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3A REVISION > NEUROLOGY > Flashcards

NEUROLOGY Flashcards

1
Q

What is a migraine?

A

Primary brain disorder, resulting from altered modulation of normal sensory stimuli - neuronal hyperexcitability
Causes aura for 15-30 min followed by unilateral, throbbing headache

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2
Q

Mechanism of migraine?

A 
Neurogenic basis
Wave of neuronal depolarisation followed by depressed activity from the occipital region across the cerebral cortex
Activation of trigeminal pain neurones
Cerebral oedema
Dilatation of vessels
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3
Q

Causes/triggers of migraine?

A 
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptives
Lie-ins
Alcohol
Tumult
Exercise
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4
Q

Symptoms of migraine without aura?

A

Photo/phonophobia
Motion sensitivity
Nausea/vomiting
Disabling pain - unilateral, throbbing

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5
Q

Symptoms of migraine with aura (25%)?

A

Visual aura - shimmering, zig zag lines, image fragmentation, possible hemaniopia
Tingling, dysphasia
Loss of motor control
Dizziness, vertigo

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6
Q

What is a hemiplegic migraine?

A

Causes hemiparesis with possible coma with the headache, rare

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7
Q

Treatment of migraine? (4)

A

NSAIDs
Triptans (5HT agonists) e.g. sumatriptan
Ergotamine as headache starts
Botulinum toxin type A last resort injections

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8
Q

When are triptans contraindicated?

A

IHD, coronary spasm, uncontrolled hypertension

Recent lithium or SSRI use

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9
Q

Prevention of migraine?

A

Remove triggers
Propanalol or amitriptyline or topiramate or CCBs 1st line
Valproate, pregabalin, gabapentin 2nd line

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10
Q

How do triptans work?

A

5HT agonists
Constrict arteries
Inhibit release of pro-inflammatory neuropeptides

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11
Q

What are the characteristics of a tension type headache?

A

Bilateral, non pulsatile headache, tight band sensation
Possible scalp muscle tenderness
No nausea or sensitivity to movement

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12
Q

How are tension type headaches treated?

A

Simple analgesics

Massage, ice packs, relaxation

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13
Q

Treatment of chronic tension headaches?

A

Tricyclic antidepressants

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14
Q

What is a cluster headache?

A

Recurrent bouts of excruciating pain lasting 30-90 minutes

Unilateral, retro-orbital

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15
Q

Cause of cluster headaches?

A

Possible superficial temporal artery smooth muscle hyperreactivity to 5HT
Hypothalamic grey matter abnormalities

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16
Q

Symptoms of cluster headaches? (3)

A

Excruciating pain around 1 eye
Watery eye, swollen, bloodshot
Rhinorrhoea

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17
Q

Frequency of cluster headaches?

A

Can occur multiple times a day, often at night

Clusters last 1-3 months and are followed by pain free periods of months before the next cluster

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18
Q

Treatment of cluster headache?

A

Oxygen for 15 min
Sumatriptan at onset
Preventative - steroid injections, verapimil, lithium, melatonin

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19
Q

What would cause acute single episode headache? (5)

A 
Meningitis/encephalitis
Trauma - intracranial haemorrhage
Venous sinus thrombosis
Sinusitis
Acute glaucoma
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20
Q

What would cause recurrent acute attacks of headache? (3)

A

Migraine
Cluster headache
Trigeminal neuralgia

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21
Q

What would cause headache of subacute onset?

A

Giant cell arteritis

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22
Q

What causes chronic headaches?

A

Tension headache
Raised ICP
Medication overuse headache

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23
Q

Features of raised intracranial pressure?

A

Worse on waking, lying, bending forward or coughing
Vomiting, papilloedema present
Exclude SOL
Consider idiopathic intercranial hypertension

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24
Q

What is trigeminal neuralgia?

A

Paroxysms of intense stabbing pain in the trigeminal nerve distribution

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25
Q

Cause of trigeminal neuralgia?

A

Commonly starts in older age, hypertension main risk factor

Compression of the trigeminal nerve by intracranial vessels or a tumour, or inflammation

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26
Q

Symptoms of trigeminal neuralgia? (3)

A

Sudden attacks of knife like/electric shock pain lasting a few seconds
Unilateral
Commonly mandibular or maxillary divisions

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27
Q

Triggers of trigeminal neuralgia?

A

Washing face, shaving, eating, talking

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28
Q

Treatment of trigeminal neuralgia? (3)

A

Carbamazepine
Or lamotrigine, phenytoin, gabapentin
Surgery - microvascular decompression where vessels are separated from nerve root

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29
Q

What is giant cell (temporal) arteritis?

A

Systemic granulomatous arteritis that usually affects large and medium sized vessels
Common in elderly, associated with polymyalgia rheumatica

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30
Q

Symptoms of GCA? (4)

A

Headache
Temporal artery/scalp tenderness
Jaw claudication
Amaurosis fugax or sudden blindness in on eye

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31
Q

Treatment of GCA?

A

Start high dose prednisolone immediately to avoid irreversible vision loss

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32
Q

Investigations of GCA?

A

ESR and CRP high
Platelets and alkaline phosphatase high, Hb low
Temporal artery biopsy

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33
Q

What is a stroke?

A

Rapid onset of focal CNS signs and symptoms due to infarction or bleeding into part of the brain

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34
Q

Causes of stroke?

A

Ischaemic stroke - thrombosis of cerebral vessel, embolism

Haemorrhagic - intracerebral haemorrhage, subarachnoid haemorrhage

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35
Q

Risk factors for stroke? (10)

A 
Age
Male
Family history
Hypertension
Smoking
Diabetes
Heart disease
Peripheral vascular disease
COCP
Alcohol
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36
Q

What symptoms would more indicate a haemorrhagic stroke? (3)

A

Meningism
Severe headache
Coma

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37
Q

What symptoms would more indicate an ischaemic stroke? (4)

A

Carotid bruit
Atrial fibrillation
Past TIA
IHD

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38
Q

Mechanism of an ischaemic stroke?

A

Embolus or thrombus cuts off the blood supply so oxygen can’t reach the neurons, so they infarct causing symptoms dependent on site

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39
Q

Mechanism of a haemorrhagic stroke?

A

Bleed due to aneurysm or trauma or BP, accumulates and compresses surrounding tissue so loss of function but neurons still receive oxygen

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40
Q

Anatomical locations of stroke?

A

Cerebral
Lacunar
Brainstem

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41
Q

General symptoms of cerebral infarcts? (3)

A

Contralateral sensory loss or hemiplegia (initially flaccid then spastic - UMN)
Dysphasia
Homonymous hemianopia

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42
Q

General symptoms of brainstem infarcts? (3)

A

Quadriplegia
Disturbances of vision
Locked in syndrome

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43
Q

General symptoms of lacunar infarcts? (5)

A 
Ataxic hemiparesis
Pure motor
Pure sensory
Sensorimotor
Dysarthria
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44
Q

Site of lacunar infarcts? (4)

A

Basal ganglia
Internal capsule
Thalamus
Pons

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45
Q

Immediate management of stroke?

A 
Protect airway
Do pulse, BP, ECG - careful about treating BP as may cause fall in cerebral pressure
Glucose
CT/MRI urgent if thrombolysis considered
Thrombolysis within 4.5hrs if ischaemic
Aspirin 300mg when haemorrhagic excluded
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46
Q

What is used for thrombolysis in non-haemorrhagic stroke?

A

Alteplase - tissue plasminogen activator

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47
Q

Contraindications for thrombolysis? (7)

A 
Past intracranial haemorrhage
Seizures
Major infarct or haemorrhage
Recent surgery/trauma
On anticoagulants or INR >1.7
Low platelets
Very high BP
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48
Q

Primary prevention of stroke?

A

Control risk factors - hypertension, DM, high lipids (statins), cardiac disease
Exercise
Quit smoking
Lifelong anticoagulation if left sided prosthetic valves, or if AF (warfarin)

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49
Q

Secondary prevention of stroke?

A

Control risk factors
Clopidogrel (antiplatelet) after a stroke if no haemorrhage
Warfarin (or NOAC) after stroke if AF - use antiplatelet until anticoagulated
Aspirin instead of warfarin if lower risk

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50
Q

What is carotid endarterectomy?

A

Surgery to remove atherosclerotic plaque causing narrowing of the carotid artery
Done when carotid Doppler ultrasound shows >70% stenosis

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51
Q

MDT management after a stroke? (5)

A 
Stroke unit
Feeding techniques
Physiotherapy
Home adaptations - occupational therapy
Speech and language therapy
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52
Q

What is the CHA2DS2-VASc score?

A 
Risk of stroke in patients with AF
Congestive heart failure
Hypertension
Age >75 (2)
Diabetes
Stroke, TIA, VTE previously (2)
Vascular disease
Age >65
Sex - female
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53
Q

What is the HAS-BLED score?

A 
Assess 1 year risk of major bleeding in patients with AF who are anticoagulated
Hyperension
Abnormal renal/liver function
Stroke
Bleeding
Labile INR
Elderly
Drugs/alcohol
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54
Q

Give some NOACs and their disadvantage

A

Rivaroxaban
Apixaban
No antidote if bleed - warfarin has vitamin K

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55
Q

Where do the anterior cerebral arteries supply?

A

Medial side of the frontal/parietal lobes and anterosuperior part of the cerebrum - cerebrum, opthalmic artery

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56
Q

Where do the middle cerebral arteries supply?

A

Majority of the lateral cerebrum

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57
Q

Where do the posterior cerebral arteries supply?

A

Medial and lateral areas of the posterior cerebrum - occipital lobes, cerebellum, brainstem

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58
Q

What supplies Broca’s and Wernicke’s areas?

A

Broca - expressive speech, normally in dominant hemisphere (left hemisphere if right handed)
Wernicke - receptive speech
Middle cerebral artery

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59
Q

What is TACI and PACI?

A

Total and partial anterior circulation infarct
Total - affects areas of the brain supplies by ACA and MCA
Partial - only ACA

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60
Q

When are TACI and PACI diagnosed?

A

TACI is all 3, PACI is 2:
Unilateral weakness +/- sensory deficit of face, arm, leg
Homonymous hemianopia
Higher cerebral dysfunction - dyphasia, visuospatial

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61
Q

What is a homonymous hemianopia?

A

Loss of half the field of view on the same side in both eyes

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62
Q

What does proximal infarction of the anterior cerebral artery cause?

A

Paraplegia of lower limbs
Sensory loss
Incontinence

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63
Q

What does distal infarction of the anterior cerebral artery cause?

A

Contralateral hemiplegia and hemisensory loss with upper limb/face sparing

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64
Q

What does occlusion of the middle cerebral artery cause?

A

Contralateral hemiplegia with lower limb sparing
Contralateral hemisensory loss and hemianopia
Dysphagia if dominant hemisphere

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65
Q

What is a posterior circulation infarct?

A

Damage to cerebellum, brainstem

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66
Q

Features of a POCI?

A 
CN palsy
Contralateral or bilateral motor/sensory deficit
Cerebellar dysfunction - nystagmus, ataxia
Homonymous hemianopia (isolated)
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67
Q

What is locked-in syndrome caused by?

A

Infarction of the basilar artery

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68
Q

What are the 4 types of stroke in the bamford classification?

A

TACI
PACI
POCI
Lacunar syndrome

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69
Q

What is a TIA?

A

Sudden onset of focal CNS phenomena due to temporary occlusion of part of the cerebral circulation, usually by emboli, lasting <24hrs with no permanent damage

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70
Q

Cause of TIA?

A

Atherothromboembolism from the carotid artery
Cardioembolism post MI or in AF
Hyperviscosity - sickle cell, polycythaemia

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71
Q

Signs of TIA?

A

Mimic same arterial territory of stroke

Amaurosis fugax- transient loss of vision in one eye, like a curtain caused by retinal artery emboli

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72
Q

Tests in TIA?

A 
FBC, ESR, U+E, glucose, lipids
CXR
ECG
Carotid doppler USS
CT/MRI
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73
Q

Treatment of TIA? (5)

A

Control CV risk factors - BP 140/85, statins, diabetes, stop smoking
Clopidogrel antiplatelet/aspirin
Warfarin if AF
Carotid endarterectomy

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74
Q

What is ABCD2 score?

A

Used to predict risk of stroke after TIA
Age >60 1
Blood pressure >140/90 1
Clinical - unilateral weakness 2, speech disturbance without weakness 1
Duration of symptoms - >1hr 2, 10-60 min 1
Diabetes 1
If >4 see stroke unit within 24hr

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75
Q

What is a subarachnoid haemorrhage?

A

Type of haemorrhagic stroke - spontaneous bleeding into the subarachnoid space

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76
Q

Causes of SAH?

A

Rupture of saccular aneurysms e.g. Berry

Arteriovenous malformations

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77
Q

Risk factors for SAH? (5)

A 
Smoking
Alcohol
Hypertension
Bleeding disorders
Post menopausal loss of oestrogen
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78
Q

Common sites for Berry aneurysms?

A

Posterior communicating with the internal carotid
Anterior communicating with the ACA
Bifurcation of the MCA

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79
Q

Associated conditions with SAH?

A

Polycystic kidneys
Coarctation of the aorta
Ehler Danlos syndrome

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80
Q

Pathogenesis of SAH?

A

Release of blood into subarachnoid space leads to rise in ICP which may limit bleeding
Bleed sealed by clot but large risk of rebleed

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81
Q

Symptoms of SAH?

A

Sudden painful THUNDERCLAP usually occipital headache

Vomiting, collapse, seizures, coma

82
Q

Signs of SAH?

A

Neck stiffness
Kernigs sign - meningism
Retinal, vitreous bleeds
Focal neurology

83
Q

What is Kernigs sign?

A

Extension of knee painful when thigh flexed at hip

84
Q

What is a sentinel headache?

A

SAH patients may have experienced earlier milder headache - warning leak from aneurysm

85
Q

Tests for SAH?

A

CT - STAR SIGN

LP if CT negative

86
Q

What does LP look like in SAH?

A

Bloody early on

Xanthochromic - yellow - after several hours due to breakdown of Hb

87
Q

Management of SAH? (4)

A

Support - fluids, aim for BP >160 to maintain perfusion
Nimodipine to reduce vasospasm
Endovascular coiling - cathether/CT angiography
Intracranial stents/balloon for large aneurysms

88
Q

Complications of SAH? (4)

A

Rebleeding
Cerebral ischaemia
Hydrocephalus
Hyponatraemia

89
Q

What is the GCS?

A

Glasgow coma scale to assess level of consciousness

90
Q

Components of the GCS?

A

EYE OPENING - none, to pain, to speech, spontaneous
VERBAL RESPONSE - none, incomprehensible, inappropriate, confused, oriented
MOTOR RESPONSE - none, extending, flexing, withdrawal, localising, obeying
15 = fully alert. 3= coma/death.

91
Q

What is a subdural haemorrhage?

A

Bleeding from bridging veins between the cortex and venous sinuses - vulnerable to deceleration injury, resulting in accumulating haematoma between the dura and arachnoid

92
Q

Pathogenesis of SDH?

A

Haematoma raises ICP
Shifts midline structures away from the side of the clot
Tentorial herniation and coning if untreated

93
Q

Cause of SDH?

A

Trauma - particularly deceleration but can be minor/long ago trauma - up to 9 months
Can occur from dural metastases

94
Q

What are the cortical bridging veins?

A

Veins which drain the underlying neural tissue and puncture the dura mater to enter dural sinuses

95
Q

Layers of meninges?

A

Skull - dura mater - arachnoid mater - pia mater - brain

96
Q

Risk factors for SDH? (4)

A

Elderly - brain atrophy makes veins vulnerable
Alcoholics
Epilepsy
Anticoagulation

97
Q

Symptoms of SDH? (5)

A 
Fluctuating level of consciousness
Insidious physical/cognitive slowing
Sleepiness
Headache
Personality change
98
Q

Signs of SDH? (3)

A

Raised ICP
Seizures
Localising neuro symptoms late onset i.e. unequal pupils

99
Q

Tests for SDH?

A

CT/MRI shows clot and midline shift

CRESCENT SHAPED BLOOD OVER 1 HEMISPHERE

100
Q

Management of SDH?

A

Irrigation/evacuation - burr hole craniostomy

101
Q

What is epidural haemorrhage?

A

Extradural bleed - between bone and dura - usually due to rupture of middle meningeal artery

102
Q

Causes of EDH?

A

Fractured temporal or parietal bone lacerating MMA
Typically after trauma to a temple lateral to the eye
Tear in dural venous sinus

103
Q

Clinical features of EDH? (5)

A 
Deteriorating consciosness after head injury that initally had no loss of consciousness, or initial drowsiness that resolves
LUCID INTERVAL hours/days
Then decreased GCS from rising ICP
Vomiting, fits, confusion, headache
Brisk reflexes, upgoing plantar
104
Q

Late features of EDH? (5)

A 
Bilateral limb weakness
Ipsilateral pupil dilation
Coma
Irregular breathing
Death
105
Q

Tests in EDH? (2)

A

CT BICONVEX rounded SHAPE from skull
Skull XR may show fracture
LP CONTRAINDICATED - decrease in ICP = herniation

106
Q

Management of EDH? (2)

A

Stabilise

Clot evacuation +/- ligation of vessel

107
Q

Features of frontal lobe damage? (4)

A 
Personality change
Loss of executive function
Confabulation
Motor problems
Broca's aphasia
108
Q

Features of temporal lobe damage? (5)

A 
Vision problems
Hallucinations
Wernicke's aphasia
Impaired memory/learning
Deafness
109
Q

Features of parietal lobe damage? (6)

A 
Sensory loss
Loss of proprioception
Vision problems
Dyslexia, dyscalcula
Agnosia
Spatial disorientation
110
Q

Features of occipital lobe damage? (5)

A 
Homonymous hemianopia
Hallucinations
Color agnosia
Movement agnosia
Blindness
111
Q

Features of cerebellar damage?

A 
DASHING
Dysdiadochokinesis (impaired rapidly alternating movement)
Dysmetria (past pointing)
Ataxia
Slurred speech
Hypotonia
Intention tremor
Nystagmus
Gait abnormality
112
Q

What is cataplexy?

A

Sudden and transient episode of muscle weakness, triggered by emotions such as laughing or crying
Normally coexists with narcolepsy

113
Q

What is narcolepsy?

A

Irresistible attacks of inappropriate sleep, possibly with hypnogogic hallucinations and sleep paralysis

114
Q

What is raised ICP?

A

Increase in the contents of the cranium

115
Q

Causes of raised ICP? (6)

A 
Tumours
Head injury
Haemorrhage
Infection
Hydrocephalus
Cerebral oedema
116
Q

Signs/symptoms of raised ICP? (5)

A 
Headache worse on coughing, leaning forward
Vomiting
Altered GCS - drowsy
Falling pulse and rising BP
Papilloedema
117
Q

Investigation of raised ICP?

A

Bloods, CXR
CT head
LP if safe

118
Q

Management of raised ICP? (5)

A 
Stabilise - if intubated, hyperventilate
Mannitol - osmotic agent
Corticosteroids if oedema
Neurosurgery if focal cause such as bleeding - craniotomy
Treat cause
119
Q

What is hydrocephalus?

A

Accumulation of CSF in the brain, causing raised ICP
Can be congenital or caused by infection, tumour, trauma
Drain

120
Q

What is neurofibromatosis?

A 
Genetic disorder (autosomal dominant) causing benign tumours to form on nerve tissue, Nf1 and Nf2
NF1 much more common
121
Q

Diagnosis of NF1? 2 of…

A 
>6 cafe au lait spots
>2 neurofibromas
Freckling of axillae or inguinal regions
Optic glioma
>2 lisch nodules
Distinctive osseous lesion i.e. sphenoid dysplasia
First degree relative with NF1
122
Q

What are cafe au lait spots?

A

Flat, coffee coloured patches of skin seen in 1st year of life, increasing in size and number with age

123
Q

What are neurofibromas?

A

Dermal - small gelatinous nodules, may itch

Nodular - arise from nerve trunks, firm, clearly demarcated, may cause paraesthesia

124
Q

What are lisch nodules?

A

Brown/translucent mounds on the iris

125
Q

Complications of NF1? (6)

A 
Learning disability
Nerve root compression
GI bleeds
Scoliosis
Renal artery stenosis
Malignancy - optic glioma, sarcoma
126
Q

Management of NF1? (3)

A

MDT
Yearly cutaneous survey and BP
Can excise some troubling lesions

127
Q

Diagnosis of NF2?

A

Bilateral vestibular Schwannoma on MRI/CT
AND
First degree relative with NF2 with
Either unilateral vestibular Schwannoma, or one of
Neurofibroma/meningioma/glioma/schwannoma

128
Q

What is a Schwannoma?

A

Schwann cell tumour - vestibular is on vestibular nerve (=acoustic neuroma) affecting balance and hearing
Sensorineural hearing loss

129
Q

Complications of NF2?

A

Tender Schwannomas of cranial/peripheral nerves

Meningiomas, gliomas

130
Q

Management of NF2?

A

Hearing tests annually
MRI brain if hearing problems
Surgery for vestibular Schwannomas

131
Q

Features of encephalitis?

A

Odd behaviour, decreased consciousness, focal neurology or seizure
Preceded by infectious prodrome, usually viral

132
Q

Causes of encephalitis?

A

Viral - HSV, CMV, EBV, VZV

Non viral - bacterial meningitis, TB, malaria

133
Q

Tests for encephalitis? (5)

A

Blood cultures, throat swab, MSU
CT with contrast
LP - increased protein, WCC, decreased glucose
EEG

134
Q

Management of encephalitis? (3)

A

Aciclovir IV for 2 weeks
Supportive
Symptomatic - phenytoin for seizures

135
Q

Emergency features of meningitis? (4)

A

Headache
Pyrexia
Neck stiffness
Altered mental state

136
Q

Common causative organisms of meningitis?

A

Neisseria meningitidia or streptococcus pneumoniae

137
Q

Early features of meningitis? (4)

A

Headache
Leg pains
Cold peripheries
Abnormal skin colour

138
Q

Late features of meningitis? (5)

A 
Meningism
Decreased consciousness
Seizures
Non blanching purpuric rash
Signs of sepsis
139
Q

What are signs of meningism? (3)

A

Neck stiffness
Photophobia
Kernigs sign

140
Q

Signs of sepsis?

A 
Temp >38 or <36
Tachycardia >90
Resp rate >60
High or low WBC
Presence of infection
141
Q

Management of meningitis?

A

IM Benzylpenicillin in community
Cefotaxime IV
Rifampicin for contacts

142
Q

What is Horner’s syndrome?

A

Triad of miosis (pupil constriction), partial ptosis (drooping upper eyelid), anhydrosis (ipsilateral loss of sweating)

143
Q

Cause of Horner’s syndrome?

A

Interruption of facial sympathetic supply

e.g demyelination, thoracic outlet obstruction (lung tumour)

144
Q

What is bulbar palsy?

A

Diseases of the nuclei of the cranial nerves 9-12 in the medulla

145
Q

Signs of bulbar palsy?

A 
LMN lesion of tongue and muscles of talking and swallowing
Flaccid fasciculating tongue
Jaw jerk normal/absent
Quiet, hoarse speech
Difficulty chewing, choking
146
Q

Causes of bulbar palsy? (4)

A

MND
Guillian Barre
MG
Brainstem tumours

147
Q

What is corticobulbar palsy (pseudobulbar)?

A

UMN lesion of the muscles of talking/swallowing

148
Q

Cause of corticobulbar palsy? (3)

A

Bilateral lesions above the mid pons - MS, MND, stroke

149
Q

Signs of corticobulbar palsy? (6)

A 
Slow tongue movements
Slow deliberate speech
Increased jaw jerk
Increased pharyngeal/palatal reflexes
Weeping unprovoked
Incongruent giggling
150
Q

What is Bells palsy?

A

Abrupt onset of complete unilateral facial weakness - CN 7 - and other symptoms, diagnosis of exclusion

151
Q

Symptoms of Bells palsy? (8)

A 
Facial weakness
Numbness/pain around ear
Hypersensitivity to sound
Decreased taste
Sagged mouth one side, upturned the other
Drooling
Speech difficulty
Watery eye
152
Q

Tests in Bells palsy?

A

Bloods (viral antibodies)
MRI (SoL, stroke, MS)
Nerve conduction tests

153
Q

Management of Bells palsy? (5)

A

Most fully recover spontaneously
Prednisolone within 72hr speeds recovery
Protect eye - dark glasses, artificial tears if drying, tape to close at night
Surgery if eye closure is long term problem
Plastic surgery if no recovery
Botulinum toxin

154
Q

What is Guillain Barre syndrome?

A

Acute inflammatory demyelinating polyneuropathy

Most common acute polyneuropathy

155
Q

Cause/mechanism of GBS? (3)

A

Immune mediated, post infectious
Campylobacter jejuni, CMV, EBV…
Infection causes antibodies that attack nerves

156
Q

Symptoms of GBS? (5)

A

1-3 weeks after an infection, symmetrical ascending muscle weakness in limbs
Paralysis
Proximal muscles more affected - trunk, resp, CNs
Back pain, limb pain
Sweating, arrhythmias
Progressive phase 4 weeks then recovery

157
Q

Investigations for CBS? (2)

A

Nerve conduction studies - slow

LP - high protein

158
Q

Management of GBS? (3)

A

Ventilatory support if respiratory paralysis
IV immunoglobulin for 5 days
Possible plasma exchange

159
Q

Prognosis of GBS?

A

85% recover, 10% unable to walk at 1 year, 10% overall mortality

160
Q

What is Parkinsonism?

A

Triad of tremor, rigidity and bradykinesia

161
Q

What type of tremor is common in Parkinson’s?

A

Pill rolling of thumb over fingers

Worse at rest

162
Q

What type of rigidity is common in Parkinson’s?

A

Cogwheel rigidity - jerking stop-start during passive movement
Increased when asked to perform an action with the opposite limb
Leadpipe rigidity - sustained stiffness

163
Q

What features of bradykinesia are common in Parkinson’s?

A

Slow to initiate movement
Slow, low amplitude repetitive actions i.e. blinking
Mask like expressionless face

164
Q

What is the typical Parkinson’s gait?

A

Reduced arm swing
Shuffling steps with flexed trunk
Freezing at obstacles/doors

165
Q

Causes of Parkinsonism?

A 
Antipsychotics
Parkinson's disease
HIV
Post flu encephalopathy
Trauma
166
Q

What is Parkinson’s disease?

A

Extrapyramidal movement disorder characterised by resting tremor, rigidity and bradykinesia

167
Q

Motor symptoms of PD? (6)

A 
Cogwheel rigidity
Pill rolling tremor
Postural instability
Shuffling gait
Reduced arm swing
Difficulty initiating movement
168
Q

Non motor symptoms of PD? (9)

A 
Reduced smell
Constipation
Hallucinations
Frequency/urgency
Drooling
Depression
REM sleep disorder
Dementia
Mask like expression
These can present years before motor symptoms.
169
Q

Peak age of onset of Parkinsons?

A

65

170
Q

Risk factors for Parkinsons? (4)

A 
Age
Male
Pesticides
Genetics if early onset
NON SMOKERS
171
Q

Pathology of Parkinsons?

A

Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurons in the substantia nigra, associated with lewy bodies
Decreases striatal dopamine levels

172
Q

Management of Parkinsons?

A

Exercise
Medications
Treat neuropsychiatric complications e.g. depression, dementia
Deep brain stimulation
Surgical ablation of overactive basal ganglia circuits

173
Q

What genes are associated with early onset Parkinsons?

A

PARK 1-11 genes

174
Q

What are Lewy bodies?

A

Tangles of alpha synuclein and ubiquitin

175
Q

What medical therapy is used in Parkinson’s? (5)

A 
Levodopa with dopa-decarboxylase inhibitor
Dopamine agonists
Anticholinergics - help tremor
MAO-B inhibitors
COMT inhiibtors
176
Q

What is levodopa? Side effects?

A

Dopamine precursor, replacing lost dopamine
Dyskinesia, on/off effect, psychosis
Efficacy decreases with time and need bigger doses, with more side effects

177
Q

What is levodopa given with?

A

Dopa-decarboxylase inhibitor prevents PERIPHERAL metabolism of levodopa into dopamine

178
Q

Give some dopamine agonists, why are they used?

A

Ropinirole, bromocriptine

Can delay starting l-dopa and allow lower doses of it

179
Q

What is apomorphine?

A

Strong dopamine agonist

Even out end of dose effects

180
Q

What are MAO-B inhibitors?

A

Rasagiline

Inhibit dopamine breakdown, alternative to dopamine agonists

181
Q

What are COMT inhibitors?

A

Entecapone

Lesson off time in end of dose effects, inhibit dopamine breakdown

182
Q

What is Parkinson’s plus syndrome?

A

Parkinson’s disease features, with atypical features and poor response to l-dopa

183
Q

What is Huntingtons disease?

A

Autosomal dominant progressive neurodegenerative disorder presenting in middle age

184
Q

Early symptoms of Huntingtons disease? (3)

A

Irritability
Depression
Poor coordination

185
Q

Later symptoms of Huntingtons disease? (4)

A

Chorea
Dementia
Fits
Death within 15 years

186
Q

Pathology of Huntingtons disease?

A

Atrophy and neuronal loss of striatum of basal ganglia and cortex
Genetics - expansion of CAG repeat on chromosome 4

187
Q

What is chorea?

A

Excessive irregular movements flitting from one body part to another - dance like

188
Q

What is genetic anticipation?

A

Found in trinucleotide repeat disorders

Successive generations have earlier onset and more severe disease

189
Q

Management of Huntingtons?

A

Genetic testing and counselling
No treatment affects progression - possible antipsychotics
Tetrabenazine for movement
Antidepressants

190
Q

What is myasthenia gravis?

A

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

191
Q

Mechanism of mysasthenia gravus?

A

Antibodies to nicotinic acetylcholine receptors
Deplete working post-synaptic receptor sites at the neuromuscular junction
Prevents the end plate potential becoming large enough to trigger muscle contraction

192
Q

Antibodies in myasthenia gravis?

A

ACh-R (against acetylcholine receptor?

MuSK (against muscle specific receptor kinase)

193
Q

Associations of myasthenia gravis?

A

If under 50, commoner in women and other autoimmune diseases and thymic hyperplasia
If over 50 commoner in men and associated with thymic atrophy, RA, SLE

194
Q

Presentation of myasthenia gravis? (7)

A

Increasing muscular fatigue
Ptosis
Diplopia
Myasthenic snarl (corners of mouth cant pull up)
Peek sign (separation of eyelids when eyes closed)
Voice fades when talking
Wasting long term

195
Q

Order of muscles affected in myasthenia gravis? (6)

A 
Extraocular
Bulbar (chewing/swallowing)
Face
Neck
Limb girdle (hips/shoulders)
Trunk
196
Q

Investigations of myasthenia gravis? (5)

A

Antibodies - Anti-AChR, MUSK
Decreased muscle response to repetitive nerve stimulation
CT thymus
Ice test - ptosis improves by >2mm after ice to shut lid
Tensilon test - give edrophonium and weakness improves if MG

197
Q

Treatment of myasthenia gravis? (3)

A

Symptom control - anticholinesterase (pyridostigmine)
Relapses with prednisolone, possibly with azathioprine/methotrexate (immunosuppress)
Thymectomy if <50 and badly controlled disease

198
Q

Why give anticholinesterases in myasthenia gravis?

A

Prolongs acetylcholine action by inhibiting cholinesterase

199
Q

What is a myasthenic crisis?

A

Weakness of the respiratory muscles during a relapse, triggered by lack of medication, infection, stress

200
Q

Management of a myasthenic crisis?

A

Ventilatory support
Give plasmapharesis/IB immunoglobulins
Treat trigger i.e. infection

3A REVISION (17 decks)

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