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NEUROLOGY Flashcards

1
Q

What are the red flag symptoms for a patient presenting with a headache?

A
  1. Thunderclap - SAH
  2. Waking at night (+ weight loss + focal signs) = malignancy
  3. Fever w worsening headache, neck stiffness + rashes = meningism
  4. Scalp tender, visual changes, jaw claudication = GCA
  5. New-onset focal neurological deficits, personality change or cognitive decline = intracranial haemorrhage, stroke, SOL
  6. Headache that is posture dependent = raised ICP
  7. Headache associated with severe eye pain/blurred vision/N+V/red eye = AACG
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2
Q

What are the features of a migraine with NO aura?

A
  • recurrent attacks lasting 4-72hrs
  • unilateral
  • fully reversible
  • pulsating character
  • nausea + photophobia
  • pt prefers to be still in dark room
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3
Q

What are the features of a migraine with aura?

A
  • 15-30mins aura followed by 1hr unilateral throbbing headache
    Auras:
  • sparks in vision, blurring vision, lines across vision, lots of different visual fields
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4
Q

What is the acute management for a pt with a migraine?

A
  1. Oral triptan plus NSAID/paracetamol
  2. Consider nasal triptan in young people
  3. Prochlorperazine
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5
Q

When is the use of triptans contraindicated?

A
  • IHD
  • coronary spasm
  • uncontrolled HTN
  • SSRI use
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6
Q

When would you give prophylaxis for migraines? What do you give?

A

Offer to pts experiencing 2 or more migraines/month

  1. Propranolol (unless asthmatic)
  2. Topiramate (unless pregnant)
  3. Amitriptyline
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7
Q

How are tension headaches managed?

A
  1. Reassurance
  2. Basic analgesia
  3. Relaxation techniques
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8
Q

What is the acute management for cluster headaches?

A
  1. Triptans SC

2. High flow oxygen for 15-20 mins

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9
Q

What can be used as prophylaxis from cluster headaches?

A
  1. Verapamil
  2. Lithium
  3. Prednisolone (2-3 wks short course can break cycle)
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10
Q

What condition is commonly associated with giant cell arteritis?

A

Polymyalgia rheumatica

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11
Q

What is the gold standard test to diagnose GCA?

A

Temporal artery biopsy

  • must be taken within 7 days of starting steroids
  • skip lesions may be present
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12
Q

How do you manage GCA?

A
  1. High dose prednisolone - 6mg/day
  2. PPI + aspirin
  3. URGENT opthalmology r/v for pts with visual changes
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13
Q

What pre-hospital management can be given for suspected meningitis? (e.g. in primary care setting)

A
  • if NO RASH present, transfer urgently to hospital with no Abx
  • if rash present, give IM benzylpenicillin
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14
Q

What investigations should be performed in suspected meningitis?

A
  1. Bloods - U+E, FBC, LFT, glucose, coag screen, ABG, CRP
  2. Blood cultures + throat swab
  3. Whole blood PCR for N -meningitides
  4. LP - only if NO raised ICP signs
  5. CXR to r/o TB
  • only perform CT head if reduced GCS or focal neurological signs
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15
Q

What is the treatment for pts presenting to hospital with suspected bacterial meningitis (over 3months age)?

A

Dexamethasone + ceftriaxone or cefotaxime

  • tend to continue Abx for about 10 days
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16
Q

What Abx treatment is given to pts under 3 months presenting with bacterial meningitis?

A

cefotaxime + amoxicillin

- all those with bacterial meningitis should have hearing assessment within 4 months of discharge

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17
Q

What are the 3 branches of the trigeminal nerve?

A 
V1 = ophthalmic
V2 = maxillary 
V3 = mandibular
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18
Q

What are the main causes of trigeminal neuralgia?

A

Can be idiopathic

  • MS can cause it
  • Can be caused by compression by SOL = MRI is key to exclude this!!
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19
Q

How do you manage trigeminal neuralgia?

A
  1. Carbamazepine
  2. Refer to neuro if failed medical treatment or under 40
  3. Surgical decompression
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20
Q

What is the most common + severe cause of encephalitis? Name a few others also.

A

HSV-1

- others = echoviruses, VZV, EBV, coxsackie, mumps, measles, influenza

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21
Q

What investigations should be performed in a pt with suspected encephalitis?

A
  1. CSF - lymphocytosis, raised protein
  2. PCR for HSV
  3. CT head
  4. EEG
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22
Q

How is encephalitis managed?

A
  1. IV aciclovir for 2-3 weeks if HSV encephalitis
  2. Anticonvulsants if experiencing seizures
  3. Dexamethasone if features of raised ICP
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23
Q

What treatment can be used to help with hormonal headaches?

A

COCP

- hormonal headaches occur normally due to low oestrogen

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24
Q

What is cervical spondylosis? What are the typical symptoms?

A

Common condition caused by degenerative changes in cervical spine
- causes neck pain, usually made worse by movement BUT can often present with a headache

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25
Q

What are some risk factors for developing SAH?

A
  • smoking
  • HTN
  • alcohol misuse
  • cocaine use
  • post-menopausal
  • low oestrogen
  • neurofibromatosis
  • CTDs
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26
Q

What investigations should be performed in suspected SAH?

A
  1. CT head - blood will cause hyper attenuation in subarachnoid space
  2. LP - do if CT neg. Will have raised RCC (+ xanthochromia after 12hrs)
  3. Angiography used later to identify source of bleeding
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27
Q

How do you manage SAH?

A

IMMEDIATE NEUROSURGICAL REFERRAL

  1. Maintain cerebral perfusion
  2. Nifedipine given to reduce vascular spasm
  3. Endovascular coiling
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28
Q

What will the CT be like for an extradural haemorrhage?

A

They have a biconvex (lemon) shape, limited by cranial suture lines

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29
Q

How do you manage extradural haemorrhage?

A
  1. Reduce ICP
    - 30 deg head tilt
    - mannitol
    - hyperventilate + sedation
  2. Definitive management = craniotomy + evacuation of haematoma
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30
Q

What will the CT be like for subdural haemorrhage?

A 
Crescent shaped (banana)
- not limited by cranial suture lines
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31
Q

What are some arrhythmic causes of syncope?

A
  • sick sinus syndrome
  • 2nd degree AV block
  • 3rd degree AV block
  • dysfunctional pacemaker
  • Supraventricular = AF, flutter, AVN re-entry tachycardia
  • VT = more likely to cause syncope than SVT
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32
Q

What are some structural cardiogenic causes of syncope?

A
  • Valvular disease e.g. aortic stenosis
  • Cardiac masses e.g. atrial myxoma
  • Cardiomyopathy e.g. HOCM
  • Pericardial disease e.g. constrictive pericarditis
  • Non-cardiac = PE, aortic dissection
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33
Q

What are red flag features of cardiogenic syncope which requires urgent CV assessment within 24hrs?

A
  1. ECG abnormality
  2. TLOC during exertion
  3. New/unexplained breathlessness
  4. Heart failure
  5. FHx of sudden cardiac death in those under 40y
  6. Presence of heart murmur
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34
Q

How do you manage AV node block if pt is unstable or risk of asystole?

A

Risk of asystole = mobitz type 2, complete heart block, prev asystole
1. IV Atropine 500mcg

If high risk of asystole:

  1. temporary transvenous cardiac pacing
  2. Permanent pacemaker
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35
Q

How do you manage a pt with VT who has (i) signs of shock (ii) haemodynamically stable?

A

(i) Immediate cardioversion is indicated if sBP under 90, chest pain, HF or syncope
(ii) Amiodarone, if this fails use cardioversion

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36
Q

What is the acute management for SVT?

A
  1. Vagal maneouvres
  2. IV adenosine
  3. Electrical cardioversion
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37
Q

What preventative management can be given to pts with SVT?

A
  1. Beta-blockers

2. Radio-frequency ablation

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38
Q

What are the 3 main causes of neurally mediated syncope?

A
  1. Vasovagal
  2. Situational syncope
  3. Carotid sinus hypersensitivity
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39
Q

What is carotid sinus hypersensitivity?

A

Syncope after manual manipulation of carotid sinus, which can happen accidentally whilst shaving, wearing a tight shirt collar or even certain head movements.

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40
Q

What are some causes of postural (orthostatic) syncope?

A
  1. Autonomic nervous failure secondary to drugs = most common cause
  2. Hypovolaemia
  3. Primary autonomic nervous disorder
  4. Secondary autonomic nervous disorder
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41
Q

With lying + standing BP, what is a significant drop in BP?

A

Drop of more than 20/10 mmHg within 3 mins of standing

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42
Q

What advice should you give for pts with postural syncope? What medical treatment can be used last line?

A
  1. Address cause
  2. Pt education re posture change, alcohol, heat + dehydration
  3. Raise head of bed, get up gradually
  4. BP monitoring
  5. Salt + water intake increased
  6. Medical treatment = fludrocortisone, midodrine
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43
Q

What clinical features are suggestive of epilepsy?

A
  • attacks when lying down/sleeping
  • aura before
  • altered breathing, cyanosis
  • obvious trigger e.g. TV
  • tonic-clonic movements
  • incontinent of urine, tongue biting
  • prolonged post-ictal drowsy/confusion/amnesia
  • transient focal paralysis (Todd’s palsy)
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44
Q

If seizure starts focally + then progresses to GTCS, what type of seizure is it?

A

Focal seizure

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45
Q

How are generalised tonic clonic seziures managed?

A
  1. Sodium valproate or lamotrigine

2. Carbamazepine or topiramate

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46
Q

What are the further classifications of focal seizures?

A
  1. Focal aware
  2. Focal unaware
  3. Awareness unknown
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47
Q

How are focal seizures managed?

A
  1. Carbamazepine

2. Sodium valproate or lamotrigine

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48
Q

What are absence seizures?

A

Usually in children

  • pt becomes blank, stares in space + then abruptly returns to normal
  • loss of awareness + unresponsive
  • vacant expression for about 10seconds

Majority stop having once they get older
- treat with sodium valproate or ethosuximide

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49
Q

What are atonic seizures? How do you manage them?

A

DROP ATTACKS
- characterised by brief lapses in muscle tone usually last less than 3 mins

Management = sodium valproate then lamotrigine

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50
Q

What investigations should you perform in a patient with seizures?

A
  1. ABCDE, vitals, SaO2
  2. Neuro exam
  3. ECG
  4. EEG
  5. Blood glucose
  6. FBC to r/o infection
  7. U+E, bone profile - Na, Ca, Mg
  8. Toxicology screen
  9. Head CT
  10. Serum prolactin (doubled in GTCS)
  11. Serum CK (may be raised in GTCS)
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51
Q

What are some side effects of sodium valproate?

A
  • teratogenic so avoid in women of child-bearing age
  • liver damage/hepatitis/pancreatitis
  • hair loss
  • tremor
  • increased appetite + weight gain
  • nausea
  • thrombocytopenia
  • hyponatraemia
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52
Q

What are some examples of cytochrome P450 inducers? What effect shall they have on drugs metabolised by cytochrome p450?

A 
CRAPS out drugs
C - carbamazepine
R - rifampicin
A - barbituates (phenobarbitone)
P - phenytoin
S - St Johns Wort 
Others = chronic alcohol intake, smoking
  • they reduce the concentration of drugs metabolised by cP450 system
53
Q

What are some examples of cytochrome P450 inhibitors? What effect shall they have on drugs metabolised by cP450 system?

A

Some Certain Silly Compounds Annoyingly Inhibit Enzymes Grr

S - sodium valproate, SSRIs (fluoxetine, sertraline)
C - ciprofloxacin
S - sulphonamide
C - cimetidine/omeprazole
A - antifungals, amiodarone, allopurinol
I - isoniazid 
E - erythromycin/clarithromycin
G - grapefruit juice 
Others = acute alcohol intake
  • increase concentration of drugs
54
Q

What drugs are metabolised by the p450 system?

A
  • warfarin
  • COCP
  • theophylline
  • corticosteroids
  • tricyclics
  • pethidine
  • statins
55
Q

What is the definition of status epilepticus?

A

Seizure lasts longer than 5 mins or repeated seizures without intervening consciousness (more than 3 in 1hr)

56
Q

How is status epilepticus managed in the (i) community (ii) secondary care?

A

(i) buccal midazolam or rectal diazepam
(ii) 1. Secure airway + high-flow O2
2. Assess CV + RS
3. Check BM
4. Gain IV access
5. IV Lorazepam 4mg - repeat after 10 mins if seizures persist
6. IV phenytoin if seizures persist - requires cardiac monitoring

57
Q

What are some risk factors for stroke?

A
  • HTN
  • PVD
  • hypercholesterolaemia
  • AF
  • smoking
  • Hx of TIA
  • Alcohol excess
  • COCP
  • DM
  • Syphillis
  • Heart disease
  • Carotid bruit
  • increased clotting e.g. Factor V Leiden
58
Q

What are the features of a total anterior circulation stroke? Where does it occur?

A

ACA or MCA
All 3 of:
1. Unilateral weakness (and/or sensory loss) of face, arm + leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction (dysplasia, visuospatial disorder)

59
Q

What are the features of a partial anterior circulation stroke?

A

Cortical stroke in ACA or MCA
2 of the following:
1. Unilateral weakness (and/or sensory loss) of face, arm + leg
2. Homonymous hemianopia
3. Higher cerebral dysfunction (dysplasia, visuospatial disorder)

60
Q

What are the features of a posterior circulation stroke?

A

At least 1 of:

  1. Cerebellar or brainstem syndrome
  2. LoC
  3. Ataxic hemiparesis
61
Q

What are the features of Lacunar syndrome?

A 
Subcortical stroke due to small vessel disease
1 of:
1. Unilateral weakness
2. Pure sensory stroke
3. Ataxic hemiparesis
62
Q

What are the symptoms of a cerebellar stroke? (HINT: DANISH)

A 
D - dysdiadokokinesia 
A - ataxia 
N - nystagmus
I - intention tremor
S - slurred speech
H - hypotonia/hyporeflexia
  • intense headache, N+V, vertigo
63
Q

What does the NIHSS score do?

A

quantifies impairment caused by stroke

64
Q

What investigations should you perform in suspected stroke?

A
  1. Non-contrast CT head - to r/o haemorrhage
  2. MRI - shows changes early in infarction + later, the extent of damage
  3. Bloods - r/o hypoglycaemia, infection + other stroke mimics, assess risk factors for stroke (cholesterol, clotting)
  4. ECG + 24h tape to look for arrhythmias
  5. Carotid artery doppler - look for carotid artery stenosis
65
Q

What are some causes of ischaemic stroke?

A
  1. HTN - retinopathy? Nephropathy? Cardiomegaly?
  2. Cardiac source of Emboli - do echo + 48h tape
  3. Carotid artery stenosis - carotid USS or CT angio
  4. Hypo/hyper-glycaemia, dyslipidaemia, hyperhomocystinaemia
  5. Vasculitis - do ESR, ANA
  6. Prothrombotic states e.g. thombophilia, antiphospholipid syndrome
  7. Hyperviscocity e.g. polycythaemic, sickle cell
66
Q

How do you immediately manage a suspected stroke?

A
  1. Admit to stroke unit?
  2. A-E assessment (remember to assess swallowing)
  3. CT head
  4. If CT rules out haemorrhage:
    - thrombolysis (alteplase) if less than 4.5h since onset
    - aspirin 300mg for 2 weeks
  5. If haemorrhage present:
    - refer to neurosurgery
    - AVOID drugs that interfere with clotting
  6. Stroke rehab with MDT
67
Q

What secondary prevention is required post-ischaemic stroke?

A
  1. Clopidogrel 75mg OD
  2. Atorvastatin 80mg OD
  3. Carotid endarterectomy if stenosis over 70%
  4. Treat modifiable risk factors = HTN, lipids, smoking cessation, DM
  5. Anticoagulate if AF is cause
68
Q

What are the causes of TIA?

A
  1. Atherothromboembolism from carotid artery is chief cause
  2. Cardioembolism - post-MI, AF, valve disease, prosthetic valves
  3. Hyperviscocity - polycythaemia, sickle cell, myeloma
  4. Vasculitis
69
Q

What are some conditions which can mimic a TIA?

A
  • syncope
  • migraine
  • retinal haemorrhage/detachment
  • hypoglycaemia
  • atypical seizure
  • temporal arteritis
  • labyrinthine disorders (present as vertigo + can be confused with posterior circulation TIA)
70
Q

What investigations should be performed in a pt with suspected TIA?

A

Find cause + define vascular risk!

  1. FBC, U+E, ESR
  2. Glucose + lipids
  3. CXR
  4. ECG
  5. Carotid artery doppler + angiogram
  6. CT if high risk
  7. Echo
71
Q

What is the ABCD2 score for assessing TIA? What does it compose of? How do you interpret the results?

A

Assesses 2-day risk of stroke. Pts with score of 4 or more should be seen by specialist within 24hrs. All others can be seen within 7 days

A - Aged over 60 (1)
B - BP 140/90mmHg and above (1)
C - Clinical features; unilateral weakness (2), speech disturbance without weakness (1)
D - Duration of symptoms; over 60 mins (2), 10-60mins (1)
D - Diabetes (1)

72
Q

How do you manage pts post TIA?

A
  1. Control CV risk factors
    - lower BP to below 140/85 mmHg
    - 80mg atorvastatin
    - help to stop smoking
  2. Antiplatelets
    - aspirin 300mg for 2 weeks
    - clopidogrel 75mg OD
  3. Carotid enderterectomy
    - performed if at least 70% stenosis present
    - perform within 2wks of first presentation
    - do NOT stop aspirin during this time
73
Q

What drugs can cause peripheral neuropathy?

A
  • isoniazid
  • amiodarone
  • cisplatin
74
Q

What type of disease is Guillain-Barre Syndrome?

A

Acute inflammatory demyelinating polyradiculopathy (AIDP)

75
Q

What condition commonly precedes GBS?

A

2/3rds of patients will have a hx of gastroenteritis or flu-like symptoms in the preceding weeks
- associated with c. jejuni, CMV, EBV

76
Q

What clinical features are present in GBS?

A
  1. Muscle weakness
    - progressive symmetrical weakness
    - affects lower limbs first
    - moves from distal to proximal
    - flaccid paralysis + areflexia
    - maximal weakness reached in 4wks
  2. Paraesthesias:
    - pins + needles in legs + feet
    - sensory abnormalities are mild
  3. Areflexia - deep tendon reflexes lost. Plantars are downgoing
  4. Speech problems + facial weakness - may progress to cranial nerves
  5. Back + leg pain - prominent in children
  6. Respiratory distress
    - dyspnoea on exertion + SOB
    - 30% will require ventilation
77
Q

What investigations are performed in suspected GBS?

A
  1. LP - raised protein + normal WCC
  2. Spirometry - reduced FVC
  3. Nerve conduction studies - slowed conduction velocity
  4. LFT - raised AST/ALT in 10-20%
78
Q

How do you manage pts with GBS?

A
  1. IVIG + plasma exchange (plasmapheresis)
  2. Supportive treatment:
    - respiratory = perform spirometry 6 hrly + ventilate if necessary
    - cardiovascular = if dysautonomia present, insert Foley catheter
    - DVT PROPHYLAXIS (PE is leading cause of death)
    - pain management = gabapentin, carbamazepine
79
Q

What are the classical clinical features of Charcot-Marie Tooth disease?

A
  • high foot arches (pes cavus)
  • weakness in hands
  • distal muscle wasting causing ‘inverted champagne bottle legs’
  • weakness in lower legs, particularly loss of dorsiflexion
  • reduced muscle tone
  • peripheral sensory loss
  • steppage gait - foot hangs down causing toes to scrape ground = pt needs to lift leg higher than normal when walking
80
Q

How is charcot-marie-tooth disease managed?

A

No treatment to alter underlying disease or to prevent it from progressing = Management is supportive from MDT

  • neuro + geneticists to make diagnosis
  • physio - maintain muscle strength + ROM
  • OTs to assist ADLs
  • Podiatrists assist with foot care + orthotics
  • Orthopods correct disabling foot deformities
81
Q

How do you differentiate between common peroneal nerve (L4-S1) palsy + tibial nerve palsy (L4-S3)?

A

In peroneal palsy there is weak ankle eversion

in tibial nerve palsy, you cannot invert the foot or flex toes

82
Q

What are the clinical features of carpal tunnel syndrome?

A
  • Aching pain in hand + arm, especially at night
  • Paraesthesias in thumb, index + middle fingers, relieved by dangling hand over edge of bed + shaking it
  • wasting of thenar eminence
83
Q

What is (i) Phalen’s test (ii) Tinels test?

A

(i) Phalens = maximal wrist flexion for 1 min - induces pain of carpal tunnel
(ii) Tinels = tapping over median nerve ilicits symptoms

84
Q

How is carpal tunnel syndrome managed?

A
  1. Splinting
  2. Steroid injection
  3. Decompression surgery
85
Q

What are the key questions you should ask a pt who has presented with foot drop?

A
  1. Back pain - any radiation to leg?
  2. Leg numbness + tingling?
  3. Hx of trauma?
  4. Any change in activity prior to onset e.g. kneeling or crossing legs
86
Q

What is the difference clinically between L5 root compression + common peroneal palsy?

A

L5 root compression: weak ankle dorsiflexion + eversion
- significant L5 compression will also cause S1 compression = ankle reflex is lost

Common peroneal nerve = ankle reflex is NOT los. Manage with foot drop splint

87
Q

What is multiple sclerosis?

A

A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time + space

88
Q

What are the typical features/presentation of MS?

A
  1. VISUAL
    - optic neuritis
    - optic atrophy
    - B/L INO (weak adduction of ipsilateral eye, nystagmus of contralateral, convergence preserved)
    - diploplia
  2. SENSORY
    - paraesthesias
    - decreased vibration sense
    - trigeminal neuralgia
    - L’hermitte’s (paraethesia in limbs following neck flexion)
  3. MOTOR
    - spastic weakness (most commonly in legs)
    - transverse myelitis
  4. CEREBELLAR
    - ataxia
    - tremor
  5. OTHERS
    - swallowing disorders, constipation
    - sexual dysfunction, urinary retention/incontinence
89
Q

What is uhthoff’s phenomenon?

A

Transient worsening of vision when body gets overheated in hot weather, exercise, fever, saunas or hot tubs

90
Q

How do you manage acute attacks of MS?

A
  1. IV methylprednisolone 1g/24h for 3-days
    - does not influence long-term outcome but decreases duration + severity of attacks
  2. Plasma exchange
91
Q

What medication can be given to prevent relapses in MS?

A
  1. Interferons (IFN-B) - no role in primary progressive
  2. Monoclonal antibodies (natalizumab) - decreases relapses by 2/3 in RR
  3. Glatiramer - good for 2ndary progressive
92
Q

What can polymyositis + dermatomyositis be associated with?

A

Malignancy

  • lung
  • breast
  • ovarian
  • gastric
93
Q

What are the antibodies for polymyositis + dermatomyositis?

A 
Polymyositis = anti-Jo-1
Dermatomyositis = Anti-Mi-2 and ANA
94
Q

What are the typical clinical features of polymyositis?

A
  • muscle pain, fatigue, weakness
  • progressive, symmetrical proximal muscle weakness (shoulder or pelvic girdle)
  • develops over weeks
  • more common in females
95
Q

What are the skin signs seen in dermatomyositis?

A
  • Heliotope rash on eyelids
  • macular rash (shawl sign over back + shoulders)
  • Nailfold erythema
  • Gottron’s papules on knuckles, elbows, knees
  • Mechanics hands = painful, rough skin cracking of fingertips
  • Retinopathy, haemorrhages, cotton wool spots
96
Q

What are the extra-muscular features of dermatomyositis + polymyositis?

A
  • fever
  • arthritis
  • bibasal pulmonary fibrosis
  • Raynaud’s phenomenon
  • Myocardial involvement = myocarditis or arrhythmias
97
Q

What investigations are to be performed in poly/dermatomyositis?

A
  1. Muscle enzymes = raised CK, raised AST, ALT, LDH
  2. EMG
  3. Muscle biopsy provides definitive diagnosis
  4. Screen for MALIGANCY
    - tumour markers, CXR, mammogram, pelvic/abdo USS, CT
98
Q

Who is at risk of developing shingles?

A

Immunocompromised

  • decline in immune function with advancing age
  • chronic stress
  • malignancy
  • HIV, AIDS
  • immunosuppressive therapy
  • malnutrition
99
Q

Who is given the shingles vaccine? Who can it NOT be given to + why?

A

Offered to all aged 70-79

- not given to those who are immunocompromised as it is a live vaccine given SC

100
Q

What are the 4 types of motor neurone disease?

A
  1. Amyotrophic lateral sclerosis - most common
    - UMN signs + LLMN fasciculations
  2. Progressive Bulbar Palsy
    - speech is quiet or nasal (donald-duck)
    - MND, GBS, MG, central pontine myelinolysis all causes
  3. Progressive Muscular Atrophy
  4. Primary lateral sclerosis
101
Q

How is MND diagnosed?

A

Based on clinical findings + r/o other diagnoses

  1. MRI - r/o structural lesions
  2. LP - r/o inflammation
  3. EMG shows acute degeneration (reduced action potentials with increasing amplitude)
102
Q

What drug can be used in MND to prolong life by about 3 months?

A

Riluzole

103
Q

What is the prognosis of patients with MND?

A

most die within 3yrs

- of bronchopneumonia + respiratory failure

104
Q

What conditions/ages are associated with development of myasthenia gravis?

A

Under 50yrs is more common in women + associate with other AI disease
Over 50 more common in men + associated with THYMOMA

105
Q

What investigations should be performed in suspected MG?

A
  1. Antibodies = ACh-R antibodies, MuSK antibodies
  2. Tensilon test (rarely done anymore, give edrophonium IV + power will return within 1min)
  3. EMG - decreasing response to a train of impulses
  4. Reduced FVC
  5. Thymus CT
  6. TFTs
106
Q

How do you manage myasthenic crisis?

A

IVIG or plasma exchange

- treat cause/trigger of relapse (usually respiratory tract infection)

107
Q

How do you treat symptoms of MG?

A

pyridostigmine (anticholinesterase)

108
Q

What are the different types of tremor? (RAPID)

A
  1. R - resting tremor
    - goes on voluntary movement or distraction
  2. A - Action/Postural
    - absent at rest, worse on movement
  3. I - Intention
    - worse at end of movement (cerebellar damage)
  4. D - Dystonic
109
Q

What are the causes of an Action tremor? (BEATS)

A

B - benign essential tremor
E - endocrine = thyrotoxicosis, hypoglycaemia, phaeochromocytoma
A - Alcohol/caffeine/opioid withdrawal
T - Toxins (beta-agonists, theophylline, valproate)
S - Sympathetic (e.g. anxiety)

110
Q

What is given to manage benign essential tremor?

A
  1. Propranolol

2. Primidone

111
Q

What is multi-systems atrophy?

A
  • early autonomic dysfunction = postural hypotension, bladder dysfunction
  • cerebellar and pyramidal signs
  • rigidity more than tremor
112
Q

What is progressive supranuclear palsy?

A
  • postural instability = falls
  • speech disturbance (+ dementia)
  • vertical gaze palsy
113
Q

What is normal pressure hydrocephalus? How is it managed?

A

Triad of dementia, gait disorder + bladder instability
- enlarged ventricles on MRI + other signs of hydrocephalus

Management = Diagnostic LP + CSF removal, then VP shunt

114
Q

What is the classical triad of Parksinsons?

A
  1. TREMOR
    - resting tremor, 4-6Hz, pill-rolling
  2. RIGIDITY
    - lead-pipe rigidity, cog-wheel rigidity
  3. BRADYKINESIA
    - slow initiation of movement, reduction of amplitude on repetition
    - monotonus voice
    - micrographia
    (GAIT = reduced arm swing, festinance, freezing)
115
Q

What are the side effects of levodopa?

A 
D - dyskinesia
O - on-off phenomenon 
P - psychosis 
A - ABP reduced
M - mouth dryness
I - insomnia 
N - nausea + vomiting
E - EDS (excessive daytime sleepiness)
116
Q

If pts with PD have a relatively young onset + biologically fit, what treatment is given in PD?

A
  1. Dopamine agonists = ropinirole, pramipexole
    - increased risk of hallucinations in elderly
  2. MAO-B inhibitors = rasagiline, selegiline
  3. L-dopa = co-careldopa, co-beneldopa
    - risk of gambling etc
117
Q

If a patient is frail/has comorbidities, how do you treat their parkinson’s disease?

A
  1. L-dopa

2. MAO-B inhibs

118
Q

What happens if patients suddenly stop taking dopamine agonists?

A

Neuroleptic malignant syndrome

  • altered mental stare
  • muscle rigidity
  • autonomic instability
  • hyperthermia
119
Q

What is genetic anticipation? What disease is it seen in?

A

Feature of trinucleotide repeat disorders whereby successive generations have more repeats in gene, resulting in

  • earlier age of onset
  • increasing severity of disease

Occurs in Huntington’s chorea

120
Q

What are some causes of vertigo? (IMBALANCE)

A

I - infection/injury (= labyrinthitis, Ramsay-Hunt, Trauma to petrous temporal bone)
M - Meniere’s disease
B - BPPV
A - Aminoglycosides
L - lymph
A - arterial = migraine or TIA/stroke
N - nerve = acoustic or vestibular Schwannoma
C - central lesions (demyelination, tumour, infarct)
E - epilepsy

121
Q

What are important negatives for BPPV?

A

NO persistent vertigo (only lasts about a minute)
No speech/visual/motor/sensory disturbances
No tinnitus, headache, ataxia, facial numbness or dysphagia

122
Q

What are the features you would suspect in a vestibular/acoustic neuroma?

A

Classic history of a combination of:

  • vertigo
  • hearing loss
  • tinnitus
  • absent corneal reflex
123
Q

What is the gold standard investigation to diagnose acoustic neuroma?

A

MRI of cerebellopontine angle

124
Q

What are the symptoms of Meniere’s disease?

A
  • recurrent vertigo attacks lasting 2-4 hrs
  • increasing aural fullness + tinnitus
  • sensorineural hearing loss
  • nystagmus always present
  • positive Romberg’s test
125
Q

What is the treatment of meniere’s disease?

A
  1. ENT assessment
  2. Acute attacks = prochlorperazine
  3. Prophylaxis = betahistine
  4. Inform DVLA (must stop driving until adequate symptom control achieved)
126
Q

What are the features of vestibular neuronitis?

A

Often develops following viral infection e.g. URTI

  • recurrent vertigo attacks lasting hours to days
  • N+V
  • horizontal nystagmus

NO HEARING LOSS OR TINNITUS

127
Q

How is vestibular neuronitis managed?

A

Most are managed at home + tend to resolve themselves after 1 week

  • may need prochlorperazine for acute episodes
  • if persistent, long term rehab with vestibular exercises can be done (Cawthorne-Cooksey exercises)
128
Q

What is the difference between vestibular neuronitis and labyrinthitis?

A

In labyrinthitis you will experience hearing loss
- there is no hearing loss in vestibular neuronitis

  • treated the same

FINALS (14 decks)

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