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YOU BETTER WERK > NEURO > Flashcards

NEURO Flashcards

1
Q

Definition of status epilepticus

A
  • most seizures are brief and end within 1-3min without treatment - status refers to continual seizure activity or repeated seizures without full recovery between attacks - traditionally lasting for 30min - however need to treat after 5 minutes of continued seizure activity
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2
Q

Causes of acute seizures

A
  • metabolic: hypoglycaemia, hyponatraemia, hypocalcaemia, renal failure - intoxication: drugs or poisons - stroke: haemorrhagic or ischaemic - brain trauma - intracranial infections: meningitis, encephalitis, cerebral abscess - autoimmune encephalitis - hypertensive encephalitis - severe cerebral hypoxia - eclampsia
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3
Q

Antiepileptic management of reversible seizures (i.e. meningitis/eclampsia)

A

Considering withdrawal of antiepileptic therapy when a minimum for 3 months has elapsed without further seizure activity

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4
Q

Management of acute seizure

A
  • supportive mx: left lateral, protect airway, maintain oxygenation - connect monitoring equipment and gain IVC access - if unable to r.o alcoholic withdrawal give thiamine - if ongoing seizure activity after 5 minutes give 5-10mg IV midazolam or 10mg IM - given antiepileptic: phenytoin and sodium valproate are both first line - if continues to seizure need to intubate
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5
Q

What are the doses of the first line anti-epileptics?

A

Phenytoin: 20mg/kg IV Sodium valproate: 40mg/kg Same doses for children!

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6
Q

Complications of seizures

A
  • aspiration - trauma - if prolonged: CNS injury, noncardiogenic pulmonary oedema, rehabdo/acidosis/acute renal failure, hyperthermia
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7
Q

Management of acute seizures in pregnancy in eclampsia

A
  • magnesium sulfate 4g IV over 20 min - hydralazine 5-10mg IV over 3-10min, repeat every 20min if needed - midazolam 5-10mg IV - plan birth ASAP - do not give ergometrine
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8
Q

Post seizure follow up

A
  • first episode: FBC, full biochem panel, BSL, UDS and CT head - consider LP if infection suspected and treat with abx - if nil acute cause consider epilepsy - consider anti-epileptic if 2 unprovoked seizures - may need to measure anti-epileptic drug level if able
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9
Q

Classification of epileptic syndrome

A
  1. Generalised: idiopathic epilepsy, symptomatic (infection, metabolic, structural, immune) 2. Focal: self limited (benign childhood epilepsy), symptomatic (temporal lobe epilepsy) 3. Focal or generalised: neonatal seizures, West syndrome (infantile spasms) 4. Special syndromes: febrile seizures, status epilepticus, metabolic/toxin induced seizures
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10
Q

Diagnosing epilepsy

A
  • refer to expert to confirm diagnosis and consider rx - diagnosis relies on description of seizures with EEG to support diagnosis - normal EEG does not rule out epilepsy, nor does abnormal EEG confirm diagnosis necessarily - type of seizure influences the choice of drug
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11
Q

Deciding when to treat epilepsy

A
  • seizures are more likely to be recurrent if: partial seizures, abnormal EEG, lesion on neuro-imaging or if abnormal neurological examination > consider starting rx on first seizure in these cases - otherwise generally consider after second unprovoked seizure ** prophylactic treatment in situations of high risk of epilepsy (TBI, tumours or neurosurg) is not recommended*
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12
Q

Initial management of tonic clonic seizures

A
  • First seizure –> investigate cause, EEG + treat cause if able –> is recurrence high risk? NO: observe and treat if further seizure YES: treat after first seizure
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13
Q

Which anti-epileptic would you start after a focal/partial seizure?

A

Carbamazepine

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14
Q

Which anti-epileptic would you start after a generalised or uncertain seizure?

A

Sodium valproate

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15
Q

Factors which affect choice of antiepileptic

A
  • type of seizure - pregnancy - adverse effects: weight gain, impaired cognition, hypersensitivity - age (valproate hepatotoxicity more common in infants - cost/ease of use - drug interactions
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16
Q

Which anti-epileptic should be avoided in pregnancy?

A

Sodium valproate!

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17
Q

Starting an antiepileptic

A
  • start at low dose and slowly increase to target - especially important with lamotrigine to reduce risk of serious skin adverse reactions - exception is phenytoin which can be started at the initial target dose or even with a loading dose - start with a single drug, increase dose until seizure stop or at max dose
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18
Q

When would you add a second antiepileptic drug for epilepsy?

A
  • if seizures are not controlled on first antiepileptic add a second drug - the first drug may be gradually withdrawn to find out if monotherapy is effective with second drug - many patients prefer to stay on combination therapy
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19
Q

How do you withdraw an anti-epileptic drug?

A
  • slow and gradual - usually done over 6 weeks but up to 6 months if clonazepam or barbiturate - driving is not permitted when the dose of anti-epileptic drug is being reduced - driving must not resume until 3 months after completely dose reduction or withdrawal
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20
Q

Ceasing anti-epileptic drug therapy

A
  • driving must stop during dose reduction and for 3 months after the last dose, hence many patients opt to continue therapy indefinitely - do not try and withdraw until at least 2 years after last seizure - risk of seizure recurrence after withdrawal of therapy after 2 years seizure free is ~50% - if seizure after withdrawal or drug decrease restart on previous effective dose (can resume driving within 1 month after this) - juvenile myoclonic epilepsy high high recurrence rate so best not to withdraw therapy
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21
Q

What are the serious adverse effects of specific anti-epileptics?

A
  • sodium valproate: hepatic failure - carbamazepine: agranulocytosis - serious skin reactions (SJS, TEN, DRESS) higher risk in patients of Asian origin - monitor vitamin D concentration in patients on long term anti-epileptics
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22
Q

When to measure serum concentration of anti-epileptics

A
  • for many correlation between serum concentration and efficacy or toxicity is poor - may need to use to check compliance/concordance with therapy, help diagnose if symptoms/signs are due to toxicity - guide dosage for phenytoin - adjust dosage of lamotrigine in pregnancy - when dose is change need to wait 5 half lives before re-checking
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23
Q

Phenytoin monitoring

A
  • nonlinear pharmacokinetics makes monitoring and dose adjustment difficult - small change in dose can cause a large change in steady state serum concentration - if serum concentration <30mcgmol/L (<7mg/L) can increase by 100mg, if concentration >30mcg/mol only increase by 50mg
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24
Q

Advice for patients with epilepsy

A
  • seizures can be provoked by sleep deprivation, ETOH, illegal stimulants, psychological stress, some drugs - avoid situations where a seizure may be dangerous (unsupervised swimming, climbing, operating machinery) - legal obligation to report condition to transport
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25
Q

Contraception in patients with epilepsy

A
  • drugs used to treat epilepsy reduce efficacy of hormonal contraception by induction of hepatic enzymes - carbamazepine, phenytoin, topiramate all reduce OCP efficacy - lamotrigine may also reduce efficacy of COC and the pill may increase lamotrigine metabolism
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26
Q

Which common anti-epileptics do not affect hormonal contraception?

A
  • levetiracetem (keppra) - sodium valproate
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27
Q

Which common anti-epileptics make OCP less effective?

A
  • carbamazepine, phenytoin, topiramate, lamotirigine
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28
Q

Planning pregnancy with epilepsy

A
  • refer all to specialist! - babies born to mother on anti-epileptics have a 4-6% risk of major congenital malformations (2 x the baseline risk) - there is no “drug of choice” in pregnancy but priority is to avoid seizures - use monotherapy if possible, minimise antiepileptic dose - avoid sodium valproate if able, wait 3 months prior to planning conception! - advise 5mg folic acid daily for at least 3 months prior to conception
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29
Q

Monitoring of antiepileptic dose during pregnancy

A
  • concentrations of some drugs will fall in pregnancy - may need to increase dose of lamotrigine - should establish baseline concentration pre-preg - check serum concentration at least every 2 months during pregnancy and aim to keep level near baseline
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30
Q

Teratogenic effects of anti-epileptic drugs

A
  • sodium valproate increases risk fo spinal bifida 10 fold - also associated with lower intelligence and greater risk of learning difficulties - effects are dose related, at daily doses 600-800mg sodium valproate’s teratogenicity are similar to other anti-epileptics - however valproate is often the only drug which controls idiopathic generalised epilepsy, but usually low doses are sufficient - phenytoin increases the risk of congenital abnormalities -
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31
Q

Management of known prolonged/repetitive seizures

A
  • management plan to be formed - if seizure > 5 min or seizure seizures (3 or more in 1 hour) can give 5-10mg midazolam buccally or intranasally
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32
Q

Juvenile absence epilepsies

A
  • genetic/idiopathic generalised seizures - onset for absence epilepsy is 4-9 years old or 10-15 - ethosuximide and sodium valproate are equally effective but ethosuximide is better tolerated and better in girls of child bearing potential - need to ensure girls have reliable contraception!
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33
Q

Juvenile myoclonic epilepsy

A
  • most common form of genetic/idiopathic generalised epilepsy in adults despite its name - typically presents with tonic clonic seizure with background of myoclonic jerks - respond to sodium valproate - if possible try to avoid sodium valproate in young females of childbearing potential who do not have relative contraception - levetiracetam and lamotrigine are alternatives
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34
Q

What is Lennox-Gastaut syndrome

A
  • symptomatic generalised epilepsy characterised by > significant intellectual disability > slow spike-wave pattern on EEG - multiple seizure types - first line therapy is sodium valproate
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35
Q

Management of focal/partial seizures

A
  • patient may be aware (simple partial seizure) or have impaired awareness (complex partial seizure) - treatment of choice = carbamazepine
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36
Q

What is the most common form of structural focal epilepsy?

A

Mesial temporal love epilepsy due to hippocampal sclerosis

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37
Q

What is the earlier sign of dose related carbamazepine toxicity?

A
  • diplopia starting 30-60min after morning dose
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38
Q

Management of seizure when generalised or focal onset is unclear

A

Sodium valproate in children/adults and females who have reliable contraception or are unable to have children Levetiracetem in females of childbearing potential who do not have reliable contraception is first line

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39
Q

What is West syndrome?

A
  • infantile spasm - onset usually 4-12 months - sudden brief contraction of head/neck/trunk usually in flexion but sometimes in extension - characteristically spasms occur in runs lasting several minutes - rx: prednisolone
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40
Q

Most common cause of neonatal seizure?

A
  • hypoxic-ischaemic encephalopathy - intracranial haemorrhage - perinatal ischaemic strokes - treatable causes: meningitis, hypoglycaemia, electrolyte disturbances, metabolic conditions - some are benign and familial
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41
Q

What is first line treatment for neonatal seizures?

A
  • phenobarbitone
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42
Q

Febrile seizures

A
  • febrile convulsion is a seizure that occurs from 3 months to 6 years associated with fever > 38 without concurrent acute intracranial disease, metabolic disturbance or CNS infection - reducing temp does not prevent or stop febrile seizures - most are self limiting and end within 1-3 minutes - treat with midazolam if > 5 min
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43
Q

What is the paediatric dose of midazolam for complex febrile seizures?

A
  • buccally/intranasal midaz: 0.2-0.3mg/kg - IM 0.15-0.2mg/kg If seizure ongoing for 10 minutes after second midaz dose treat with anti-epileptic rx
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44
Q

Benign childhood epilepsy with centrotemporal spikes

A
  • starts mid childhood - seizures generally occur during sleep and begin in face or mouth - produce typical “glugging” sounds - speech arrest is common - excellent prognosis, most children seizure free by adolescence - rx: carbamazepine/sodium valproate but rx is not always indicated
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45
Q

Differential diagnosis of epileptic seizure

A
  • syncope - psychogenic non-epileptic seizures - migraine - TIA - paroxysmal dyskinesia - parasomnia
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46
Q

Describe how a generalised absence seizure may present

A
  • “petite mal seizure” - frequent (more than daily) - brief (<30sec) - episodes of behavioural arrest without prominent motor features and immediate recovery of alertness
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47
Q

What is a focal seizure?

A
  • seizures confirmed to one cerebral hemisphere - can evolve to become generalised/bilateral - can have motor, somatosensory, autonomic, visual, auditory disturbances - focal seizures may not impair consciousness (simple focal) but if they do they are “complex focal seizures”
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48
Q

Common causes of provoked epileptic seizures

A
  • acute neurological insult: stroke, trauma, infection, inflammation - biochem: hyper/hypo glucose + sodium + calcium, hypomagnesaemia
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49
Q

What are the common side effects of phenytoin?

A
  • hirsuitism - acne - gum hypertrophy - rash/SJS
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50
Q

AED and SJS

A
  • severe cutaneous adverse reaction seen with carbamazepine, phenytoin, phenobarbiton, primidone, lamotrigine - occurs generally in the first 8 weeks of exposure - to prevent this in patients on lamotrigine need to start low and slowly increase - patients of Chinese heritage have a higher risk (need to consider HLA testing in these patients prior to starting carbamazepine)
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51
Q

Which AEDs can be monitored in serum?

A

Carbamazepine, phenytoin, valproate, lamotrigine - however the best dose is the one at which seizures are controlled and nil adverse effects are seen - may need to monitor drug levels when adherence is in question or altered pharmacokinetics are expected (pregnancy)

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52
Q

Epilepsy and driving

A
  • patients with epilepsy on AEDs and patients after their first seizure are fit to return to driving after being seizure free for 6 months
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53
Q

What are the enzyme inducing AEDS?

A
  • carbamazaepine - topiramate - oxycarbaxepine - phenytoin These all reduce the efficacy of the OCP by increasing oestrogen and progesterone clearance - strategies include: double dosing bills, using active pills continuously - depot and IUD remain effective however implanon efficacy will be reduced by the above AEDs
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54
Q

What are the 4 classifications of dizziness?

A
  1. vertigo: spinning sensation 2. disequilibrium: feeling of imbalance 3. light-headed: sensation of giddiness 4. presyncope: sensation of feeling faint
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55
Q

What are the 2 broad classifications of vertigo?

A

Central (cerebellum, brain stem) Peripheral (inner ear and vestibular nerve)

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56
Q

What serious causes must be considered in patients presenting with vertigo?

A
  • CVA - tumour - MS
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57
Q

What features associated with vertigo suggest a central cause?

A
  • suspect a central cause if associated with weakness, dysarthria, sensory changes, ataxia or confusion - always think about the vascular risk factors: smoking, diabetes, obesity, HTN, high cholesterol
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58
Q

What features associated with vertigo suggest a peripheral pathology?

A
  • nausea, vomiting - hearing loss
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59
Q

Whihc medications can affect the vestibular system and in turn cause vertigo?

A
  • Frusemide - salicylates - antihypertensive agents
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60
Q

What is Tullio phenomenon?

A
  • loud noises precipitating vertigo in patients with peripheral causes
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61
Q

When would you suspect a perilymphatic fistula in patients with vertigo?

A

After recent head injury - signs: vertigo induced by valsalva manouvres or by pushing tragus

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62
Q

What are the 2 conditions in which vertigo with hearing loss in seen?

A

Labrynthitis or Meniere’s disease - hearing loss in not seen in BPPV or vestibular neuronitis

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63
Q

Physical examination of vertigo

A
  • ear examination: should check for vesicles or reaction as seen in cholesteotoma - vertigo triggered by pushing the tragus or with valsalva is seen in perilymphatic fistula - check hearing - neurological examination: focusing on gait, balance, coordination with Romberg’s and heel toe, cerebella examination - eye examination: looking for nystagmus
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64
Q

What does vertical nystagmus indicate?

A

Central vertigo cause ONLY - can also cause horizontal, rotational and doesn’t disappear on fixing the gaze

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65
Q

When nystagmus is seen with peripheral causes

A
  • nystagmus will disappear with fixation of gaze in peripheral causes
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66
Q

What specialised tests can be done for vertigo?

A

Dix-Hallpike: sitting on edge of bed, examined turns patients head 30-45 degrees to side being tested and quickly lies supine and hyperextends the neck (horizontal nystagmus is a positive test) Orthostatic BP check: 20mmHg is a significant postural drop Head impulse test: pt looks at examiners nose and examiner quickly turns patients head 10-20 degrees, if abnormal eyes move rapidly and repetitively failing to re-fixate on nose

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67
Q

What are the most common causes of vertigo seen in primary care? (4)

A
  1. Labrynthitis 2. Vestibular neuronitis 3. BPPV 4. Meniers BPPV is THE most common cause seen
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68
Q

Which causes of peripheral vertigo cause hearing loss and tinnitis?

A

Labrynthitis and Menier’s - Menier’s occurs spontaneously and lasts for hours - Labrythitis is provoked by change in head positive and episodes last for few seconds to minutes

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69
Q

What are the diagnostic features of vestibular neuronitis

A
  • usually provoked by recent URTI - attacks last for seconds to minutes - often will be very unbalances - nil hearing loss
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70
Q

What causes BPPV?

A
  • accumulation of calcium crystals in the posterior semicircular canal - crystals effects movement of endolymph causing vertigo - causes brief episodes of vertigo and are associated with nausea and nystagmus - episodes are triggered by rapid changes in head position - nystagmus in BPPV has a rotation nature - diagnosed by Dix-hallpike
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71
Q

Which manoeuvre is used to treat BPPV?

A

Epley’s 1. Sit with patient on the bed 2. With neck hyperextended and laterally rotated to 45 deg patient is asked to lie supine 3. Remain supine for 1 minute 4. Head is then turned to the opposite side with lateral rotation of 45 deg, remain in this position for further 1 min 5. Rotate head, chest and pelvis to almost prone, hold for further 1 minute 6. quickly sit patient up right with head tilted to the affected side

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72
Q

When should Epley manouvre NOT be performed?

A
  • in patients with neck injury, carotid stenosis and heart disease
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73
Q

Acute labrynithitis

A
  • inflammation of the labyrinth - presents with vertigo, hearing loss, often preceded by a viral infection - middle ear infections can spread to the inner ear and cause labrynthitis - symptoms range from days to weeks - hearing loss is main distinguishing factor - no treatment but if suppurative should drain OM
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74
Q

Meniere’s disease

A
  • uncommon cause of vertigo - thought to be due to increased fluid in endolymph - commonly seen in women - classically presents with episodes > 20min, tinnitus, sensorineural hearing loss and aural fullness - eventually hearing loss becomes permanent - not cure and treatment is symptomatic - mainstay of treatment is betahistine
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75
Q

What is the treatment for Meniere’s?

A

Betahistine

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76
Q

Vestibular neuronitis

A
  • inflammation of vesticular nerve - precedes viral UTI or herpes zoster infection - common in middle ages adults - acute onset vertigo without hearing loss or tinnitus - vertigo symptoms are aggravated by change in position -loss of balance is more prominent in VN, commonly patients will present after a fall - vertigo is initially severe and lasting fro 2-3 days followed by a gradula recovery which can take 2-6 weeks - bed rest and antiemetics used from 24-72 hours
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77
Q

Indication for neuroimaging in vertigo

A
  • examination not fitting with peripheral lesion - prominent risk factors for CVA are present - neurological signs and symptoms present - vertigo with accompany headache
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78
Q

What lifestyle changes are recommended in patients with vertigo?

A
  • salt restriction - avoid alcohol and coffee - referral to physio for vestibular rehab
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79
Q

Pathophysiology of multiple sclerosis

A
  • multifocal CNS disorder characterised by inflammatory demyelinating lesions affecting white and grey matter - thought to be mediated by autoreactive T cells - causes irreversible axonal injury from outset - steady accumulation of CNS damage leads to irreversible disability
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80
Q

Aetiology of MS

A
  • complex interaction of environmental and genetic factors - environmental: EBV exposure and smoking - later age of exposure to EBV is associated with a higher incidence of disease - HLA-DRB1 has strongest genome correlation
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81
Q

Describe the natural history and disease phases of MS

A
  1. Clinically isolated syndrome: first demyelinating event, most commonly isolated episode of long tract motor and sensory deficits, optic neuritis, brain stem syndrome 2. Relapsing remitting MS: relapse shows by symptoms of acute inflammatory demyelinating event in CNS lasting at last 24 hours, complete resolution may occur but mild residual symptoms persist in up to 40% of attacks 3. Secondary progressive MS: after 10 years ~40% of patients with RRMS transition to progressive accumulation of disability without relapses, risk of this transition is greater to 80% 4. Primary progressive MS: 15-20% of patients have progressive disease from onset without relapse or remission, commonly see slow progressive spastic parapresis followed by cerebellar or hemiplegic syndromes. This stage/disease does not respond to rx
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82
Q

Investigation and diagnosis of MS

A
  • clinical diagnosis supported by MRI and CSF findings of oligoclonal bands and raised IgG index with evoked potential studies - diagnosis can only be confirmed histopathologically but need to resort to biopsy is rare
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83
Q

What criteria is used to diagnose MS?

A

McDonald criteria - > 2 clinical attacks with > 2 lesions = diagnostic - > 2 clinical attacks, with 1 lesion with history suggestive of previous lesion = diagnostic - > 2 clinical attacks, with 1 lesion and dissemination in space evident on MRI without evidence of previous lesion Clinically isolated syndrome = 1 attack with > 2 lesions with objective clinical evidence, with dissemination on MRI or CSF oligoclonal bands

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84
Q

What are the common sites and signs of acute inflammatory dyemyelinating events of MS?

A
  1. Optic nerve: pain in eye, blurred vision, reduce visual acuity 2. Cerebellum: unsteadiness, ataxia, evoked nystagmus 3. Spinal cord: usually multifocal and asymmetric, upper or lower limb weakness or parasthesia 4. Brainstem: blurred or double vision, opthalmoplegia 5. Bladder/bowel: constipation, urge incontinence, erectile dysfunction, urinary frequency
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85
Q

Typical sites of lesion on MRI in MS

A
  • periventricular white matter - juxtacortical white matter - corpus callosum - optic nerve - infratentorial structures (pons, peduncles, cerebellum) - spinal cord
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86
Q

DDx of MS

A
  • Neuromyelitis optica (Devic disease) - Acute disseminated encephalomeylitis (monophasic autoimmune disease seen more commonly in paeds, can be triggered by viral illness or vaccination) - migraine - cerebral neoplasma - nutritional deficiencies: B12 or copper - spinal cord compression - infections: syphilis and HIV - SLE - paraneoplastic syndromes - functional symptoms - recurrent infarction
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87
Q

How are acute MS relapses treated?-

A

IV methylprednisolone 1g/day for 3 days - only required if relapse impacts significantly on QOL - hastens recovery but does’t improve likelihood of recovery

88
Q

Adverse effects of high dose steroids in acute MS relapse?

A
  • psychosis - mood changes - aseptic hip necrosis - hyprglycaemia
89
Q

Symptomatic management of MS

A
  • spasticity: baclofen, diazepam, dantrolene - paroxysmal symptoms: carbamazaepine - fatigue: amantadine - intention tremor: clonazepam, propranolol, carbamazepine - urinary urgency: oxybutynin - erectile dysfunction: sildenafil
90
Q

What are the first line agents used for relapsing and remitting MS?

A
  • interferon-Bs and glatiramer acetate
91
Q

Pregnancy and MS

A
  • all drugs for MS are category D - except glatiramer (cat b1) - pregnancy reduces disease activity, particularly in 3rd trimester - high risk of relapse in 3 months post partum
92
Q

MS prognosis

A
  • less than 5% of patients have very severe disability within the first 5 years onset - 10-20% of patients remained unimpaired without therapy over20 years - medial survival time is approx 5-10 years shorter for MS patients
93
Q

What is normal pressure hydrocephalus?

A
  • excess CSF in ventricles - normal ICP measured with lumbar puncture - brain ventricles enlarge with CSF and can disrupt damage of nearby brain tissue causes difficulty walking, problems with thinking/reasoning and loss of bladder control - generally affects people in their 60-70s - often misdiagnosed as Alzheimer’s or Parkinson’s
94
Q

Classical triad of symptoms of normal pressure hydrocephalus?

A
  • ataxic gait - mild dementia: short term memory loss, forget-fullness, loss of interest in daily activities, changes in personality and behaviour - loss of bladder control, generally seen after difficulty walking and cognitive decline
95
Q

Diagnosis of normal pressure hydrocephalus

A
  1. Neuroimaging: MRI or CT 2. Clinical examination 3. CSF testing
96
Q

Treatment of normal pressure hydrocephalus

A
  • high volume spinal tap - surgical insertion of VP shunt
97
Q

What are the blue flags for headaches?

A

A blue flag indicates secondary headaches that do not require urgent investigation - occipital headache, which sometimes radiates to temple, exacerbated by neck mobility (cervicogenic headaches or cervical spondylosis) - headaches linked to whiplash injury - headache related to reading (eye strain) - headache clearly linked to medications (i.e. GTN) - headaches associated with systemic viral illness (influenza)

98
Q

What are the red flags for headaches?

A
  • new onset in setting of cancer (met), HIV (opportunistic infection), post manipulation or trauma of neck, or associated with mild head trauma in elderly pt (subdural) - new persistent headache - focal signs or symptoms - headaches with focal neurological signs that precede or outlast the headache - progressive headache (? mass lesion) - acute onset/thunder clap (SAH) - headache with rash (meningococcal) - persistent unilateral temporal headache (?temporal arteritis) - headache with raised ESR –> infection, vasculitis, collagen disease - headache with papilloedema: ? raised ICP - non migrainous headaches in pregnancy or postpartum (cerebral vein thrombosis) - headache triggered by cough or straining (SAH/SOL) - postural headache changes (spont CSF leak) - headache + pressing visual changes (glaucoma/optic neuritis)
99
Q

How can primary headache disorders be classified?

A

Primary episodic (<15 headache days/month) - migraine, tension type, cluster, trigeminal autonomic cephalagias Primary frequent (chronic daily, >15 headache days/month) - transformed migraine, chronic tension, new daily persistent headache, hemicrania continua

100
Q

Episodic headaches - short vs long duration headaches

A

Long duration episodic: migraine, tension >4 hours/day Short duration episodic: cluster, trigeminal autonomic cephalagias <4 hours/day Shorter duration with special features: primary cough, primary exertional, hypnic, organismc and pre-orgasmic headaches) ** short stabbing headaches < 15 days/month

101
Q

Causes of secondary headaches

A
  • skull: Pagets, mastoiditis, secondary malignancy - ears: OM/OE - eyes: glaucoma, ocular strain, iritis - nose: sinusitis - teeth: abscess - neck: spondylosis - cranial nerves: herpes zoster, occipital neuralgia - intracranial vascular: venous sinus thrombosis, ruptured aneurysm, ICH - extracranial vascular: carotid artery dissection - CSF: raised ICP, post dural puncture - infection: encephalitis, meningitis
102
Q

Clinical features of episodic headaches: migraine

A
  • female predominance - often starts in adolescence - often associated with positive family history - associated visual, sensory, motor or cortical symptoms - unilateral throbbing headache - associated with nausea and vomiting - associated with light and sound sensitivity - can last for days (4-72 hrs) - often recurrent with predictable triggers
103
Q

Clinical features of episodic headaches: tension

A
  • often begins in young adulthood - nil aura - tight band like pressure - nil GIT features, phono or photo-phobia - usually not as incapacitating as migraine or cluster headache - can last for 30minutes to 7 days
104
Q

Clinical features of episodic headaches: cluster

A
  • male predominance - severe, often excruciating - unilateral and seldom side shifts - location of pain behind the eye - shorter duration with typically abrupt onset (15-180min) - seldom triggers: except for ETOH during a cluster - will normally see conjunctival injections, lacrimation, nasal blockage and basal discharge ipsilateral to headache
105
Q

What are the main categories of high frequency primary headaches? (long and short duration)

A

LONG duration - chronic migraine - chronic tension headache - new daily persistent headache - hemicrania continua SHORT duration - chronic cluster - chronic paroxysmal haemicrania - unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) syndrome - short stabbing headaches

106
Q

How can primary headaches be classified?

A

By frequency: - episodic (<15 headache days/month) - frequent (>15 headache days/month) By duration - long duration (> 4 hours) - short duration (< 4 hours)

107
Q

Chronic migraine diagnosis

A
  • headaches for > 15 days/month - lasting for more than 4 hours for at least 3 months - clinical features of migraine: throbbing, unilateral, nausea/vomiting, light and sound sensitivity
108
Q

Chronic tension type headache

A
  • chronic daily headache - less frequent than chronic migraines - gradually escalating headache frequency coalescing into chronic daily headache pattern without features suggesting of migraine - daily dull bilateral headache characterised by pressure
109
Q

New daily persistent headache

A
  • key feature is that this headache does not evolve from an intermittent episodic headache pattern - begins and simply continues as a daily headache
110
Q

Hemicrania continua

A
  • rare - strictly unilateral headache - sometimes evolving from intermittent pattern - has the features of a cluster headache - moderate severity - autonomic features are not as pronounced as in cluster headaches - dramatically responsive to indomethacin
111
Q

Trigeminal autonomic cephalagias

A
  • primary headache disorders which are characterised by both trigeminal parasympathetic activation - include: cluster, paroxysmal hemicrania, SUNCT syndrome - recurrent attacks of obritotemporal pain associated with parasympathetic features - Chronic paroxysmal hemicrania: features of cluster headache but more frequent attacks, > 5/day lasting for 2-30min
112
Q

Primary stabbing headache

A
  • recurrent stabs of sharp, jabbing pain in distribution of first division of trigeminal nerve - recurrent attacks are very alarming for patients and often stops them in their tracks - nil autonomic features
113
Q

What are the divisions of the trigeminal nerve?

A

Ophthalmic nerve (V1) Maxillary nerve (V2) Mandibular nerve (V3)

114
Q

Hypnic headache

A
  • occurs primarily in elderly - short lives headache which wakes patients from sleep often in early hours of the morning - no autonomic features
115
Q

Headaches related to cough/exertion/sexual activity

A

Need to exclude structural pathology! - Arnold-Chiari malformations - Vascular lesions (aneurysms or dissections)

116
Q

Which type of tremor is typically improved by ETOH?

A

Essential tremor!

117
Q

Name the 12 cranial nerves

A

I: olfactory II: optic III: oculomotor IV: trochlea V: trigeminal VI: abducens VII: facial VIII: vestibulocochlear IX: glossopharyngeal X: vagus XI: accessory XII: hypoglossal Oh Oh Oh To Touch And Feel A Girls Vagina Ah Heaven

118
Q

What is the name for CN VI?

A

Abducens

119
Q

What is the innervation of the extra-ocular muscles?

A
  • three cranial nerves innervate the 6 extraocular muscles - CN III (oculomotor), IV (trochlea) and VI (abducens) 1. superior rectus: III (oculomotor) 2. inferior rectus: III (oculomotor) 3. medial rectus: III (oculomotor) 4. lateral rectus: VI (abducens) 5. superior oblique: IV (trochlea) 6. inferior oblique: III (oculomotor)
120
Q

Which extraocular muscle does CN VI innervate?

A

Abducens innervates the lateral rectus - lateral rectus acts to abduct the eyeball hence if paralysed will cause adduction

121
Q

What is the clinical presentation of abducens/6th CN palsy?

A
  • usually present with binocular horizontal diplopia - esotropia/stabismus/turning in of affected eye - pts may present with a head turn to minimise diplopia - need to exclude papiloedmea, examine other extra-ocular muscles and rule out involvement of CN V, VII, VIII - need to exclude meningitis in young patients without a history of diabetes - should also screen for temporal arteritis (ESR/CRP)
122
Q

What are the common causes of abducens palsy?

A
  • post viral syndrome in younger patients - ischaemic mononeuropathy in adult population - linked to HTN and diabetes
123
Q

Where are the thenar muscles located?

A

Base of the thumb - innervated by the median nerve - control abduction of thumb, and flexion at MCP of thumb

124
Q

Where are the hypothenar muscles located?

A

Base of the 5th finger - innervated by the ulna nerve - 5th finger opposition, abduction, and flexion at MCPJ

125
Q

Which nerve innervates the lumbricals?

A
  • innervation: lateral 2 = median, medial 2 = ulna - action: flexion at MCPJ and extension at IP joints of each digits
126
Q

Which never innervates the interossei?

A

Dorsal interossei > ulna innervation > abduction of fingers a MCPJ - palmar interossei - unla innervation - adduction of fingers at MCPJ

127
Q

What are the following red flags concerning for in headaches… a) sudden onset b) first ever headache, focal neurology, confusion, ALOC c) patients >50 d) onset after head trauma e) increasing frequency/severity f) new onset in pt with HIV or cancer g) signs of systemic illness and neck stiffness h) papilloedema i) positional headache, worse when lying down and cough headache

A

A) subarachnoid, pituitary apoplexy, haemorrhage into mass, arterial dissection B) stroke, venous sinus thrombosis, meningitis/encephalitis C) giant cell arteritis, mass lesion, stroke D) subdural/epidural haemorrhage E) mass lesin, subdural haemorrhage, analgesic rebound F) meningitis, abscess, metasasis H) mass lesion, raised ICP, venous sinus thrombosis I) space occupying lesion , Ciari malformation

128
Q

Can a tension headache be associated with photophobia and phonophobia?

A

Yes! But will not be associated with nausea

129
Q

Trigeminal autonomic cephalgias

A
  • unilateral and side locked - unilateral autonomic features: tearing, conjunctival injections, ptosis, rhinorrhoea, fullness of ear, tinnitus, facial flushing or sweating - may present with unilateral photophobia or phonophobia - patients present agitated and restless
130
Q

What needs to be excluded in causes of primary headache associated with sexual activity?

A
  • space occupying lesion or aneurysm
131
Q

What is a primary stabbing headache?

A
  • transient localised stabs of pain in the head - occur spontaneously in absence of organic disease - lasts for seconds and recur irregularly - nil autonomic features - treatment often not warranted but may respond to indomethacin
132
Q

How to treat a hypnic headache

A
  • 1-2 cups of coffee before bed - lithium, melatonin, indomethacin - headache in age >50 which wakes patients from sleep and often associated with nausea
133
Q

Which headache features would be concerning for raised ICP

A
  • headache worse in the morning - worse when lying down and improved by upright posture - aggravated by cough, straining and valsalva - need to exclude: SOL, venous sinus thrombbosis or obstruction and use of tetracyclines and retinals - consider idiopathic intracranial HTN especially if recent weight gain
134
Q

Which drugs commonly cause drug-induced headaches?

A
  • alcohol - marijuanna - cocaine - nitrates - ciclosporin
135
Q

Clinical features of trigeminal autonomic cephalgias

A
  1. cluster
  2. paroxysmal hemicrania
  3. SUNCT
  4. hemicrania continua
136
Q

Pain characteristics of trigeminal neuralgia

A
  • recurrent, unilateral, shock like pain in one or more division of trigeminal nerve (especially V2/V3)
  • can be triggered by simple stimuli or cold
  • attacks last seconds to minutes
  • typically followed by brief refractory peroid
  • may be asociated with MS or neurovascular compression
137
Q

Pain characteristics of greater occipital neuralgia

A
  • shooting or stabbing pain over occiput
  • typically unilateral
  • may radiation to ipsilateral fronto-orbital region
  • pressure over site of the nerve often evokes pain
138
Q

Pain characteristics of TMJ dysfunction

A
  • pain aggrevated by active and passive jaw movements or pressure over affected structures
139
Q

How often should triptans be limited to in treatment of migraine

A

10 days per month

  • if used more often can cause medication overuse headache
140
Q

When should you consider migraine prophylaxis?

A

If needing treatment for acute migraine on more than 2-4 days per month

141
Q

Non-pharmacological therapies for migraine

A
  • regular sleep schedule
  • regular meals, avoid simple carbs
  • adeqate hydration
  • limited caffiene
  • regular exercise
  • relaxation techniques
  • avoidance of triggers
  • could trial magnesium trial for 3 months
142
Q

Non pharmacological management of ACUTE migraine

A
  • cold pack on forehead or back of skull
  • hot packs on neck and shoulders
  • neck stretches and self mobilisation
  • rest in a dark quiet room
143
Q

Acute migraine management with nonopioid analgesics and antiemetics

A

ASPIRIN 900-100mg, repeat dose 4-6 hours later if needed (max 4g in 24 hours)

BRUFEN 400-600mg, repeat dose 4-6 hours later if needed (max 2.4g in 24 hours)

* aim to limit non-opioid analgesia to less than 15 days/month*

If additional nausea

METOCLOPRAMIDE 10mg, TDS if required

144
Q

Acute treatment for migraine with triptan

A
  • if nonopioid analgesics do not relieve migraine prescribe triptan for next attack

ELETRIPTAN 40-80mg, if symptoms recur wait Q2H before repeating dose (max 160mg dose in 24 hrs)

SUMATRIPTAN 50-100mg PO, if symptoms recur wait Q2H before repeating dose (max 300mg dose in 24 hrs)

RIZATRIPTAN 10mg PO if symptoms recur wait Q2H before repeating dose (max 30mg dose in 24 hrs)

Educate patients on SSRIs/SNRIs about seretonin syndrome

145
Q

Migraine in pregnancy

A
  • paracetamol
  • avoid NSAIDs
  • if required a sparing dose of codiene may be considered
146
Q

Migraine prophylaxis

A
  • consider if getting 2-4 migraines/month
  • avoid beta blockers in asthma

Should trial prophylaxis for aleast 8-12 weeks

AMITRIPTYLINE
CANDESARTAN
NORTRIPTYLINE
PIXOTIFEN
PROPRANOLOL
SODIUM VALPROATE

147
Q

Acephalgic migraine

A
  • aura without headache
  • ddx: TIA, epilepsy
  • consider neuroimaging and be suspicous for another diagnosis
148
Q

Medication overuse headache

A
  • medication overuse can cause rebound headache as dose wears off
  • limits the efficacy of migraine prophylaxis
  • causes a secondary headache disorder which is superimposed on the primary headache
  • patients with migraines and tension headache are more susceptible to overuse headaches
  • common drugs: opioids, tryptants, ergots
  • NSAIDs can induce medication overuse headache if for more than 15 days/month
149
Q

Management of tension-type headache

A
  • lifestyle modification
  • CBT and relaxation training may be effective
  • acupuncture may be effective but need 6 sessions min
  • physiotherapy can also help

ASPIRIN 600-900mg repeat Q4-6H if needed
DICLOFENAC 50mg, repeat Q4-6H if needed
IBUPROFEN 400mg, repeat Q4-6H if needed
NAPROXEN 500-750mg, repeat Q4-6H if needed

If more frequent tension-type headache
AMITRIPTYLINE 10mg NOCTE, increase to max 75mg
Continue for 6 months if effective and then consider trial of withdrawal, if nil response consider

MIRTAZAPINE 15-30mg nocte for 8-12 weeks

150
Q

What imaging is required after diagnosis of cluster headaches?

A

MRI with pituitary views to r/o structural lesion of pituitary

151
Q

Acute treatment for cluster headaches

A
  1. SUMATRIPTAN 6mg S/C
  2. SUMATRIPTAN 20mg intranasally

Plus

HIGH FLOW OXYGEN 100% at 15L
> via nonrebreather for 15-20 min

Consider prophylaxis if recurrent: verapamil (first line)

  1. VERAPAMIL IR 80mg TDS for 2 weeks and uptitrate
152
Q

What is SUNCT?

A

Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing

  • subtype of trigeminal autonomic cephalgia
  • can be treated with gabapentin, lamotrigine, topiramate
153
Q

What is the treatment of rheicrania continua and paroxysmal hemicrania?

A

INDOMETHACIN 25mg TDS for 3 days, 50mg TDS for 3 days and then 75mg TDS for 3 days

154
Q

Idiopathic intracranial hypertension

A
  • presents in overweight young women, often after recent weight gain with features of raised ICP
  • drugs can cause raised ICP: OCP, tetracyclines, vitamin A analogues
  • can cause permenant vision loss
  • exclude venous obstruction and SOL on MRI and confirm raised opening pressure on lumbar puncture
  • management: weight loss and acetazolamide 250mg BD
155
Q

Managament of trigeminal neuralgia

A
  • can be de to demyelination or neurovascular compression, request imaging to r/o structural case especially in setting of sensory loss

CARBAMAZEPINE MR 100mg BD, up to 400mg BD

156
Q

Mangement of greater occipital neuralgia

A
  • shooting/stabbing pain over occiput
  • initial treatment is nerve block, can be repeated 3/12
  • if nerve block not effective can trial rx

GABAPENTIN 300mg nocte (max 1200mg TDS)

PREGABALIN 65mg nocte (max 300mg BD)

157
Q

Which clinical symptoms would be concerning for carotid artery dissection?

A 
Frontotemporal headache (gradual or thunderclap)
Neck pain with associated ipsilateral horners syndrome
158
Q

Diagnosis of Parkinson’s

A
  • bradykinesia PLUS one of the following
    > muscular rigidity
    > 4-6 Hz rest tremor
    > postural instability

Many causes but sporadic is most common

159
Q

What are the non-motor complications of Parkinsons?

A
  • fatigue
  • neuropsychiatric symptoms: depression, anxiety, psychosis
  • sleep disturbance
  • autonomic symptoms: orthostatic hypotension, bladder dysfuction, dysfunction, sexual dysfunction
  • dysphagia
160
Q

What are the broad options for Parkinsons’ management?

A
  • levodopa + dopamine agonist are the main drugs
  • allied health input
  • physical therapy
161
Q

What are the behavioural adverse effects of dopamine agonists as monotherapy?

A
  • pathological shopping
  • eating
  • hoarding
  • gambling
  • sexual preoccupation
  • medicatio nabuse
  • punding: doing and re-doing

Do not use dopamine agonists in patients with history of impulse control disorders

162
Q

First line treatment for eary Parkinson’s

A
  • preferred drug = levodopa rather than dopamine agonists
  • start low dose and increase gradually increase over weeks

LEVODOPA+BENSERAZIDE 50/12.5mg TDS

LEVODOPA+CARBIDOPA 50/12.5mg TDS

All antiparkinsons drugs cause nausea but tolerance rapidly develops and taking with food can help

Need to avoid metoclopramide/prochlorperazine (dopamine antagonists)

163
Q

What drug can be used to treat nausea in patients with Parkinson’s?

A

Domperidone 10mg TDS for up to 7 days

DO NOT USE metoclopramide or prochlorperazine

164
Q

What are the motor complications experienced as Parkinson’s disease progresses?

A
  • motor fluctuation (i.e. wearing off effect or intermittent dose failure or delayed or reduce drug effect of individual doses)
  • drug induced chorea or dystonia
  • may need smaller more frequent evenly spaced doses of levodopa to manage motor complications
  • high protein meals may also interfere hence modify diet and avoid dosing at mealtimes (give drugs 1 hour before eating)

-

165
Q

Management of orthostatic hypotesion in Parksinson’s disease

A

Fludrocortisone 0.1mg daily, up to 0.2mg daiy if needed

Non pharmacological advice: avoid extreme heat, ETOH, rising rapidly, increase sodium and water intake, eat smaller more frequent meals, regular swimming, compression stocking, sleep with bed head raised

166
Q

Dementia in Parkinsons’

A
  • pattern of cognitive impairmenet is executive dysfunction and impaire visospatial function
  • language is prefered and fewer memory deficits are seen
  • benefits of acetylcholinesterase inhibitors are modest and can be trialed for 2-3 months

DONEPEZIL 5mg nocte for 4 weeks

RIVASTIGMINE 4.6mg transdermally daily

167
Q

Parkinson plus disorders

A
  • progressive supranuclear palsy
  • corticobasal syndrome
  • Lewy body dementia
168
Q

Essential tremor

A
  • oistural or kinetic tremor in frequency between 4-12Hz
  • family history and temporary benefit after ETOH is cmmon
  • exclude drugs or systemic causes: hyperthyroidism
  • mild tremors do not require treatment

PROPRANOLOL 10mg BD

169
Q

Causes of chorea

A
  • Sydenham’s chorea –> ARF
  • Parkinson’s –> drug iduced
  • Severe chorea –> Huntington’s
170
Q

Emergecy treatment of severe chorea

A

CHLORPROMAZINE 25mg once to twice daily

OR

HALOPERIDOL 1-2mg up to 4 times daily

171
Q

Sydenham’s Chorea

A
  • neuropsychiatric disorder trigged by GAS

Treatment: CARBAMAZEPINE

172
Q

Acute drug induced dystonia

A

BENZATROPINE 1-2mg IV or IM

Can repeat Q20min if nil response

173
Q

Symptoms strongly suggestive of MS

A
  • acute painful loss of vision in one eye (optic neuritis
  • limb weakness and numbness with or without bladder/bowel dysfunction and sometimes with acute pain (transverse myelitis)
  • ataxia, facial numbness, diplopia (brain stem syndrome)
174
Q

What are the symptoms of brain stem syndrome in MS?

A
  • ataxia
  • diplopia
  • facial numbness
175
Q

Management of spasticity in MS

A

BACLOFEN 5mg TDS

176
Q

MS and vitamin D

A
  • low serum vitamin D concentration has been associated with increased relapse frequency and MRI activity in early MS
  • check vitamin D at diagnosis and supplement if <50
177
Q

Causes of myopathy

A
  • immune disorders: polymyositis, NAM, dermatomyositis
  • connective tissue disorders: SLE, sjogren
  • drugs: statins, firbates
  • endocrine disorders: thyroid, diabetes, adrenal dysfunction, vitamin D deficiency, –> all assoc with proximal myopathy
  • infections: HIV, viral myositis
  • malignancy: may be associated with dermatomyositis
178
Q

Classification of immune-mediate myopathy

A

DERMATOMYOSITIS
POLYMYOSITIS
OVERLAP MYOSITIS: associated w/ SLE, Sjogren, rheumatoid
NECROTISING AUTOIMMUNE MYOPATHY: statin associated, associated with HIV/Hep C, malignancy
INCLUSION BODY MYOSITIS

179
Q

Management of immune mediately myopathies

A

First line: corticosteroid + steroid sparing agent

If severe: STAT methylprednisolone 1g daily for 3 days

Otherwise

PREDNISOLONE 1mg/kg (up to 75mg) daily for 6 wees + taper

+

AZATHIOPURINE/METHOTREXATE

180
Q

Myasthenia gravis

A
  • autoimmune disorder with antibodies against the postsynaptic acetylcholine recetors (Ach-R) or less commonly MuSK
  • presents most often in females between age 10-30 and men 50-70
  • to diagnose need to show fatigability of muscles
  • patients who show ocular myasthenia are at risk of developing generalised disease within 2 years of onset
  • if myasthenia gravis is suspected: blood tests of anti-AchR + MuSK if bulbar symptoms
  • neurophysiological testing
  • check thyroid and B12 in all patients as links with thyroid/coeliac diseases
  • also need to do CT to r.o thymoma
181
Q

Approach to treatment of myasthenia gravis

A
  • do not treat until diagnosis confirmed unless emergency
  • always assess breathing and swallowing
  • isolated ocular symptoms or mild to moderate limb/bulbar weakness can be managed as outpatient
  • If rapidly prgressive weakness or resp involvement needs admission, use FVC to guide admission to ICU
182
Q

First line maagement for myasthenia gravis

A

PYRIDOSTIGMINE (anticholinesterase inhibitor)

  • time dose for when patient is most fatigued
  • if muscarinic adverse effects can add anticholinergic

In ICU settings can use IV neostigmine

183
Q

Immunosuppression for myasthenia gravis

A
  • indicated in moderat to severe cases when response to pyridostigmine (anticholinesterase inhibitor) is incomplete
  • high dose steroids can worsening symptoms in forst 3-7 days but this is transient
184
Q

Myasthenia crisis

A
  • IVIG or plasma exchange may be used
185
Q

Drugs to avoid/caution in patients with myasthenia gravis

A
  • neuromuscular blockers: depolarising and non-depolarising
  • aminoglycosides
  • macrolindes
  • quinine
  • fluoroquinolones
186
Q

What is the more common name for idiopathic facial nerve palsy?

A

Bell’s palsy

187
Q

Bell’s palsy

A
  • facial nerve palsy
  • most common cranial neuropathy
  • cause in uncertain, may be related to viral infection
  • DDx: diabetes, HTN, parotid tumour, tick bites, trauma
  • many patients return to normal with nil residual weakness
  • can take several weeks or months to recover
  • if symptoms <72H can start steroid

PREDNISOLONE 1mg/kg (max 75mg) mane for 5 days

188
Q

Treatable causes of peripheral neuropathy

A
  • immune mediated neuropathy
  • diabetes
  • vitamin B1 deficiency
  • B12 decifiency
  • sarcoidosis
  • drugs
  • vasculitis
  • porphyria

However most cases no cause if found!

189
Q

What is the other name for Guillain Barre syndrome

A

Acute inflammatory polyradiculoneuropathy

190
Q

Presentation of GBS

A
  • presents as widespread weakness and sensory disturbance the progresses rapidly
  • starts peripherally with impaired of loss of tendon reflexes
  • autonomic instability can occur: BP changes, arrhythmia, retention
  • some cases are triggered by infection: campylobacter, mycoplasma pneumoniae, EBV, CMV
191
Q

Which infections are known to trigger GBS?

A

Mycoplasma pneumonia

Campylobacter

EBV

CMV

192
Q

Diagnosis of GBS

A
  • CSF: raised protein concentration with minimal cellular response
  • nerve conduction studies: early in disease will show absence of F waves but later nerve conduction slows
193
Q

GBS management

A
  • inpatient management
  • Q4H FVC, if falls to 20ml/kg or rapidly declines ADMIT ICU
  • treatment = IVIg and plasma exchange
  • require VTE prophylaxis
194
Q

Motor neurone disease

A
  • progressive neurodegenerative disorder of upper and lower motor neurones
  • present with limb, bulbar and or resp muscle weakness
  • disease is fatal usually within 3-4 years of onset
  • no cure but riluzole slows disease modestly (improve survival by 3-6 months)
195
Q

Acute brachial neuritis

A
  • acute severe pain in shoulder and upper arm on one side
  • may follow URTI, vaccination or local trauma
  • pain persists for days or weeks
  • may be associated with muscle wasting
196
Q

Management of restless leg syndrome

A
  • physical exercise and good sleep exercises
  • exclude iron deficiency as this can aggrevate
  • if mild movements at sleep: levodopa + carbidopa
  • if severe symptom: gabapentin, pregabalin
197
Q

Classification of stroke

A

ISCHAEMIC 75%

  • large vessel: artery to artery embolism (30%)
  • cardioembolic: heart to artery embolism
  • small vessel disease: lacunar infarcts
  • rare: dissection, venous infarction, vasculopathies

HAEMORRHAGIC 10%
SUBARACHNOID HAEMORRHAGE 5%

198
Q

What are “stroke mimics”

A
  • hypglycaemia
  • tumour
  • subdural haematoam
  • migraine
  • postictal paralysis
  • cerebral abscess
199
Q

Patients at high risk of stroke after TIA

A
  • age > 60
  • raised BP > 140/90
  • motor or speech symptoms
  • symptoms lasting > 1 hours
  • diabetes

Patients at greatest risk are those with established infarction, AF or known high grade carotid stenosis

200
Q

Immediate management of acute ischaemic stroke

A
  • IV thrombolysis can be given within 4.5 hours of onset of acute ischaemic stroke
  • alteplase is preferred
  • treat hypertension prior to thrombolysis (needs to be <185/110) using GTN and labetalol
  • endovascular thrombectomy: highly effective in patient who present 6-24 hours after onset of symptoms
201
Q

Secodary prevention of ischemic stroke and TIA

A

ASPIRIN 100mg daily or CLOPIDOGREL or ASSASANTIN

ANTIHYPERTENSIVE

STATIN

Management of carotid stenosis

202
Q

Rarer causes of ischaemic stroke

A
  • bacterial endocarditis
  • cerebral venous thrombosis
  • carotid or vertebrobasilar arterial dissection
  • patent foramen ovale
203
Q

SAH

A
  • present either with acute severe headache or loss of consciousness
  • 20% of patients may have a sentinel bleed
204
Q

Driving after TIA/stroke

A
  • unable to drive for atleast 4 weeks after stroke for private vehicle and at least 3 months if commercial driver
  • after TIA unable to drive for 2 weeks if private license or 4 if commercial driver
205
Q

Central vs peripheral causes of vertigo

A

Peripheral features: tinnitus, hearing loss, aural fullness, positive head impulse test

Central features: ataxia, visual field loss, diplopia, sensory loss, limb weakness, slurred speech, dysphagia

206
Q

DDx of vertigo

A

Spontaneous vetigo (when head in stationary)
> acute vestibular syndrome: possible stroke or vestibular neuritis
> episodic vertigo: meniers or vestibular migraine

Motion induced vertigo (only when head is moving)
> short lives attacks in horizontal plane : peripheral vestibular lesion
> trigged by movement in vertical plan: BPPV

207
Q

Symptomatic treatmemt of acute vertigo

A
  • only indicated for up to 48 hours

PROCHLORPERAZINE 5-10mg Q6-8H

PROMETHAZINE 25-50mg Q8-12H

Do not continue these drugs long term du eto risk of tardive dyskinesia and drug induced parkinsonism

208
Q

Vestibular neuronitis

A
  • common cause of severe spontaneous vertigo
  • many cases due to HSV1 reactivation
  • history of acute or subacute onset of severe rotary vertigo, nausea, postural imbalance W/OUT hearing loss
  • fiding of unidirectionaly mixed horixontal and torsional nystagmus with positive head impulse test
  • usually self limiting improving over hours to day but 30% of caes may not resolve completely
  • if severe can use prednisolone
209
Q

Stroke and vertigo

A
  • vertebrobasilar circulation stroke can cause spontaneous vertigo
  • always check for vascular risk factors
  • examination: head impulse negative, direction changing nystagmus, test of skew positive and positive for new hearing loss
  • CT is not sensitive in posterior circulation strokes
210
Q

What is the HINTS+ examination?

A
  1. Head Impulse: abnormal in peripheral causes
  2. Nystagmus: primary gaze and lateral gaze

> unidirectional nystagmus = peripheral
> bidirectional nystagmus = central

  1. Test of Skew: cover an eye and check for vertical movement of eye when uncovered eye

+ hearing loss

211
Q

Meniere’s disease

A
  • idiopathic endolymphatic hydrops
  • episodic vertigo accompanied by tinnitus, hearing loss and aural fullness
  • cause is unknown
  • treatment:

HYDROCHLOROTHIAZINE 25mg daily

212
Q

Vestibular migraine

A
  • episodic spontaneous vertigo
  • accompanies migraine headache in 25% of patients
  • treat with migraine prophylaxis and acute symptomatic vertigo treatment
213
Q

Uncompensated peripheral vestiular lesion

A
  • motion-induced vertigo
  • persisent, short bouts of dizziness and vertigo triggered by horizontal movement and balance dysfunction
  • occurs after unilateral loss of vestibular function: vestibular neuritis, Menier’s disease, after acute symptoms have resolved
214
Q

BPPV

A
  • suspect BPPV when vertigo is triggered by head movement in verticlar plane i.e. lying down, head in extension or when rolling out of bed
  • diagnosed by Hallpike manouvre which will induce positional nystagmus
215
Q

What are the 3 treatment manovres for BPPV?

A
  1. Epley
  2. Semont
  3. Brandt-Daroff
216
Q

What needs to be ruled out in cases of unilateral tinnitus or hearing loss?

A

Acoustic neuroma

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