>50

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8
Q

Tension headache treatment

A

Ibuprofen, Aspirin, Amitriptyline, avoid triggers

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9
Q

Migraine pathophysiology

A

Intracranial vasoconstriction, meningeal and extra cranial vasodilation mediated by bradykinin and 5-HT

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10
Q

Migraine triggers

A

Cheese, alcohol, chocolate, hormones, salt, caffeine, stress, bright lights, loud sounds, lack of sleep

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11
Q

Name 3 Migraine differentials

A

Meningoencephalitis, idiopathic intracranial hypertension, SAH, SOL, Temporal arteritis, stroke/TIA

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12
Q

Migraine medical management (Acute vs Prophylaxis)

A

Acute

  • NSAIDs (Ibuprofen)
  • Paracetamol
  • Codeine
  • Antiemetics (eg. metoclopramide)
  • Triptans (eg. Sumatriptan) can act on: smooth muscle in arteries to cause vasoconstriction / Peripheral pain receptors to inhibit activation of pain receptors / Reduce neuronal activity in the central nervous system

Prophylaxis

  • B-blockers
  • Amitriptyline
  • Topiramate (this is teratogenic and can cause a cleft lip/palate so patients should not get pregnant)
  • Valproate

(Acupuncture and Vit B2

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13
Q

Migraine investigations

A

CT/MRI/LP (exclude other causes)

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14
Q

Migraine presentation

A

Pulsing headache with/without aura lasting 4-72 hours

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15
Q

Trigeminal Neuralgia presentation

A

Electric shock-type pain lasting up to 2 minutes, dull ache afterwards (may be triggered by touching skin supplied by nerve distribution)

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16
Q

Trigeminal Neuralgia management (1 drug, 2 operations)

A

Carbamazepine/surgical decompression/glycerol injection/radiofrequency lesioning/balloon compression

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17
Q

Thrombotic Stroke acute Mx

A

Alteplase (within 4.5hrs) + Thrombectomy (within 6 hrs if proximal anterior) + 300mg Aspirin and 75mg Clopidogrel for 2 weeks

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18
Q

Haemorrhagic Stroke acute Mx

A

Stop anticoagulants/antiplatelets + correct coagulation problems

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19
Q

6 Investigations for Stroke

A

CT(exclude haemorrhage)/MRI(Dx)/Carotid doppler(stenosis?)/Ca2+/U+E/LFTs/FBC/Creatinine/TFTs/Cholesterol/Clotting/BM

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20
Q

TIA definition (+ how long?)

A

Sudden onset global neurological deficit lasting <24 hours with complete clinical recovery

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21
Q

TIA management (drugs)

A

300mg Aspirin, 40mg Simvastatin

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22
Q

Epilepsy definition

A

Recurrent tendency to have spontaneous, intermittent and abnormal electrical activity in a part of the brain or generalised across the brain, leading to seizures

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23
Q

Temporal seizure presentation

A

Smell/taste abnormality, auditory phenomena, automatism, lip smacking, memory phenomena, deja-vu

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24
Q

Frontal seizure presentation

A

Motor phenomena (Jacksonian march -spreading clonic movements)

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25
Q

Occipital seizure presentation

A

Visual phenomena, occulomotor (eye closure/eyelid fluttering, nystagmus)

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26
Q

Parietal seizure presentation

A

Sensory disturbances (tingling/numbness)

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27
Q

Absence seizure Presentation + Management

A
  • Typically in children
  • TLoC (<10s, abrupt onset +termination)
  • patient becomes blank, stares into space and then abruptly returns to normal
  • Typically only lasts 10-20 seconds.
  • Most patients stop having absence seizures as they get older.

Management is:
- First line: sodium valproate or ethosuximide

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28
Q

Myoclonic seizure presentation + management

A
  • sudden, brief jerking/muscle contractions in limb/face/trunk, like a sudden ‘jump’
  • patient usually remains awake during the episode
  • typically happen in children as part of juvenile myoclonic epilepsy

Management is:

  • First line: sodium valproate
  • Other options: lamotrigine, levetiracetam or topiramate
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29
Q

Tonic seizure presentation

A

Sudden stiffness or tension in arms/legs/trunk

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30
Q

Generalised tonic-clonic seizure presentation + Management

A
  • Tonic phase (LoC + tensing/stiffness in limbs)
  • Clonic phase (rhythmical jerking of limbs)
  • There may be associated tongue biting, incontinence, groaning and irregular breathing.
    (there is a post-ictal period after the seizure where the person is confused, drowsy and feels irritable or depressed)

Management of tonic-clonic seizures is with:

  • First line: sodium valproate
  • Second line: lamotrigine or carbamazepine
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31
Q

Atonic seizure presentation + management

A
  • also known as “drop attacks”
  • Sudden loss of muscles tone (eg. fall/drop of hand or foot)
  • don’t usually last more than 3 minutes
  • typically begin in childhood
  • may be indicative of Lennox-Gastaut syndrome.
    Management is:
  • First line: sodium valproate
  • Second line: lamotrigine
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32
Q

where do pyramidal tracts originate and what are they responsible for?

A

Cerebral cortex and voluntary movements

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33
Q

where do extrapyramidal tracts originate and what are they responsible for?

A

Brain stem and involuntary movements

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34
Q

What are the differences between pyramidal and extrapyramidal tracts and what are they responsible for?

A

Pyramidal origin at cerebral cortex, responsible for voluntary movements
Extrapyramidal origin at brain stem, responsible for involuntary movements

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35
Q

Where does the lateral corticospinal tract decussate

A

Medulla

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36
Q

Name the 4 extrapyramidal tracts

A

Rubrospinal, Reticulospinal, Olivospinal, Vestibulospinal

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37
Q

median nerve entrapment causes what?

A

Carpal Tunnel Syndrome

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38
Q

Which nerve is responsible for Carpal Tunnel Syndrome

A

Median nerve entrapment

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39
Q

Typical Charcot-Marie Tooth features?

A

distal limb muscle wasting and sensory loss, with proximal progression over time slowly
(weakness of feet+ankles, bilateral foot drop, per cavus, atrophy of hand muscles)

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40
Q

a disorder of neuromuscular transmission, resulting from binding of autoantibodies to components of the neuromuscular junction, most commonly the acetylcholine receptor

A

Myasthenia Gravis

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41
Q

Name 2 investigations for MG

A

AChR antibodies, EMG, CT thorax, Tension test

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42
Q

Name a form of management for MG

A
  • Acetylcholinesterase inhibitors (Pyridostigmine)
  • Steroids (Prednisolone)
  • Immunosuppression (Azathioprine)
  • Thymectomy

Emergency:

  • O2
  • IVIg
  • Plasmapheresis
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43
Q

a disorder causing demyelination and axonal degeneration resulting in acute, ascending and progressive neuropathy, characterised by weakness, paraesthesiae and hyporeflexia

A

Guillain-Barré Syndrome

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44
Q

What is the inheritance pattern of Duchenne muscular dystrophy?

A

X-linked recessive

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45
Q

Name a feature of Guillain-Barré syndrome

A

ascending pattern of progressive symmetrical weakness, starting in the lower extremities; Neuropathic leg/back pain; Reduced or absent reflexes; Paraesthesia/Sensory loss; autonomic symptoms (reduced sweating/urinary hesitancy)

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46
Q

An inherited disorder characterised by progressive muscle wasting and weakness

A

Duchenne Muscular Dystrophy

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47
Q

Name an investigation for a suspected muscle disorder (DMD/FSHD)

A

CK, EMG, ESR/CRP

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48
Q

clinical manifestation of abnormal and excessive discharge of cerebral neurones

A

Epileptic seizures

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49
Q

Transient global hypoperfusion

A

Syncope

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50
Q

Name a common and an uncommon cause of coma

A

Common: Drugs/toxins, anoxia, mass lesions, infection, infarct, metabolic, SAH
Uncommon: venous sinus occlusion, hypothermia, fat embolism

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51
Q

Status epilepticus is persistent seizure activity for how long?

A

30 mins or more

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52
Q

Myotome, Dermatome and Reflex for:

C5+6, C7, C8+T1, L5, S1

A

C5+6 - Elbow flexion, Thumb, Biceps
C7 - Elbow extension, Middle finger, Triceps
C8+T1 - Hand, Forearm (no reflex)
L5 - dorsiflexion, big toe (no reflex)
S1 - plantar flexion, little toe/sole/heel, ankle jerk

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53
Q

Does the deficit present on the same or opposite side of a cerebellar lesion?

A

Same

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54
Q

Total CSF volume?

A

120ml

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55
Q

Discrete plaques of demyelination disseminated in time and space causes what condition?

A

Multiple Sclerosis

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56
Q

Name 3 types of motor neurone disease

A
  • Amyotrophic Lateral Sclerosis (ALS)
  • Progressive Muscular Atrophy (LMN signs)
  • Progressive Bulbar + Pseudobulbar palsy (LMN signs)
  • Primary Lateral Sclerosis (UMN signs)
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57
Q

Clinical syndrome consisting of rapidly developing focal disturbance of cerebral function lasting >24 hours or leading to death

A

Stroke

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58
Q

What are symptoms of a stroke in carotid artery vs posterior circulation

A

carotid artery - weakness of face, leg, arm / impaired language / amaurosis fugax
posterior circulation - dysarthria / dysphagia / diplopia / dizziness / diplegia / ataxia

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59
Q

What is the most common type of stroke?

A

Ischaemic (85%)

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60
Q

What is the cause of Subarachnoid Haemorrhage?

A

Cerebral aneurysm

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61
Q

Upper motor neurone signs

A

Hyperreflexia, muscle weakness, lack of coordination with movements, poor balance, positive babinski sign

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62
Q

Lower motor neurone signs

A

Hyporeflexia, Fasciculations, Flaccid paralysis, muscular atrophy, negative babinski sign

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63
Q

What is the most common heart lesion associated with Duchenne muscular dystrophy?

A

dilated cardiomyopathy

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64
Q

By what age do children typically stop having Febrile Convulsions?

A

5 years old

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65
Q

What is a Febrile Seizure/Convulsion? (+ how old?)

A

A febrile seizure can be defined as a seizure accompanied by fever (temperature higher than 38°C by any method), without central nervous system infection, which occurs in infants and children aged 6 months to 5 years.

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66
Q

Wernicke’s vs Korsakoff’s encephalopathy?

A

Wernicke’s encephalopathy represents the “acute” phase of the disorder and Korsakoff’s amnesic syndrome represents the disorder progressing to a “chronic” or long-lasting stage.

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67
Q

How might Wernicke-Korsakoff Syndrome present?

A

Features of Wernicke’s:

  • Confusion
  • Oculomotor disturbances (disturbances of eye movements, diplopia, ptosis)
  • Ataxia (difficulties with coordinated movements)

Features of Korsakoffs syndrome

  • Memory impairment (retrograde and anterograde)
  • Behavioural changes
  • Psychosis - Hallucinations.
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68
Q

At least two of the four following criteria should be present to diagnose encephalopathy

A
  • Dietary deficiencies.
  • Oculomotor abnormalities.
  • Cerebellar dysfunction.
  • Either an altered mental state or mild memory impairment.
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69
Q

What is the pharmacological treatment for Wernicke’s-Korsakoff’s syndrome?

A

Thiamine orally (IM or IV may be used in secondary care) plus vitamin B complex or multivitamins, which should be given indefinitely

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70
Q

Stroke by site of lesion (ant, mid, post, ant+post cerebellar…)

A
  • Anterior cerebral artery => Contralateral hemiparesis and sensory loss, lower extremity > upper
  • Middle cerebral artery => Contralateral hemiparesis and sensory loss, upper extremity > lower
    (Contralateral homonymous hemianopia and Aphasia)
  • Posterior cerebral artery => Contralateral homonymous hemianopia with macular sparing
    (Visual agnosia)
  • Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain) => Ipsilateral CN III palsy
    (Contralateral weakness of upper and lower extremity)
  • Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome) => Ipsilateral: facial pain and temperature loss
    (Contralateral: limb/torso pain and temperature loss
    Ataxia, nystagmus)
  • Anterior inferior cerebellar artery (lateral pontine syndrome) => Symptoms are similar to Wallenberg’s (see above), but: Ipsilateral: facial paralysis and deafness
  • Retinal/ophthalmic artery => Amaurosis fugax
  • Basilar artery => ‘Locked-in’ syndrome
  • Lacunar strokes
    present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
    strong association with hypertension
    common sites include the basal ganglia, thalamus and internal capsule
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71
Q

What is a crescendo TIA? (/how many?)

A

A crescendo TIA is where there are two or more TIAs within a week. This carries a high risk of developing in to a stroke.

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72
Q

Stroke features + risk factors

A

Stoke symptoms are typically asymmetrical:

  • Sudden weakness of limbs
  • Sudden facial weakness
  • Sudden onset dysphasia (speech disturbance)
  • Sudden onset visual or sensory loss

Risk Factors

  • Cardiovascular disease such as angina / MI
  • Previous stroke or TIA
  • Atrial fibrillation
  • Carotid artery disease
  • Hypertension
  • Diabetes
  • Smoking
  • Vasculitis
  • Thrombophilia
  • Combined contraceptive pill
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73
Q

Management of Stroke vs TIA

A

Management of Stroke

  • Admit patients to a specialist stroke centre
  • Exclude hypoglycaemia
  • Immediate CT brain to exclude primary intracerebral haemorrhage
  • Aspirin 300mg stat (after the CT) and continue for 2 weeks
  • Thrombolysis with Alteplase (tissue plasminogen activator that rapidly breaks down clots and can reverse the effects of a stroke ) can be used after the CT brain scan has excluded an intracranial haemorrhage.
  • Thrombectomy (mechanical removal of the clot) may be offered if an occlusion is confirmed, depending on the location and the time since the symptoms started.
    (It is not used after 24 hours since the onset of symptoms)

Management of TIA

  • Start aspirin 300mg daily. Start secondary prevention measures for cardiovascular disease. They should be referred and seen within 24 hours by a stroke specialist.
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74
Q

What is the gold standard imaging technique for stroke?

A
  • Diffusion-weighted MRI is the gold standard imaging technique (CT is an alternative)
  • Carotid ultrasound can be used to assess for carotid stenosis. Endarterectomy to remove plaques or carotid stenting to widen the lumen should be considered if there is carotid stenosis.
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75
Q

Secondary prevention of Stroke

A
  • Clopidogrel 75mg once daily (alternatively dipyridamole 200mg twice daily)
  • Atorvastatin 80mg should be started but not immediately
  • Carotid endarterectomy or stenting in patients with carotid artery disease
  • Treat modifiable risk factors such as hypertension and diabetes
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76
Q

Layers of meninges from brain to skull

A

Brain > Pia mater > Subarachnoid space > Arachnoid mater > Dura mater > Skull

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77
Q

Glasgow coma scale (Eyes, Verbal, Motor)

A

Eyes

  • Spontaneous = 4
  • Speech = 3
  • Pain = 2
  • None = 1

Verbal response

  • Orientated = 5
  • Confused conversation = 4
  • Inappropriate words = 3
  • Incomprehensible sounds = 2
  • None = 1

Motor response

  • Obeys commands = 6
  • Localises pain = 5
  • Normal flexion (flexion to withdraw from pain) = 4
  • Abnormal flexion = 3
  • Extends = 2
  • None = 1
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78
Q

When someone has a GCS score of what or below then you need to consider securing their airway as there is a risk they are not able to maintain it on their own?

A

8/15 or below

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79
Q

Subdural haemorrhage occurs between which layers?

+ do they cross sutures?

A

Dura mater and subarachnoid mater

+ cross over sutures

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80
Q

Extradural haemorrhage occurs between which layers?
(+ usually rupture of which artery?)
(+ do they cross sutures?)

A

Between skull + Dura mater
(+ rupture of the middle meningeal artery in the temporo-parietal region. It can be associated with a fracture of the temporal bone)
(+ do not cross sutures)

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81
Q

Subarachnoid haemorrhage occurs between which layers?

A

Between pia mater and arachnoid membrane

usually the result of a ruptured cerebral aneurysm

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82
Q

First line investigation for SAH (+ others?)

A

First-line = CT head

  • If CT head is negative, Lumbar Puncture is used to collect a sample of the CSF: Red cell count will be raised + Xanthochromia (the yellow colour of CSF caused by bilirubin)
  • Angiography (CT or MRI) can be used once a subarachnoid haemorrhage is confirmed to locate the source of the bleeding.
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83
Q

Surgical + Medical interventions for an aneurysm (eg SAH)?

A
  • Coiling involves inserting a catheter into the arterial system (taking an “endovascular approach”), placing platinum coils into the aneurysm and sealing it off from the artery.
  • An alternative is clipping, which involves cranial surgery and putting a clip on the aneurysm to seal it.
  • Nimodipine is a calcium channel blocker that is used to prevent vasospasm.
  • Lumbar puncture or insertion of a shunt may be required to treat hydrocephalus.
  • Antiepileptic medications can be used to treat seizures.
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84
Q

MS is more common in what age / sex?

A
  • MS typically presents in young adults (under 50 years) and is more common in women.

(Symptoms tend to improve in pregnancy and in the postpartum period)

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85
Q

Multiple sclerosis typically only affects the central nervous system

Which cells wrap around axons to provide myelin sheath?

A

the oligodendrocytes - CNS

Schwann cells in PNS

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86
Q

The key expression to remember to describe the way MS lesions change location over time?

A

“disseminated in time and space”

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87
Q

Signs/Symptoms of MS

A

Symptoms usually progress over more than 24 hours. At first presentation, symptoms tend to last days to weeks and then improve. There are a number of ways MS can present. These are described below.

  • Optic neuritis
    Most common presentation of multiple sclerosis - demyelination of the optic nerve and loss of vision in one eye
  • Eye movement abnormalities
    Double vision due to lesions with the sixth CN (abducens nerve). Describing a sixth CN palsy: internuclear ophthalmoplegia and conjugate lateral gaze disorder
    (Internuclear ophthalmoplegia due to unilateral lesions in the sixth nerve. Internuclear nerve fibres coordinate eye movements to ensure eyes move together + Ophthalmoplegia means a problem with the muscles around the eye)
    (Conjugate Lateral Gaze Disorder due to lesions in the sixth cranial nerve. Conjugate means connected. Lateral gaze is where both eyes move together to look laterally. When looking laterally, the affected eye will not be able to abduct. For example, when looking to the left in an affected left eye, the right eye will adduct (move towards the nose) and the left eye will remain in the middle as the muscle responsible for making it move laterally is not functioning)
  • Focal weakness
    (Bells palsy, Horners syndrome, Limb paralysis, Incontinence)
  • Focal sensory symptoms
    (Trigeminal neuralgia, Numbness, Paraesthesia, Lhermitte’s sign)
  • Ataxia
    (Sensory ataxia is the result of loss of the proprioceptive sense, which is the ability to sense the position of the joint (e.g. is the joint flexed or extended). Leads to positive Romberg’s test and can cause pseudoathetosis)
    (Cerebellar ataxia is the result of problems with the cerebellum coordinating movement)
88
Q

What is Lhermitte’s sign?

A

Lhermitte’s sign is an electric shock sensation that travels down the spine and into the limbs when flexing the neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column (MS!)

89
Q

Name a disease pattern of MS

A

Clinically isolated syndrome, Relapsing-remitting, Primary Progressive, Secondary Progressive

90
Q

Features of Optic Neuritis in MS

A
  • Central scotoma (enlarged blind spot)
  • Pain on eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect
91
Q

Symptoms have to be progressive over a period of how long to diagnose primary progressive MS?

A

1 year

92
Q

MS Management (Relapses + Symptomatic Tx)

A
  • Disease-modifying with Interleukins, cytokines, immune cells
  • Relapse Tx: Methylprednisolone 500mg OD
  • Symptomatic Tx:
    (Exercise, Amitriptyline or Gabapentin for neuropathic pain, SSRIs for depression,baclofen, gabapentin and physiotherapy for spasticity, anticholinergic medications such as Tolterodine or Oxybutynin for urge incontinence (although these can cause or worsen cognitive impairment!)
93
Q

Are there any sensory symptoms in MND?

A

No

94
Q

Can MND be inherited?

A

Yes (around 5-10% of cases are inherited)

95
Q

Does MND affect upper or lower motor neurones?

What are the Signs/Symptoms?

A

Both
Signs of lower motor neurone disease:
- Muscle wasting
- Reduced tone
- Fasciculations (twitches in the muscles)
- Reduced reflexes
(Can often present with weakness and dysarthria

Signs of upper motor neurone disease:

  • Increased tone or spasticity
  • Brisk reflexes
  • Upgoing plantar responses
96
Q

MS management (Medications to slow progression / Support)

A
  • Riluzole slows progression and extends survival by a few months in ALS
  • Edaravone is used in US but not UK and has potential to slow the progression of the disease.
  • Non-invasive ventilation (NIV) used at home to support breathing at night improves survival and quality of life.

Support:

  • Effectively breaking bad news
  • Involving the MDT in supporting and maintaining their quality of life
  • Advanced directives to document the patient’s wishes as the disease progresses
  • End of life care planning
  • Patients usually die of respiratory failure or pneumonia
97
Q

Parkinson’s disease involves progressive reduction of what chemical where in the brain?

A

dopamine in the basal ganglia (substantial nigra)

98
Q

Triad of Parkinson’s (+ other symptoms)

A

Resting tremor
- ‘Pill-rolling’ unilateral tremor

Cogwheel rigidity
- Resistance to passive movement in increments

Bradykinesia

  • Handwriting smaller and smaller
  • “shuffling gait”
  • difficulty initiating movement (e.g. standing to walking)
  • difficulty turning around when standing
  • reduced facial movements and facial expressions (hypomimia)

Also:

  • Depression
  • Sleep disturbance and insomnia
  • Loss of the sense of smell (anosmia)
  • Postural instability
  • Cognitive impairment and memory problems
99
Q

Parkinson’s tremor vs Essential tremor

A

Parkinson’s Tremor

  • Asymmetrical
  • 4-6 Hz
  • Worse at rest
  • Improves with intentional movement
  • Other Parkinson’s features
  • No change with alcohol

Benign Essential Tremor

  • Symmetrical
  • 5-8 hertz
  • Improves at rest
  • Worse with intentional movement
  • No other Parkinson’s features
  • Improves with alcohol
100
Q

Name a Parkinson’s-plus syndrome

A
  • Multiple System Atrophy
    (rare) neurones of multiple systems in the brain degenerate leading to autonomic dysfunction (postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia).
  • Dementia with Lewy Bodies
    Dementia associated with features of Parkinsonism. Progressive cognitive decline with associated symptoms of visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness.

Others:

  • Progressive Supranuclear Palsy
  • Corticobasal Degeneration
101
Q

Management of Parkinson’s

A
  • Levodopa
    Oral synthetic dopamine usually combined with a drug that stops levodopa being broken down in the body before it gets the chance to enter the brain (peripheral decarboxylase inhibitors) - Carbidopa and Benserazide.
    Combination drugs = Co-benyldopa (levodopa and benserazide) or Co-careldopa (levodopa and carbidopa)
    (Too much causes dyskinesia like chorea or dystonia)
  • COMT Inhibitors
    Inhibitors of catechol-o-methyltransferase (COMT) enzyme, which metabolises levodopa in both the body and brain. Entacapone is taken with levodopa (and a decarboxylase inhibitor) to slow breakdown of the levodopa in the brain.
  • Dopamine Agonists
    Mimic dopamine and stimulate dopamine receptors. Less effective than levodopa. Usually used to delay the use of levodopa and are used in combination reduce the dose of levodopa that is required to control symptoms. One notable side effect with prolonged use is pulmonary fibrosis.
    Examples are: Bromocryptine, Pergolide, Carbergoline
  • Monoamine Oxidase-B Inhibitors
    Monoamine oxidase breaks down neurotransmitters such as dopamine, serotonin and adrenaline. These medications block this enzyme and help increase circulating dopamine. They are also used to delay the use of levodopa and then in combination with levodopa to reduce the required dose. Examples are: Selegiline and Rasagiline
102
Q

What is a common side effect of a high levodopa dose

A

Dyskinesias - abnormal movements associated with excessive motor activity.

Examples are:

  • Dystonia: This is where excessive muscle contraction leads to abnormal postures or exaggerated movements.
  • Chorea: These are abnormal involuntary movements that can be jerking and random.
  • Athetosis: These are involuntary twisting or writhing movements usually in the fingers, hands or feet.
103
Q

What is one notable side effect with prolonged use of Dopamine Agonists (Carbergoline)?

A

pulmonary fibrosis.

104
Q

Benign essential tremor features

A
  • Fine tremor
    (most notable in the hands but affects other areas like head tremor, jaw tremor and vocal tremor)
  • Symmetrical
  • More prominent on voluntary movement
  • Worse when tired, stressed or after caffeine
  • Improved by alcohol
  • Absent during sleep
105
Q

2 medications that can improve symptoms of benign essential tremor?

A
  • Propranolol (a non-selective beta blocker)

- Primidone (a barbiturate anti-epileptic medication)

106
Q

2 investigations for Epilepsy

A

EEG + MRI brain

107
Q

Focal seizure Presentation + Management

A

Focal seizures start in temporal lobes.

  • affect hearing, speech, memory and emotions
  • Hallucinations
  • Memory flashbacks
  • Déjà vu
  • Doing strange things on autopilot

Management is the reverse of tonic-clonic seizures:

  • First line: carbamazepine or lamotrigine
  • Second line: sodium valproate or levetiracetam
108
Q

Infantile spasms are also know by what name?

A

West Syndrome

109
Q

Infantile spasms presentation and management

A
  • starting in infancy at around 6 months of age
  • characterised by clusters of full body spasms
  • poor prognosis: 1/3 die by age 25, however 1/3 are seizure free.

First line treatments are:

  • Prednisolone
  • Vigabatrin
110
Q

Name some Epilepsy maintenance medications

+ side effects?

A
  • Sodium Valproate
    First line option for most forms of epilepsy (except focal seizures). Increases activity of GABA, which has a relaxing effect on the brain.
    (Side effects: Teratogenic so patients need careful advice about contraception, Liver damage and hepatitis, Hair loss, Tremor)
    (It must be avoided in girls or women unless there are no suitable alternatives and strict criteria are met to ensure they do not get pregnant)
  • Carbamazepine
    First line for focal seizures.
    (Side effects are: Agranulocytosis, Aplastic anaemia, Induces the P450 system so there are many drug interactions)
  • Phenytoin
    Side effects: Folate and vitamin D deficiency, Megaloblastic anaemia (folate deficiency), Osteomalacia (vitamin D deficiency)
  • Ethosuximide
    Side effects: Night terrors + Rashes
  • Lamotrigine
    Notable side effects:
    Stevens-Johnson syndrome or DRESS syndrome (These are life threatening skin rashes) Leukopenia
111
Q

Name a side effect of Sodium Valproate

A
  • Teratogenic so patients need careful advice about contraception
  • Liver damage and hepatitis
  • Hair loss
  • Tremor
112
Q

Status Epilepticus is defined as seizures lasting more than how long? (Or how many?)

A

5 minutes or more than 3 seizures in one hour.

113
Q

Status Epilepticus Management

A

ABCDE

  • Secure the airway
  • High-concentration oxygen
  • Assess cardiac and respiratory function
  • Check blood glucose levels
  • Gain intravenous access (insert a cannula)
  • IV lorazepam 4mg, repeated after 10 minutes if the seizure continues
  • If seizures persist: IV phenobarbital or phenytoin

Medical options in the community:

  • Buccal midazolam
  • Rectal diazepam
114
Q

What does neuropathic pain feel like?

A
  • Burning
  • Tingling
  • Pins and needles
  • Electric shocks
  • Loss of sensation to touch of the affected area
115
Q

What questionnaire assesses characteristics of neuropathic pain?

A

DN4 Questionnaire - A score of 4 or more indicates neuropathic pain.

116
Q

What are the 4 first line treatments for neuropathic pain?

A
  • Amitriptyline is a tricyclic antidepressant
  • Duloxetine is an SNRI antidepressant
  • Gabapentin is an anticonvulsant
  • Pregabalin is an anticonvulsant
117
Q

Features of Complex Regional Pain Syndrome

A
  • Neuropathic pain
  • Colour change
  • Skin flushing
  • Temperature change
  • Swelling
  • Abnormal sweating
  • Abnormal hair growth
118
Q

Where does the facial nerve exit the brainstem?

+ what does it go through before it splits into 5 main divisions?

A

Cerebellopontine angle

(passes through the temporal bone and parotid gland)

It then divides into five branches that supply different areas of the face:

  • Temporal
  • Zygomatic
  • Buccal
  • Marginal mandibular
  • Cervical
119
Q

Motor, Sensory and Parasympathetic functions of facial nerve

A
  • Motor: Supplies muscles of facial expression, the stapedius and the posterior digastric, stylohyoid and platysma muscles in the neck.
  • Sensory: carries taste from the anterior 2/3 of the tongue.
  • Parasympathetic: it provides parasympathetic supply to submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production).
120
Q

Upper vs lower motor neurone facial nerve lesion

A

Upper:

  • new onset upper motor neurone facial nerve palsy should be referred urgently with a suspected stroke.
  • Each side of the forehead has upper motor neurone innervation by both sides of the brain
  • Forehead will be spared and the patient can move their forehead on the affected side

Lower:

  • Pt can be reassured and managed in the community.
  • Each side of the forehead only has lower motor neurone innervation from one side of the brain.
  • the forehead will NOT be spared and the patient cannot move their forehead on the affected side.
  • Drooping of eyelid, exposing eye
  • Loss of nasolabial fold
121
Q

What conditions would cause unilateral vs bilateral upper motor neurone facial nerve lesions?

A

Unilateral upper motor lesions occur in:

  • Cerebrovascular accidents (strokes)
  • Tumours

Bilateral upper motor neurone lesions are rare. They may occur in:

  • Pseudobulbar palsies
  • Motor neurone disease
122
Q

Bell’s palsy is the result of damage to which cranial nerve?

A

7th - Facial nerve

123
Q

Is Bell’s palsy uni- or bilateral and upper or lower motor neurone?

A

Unilateral lower motor neurone

124
Q

What can be prescribed how soon after developing symptoms of Bell’s palsy?
(+ treatment for a dry eye in Bell’s palsy?)

A

Prednisolone within 72 hours of developing symptoms

(also require lubricating eye drops to prevent the eye on the affected drying out and being damaged. If they develop pain in the eye they need an ophthalmology review for exposure keratopathy)

125
Q

Ramsay-Hunt Syndrome is caused by what virus?
(+ what rash?)
(+ what treatment?)

A
  • Varicella zoster virus
  • vesicular rash in the ear canal, pinna and around the ear on the affected side (can extend to the anterior 2/3 of the tongue and hard palate)
  • Treatment should be initiated within 72 hours with:
    Prednisolone / Aciclovir (Also lubricating eyedrops)
126
Q

Name a condition that causes a lower motor neurone facial nerve palsy

A 
- Infection:
Otitis media
Malignant otitis externa
HIV
Lyme’s disease
 - Systemic disease:
Diabetes
Sarcoidosis
Leukaemia
Multiple sclerosis
Guillain–Barré syndrome
  • Tumours:
    Acoustic neuroma
    Parotid tumours
    Cholesteatomas
  • Trauma:
    Direct nerve trauma
    Damage during surgery
    Base of skull fractures
127
Q

Raised ICP (brain tumour?) features

A

Headache:

  • Constant
  • Nocturnal
  • Worse on waking
  • Worse on coughing, straining or bending forward
  • Vomiting

Other features of raised intracranial pressure may be:

  • Altered mental state
  • Visual field defects
  • Seizures (particularly focal)
  • Unilateral ptosis
  • Third and sixth nerve palsies
  • Papilloedema (on fundoscopy)

(Papilloedema is a key finding on fundoscopy!)

128
Q

Fundoscopy changes due to Papilloedema

A
  • Blurring of the optic disc margin
  • Elevated optic disc (look for the way the retinal vessels flow across the disc to see the elevation)
  • Loss of venous pulsation
  • Engorged retinal veins
  • Haemorrhages around optic disc
  • Paton’s lines which are creases in the retina around the optic disc

(Vessels are able to flow straight across a flat surface, whereas they will curve over a raised disc)

129
Q

Name a type of brain tumour

A

Glioma / Meningioma / Acoustic Neuroma / Pituitary tumour…

130
Q

Where are Gliomas found and what are the three types?

A

In glial cells in the brain or spinal cord

  • Astrocytoma (glioblastoma multiforme is the most common)
  • Oligodendroglioma
  • Ependymoma
131
Q

Are meningiomas usually benign or malignant?

A

Benign

132
Q

What visual defect does pituitary tumour cause?

A

Bitemporal hemianopia

133
Q

Where are Acoustic Neuromas found and what are the classic symptoms?

A
  • Tumours of Schwann cells surrounding the auditory nerve that innervates the inner ear.
  • They occur around the “cerebellopontine angle”
    (sometimes called cerebellopontine angle tumours)
  • Slow-growing but eventually grow large enough to produce symptoms and become dangerous.
  • usually unilateral
    (Bilateral acoustic neuromas are associated with neurofibromatosis type 2)

Classic symptoms of an acoustic neuroma are:
- Hearing loss
- Tinnitus
- Balance problems
(associated with a facial nerve palsy too)

134
Q

Treatment of pituitary tumours

A
  • Trans-sphenoidal surgery
  • Radiotherapy
  • Bromocriptine to block prolactin-secreting tumours
  • Somatostatin analogues (e.g. ocreotide) to block growth hormone-secreting tumours
135
Q

At what age do symptoms present in Huntington’s?

A

usually 30 to 50 years old

136
Q

Huntington’s chorea is what type of disorder genetically?

A

“trinucleotide repeat disorder”

137
Q

Features of Anticipation

A

successive generations have more repeats in the gene, resulting in:
- Earlier age of onset
- Increased severity of disease
(Huntington’s!)

138
Q

Features of Huntington’s Disease

A
  • Huntington’s chorea usually presents with insidious, progressive worsening of symptoms.
  • Begins with cognitive, psychiatric or mood problems
  • Followed by the development of movement disorders.
  • Chorea (involuntary, abnormal movements)
  • Eye movement disorders
  • Speech difficulties (dysarthria)
  • Swallowing difficulties (dysphagia)
139
Q

Life expectancy after onset of symptoms in Huntington’s?

A

Life expectancy is around 15-20 years after the onset of symptoms

140
Q

Medications that can suppress disordered movement in Huntington’s?

A
  • Antipsychotics (e.g. olanzapine)
  • Benzodiazepines (e.g. diazepam)
  • Dopamine-depleting agents (e.g. tetrabenazine)
141
Q

There is a strong link between MG and what type of tumour?

A

Thymoma

10-20% of patients with myasthenia gravis have a thymoma. 20-40% of patients with a thymoma develop myasthenia gravis

142
Q

Myasthenia gravis is caused by which antibodies in the neuromuscular junction?

A
  • Acetylcholine Receptor Antibodies
    (produced by the immune system - bind to the postsynaptic neuromuscular junction receptors preventing acetylcholine form stimulating the receptor and triggering muscle contraction)
    (AChR antibodies also activate the complement system in the NMJ, causing damage to cells at the postsynaptic membrane)

There are two other antibodies that cause the other 15% of MG:

  • antibodies against muscle-specific kinase (MuSK)
  • antibodies against low-density lipoprotein receptor-related protein 4 (LRP4)
143
Q

Features of Myasthenia Gravis

A
  • weakness that gets worse with muscle use and improves with rest.
  • Symptoms typically minimal in the morning and worst at the end of the day.
  • mostly affects proximal muscles and small muscles of the head and neck

It leads to:

  • Extraocular muscle weakness causing double vision (diplopia)
  • Eyelid weakness causing drooping of the eyelids (ptosis)
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
144
Q

Things to check on examination of MG patient

A
  • Repeated blinking will exacerbate ptosis
  • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
  • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
  • Check for a thymectomy scar.
  • Test the forced vital capacity (FVC).
145
Q

Diagnosis of Myasthenia Gravis

A
  • Acetylcholine receptor (ACh-R) antibodies (85% of patients)
  • Muscle-specific kinase (MuSK) antibodies (10% of patients)
  • LRP4 (low-density lipoprotein receptor-related protein 4) antibodies (less than 5%)
  • A CT or MRI of the thymus gland is used to look for a thymoma.
  • The edrophonium test can be helpful where there is doubt about the diagnosis.
    (Edrophonium blocks cholinesterase enzymes in NMJ from breaking down Acetylcholine => It briefly and temporarily relieves the weakness of MG, helping diagnosis)
146
Q

Management of Myasthenia Gravis

A
  • Reversible acetylcholinesterase inhibitors (pyridostigmine or neostigmine) increase how much acetylcholine is in the NMJ and improve symptoms
  • Immunosuppression (e.g. prednisolone or azathioprine) suppresses the production of antibodies
  • Thymectomy can improve symptoms even without thymoma
  • Monoclonal antibodies
    (eg. Rituximab targets B cells and reduces the production of antibodies)
    (+ Eculizumab targets complement protein C5, preventing complement activation and destruction of EACh receptors)
147
Q

Management of Myasthenia Crisis

A

Myasthenia crisis = Acute worsening of symptoms, often triggered by another illness such as a respiratory tract infection + can lead to respiratory failure as a result of weakness in the muscle of respiration.

  • Patients may require non-invasive ventilation with BiPAP or full intubation and ventilation.
  • Medical treatment = immunomodulatory therapies such as IV immunoglobulins and plasma exchange.
148
Q

Lambert-Eaton Syndrome typically occurs in patients with what malignancy?
(+ what is the first-line Tx?)

A
  • Small-Cell Lung Cancer
  • Amifampridine allows more acetylcholine to be released in NMJ synapses by blocking voltage-gated potassium channels in presynaptic cells, which in turn prolongs depolarisation of the cell membrane and assists calcium channels in carrying out their action
149
Q

What inheritance pattern is Charcot-Marie-Tooth?

A

Autosomal Dominant

150
Q

Symptoms of Charcot-Marie-Tooth usually start at what age?

A

before the age of 10 years but the onset of symptoms can be delayed until 40 or later.

151
Q

Features of Charcot-Marie-Tooth

A
  • High foot arches (pes cavus)
  • Distal muscle wasting causing “inverted champagne bottle legs”
  • Weakness in the lower legs, particularly loss of ankle dorsiflexion
  • Weakness in the hands
  • Reduced tendon reflexes
  • Reduced muscle tone
  • Peripheral sensory loss
152
Q

Causes of Peripheral Neuropathy (ABCDE mnemonic)

A 
A – Alcohol
B – B12 deficiency
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin)
E – Every vasculitis
153
Q

Guillan-Barré is associated with which organisms?

A

campylobacter jejuni, cytomegalovirus and Epstein-Barr virus

154
Q

Features of Guillan-Barré Syndrome

A
  • Symmetrical ascending weakness (starting at the feet and moving up the body)
  • Reduced reflexes
  • There may be peripheral loss of sensation or neuropathic pain
  • It may progress to the cranial nerves and cause facial nerve weakness
155
Q

Clinical course of Guillan-Barré syndrome

A
  • Symptoms usually start within 4 weeks of the preceding infection
  • Symptoms usually start in the feet and progresses upward
  • Symptoms peak within 2-4 weeks, then there is a recovery period that can last months to years.
156
Q

Diagnosis and management of Guillan-Barré Syndrome

A
  • Diagnosis is made clinically using the Brighton criteria.

Supported by:

  • Nerve conduction studies (reduced signal through the nerves)
  • Lumbar puncture for CSF (raised protein with a normal cell count and glucose)

Management:

  • IV immunoglobulins
  • Plasma exchange (alternative to IV IG)
  • Supportive care
  • VTE prophylaxis (pulmonary embolism is a leading cause of death)
  • In severe cases with respiratory failure, patients may need intubation, ventilation and admission to ICU.
157
Q

What criteria are used for diagnosis of GBS?

A

Brighton criteria

158
Q

What is the mortality rate in GBS

A

5%

159
Q

What chromosome is Neurofibromatosis type 1 gene found on?
What protein does it code for?
What pattern is inheritance of mutations of this gene?

A
  • chromosome 17
  • It codes for a protein called neurofibromin, which is a tumour suppressor protein.
  • Autosomal Dominant
160
Q

There must be at least 2 of the 7 Neurofibromatosis Type 1 features to indicate a diagnosis. You can remember this with the mnemonic CRABBING.

A

C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults
R – Relative with NF1
A – Axillary or inguinal freckles
BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris
N – Neurofibromas (2 or more) or 1 plexiform neurofibroma
G – Glioma of the optic nerve

161
Q

Complications of Neurofibromatosis Type 1

A
  • Migraines
  • Epilepsy
  • Renal artery stenosis causing hypertension
  • Learning and behavioural problems (e.g. ADHD)
  • Scoliosis of the spine
  • Vision loss (secondary to optic nerve gliomas)
  • Malignant peripheral nerve sheath tumours
  • Gastrointestinal stromal tumour (a type of sarcoma)
  • Brain tumours
  • Spinal cord tumours with associated neurology (e.g. paraplegia)
  • Increased risk of cancer (e.g. breast cancer)
  • Leukaemia
162
Q

What chromosome is Neurofibromatosis type 2 gene found on?
What protein does it code for?
What pattern is inheritance of mutations of this gene?

A
  • chromosome 22.
  • It codes for a protein called merlin, which is a tumour suppressor protein particularly important in Schwann cells. Mutations in this gene lead to the development of schwannomas (benign nerve sheath tumours of the Schwann cells).
  • Inheritance is autosomal dominant.
163
Q

Neurofibromatosis Type 2 is most associated with what malignancy?

A

Acoustic neuroma

164
Q

Bilateral acoustic neuromas almost certainly indicate diagnosis of which condition?

A

neurofibromatosis type 2

165
Q

What is the characteristic feature of Tuberous Sclerosis?

A

Formation of Hamartomas (benign neoplastic growths of tissue)

166
Q

Tuberous sclerosis is caused by mutations in which two genes?

A
  • TSC1 gene on chromosome 9, which codes for hamartin
  • TSC2 gene on chromosome 16, which codes for tuberin

(Hamartin and tuberin interact with each other to control the size and growth of cells. Abnormalities in one of these proteins leads to abnormal cell size and growth)

167
Q

Classic presentation of Tuberous Sclerosis

A

child presenting with epilepsy found to have skin features of tuberous sclerosis

(Ash leaf spot / Shagreen patches / Angiofibromas / Subungual fibromata / Cafe-au-lait spots / Poliosis)

168
Q

Skin signs and neurological features of Tuberous Sclerosis

A

Skin Signs:

  • Ash leaf spots (depigmented areas of skin shaped like an ash leaf)
  • Shagreen patches (thickened, dimpled, pigmented patches of skin)
  • Angiofibromas (small skin-coloured or pigmented papules on the nose and cheeks
  • Subungual fibromata (fibromas growing from the nail bed - usually circular painless lumps that grow slowly)
  • Cafe-au-lait spots are light brown “coffee and milk” coloured flat pigmented lesions on the skin
  • Poliosis is an isolated patch of white hair on the head, eyebrows, eyelashes or beard

Neurological Features:

  • Epilepsy
  • Learning disability and developmental delay

Other:

  • Rhabdomyomas in the heart
  • Gliomas (tumours of the brain and spinal cord)
  • Polycystic kidneys
  • Lymphangioleiomyomatosis (abnormal growth in smooth muscle cells, often affecting the lungs)
  • Retinal hamartomas
169
Q

Headache red flags

A
  • Fever, photophobia or neck stiffness (meningitis or encephalitis)
  • New neurological symptoms (haemorrhage, malignancy or stroke)
  • Dizziness (stroke)
  • Visual disturbance (temporal arteritis or glaucoma)
  • Sudden onset occipital headache (subarachnoid haemorrhage)
  • Worse on coughing or straining (raised intracranial pressure)
  • Postural, worse on standing, lying or bending over (raised intracranial pressure)
  • Severe enough to wake the patient from sleep
  • Vomiting (raised intracranial pressure or carbon monoxide poisoning)
  • History of trauma (intracranial haemorrhage)
  • Pregnancy (pre-eclampsia)
170
Q

What might cause a tension headache?

A
  • Stress
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
171
Q

Sinusitis features and management

A
  • Sinusitis = headache associated with inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses
  • Usually facial pain behind the nose, forehead and eyes
  • Tenderness over the affected sinus
  • Usually resolves within 2-3 weeks
  • Most sinusitis is viral
  • Nasal irrigation with saline can be helpful
  • Prolonged symptoms can be treated with steroid nasal spray.
  • Antibiotics are occasionally required.
172
Q

When might hormonal headaches related to low oestrogen occur in relation to menstrual period?
(+ what might improve symptoms?)

A
  • Two days before and first three days of the menstrual period
  • Around the menopause
  • Pregnancy (worst in first few weeks and improves in last 6 months)
    (Headaches in the second half of pregnancy should prompt investigation for pre-eclampsia)

The oral contraceptive pill can improve hormonal headaches.

173
Q

Typical Migraine headache symptoms (how long?)

A

Headaches last between 4 and 72 hours

  • Moderate to severe intensity
  • Pounding or throbbing in nature
  • Usually unilateral but can be bilateral
  • Discomfort with lights (photophobia)
  • Discomfort with loud noises (phonophobia)
  • With or without aura
  • Nausea and vomiting
174
Q

Types of aura in migraine

A
  • Sparks in vision
  • Blurring vision
  • Lines across vision
  • Loss of different visual fields
175
Q

Features of Hemiplegic Migraine

A
  • Typical migraine symptoms
  • Sudden or gradual onset
  • Hemiplegia (unilateral weakness of the limbs)
  • Ataxia
  • Changes in consciousness
176
Q

5 stages of Migraine

A
  • Premonitory or prodromal stage (can begin 3 days before the headache)
  • Aura (lasting up to 60 minutes)
  • Headache stage (lasts 4-72 hours)
  • Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping)
  • Postdromal or recovery phase
177
Q

Cluster headaches last for how long?

A

Attacks last between 15 minutes and 3 hours.

178
Q

Features of cluster headaches

A
  • Red, swollen and watering eye
  • Pupil constriction (miosis)
  • Eyelid drooping (ptosis)
  • Nasal discharge
  • Facial sweating
179
Q

Management of cluster headaches (Acute vs prophylaxis)

A

Acute management:

  • Triptans (e.g. sumatriptan 6mg injected subcutaneously)
  • High flow 100% oxygen for 15-20 minutes (can be given at home)

Prophylaxis options:

  • Verapamil
  • Lithium
  • Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)
180
Q

Which Dementia is associated with MND?

A

Frontotemporal Dementia

181
Q

Neuroleptic malignant syndrome often presents with which two abnormal blood test findings?

A

raised CK and leukocytosis

182
Q

3 findings of third nerve palsy

A

Ptosis + Outward deviation + Mydriasis

183
Q

How does a middle cerebral artery stroke present?

A
  • Contralateral hemiparesis and sensory loss, upper extremity > lower
  • Contralateral homonymous hemianopia
  • Aphasia
184
Q

What is pituitary apoplexy and how do you treat it?

A

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction:

  • sudden onset headache similar to that seen in subarachnoid haemorrhage
  • vomiting
  • neck stiffness
  • visual field defects: classically bitemporal superior quadrantic defect
  • extraocular nerve palsies

Management:

  • urgent steroid replacement due to loss of ACTH
  • careful fluid balance
  • surgery
185
Q

Migraine acute Tx + prophylaxis?

A

acute: triptan + NSAID or triptan + paracetamol
prophylaxis: topiramate (teratogenic) or propranolol

186
Q

Mid-shaft humeral injuries are associated with what nerve injury?
(+ what movement could test this?)

A

Radial nerve injury

+ innervates extensors (ie. extend wrist)

187
Q

Up to how long after a stroke can you provide thrombolysis?

A

Up to 4.5 hours after

188
Q

How is the eye deviated in a third nerve palsy?

A

Down + Out

189
Q

5 MRC power grades

A
  • Grade 0 - No muscle movement
  • Grade 1 - Trace of contraction
  • Grade 2 - Movement at the joint with gravity eliminated
  • Grade 3 - Movement against gravity, but not against added resistance
  • Grade 4 - Movement against an external resistance with reduced strength
  • Grade 5 - Normal strength
190
Q

Name a dopamine agonist

+ what condition they’re used for?

A

Ropinirole, Bromocriptine, Cabergoline

Parkinson’s

191
Q

Name a dopamine antagonist

+ what conditions might they be used for?

A
  • Antipsychotics ( First gen - Haloperidol, Second gen - Clozapine)
  • Antiemetics (Metoclopramide)
  • Identify Huntington’s progression (Raclopride)
192
Q

How long can you not drive after first seizure?

A

6 months

193
Q

Broca’s vs Wernicke’s aphasia

A

Wernicke’s (receptive) aphasia

  • Due to lesion of superior temporal gyrus. It is typically supplied by inferior division of the left MCA
  • This area ‘forms’ speech before ‘sending it’ to Broca’s area. Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent - ‘word salad’
  • Comprehension is impaired

Broca’s (expressive) aphasia

  • Due to a lesion of the inferior frontal gyrus. It is typically supplied by the superior division of the left MCA
  • Speech is non-fluent, laboured, and halting. Repetition is impaired
  • Comprehension is normal
194
Q

What section is Broca’s and Wernicke’s areas?

A

Broca’s Frontal, Wernicke’s temporal

195
Q

Which anti epileptic is commonly know for weight gain SE?

A

Sodium Valproate

196
Q

What is the mechanism of Pyridostigmine

A

Long-acting Acetylcholinesterase inhibitor

197
Q

Give a first-line treatment for neuropathic pain

A

amitriptyline, duloxetine, gabapentin or pregabalin

198
Q

Contraindication for triptans?

A

patients with a history of, or significant risk factors for, ischaemic heart disease or cerebrovascular disease

199
Q

Positive Hoffmans sign indicates what?

A

Upper motor neurone lesion

200
Q

Which 2 drugs for brain abscess management?

A

Cephalosporin (eg. Ceftriaxone) + Metronidazole

201
Q

C2 dermatome?

A

Posterior half of the skull (cap)

202
Q

C3 dermatome?

A

High turtleneck shirt

203
Q

C4 dermatome?

A

Low-collar shirt

204
Q

C5 dermatome?

A

Ventral axial line of upper limb

205
Q

C6 dermatome?

A

Thumb + index finger (make a 6 with your fingers)

206
Q

C7 dermatome?

A

Middle finger + palm of hand

207
Q

C8 dermatome?

A

Ring + little finger

208
Q

T4 dermatome?

A

Nipple (T4 at teat pore)

209
Q

T6 dermatome?

A

xiphoid process

210
Q

T10 dermatome?

A

Umbilicus (belly but-ten)

211
Q

L1 dermatome?

A

Inguinal ligament (L - ligament, 1 - inguinal)

212
Q

L4 dermatome?

A

Knee caps (down on all fours)

213
Q

S1 dermatome?

A

lateral foot (small toe - Smallest 1)

214
Q

S2/3 dermatome?

A

genitalia

215
Q

L5 dermatome?

A

Big toe, dorsal of foot (Largest of 5 toes)

216
Q

Common peroneal nerve lesion signs?

A
  • weakness of foot dorsiflexion
  • weakness of foot eversion
  • weakness of extensor hallucis longus
  • sensory loss over the dorsum of the foot and the lower lateral part of the leg
  • wasting of the anterior tibial and peroneal muscles

Phase 3a medicine (24 decks)

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