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Specialties > Neurology > Flashcards

Neurology Flashcards

1
Q

What are red flags for headaches

A 
New headache 
over >60yrs
Thunderclap headache
Hx of malignancy
Hx of infectious disease 
Altered Consciousness, memory or confusion 
Seizure
Papilloedema
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2
Q

What is the most common type of chronic daily recurrent headache

A

Tension Headache

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3
Q

How does tension headache present

A

bilateral non pulsatile headache +/- scalp tenderness
pressure or tightness around head
No N/V or photophobia

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4
Q

What is the treatment for a tension headache

A

Explanation & Reassurance
Stress Relief
Simple Analgesia e.g Paracetamol or Ibuprofen

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5
Q

What is one of the main issues of using long term analgesia to treat tension headaches

A

Analgesia overuse headaches - when you stop taking analgesia you get headaches from analgesia withdrawal
(paracetamol, codine/opiates, triptans)

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6
Q

What medication can be tried to relieve chronic tension headaches

A

Tricyclic Antidepressents e.g Amitriptyline

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7
Q

What are the two subtypes of Migraine

A

Migraine with aura

Migraine without aura

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8
Q

How does a migraine without aura present

A

Unilateral throbbing building up over minutes/hours
Nausea and Vomiting
Photophobia/Phonophobia
(patients like to sit in dark and often irritable)

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9
Q

What additional features would you see in migraine with aura and when does the aura begin

A

Aura presents before the headache (temporary warning)
Eyes: Scotoma, Unilateral Blindness, Flashes and zig-zags
Motor: Weakness
Sensory: Aphasia, tingling, numbness

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10
Q

What are the triggers of Migraine

A 
C hoclate
H angovers 
O rgasm 
C heese
O ral contraceptive  
L ie ins 
A lcohol 
T umult (loud noise)
E xercise
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11
Q

What are other premonitory changes may you get before migraine

A

Fatigue
Nausea
Change in mood or appetite

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12
Q

What may differentiate a migraine from a stroke

A

Migraines usually have +ve symptoms whilst stroke -ve

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13
Q

How can you manage migraines conservatively

A

avoid triggers

Usually resolve through sleep

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14
Q

How can you manage a mild migraine

A

Simple analgesia + Anti-emetic e.g metoclopramide

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15
Q

How can you manage a migraine which is unresponsive to simple analgesia or severe migraines

A

Triptans e.g Sumatriptan

contraindicated in vascular disease cause vasoconstriction

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16
Q

What can frequent use of Triptans lead to

A

Analgesia overuse headaches

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17
Q

What medication is used to prevent migraines

A

1st line: B-blockers e.g propanolol

2nd line: Topiramate or Amitriptyline (if B-blockers contraindicated)

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18
Q

What is a cluster headache

A

Rapid onset, severe, short lived (1-2hrs) unilateral headache with a clustering of painful attacks over weeks/months followed by periods of remission

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19
Q

Who is at risk of cluster headaches

A

Men

20 -50 yrs

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20
Q

How does a cluster headache present

A 
Short lived, severe unilateral headache
Pain begins around eye and temple 
Lacrimation and redness of eye 
Rhinorrheoa
Flushing
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21
Q

How can you manage an acute attack of a cluster headache

A

SC Sumatriptan or Intranasal Sumatriptan

100% O2

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22
Q

What can trigger cluster headaches

A

Alcohol
Strong smelling chemicals e.g perfume, petrol
Smoking

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23
Q

How can you prevent cluster headaches

A

Avoiding triggers
Verapamil - Ca2+ channel blocker
Not effective: Corticosteroids, Lithium Carbonate

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24
Q

What can cause secondary headaches

A

Subarachnoid Haemorrhage
Raised Intracranial pressure
Idiopathic Intracranial HTN
Medication/Analgesia Overuse Headache

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25
Q

How does Subarachnoid Haemmorhage headache present

A

Thunderclap headache - focal symptoms and signs, coma if severe

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26
Q

How does raised intracranial pressure present

A

Typically worse walking, lying, bending and coughing
Nausea/ Vomiting
Papilloedema
Focal signs

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27
Q

What causes idiopathic intracranial HTN

A

Caused by raised ICP

risk factors: drugs, obesity

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28
Q

What is giant cell arteritis/ temporal arthritis

A

Chronic Vasculitis - characterisied by granulomatous inflmmation in the large arteries of the scalp and neck

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29
Q

What is granulomatous inflammation

A

Inflammation with granulomas (collection of macrophages attempting to wall off foreign substances)

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30
Q

What is GCA closely related to and therefore what other symptoms may present alongside GCA

A

Polymyaligia rheumatica - Fatigue and Pain, stiffness and inflammation of the shoulders, hip and neck

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31
Q

What are the clinical features of GCA

A

Headache (usually unilateral in temporal area but may become bilateral)
Scalp Tenderness (e.g when combing hair)
Jaw Claudication
Features of polymyaligia rheumatica - arm, neck and pelvic stiffness and tenderness
Partial or Complete Blindness in one or both eyes - usually permanent
Amaurosis Fugax - temporary painless loss of vision in one or both eyes
Systemic Features: weight loss, fatigue, low grade fever

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32
Q

What may you find on examination of someone with temporal arteritis

A

If its a superfical temporal artery it may be tender, firm and pulseless - the skin overlying may be red

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33
Q

When should you suspect GCA

A

Over 50 with either:

  • new onset localised unilateral headache in temporal area
  • temporal artery abnormality - tender, firm and pulseless
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34
Q

What confirms diagnosis of GCA

A

*Temporal artery biopsy confirms diagnosis - although granulomatous changes may be patchy and missed
Always raised ESR

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35
Q

How do you manage GCA

A

High dose oral steroids e.g Prednisolone
Aspirin
PPI to protect Gut e.g Omeprazole

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36
Q

What is trigeminal neuralgia

A

Severe episodic face pain in the distribution of one or more branches of the trigeminal (5th) nerve

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37
Q

What are the clinical features of trigeminal neuralgia

A

Severe paroxysms of sharp/knife like pain in one or more divisions of the 5th nerve

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38
Q

What ‘trigger factors’ precipitate trigeminal neuralgia attacks

A

Light touch to the face
Washing
Shaving
Eating

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39
Q

What is the most common cause of trigeminal neuralgia

A

Vascular compression of the nerve - main cause

Rare causes: MS, tumours

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40
Q

What are risk factors for developing trigeminal neuralgia

A

Increasing age
MS
Family Hx

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41
Q

How is trigeminal neuralgia managed

A

Check for red flags: tumours, MS, aneurysms

Carbamazepine

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42
Q

What is a transient ischaemic attack

A

A transient episode of neurological dysfunction caused by temporary occlusion of cerebral circulation usually an emboli (less than 24hrs)

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43
Q

What is a stroke

A

Rapid onset of neurological dysfunction caused by infarction or haemorrhage in the brain lasting more than 24 hrs

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44
Q

What are the two types of stroke

A

Haemmorhagic Stroke - caused by intracerebral or subarachnoid haemorrhage
Ischaemic Stroke - caused by infarct

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45
Q

What two things can cause an ischaemic stroke

A
  • Thrombus - occurs at sight of atheromatous plaque in internal carotid, vertebral, cerebral arteries
  • Embolus - occurs from atheromatous plaque of the internal carotid artery breaking off or emboli from the heart e.g AF
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46
Q

What are TIAs usually caused by

A

Microemboli from atheromatous plaques of the internal carotid or from the heart e.g AF

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47
Q

What are risk factors for stroke/TIA

A 
HTN
Diabetes 
Smoking
Cardiovascular Disease 
Hyperlipidaemia 
Obesity 
Oestrogen oral contraceptives 
Alcohol 
AF - major risk for emboli stroke 
Rarer: Cocaine, Migraine, Vasculitis
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48
Q

What does the Frontal lobe control

A 
Movement 
Executive Function (cognitive control and behaviour)
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49
Q

What does the Parietal lobe control

A

Sensory information

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50
Q

What does the temporal lobe control

A 
Hearing 
Memory 
Smell 
Languages
Facial Recognition
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51
Q

What does the occipital lobe control

A

Vision

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52
Q

Whats does the cerebellum control

A

Balance and Co-ordination

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53
Q

What does the brain stem control

A

Heart Rate and BP
Breathing
GI function
Consciousness

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54
Q

Where is Broca’s area and what does it do

A

It is located mainly in the left hemisphere of the frontal lobe
It is the area which controls speech production

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55
Q

What is Wernickes area and what does it do

A

It is located mainly in the left hemisphere of the temporal lobe
It is the area which controls understanding speech

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56
Q

What two groups of arteries supply the brain

A 
Internal Carotid Arteries (L&R)
Vertebral Arteries (L&R) - come together to form basillar artery
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57
Q

What does the Internal carotid artery/Anterior circulation supply

A

Anterior Cerebral Artery - median portions of frontal and parietal lobes
Middle Cerebral Artery - lateral portions of frontal, parietal and temporal lobes

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58
Q

What does the Vertebral Artery/Posterior circulation supply

A

The Cerebellum
The Brainstem
The Posterior Cerebral Artery - supplies the occipital lobe, some of the temporal lobe and the thalamus

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59
Q

How can stroke be classed

A

Oxford Stroke (Bamford) Classification

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60
Q

What is the presentation of a total anterior circulation stroke

A

All three of the following:

  • Unilateral weakness &/or sensory deficit of the face, arm and leg
  • Homonymous Hemianopia
  • Higher Central Dysfunction (dysphasia, visuospatial disorder)
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61
Q

What is the presentation of a partial anterior circulation stroke

A

Two of the following: - Unilateral weakness &/or sensory deficit of the face, arm and leg

  • Homonymous Hemianopia
  • Higher Central Dysfunction (dysphasia, visuospatial disorder)
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62
Q

What is a lacunar stroke

A

Occlusion of deep penetrating arteries of the brain
It is the most common type of stroke
It only affects a small amount of subcortical white matter therefore does not present with cortical features

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63
Q

What is the presentation of a lacunar stroke

A

One of the following:

  • Pure Sensory Stroke
  • Pure Motor Stroke
  • Sensori-Motor Stroke
  • Ataxia hemiparesis
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64
Q

What is the presentation of a posterior circulation syndrome

A

One of the following:

  • Ipsilateral cranial nerve palsy and a contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (gaze palsy)
  • Cerebellar Dysfunction e.g ataxia, nystagmus, vertigov
  • Isolated homonymous hemianopia or cortical blindness
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65
Q

What is the Acronym to recognise stroke

A

F ace
A rm
S peech
T ime

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66
Q

What is the initial management of someone who presents with a stroke

A
  1. FAST
  2. ABCDE
  3. Bloods + BM
  4. Breif Hx and Examination (time of onset, risk factors, contraindications for thrombolysis)
  5. BP and ECG
  6. NIHSS (national institute of health stroke scale) - to grade severity
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67
Q

What is the key investigation for stroke

A

Urgent CT head (+/- CT angiography)

- Sensitive for haemorrhage, cannot usually diagnose stroke in the acute phase)

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68
Q

What is the emergency treatment for an ischaemic stroke once haemmorhagic stroke has been excluded

A

Thrombolysis e.g IV alteplase +/- Mechanical Thrombectomy

Aspirin

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69
Q

What is the timeframe for using thrombolysis

A

4.5 hrs from onset of symptoms

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70
Q

What are contraindications for thrombolysis

A 
Haemorrhage on CT
Active bleeding from any site
recent GI or urinary tract haemorrhage
Suspected known pregnancy 
Active pancreatitis 
Blood Pressure 185/110
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71
Q

What are the risks of thrombolysis

A

severe high blood pressure
bleeding
Haemorrhagic stroke Transformation

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72
Q

What is it essential to do post thrombolysis care

A

Aggressive blood pressure monitoring
Vigilance for complications
24hr CT head to check for haemmorhagic transformation

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73
Q

What is the timeframe for mechanical thrombectomy

A

6 hr time frame for Anterior circulation stroke (longer for posterior)

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74
Q

Can Mechanical Thrombectomy be used alongside IV Thrombolysis

A

Yes

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75
Q

What is the disadvantage of Thromectomy

A

It is a limited resource

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76
Q

Following Thrombolysis how should ischaemic stroke patients be managed

A
  1. Investigate the cause
  2. Screen and prevent further complications
  3. Rehabillitation
  4. Manage secondary prevention
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77
Q

What investigations should be performed following thrombolysis

A

Blood Tests:
FBC, ESR, U&E, Lipid Profile, LFTs, CRP, Clotting screening, Glucose
ECG: MI, Atrial flutter/fibrillation
Carotid Dopper US - carotid stenosis
Echocardiogram
MRI - confirms diagnosis of ischaemic strome

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78
Q

Who needs to be in the MDT to provide supportive care following a stroke

A 
Nursing 
SALT
OT
Physiotherapy 
Dieticans
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79
Q

What lifestyle changes can be used for secondary prevention of further strokes/TIAs

A 
Smoking cessation
Drinking and drugs cessation
Dietary modifications
Exercise
Driving Advice
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80
Q

What medication can be used for secondary prevention of further strokes/ TIAs

A

Antiplatelets e.g Clopidogrel superior to Aspirin
Anticoagulation if AF using CHADVASC score e.g warfarin
Antihypertensive Drugs to lower BP e.g B-blockers
Lower Cholesterol using Statin e.g Simvastatin

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81
Q

What medical management can be performed to prevent further complications of stroke

A 
Prevention of DVT e.g TED stockings
Hydration 
NG feeding/ PEG feeding
Botox and Physio for Spasticity 
Monitor for infection
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82
Q

What further surgical management may be performed to prevent further strokes/TIAs causes by carotid stenosis

A

Carotid Endarterectomy

Carotid Artery Stenting

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83
Q

What is the CHA2DS2 VASc Score

A

Estimates risk of stroke in AF patients
All worth one point accept A2 and S2

C HF
H ypertension
A2 ge 75 or other
D iabetes 
S2 troke/TIA

V ascular Disease
A ge 65-74
Sc sex category

0 = low risk no anticoagulation 
1 = moderate risk consider antiplatelet or anticoagulation 
2 = anticoagulation candidate
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84
Q

What is the ABCD2 score

A

Estimates the risk of a stroke following a TIA

A ge (60 or over)
B lood pressure (140/90 or greater)
C linical features (unilateral weakness +/- speech impairment = 2, only speech impairment = 1)
D uration of symptoms (60 mins or longer =2, under 60 mins = 1)
D iabetes

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85
Q

What are the two types of haemmorhagic stroke

A

Subarachnoid Haemorrhage

Intracerebral Haemorrhage

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86
Q

What is an intracerebral haemorrhage and its presentation

A

A bleed within the brain tissue itself

headache and neurological deficit

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87
Q

What is a subarachnoid haemorrhage and its presentation

A

A bleed within the subarachnoid space usually caused by saccular aneurysms
Symptoms:
Thunderclap headache
meningeal symptoms (neck stiffness, vomiting and photphobia)
Painful 3rd cranial nerve palsy
Horners Syndrome
Reduced GCS - can lead to seizures, collapse and sudden death

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88
Q

How is haemorrhagic stroke diagnosed

A

MRI/CT

Cerebral Angiography - to rule out anurysmal cause and locate anuerysm

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89
Q

In a suspected SAH what other investigation would you like to perform if the CT is -ve

A

LP - can be performed after 12 hrs after onset and can be detected up to 2 weeks after - will show xanthochromia

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90
Q

What is the emergency management of a haemmorhagic stroke

A

ABCDE
Control BP try and keep systolic between 140-160 no higher
Stop all anticoagulation and reverse any anticoagulation (Vit K for Warfarin and Protamine in Heparin/partally LMWH)
Manage underlying malformation - SAH aneurysm surgical clipping or endovascular coiling is definite management
Evaluate for neurosurgery - if continual bleeding causing brainstem compression and hydrocephalus in intracerebral haemorrhage - perform haematoma evacuation

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91
Q

What other conditions mimic strokes

A

Seizures
Tumours/Abscesses
Migraine
Metabolic (hypoglycaemia, hyponatramia)

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92
Q

What is the treatment for a SAH

A

Surgical clipping

Endovascular Coiling

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93
Q

What are the risk factors fo haemorrhagic stroke

A

Smoking
HTN
Alcohol Access
Increasing age

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94
Q

What is a subdural haemorrhage

A

accumulation of blood due to rupture of bridging veins in the subdural space between dura and arachnoid

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95
Q

What is the pathophysiology behind subdural haemorrhage

A

Bleeding causes ICP to gradually rise causing shifting of midline structures away from clot
If left untreated eventual tentorial herniation and coning

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96
Q

What is the cause of a subdural haemorrhage and who is at risk of developing one

A
  • Brain atrophy leads to tearing of bridging veins usually only from minor head trauma
  • Patients with brain atrophy high risk - alcoholics and the elderly
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97
Q

How does subdural haemorrhage present

A 
A progressively worsening headache
Fluctuating levels of consciousness 
Confusion
Personality change
Sleepiness 
Raised ICP 
seizures
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98
Q

When can a subdural haemorrhage present

A

Acute - if severe head injury

Subacute/ Chronic - over days and weeks if minor head injury

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99
Q

What could be a differential diagnosis of a subdural haemorrhage

A

Stroke
Dementia
Infection

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100
Q

What are the symptoms of raised ICP

A

Papilloedema
Vomiting
Headache
Deterioration on level of consciousness

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101
Q

What investigation would you use for suspected subdural haemorrhage and what would you see if it is a subdural haemorrhage

A

CT/MRI

Show concave collection of blood (sickle shape) +/- midline shift

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102
Q

How would you treat a subdural haemorrhage

A

Surgical evacuation of haematoma e.g burr hole craniotomy

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103
Q

What is an extradural/epidural haemorrhage

A

A bleed between the bone and dura

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104
Q

How is an extradural haemorrhage usually caused

A

fractured temporal or parietal bone causing laceration of middle meningeal artery typically after trauma to temple

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105
Q

How do extradural haemorrhage patients present

A

Triphasic:

  1. Brief deterioration in consciousness
  2. Lucid phase where they appear to recover (can last hours)
  3. Rapid deterioration - headache, falling GCS, raised ICP, vomiting, confusion, fits, hemiparesis with brisk reflexes, compression of 3rd nerve causing fixed dilated pupil, coma, breathing deep irregular (brainstem compression) - Death
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106
Q

What investigation is key for suspected Extradural haemorrhage

A

CT - Convex haematoma (Egg shape)

X-ray may show skull fracture

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107
Q

What is the management of an extradural haemorrhage

A

Stabilse and surgical evacuation/ drainage of bleed (craniotomy)

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108
Q

What is the difference between an extradural and subdural on CT

A

Extradural - Egg shaped (convex)

Subdural - Sickle shaped (concave)

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109
Q

What is Guillain -Barre Syndrome

A

An acute inflammatory demyelinating peripheral polyneuropathy

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110
Q

What is Guillain - Barre Syndrome usually cause by

A

Usually triggered by an infection

  • Campylobacter jejuni
  • EBV
  • Cytomegalovirus
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111
Q

What are the clinical features of GBS

A

Symptoms are toes to nose and symmetrical:

  • Progressively worsening limb weakness (starting in the hands and feet and spreading upwards) - eventual flaccid weakness
  • Paresthesias (tingling/numbness) - starting in hands and feet snd spreading upwards
  • Absent Reflexes
  • Eventual Paralysis of Respiratory muscles leafing to life-threatening respiratory failure
  • Autonomic Dysfunction: postural hypotension, cardiac arrythmias, sweating, flushing and urinary retention
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112
Q

At what rate does GBS reach maximum weakness

A

3 -4 weeks

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113
Q

What is miller fisher syndrome

A

A variant of GBS affecting the cranial nerves leading to opthalmoplegia and ataxia

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114
Q

What investigations should you do for suspected GBS

A

Clinical
Nerve Conduction Studies: F waves slow/absent, reduced motor conduction velocity
CSF: Usually protein is raised but may be normal
MRI to exclude cord compression

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115
Q

What is the management of GBS

A

Monitoring respiratory weakness - FVC, RR may need mechanical ventilation
ECG and BP - cardiac monitoring of arrhythmias and hypotension
Supportive Treatment - pain management opiates, physiotherapy and VTE prevention (heparin TED stockings)
Immunotherapy - IVIG or plasma exchange

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116
Q

What is the most commonly used treatment for GBS

A

IVIG - to reduce duration and severity of symptoms

Plasma exchange - may be more side effects than IVIG

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117
Q

What is a seizure

A

A transient event caused by the abnormal and excessive discharge of cerebral neurones

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118
Q

What is epilepsy

A

An increased tendency to experience recurrent unprovoked epileptic seizures

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119
Q

What type of onset can a seizure take

A

Generalised onset - affect whole brain

Focal/Partial onset - affect one part of brain may become generalised

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120
Q

What types of seizures are generalised onset

A

Generalised Tonic- Clonic Seizure
Absence Seizure
Myoclonic jerk seizures

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121
Q

What types of seizure are partial/focal onset

A

Simple partial seizures
Complex partial seizures
Secondary Generalised Tonic Clonic Seizures

122
Q

What is a generalised tonic clonic seizure (grand mal)

A
  • Sudden onset rigid (tonic phase) followed by convulsion (clonic phase) and rhythmic muscle jerking
  • Tongue Biting
  • Urinary Incontinence
  • After feel drowsy, pale, confused for several hours
123
Q

What is an absence seizure (petit mal)

A
  • Usually disorder of childhood
  • Child ceases activity and stares blanky into space
  • Lasts a few seconds
124
Q

What is a myoclonic seizure

A

When some or all of muscles in body start jerking

Usually aware of event

125
Q

What is a simple partial/focal seizure

A

Presents with aura symptoms you are fully aware of what is happening

  • Hallucinations (vision, smell)
  • Motor movements (stiffness, twitching)
  • Sensory disturbances (tingling, numbness)
  • Rising sensation in stomach
  • Feeling strange
126
Q

What can simple focal/partial seizures be a warning of

A

The development of a bigger seizure - secondary grand mal

127
Q

What is a complex focal/partial seizure

A

Loss of awareness with random symptoms such as:

  • smacking lips
  • making weird noises
  • rubbing hands
  • chewing/ swallowing
128
Q

What are secondary generalised tonic - clonic seizures

A

The development of generalised tonic- clonic seizure following a focal/partial seizure

129
Q

What is Todds Paralysis

A

Paralysis of involved limbs for several hours after the seizure can be partial or complete

130
Q

What can cause Seizures

A 
Causes:
Idipoathic
Family Hx 
Head Trauma
Genetic 
Tumours 
Structural Defects 
Alcohol and Illegal drugs
131
Q

What can precipitate seizures in epileptics

A 
Precipitates: 
Stress
Lack of sleep
Waking up
Drinking alcohol
Flashing lights
132
Q

What are the main 3 differentials for loss of consciousness

A

Epileptic seizures
Syncope - transient global cerebral hypoperfusion
Psychogenic nonepileptic seizure

133
Q

What can cause Syncope

A
  • Reflex: vasovagal (caused by your body overeacting to triggers e.g fainting at blood)
  • Cardiogenic
  • Orthostatic Hypotension (sitting to standing can be caused by medication)
134
Q

What can cause cardiac syncope

A
  1. Conditions that predispose to transient tachycardias
  2. Bradycardias
  3. Cardiac Ischaemia
  4. Structural heart disease
135
Q

If someone presents with LOC what is the key investigation to perform

A

ECG - conditions that give rise to transient tachyarryhthmias have abnormal ECGs between events!
* They are a major cause of sudden death in younger people

136
Q

What is a blackout during exercise until proven otherwise

A

Cardiogenic Syncope

137
Q

What are Psychogenic Non-epileptic Seizures

A

PNES are attacks that may look like epileptic seizures but are not caused by abnormal brain electrical discharges. Instead, they are a manifestation of psychological distress e.g childhood sexual abuse

138
Q

What are two rare but important causes of transient LOC

A

Hypoglycaemia

Acute Hydrocephalus

139
Q

What is essential for distinguishing between different causes of LOC

A 
The History:
Circumstances - trigger
Prodome - any aura 
Witness - what did they see
Duration
Post icital phase - what happened after
140
Q

What are the key investigations for LOC

A

ECG - no.1
CT head
MRI
EEG - for the diagnosis and classification of epilepsy

141
Q

What is the emergency management of someone having a seizure

A
  • Ensure patients harm themselves as little as possible environment around them is safe as possible
  • Repeated or Prolonged seizures give Rectal (if no IV access) or IV (inpatient) diazepam or lorazepam
142
Q

What anti epileptic drugs can be used to treat epilepsy

A

Generalised Tonic Clonic - Sodium Valproate and Lamotrigine
Absence Seizure - Sodium Valproate
Partial Seizure - Carbamazepine

143
Q

What is important to remember about anti epileptic drugs

A

They are highly teratogenic - especially Sodium Valproate

- Must be on some form of long term contraception

144
Q

What is the pathogenesis behind parkinsons disease

A
  1. Progressive depletion of of dopamine secreting cells in the substantria nigra
  2. Causing depletion in dopamine secretion
  3. Fall in neuronal transmission from basal ganglia to cortex
145
Q

What are the three clinical features of Parkinson disease

A

Tremor - resting tremor
Rigidity - hypertonia in limbs and trunk
Bradykinesia - difficultly initiating movement

146
Q

How is Hypertonia different in Parkinsons to UMN lesion

A

Hypertonia is present throughout extension unlike UMN where resistance falls throughout extension

147
Q

What are other symptoms/signs may you get in Parkinsons

A 
Shuffling gait
Poor balance 
Lewy Body Dementia - hallucinations 
Depression
Loss of sense of smell
148
Q

What investigations can be performed for suspected parkinsons disease

A

Diagosis is clinical

149
Q

How is parkinsons disease managed

A
  • Levodopa - 1st line: in Parkinsons whose motor symptoms impact QoL
  • Dopamine Agonists (ropinarole) - 1st line: for young patients, or not impacting QoL to prolong use of L-DOPA
  • Monoamine Oxidase B Inhibitors
  • Physiotherapy
150
Q

What is a side effect of L-Dopa and what medication can manage this

A
  • Nausea

- Carbidopa

151
Q

What happens to L-Dopa overtime

A

It becomes less effective

152
Q

What are the side effects of Dopa Agonists

A
  • Impulsive control disorders e.g impulsive shopping

- Excessive sleeping

153
Q

What is Huntingtons Chorea

A

A rare autosomal dominant condition

It is an incurable, progressive, neurodegenerative disorder presenting at middle age

154
Q

What is the average age of onset of huntingtons chorea

A

40 years

155
Q

What are the clinical features of Huntingtons Chorea

A

Prodomal phase: irritability, depression, incoordination
Progresses to:
- Chorea - jerky involuntary movements
- Dementia - memory problems
- Psychotic changes - presonality change, depression and psychosis
- fits +/- death

156
Q

What is the pathophysiology behind Huntingtons Chorea

A
  1. Expansion of CAG repeats in Huntingtons gene
  2. Causes atrophy of neurones in the striatum
  3. Less GABA
  4. Less regulation of Dopamine
  5. Increase in Dopamine - increase in movement
157
Q

What would you see on examination of someone with Huntingtons Chorea

A

Abnormal eye movements
Random unpredictable movements
Ataxia Problems
Heal to Toe walking

158
Q

What is the treatment for Huntingtons

A

Genetic test will reveal condition
No cure
MDT to manage patients e.g physio, occupational health
SSRIs - to manage depression

159
Q

What is Myasthesia Gravis

A

An autoimmune disease characterised by weakness and fatiguability of the occular, bulbar and skeletal muscles

160
Q

How may a myasthesia gravis patient present

A
  • Progressive tiredness throughout the day or through repetitive movements which improves after rest:
  • skeletal muscle fatigue of proximal limbs
  • occular: diplopia
  • bulbar: tiring from swallowing and chewing
  • face and neck: head drop, ptosis
161
Q

What may you see on examination of a myasthesia gravis

A
  • fading voice when asking patient to count to 50
  • ask patients to stretch out arms and look for downward drift
  • ask patient to look up - look for ptosis
162
Q

What investigations should you perform for myasthesia gravis

A
  • Tensilon Test
  • AchR antibodies
  • MuSK antibodies
  • EMG - may be normal but repetitive stimulation of nerve may demonstrate decrements in muscle action potential
  • CT Thorax - look for thyoma
163
Q

What is Myasthesia Gravis associated with

A
  • Thymic Hyperplasia/ Thyoma

- Other AI disease: thyroid

164
Q

What is a differential diagnosis of Myasthesia Gravis

A

Generalised muscle weakness in MND

165
Q

What is the management of Myasthesia Gravis

A
  • Acetylcholine esterase inhibitors e.g Pyridostigmine
  • Immunosupressents e.g Steroid (prednisolone) or Azathriopine/Methotrexate
  • Thymectomy
166
Q

What is a Myasthenic Crisis

A

Severe weakness including the respiratory muscles it is life threatening
Can be caused by infection, relapse, medication dosing

167
Q

How is a Myasthenic Crisis managed

A

Urgent!!
Monitor FVC
Treat with IVIG or plasma exchange
Identify and treat trigger

168
Q

What is Multiple Sclerosis

A
  • Chronic inflammatory demyelinating autoimmune disorder specific to the CNS
  • it causes multiple plaques of demyelination within the brain and spinal cord
169
Q

What is the cause of Multiple Sclerosis and who is at risk

A
  • Genetic Predispostion + Environmental Trigger (infection (EBV) or Vit D deficiency)
  • Most common in women
170
Q

What is usually the age of onset in MS

A

Early adulthood

171
Q

What are the 3 types of progression of MS

A
  • Relapsing/ Remitting - periods of relapse followed by periods of remission where they are well
  • Primary Progressive - disease progressively worsens from onset
  • Secondary Progressive - disease begins as relapsing/remitting followed by progression
172
Q

How does an MS patient usually present and how does regression occur

A
  • young adult with two or more clinically distinct episodes of CNS dysfunction followed by remission
  • resolution of inflammation and partial remyelination
173
Q

What are the symptoms of MS

A 
- Optic Neuropathy: impaired vison and 
   unilateral eye pain
- Spinal cord lesions
   \+ Sensory: numness, paraesthesia 
   \+ Motor: spastic weakness
   \+ Autonomic: Sexual Dysfunction and urine 
      retention
- Cerebellar: Charots Triad: nystagmus, 
   dysarthia and intention tremor 
- Change in mental state: memory, impaired 
  concentration
174
Q

What sign in MS causes electric shock sensations down spine when they flex their neck

A

Lhermittes Sign

175
Q

What are MS symptoms exacerbated by

A

Uthoffs Sign - Fever, physical, exersion, warm water (worsen with heat)

176
Q

What investigations should be performed in suspected MS

A
  • Detailed Hx and Examination
  • MRI - may show plaques
  • Nerve Conduction Studies - Prolonged
    evoked potential
  • LP: increased protein and cell count
    electrophoresis: Oligoclonal bands
177
Q

What is the management of Relapsing/Remitting MS

A 
Medications for relapsing/remitting 
Relapses: 
- 1st line: Steroids - IV methyprednisalone shortens 
- 2nd line: Plasmapheresis 
To prevent relapses in remission:
- 1st line: Interferon therapy: IFN-B 
- 2nd line: Natalizumab
178
Q

What is the management of Primary Progressive MS

A

No drugs to manage primary progressive

179
Q

What supportive management can be given to those with MS especially those with primary progressive

A
  • Spasticity: baclofen, diazapam, physio
  • Paraesthesia: Amitriptyline
  • Tremors: Beta Blockers
  • Urinary Incontinence: Oxybutinin
180
Q

What is Motor Neurone Disease

A

Neurodegenerative Disease of the UMN and LMN

181
Q

What is MND pathophysiology

A

LMN: Destruction of motor neurones in anterior horn of spinal cord and brainstem
UMN: Destruction of lateral corticospinal tracts in motor cortex

182
Q

How can you distinguish MND from MS

A

No sensory loss or sphincter disturbance

183
Q

What most commonly causes death in MND patients

A

Respiratory failure from bulbar palsy and pneumonia

184
Q

Who does MND most commonly present in

A

Middle aged men
Most cases are sporadic with no FHx
Rare familial cases

185
Q

What are the 4 clinical patterns of MND

A

All 4 no involvement of sensory system or motor nerves of eyes or sphincters
- Amyotrophic Lateral Sclerosis - most common
- Progressive muscular atrophy- predominantly LMN
affected
- Progressive bulbar and pseudobulbar palsy - destruction
of UMN and LMN cranial nerves (dysarthia, dysphagia)
- Primary lateral Sclerosis

186
Q

What are the features of Amyotrophic Lateral Sclerosis

A

UMN and LMN signs
UMN: spasticity, hypertonia, hyperreflexia, no fasiculations, no atrophy, babinski +ve
LMN: flaccidity, hypotonia, hyporeflexia, fasciculation’s present, severe atrophy of muscles, babinski -ve

187
Q

What are the investigations for MND

A

Clinical

Fasciculations are characteristic

188
Q

How can you differentiate between MND and cervical spine lesions with UMN and LMN signs

A

Cervical spine lesions often will have sensory signs

189
Q

How is MND managed

A

There is no cure
Riluzole delays progression of disease by a few months
Ventilatory support
NG feeding tube

190
Q

What are the features of spinal cord compression

A
  • UMN deficit below the lesion due to disruption to corticospinal pathways
  • Sensory impairment below the lesion due to disruption of spinothalamic and dorsal coulmn function
  • Acute spinal compression can present as spinal shock (flaccid weakness and no UMN signs)
  • Lhermittes Phenomenom
  • Painless Atonic Bladder
191
Q

What are the causes of spinal cord compression

A

Secondary malignancy
Infection e.g spinal TB
Cervical disc prolapse
Trauma

192
Q

What investigations should you perform for spinal cord compression

A

Urgent MRI!!! especially acute to prevent irreversible paralysis

193
Q

What spinal cord syndromes are not caused by compression

A

Inflammation
Infarction
MND
Syrinx

194
Q

What is cauda equina

A

Spinal damage distal to L1

195
Q

What does cauda equina present as

A

bilateral sciatica
leg weakness
bladder/bowel dysfunction
saddle paraesthesia/numbess

196
Q

What is the management of cauda equina

A

Medical emergency

Surgical Decompression

197
Q

What is a mononeuropathy

A

affects a single nerve OR multiple mononeuropathy/mononeuritis multiplex affects several random nerves

198
Q

What causes single mononeuropathy

A

Acute compression/entrappment of a nerve
OR
Direct damage to nerve through surgery, trauma

199
Q

What is the most common cause of single neuropathy

A

Carpel Tunnel Syndrome - pressure on median nerve

200
Q

What causes carpel tunnel syndrome

A 
Idiopathic
Pregnancy
Obesity 
DM
RA 
Hypothyroidism
201
Q

What are the clinical features of carpel tunnel

A

Pain and paraesthesia
Weakness and wasting of thenor muscles
Sensory loss of palm and palmer aspects of 3 radial and a half fingers
Tapping will cause pain: Tinnels and Phallens

202
Q

How is mononeuropathys managed

A

Treat the cause
Nocturnal Splints (carpel tunnel)
Local Steroid injections
Surgical decompression

203
Q

What other mononeuropathys

A

Ulner Nerve - Elbow - Tennis Elbow
Radial Nerve - wrist drop from pressure of humerus - Saturday night syndrome
Common Peroneal Nerve - pressure of head of fibula - lateral loss of sensation -leg crossing

204
Q

What causes multiple mononeuropathy/ mononeuritis multiplex

A

Individual nerves picked off randomally
Often inflammatory/ autoimmune mediated
e.g Vasculitis and Connective Tissue Disorders

W egners
A IDs/Amyloid 
R heumatoid
D M
S arcoidosis

P AN
L eprosy
C arcinoma

205
Q

What are the three types of the peripheral neuropathys

A

Polyneuropathy
Mononeuropathy
Mononeuropathy Multiplex

206
Q

What are polyneuropathys

A

Disorders of the peripheral nerve whos distribution is usually symmetrical and widespread
Can be sensory, motor or both
Chronic, Slow and Progressive
Starts in the most distal nerves

207
Q

What is the most common cause of peripheral polyneuropathy

A 
Diabetes 
idiopathic 
Uncommon: 
Deficiency states B12/Folate
Alcohol/Toxins/Drugs
Hereditary Neuropathies
Paraneoplastic Syndromes/Malignancy 
Metabolic Syndromes: Thyroid/ Renal Failure
208
Q

What investigations should you do for neuropathies

A 
Hx and Ex
Neuropathy Screening 
Vasculitic Screening 
EMG/NCS
CSF Study 
Nerve Biopsy
209
Q

What neuropathy screening tools are there

A

FBC, ESR
Glucose, U&E, TFT
B12/ Folate
HIV

210
Q

What Vasculitic Screening tools are there

A

FBC, ESR
ANA, ANCA, compliment, RhF
CRP

211
Q

How are neuropathys managed

A

Idiopathic - no treatment - manage pain with pregabalin/ amitriptyline
Treat remove/underlying cause e.g DM/glusose
Inflammatory Neuropathy - Prednisalone with steroid sparing agent e.g azathioprine
Vasculitis Neuropathy - Prednisalone + Immunosuppresent e.g cyclophosphamide

212
Q

What is the most common cell type of primary brain tumours

A

Majority glial cell!!!

  • Astrocytoma
  • Oligodendroglioma
213
Q

Where do secondary brain tumours originate from

A 
Breast
Prostate 
Thyroid 
Kidney 
Stomach
214
Q

What are three clinical features of brain tumours

A
  1. Progressive Neurological Deficit - dependent on site of tumour
  2. Raised Intracranial Pressure - headache, vomiting and
    papilloedema - can lead to pressure on brainstem
  3. Epilepsy
215
Q

What investigations should you perform for brain tumours

A

CT & MRI

216
Q

What is the management for brain tumours

A

Surgical resection of tumour and Radiotherapy

217
Q

What is benign ICP

A

headache and papilloedema in young obese females
Management:
Weight loss, loop diuretics and predinisalone

218
Q

What are the contraindications for a lumbar puncture

A

Raised Intracranial Pressure!!!

- Due to pressure gradient can cause coning and neurological deterioration even death!!!

219
Q

What is Hydrocephalus

A

Excessive amounts of CSF within the ventricles causing raised ICP most often due to obstruction of outflow of CSF

220
Q

What can cause Hydrocephalus

A

Congenital
Malignancy
Meningitis
Subarachnoid Haemorrhage

221
Q

What is the presentation of Hydrocephalus

A

Signs of raised ICP and ataxia

222
Q

What is the management of Hydrocephalus

A

Diagnosed on MRI/CT

Surgical insertion of a shunt

223
Q

What is meningitis

A

Inflammation of the meninges

224
Q

What are the causes of meningitis

A

Bacterial
Viral
Fungi

225
Q

What bacteria cause bacterial meningitis

A

Neisseria Meningitidis
Streptococcus Pneumoniae
Listeria Monocytogenes
Haemophilus Influenzae

226
Q

What viruses cause Viral Meningitis

A 
Enterovirus 
Mumps
Herpes Simplex (HSV)
HIV
EBV
227
Q

What is the presentation of acute bacterial meningitis

A 
Headache
Neck Stiffness
Fever 
Photophobia 
Vomiting 
Papilloedema 
Progressive Drowsiness
228
Q

What can acute bacterial meningitis lead to and what symptoms may you get

A

Meningococcal Septicaemia

- a non blanching purpuric rash and signs/ symptoms of shock

229
Q

What is the presentation of viral meningitis

A

Same symptoms except no rash or sepsis - usually self limiting condition

230
Q

What is the deifferential diagnosis of meningitis

A

Subarachnoid Haemorrhage
Migraine
Viral encephalitis

231
Q

What investigations may be done for someone with suspected meningitis

A

Head CT scan
Lumbar Puncture -B - WCC high, Protein high, low glucose
-V - WCC normal, Protein slightly raised,
glucose normal
Blood cultures
CXR

232
Q

What is the management of a pateint with suspected meningococcal septicaemia

A
  • Medical Emergency!!!!!!
  • Non blanching rash is a sign
  • LP is contraindicated in Sepsis!! - coning
  • Do blood culture instead
  • Start immediate treatment of IV benzylpenicillin or IV
    cefotaxime
  • BUFALO
233
Q

What is the management of meningitis

A

Cefotaxime IV add ampicillin if risk of listeria

Treatment depends on results from MC&S

234
Q

What is meningococcal Prophylaxis

A 
Oral Ciprofloxacin (tendon disorders and quinalones)
Vaccination
235
Q

What is Encephalitis

A

Inflammation of the brain

236
Q

What is the presentation of Encephalitis

A

Unlike meningitis - it leads to abnormal cerebral function, mental state, motor and sensory deficiencies

Mild - most common - self limiting fever, headache and
drowsy
Less common - severe focal signs, seizures and coma/death

237
Q

What is Encephalitis caused by

A

Viruses - Herpes Simplex, HIV, Mumps

Can also occur in a bacterial infection

238
Q

Who is encephalitis most common in

A

Immunosuppressed
MSM
IVDU

239
Q

What infection can be concerning in encephalitis

A

Herpes - death or brain injury follows herpes encephalitis for many in the UK

240
Q

What investigations should be performed in Encephalitis

A

CT/MRI
CSF - high WCC and high protein
Viral serology or blood cultures
EEG

241
Q

What is the treatment for encephalitis

A

Suspected HSV - start IV aciclovir immediately

242
Q

What is the Cerebellum responsible for

A

Co-ordinating movements

Maintenance of balance and posture

243
Q

What are the pathways of the the Cerebellum

A

Ipsilateral

244
Q

What causes Cerebellar Lesions

A 
MS
Primary/Secondary Tumours 
Haemorrhage/Infarct 
Chronic Alcohol use 
Anti-epileptic Drugs
245
Q

What are the clinical features of Cerebellar Disease

A 
Ataxia 
Dysarthia 
Dysphagia 
Nystagmus 
Clumsiness
Tremor
246
Q

How is Cerebellar Disease diagnosed

A

Hx and Ex

MRI

247
Q

What are muscular dystrophys

A

Inherited groups of progressive myopathic disorders affecting normal muscle function

248
Q

What is Duchenne Muscular Dystrophy

A

An X linked mutation
Presents in early childhood with weakness in proximal legs progressing to other muscle groups leading to severe disability and death in late teens
No curative treatment

249
Q

What tract relays motor response

A

The corticospinal tract

250
Q

Where does the corticospinal tract cross

A

The medulla

251
Q

What tract relays sensory response

A

Dorsal Columns - Vibration and Light Touch/proprioception

Spinothalamic - Pain and Temperature

252
Q

Where does the posterior column cross

A

The medulla

253
Q

Where does the spinothalamic cross

A

1-2 segments above point of entry

254
Q

What are the 12 cranial nerves

A

Olfactory - smell
Optic - vision
Oculomotor - eye movements and pupil reflex (inferior oblique, medial, superior and inferior rectus)
Trochlear - eye movements (superior oblique)
Trigeminal - face sensation and chewing
Abducens - eye movements (lateral rectus)
Facial - face movment and taste
Vestibulocochlear - hearing and balance
Glossopharyngeal - throat sensation, taste and swallowing
Vagus - movement, sensation and abdominal organs
Accessory - neck movements
Hypoglossal - tongue movement

255
Q

What would you get in a unilateral transverse lesion

A

Brown - Sequard Syndrome
Ipsilateral loss of vibration and proprioception
Ipsilateral weakness
Contralateral loss of pain temperature

256
Q

What would you get in central cord syndrome

A

Quadraparesis
Rare: loss of pain/temperature sensation in upper > lower extremities
+/- bladder dysfunction

257
Q

What would you get in anterior cord syndrome

A 
Paraplegia
Loss of pain/temperature 
Autonomic Dysfunction 
Bowel, Bladder and Sexual Dysfunction
Preservation of dorsal columns
258
Q

What is the most common fatal accidental poisoning

A

CO poisening

Headache, N&V, Confusion, Coma, Death

259
Q

What can Amphetamines and other stimulants cause

A 
Seizures
Psychosis
Ischaemic Stroke 
Intracranial Haemorrhage 
Coma
260
Q

What are the symptoms of alcohol overdose

A

Ataxia
Dysarthia
Nystagmus
Coma

261
Q

What are the symptoms of alcohol withdrawal

A

6-8hrs Tremor, anxiety, nausea
24hrs Delirium Tremens - Visual Hallucinations
48hrs Generalised Tonic-Clonic Seizures
3-5 days rare hyperactivity

262
Q

How should you treat alcohol withdrawal

A

Thiamine (BEFORE GLUCOSE)
Multivitamins
Benzodiazapine

263
Q

What is Wernickes Encephalopathy

A

Thiamine Deficiency
Opthalmoparesis, Ataxia and Confusion
Majority improve however some develop Korsakoffs Psychosis may emerge as Wernickes resolve
Possibly irreversible

264
Q

Apart from Wenickes Encephalopathy what else can alcohol lead to

A 
Cerebellar Degeneration 
Peripheral Neuropathy 
Colour Blindness
Dementia
Tremor 
Central Pontine Myelinolysis
265
Q

What virus causes chicken pox

A

Varicella Zoster Virus (one of the herpes viruses)

266
Q

What is is called when varicella zoster virus reactivates from latent phase

A

Herpes Zoster

267
Q

Where does herpes zoster remain dormant before reactivation

A

In dorsal root ganglia and/or cranial nerve ganglia

268
Q

What does reactivation of herpes zoster lead to

A

Shingles

269
Q

What is the risk to others with shingles

A

Could cause chickenpox in a non-immune individual after close touch or contact

270
Q

What are the clinical features of shingles

A

pain and tingling in a dermatomal distribution followed by a rash a few days later
The rash consists of papule and vesicles in the same dermatome

271
Q

What are the most common dermatomes for shingles

A

Lower Thoracic Dermatome

Ophthalmic Trigeminal Dermatome

272
Q

What is the management of shingles

A

Oral Acyclovir

273
Q

What is a complication of shingles

A

post herpatic neuralgia which can be sever and last for years
Meningitis or Encephalitis
Blindness - if near eye (ulceration)

274
Q

How can you treat PHN

A

Carbamazipine - quick treatment of acyclovir reduces risk of PHN

275
Q

What can be given to reduce risk of shingles

A

The varicella vaccine (in over 70s)

276
Q

What may lead to you developing shingles

A

Weakened Immune System:

  • Increasing age
  • HIV/AIDS
  • Stress
  • Chemotherapy
  • Immunosupression - organ transplant
277
Q

What are the symptoms of DCM

A

DCM symptoms can include any combination of :
Pain (affecting the neck, upper or lower limbs)
Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence and/or impotence) - these can occur and do not necessarily suggest cauda equina syndrome in the absence of other hallmarks of that condition
Hoffman’s sign: is a reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.

278
Q

What is Degenerative Cervical Myelopathy

A

Degenerative of the cervical intravertbrae discs in the leading to spinal cord compression in the neck

279
Q

How is DCM treated

A

Urgent referral for assessment to prevent permanent damage

Decompressive Surgery!!!

280
Q

What opiate can help with nerve pain

A

Tramadol

281
Q

What is the treatment of nerve pain

A

1st line: amitriptyline, pregablin, gabapentin

2nd line: tramadol

282
Q

What are the rules for group 1 drivers following a TIA

A

Can start driving if symptom free after 1 month and no need to inform DVLA

283
Q

What is the contraindication of Triptan

A

Cardiovascular Disease

284
Q

What is normal pressure hydrocephalus

A

Normal pressure hydrocephalus is a reversible cause of dementia seen in elderly patients. It is thought to be secondary to reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.

285
Q

What is the triad of symptoms of normal pressure hydrocephalus

A 
Wet, Wobbly and Wacky 
A classical triad of features is seen
urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson's disease)
286
Q

What is a differential for GBS

A

Charot Marie Tooth Disease

Autosomal Dominant - Sensorimotor Neuropathy

287
Q

What is the treatment of Meningococcal Septicaemia in the community

A

IM benzylpenicillin

Report to the proper officer at the local council

288
Q

What is multiple system atrophy

A

Multiple system atrophy is a cause of Parkinsonism which can be difficult to differentiate from idiopathic Parkinson’s disease. Key features to help you differentiate are the presence of unilateral symptoms, and more severe/early onset autonomic dysfunction (postural hypotension/erectile dysfunction).

289
Q

What is a pontine haemorrhage

A

Pontine haemorrhage is a life-threatening condition. It often occurs as a complication secondary to chronic hypertension. Patients often present with reduces Glasgow coma score, quadriplegia, miosis, and absent horizontal eye movements

290
Q

What lesions are homonymous quantrantinopias

A

PITS (Parietal-Inferior, Temporal-Superior)

291
Q

What dementia is associated with MND

A

Frontotemporal dementia

292
Q

How does a 3rd nerve palsy present

A

Affected eye looks down (hypotropia) and out (exotropia)
Ptosis
Diplopia

Compression - fixed dilated pupil
ischaemic microangiopathy - pupil sparing

293
Q

How does a 4th nerve palsy present

A

Extorsion of the eye

Diplopia

294
Q

How does a 6th nerve palsy present

A

Esotropia

Diplopia

295
Q

What is facial nerve palsy caused by

A 
Bells Palsy (idiopathic)
Lymes Disease 
Ramsey Hunter Syndrome 
Meningits 
TB, Viruses 
Stroke 
MS 
Tumour 
Guillian Barre (bilateral) 
Diabetes 
Sarcoidosis
296
Q

What is Ramsey Hunter Syndrome what are the symptoms and how is it treated

A

When latent varicella zoster virus reactivates in the ganglion of the 7th cranial nerve

Symptoms:

  • Painful vesicular rash on auditory canal +/- drum, pinna, tongue palate or iris
  • Ipsilateral Facial Palsy
  • Loss of taste
  • Vertigo
  • Tinnitus/Deafness
  • Dry mouth and Eyes

Treatment: Acyclovir + Prednisolone (as for Bells Palsy)

297
Q

What symptoms do you get for a facial nerve palsy

A 
Abrupt Onset: 
Complete Unilateral Face Weakness 
Unilateral sagging of the mouth 
Drooling of Saliva 
Food trapped between gum and cheek 
Speech Difficulty 
Failure of eye closure making watery/dry eye
Ipsilateral numbness or pain around the ear
Decreased Taste 
Hypersensitivity to Sound
298
Q

What are the signs of Facial Nerve Palsy

A

UMN (brainstem) lesion - Patients are able to close eyelids and frown, symptoms present as contralateral

LMN - (peripheral) lesion - Patients are unable to close eyelids fully and frown, symptoms are present ipsilateral (Bells)

299
Q

What tests are done for Facial Nerve Palsy

A

Bloods - ESR, glucose, Increased Borriella Antibodies in Lymes, Increased VZV antibiodies in Ramsey Hunter
MRI - space occupying lesions
CSF - infection
Nerve Conduction Studies

300
Q

What is the Management of Bells Palsy

A

Prednisolone

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