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Neuro Flashcards

1
Q

PACS criteria?

A
  • 2/3 of TACS

or

  • Higher cortical dysfunction alone

or

  • Isolated motor deficit not meeting LACS criteria
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2
Q

Higher cortical problems in stroke?

A

LEFT = Language dysfunction

RIGHT = Neglect of contralateral limbs Apraxia

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3
Q

POCS criteria?

A
  • Ipsilateral cranial nerve palsy + contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Disordered conjugate eye movement
  • Cerebellar dysfunction
  • Isolated hemianopia or cortical blindness
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4
Q

Investigations in stroke?

A
  • Bloods
  • ECG
  • CXR
  • CT head
  • Echo/carotid doppler/24h ECG
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5
Q

Criteria for thromboylsis in stroke?

A
  • Age <80 - <4.5 hours from start of symptoms
  • Age >80 - <3 hours from start of symptoms
  • Non-haemorrhagic stroke (excluded by CT)
  • Significant symptoms and not improving
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6
Q

Contraindications to thrombolysis?

A
  • Active bleeding
  • CNS trauma
  • Neoplasms or arteriovenous malformations
  • Previous intracerebral haemorrhage
  • Ischaemic stroke in previous 6mths
  • Major trauma/surgery in past 3wk
  • Non-compressible punctures in past 24hrs (LP etc).
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7
Q

Management of haemorrhagic stroke?

A

FFP/prothrombin complex concentrate, vitamin K and surgical review.

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8
Q

ABCD2 score?

A
  • Age >60
  • Blood pressure >140/90
  • Clinical features = unilateral weakness (2) and speech disturbance without weakness (1)
  • Duration = >60 mins (2), 10-60 mins (1)
  • Diabetes

>4 = high risk

>5 = 8% risk of stroke in 48 hours

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9
Q

Causes of bacterial meningitis in different age groups?

A

NEONATES

  • E.coli,
  • GBS
  • listeria
  • S.aureus
  • Pneumococcal

1m-15yrs

  • HIB
  • meningococcus
  • pneumococcus

ADULTS 15+

  • Pneumococcus
  • meningococcus

ELDERLY

  • Staph aureus
  • Gram -ve organisms
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10
Q

Causes of non-bacterial meningitis?

A

VIRAL

  • Mumps
  • coxsackie

FUNGAL

  • Immunosuppressed - cryptococcus
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11
Q

Contraindications to LP?

A
  • Focal neurological signs (seizures)
  • Raised ICP (low HR, high BP, papilloedema)
  • Shock/CV instability
  • Bleeding risk
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12
Q

Bacterial LP appearance?

A
  • Turbid
  • High polymorphs (neutrophils)
  • High protein
  • Low glucose
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13
Q

Viral LP appearance?

A
  • Clear
  • High lymphocytes
  • Low/normal protein
  • Low/normal glucose
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14
Q

TB LP appearance?

A
  • Turbid/clear/viscous
  • High lymphocytes
  • V high protein
  • V low glucose
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15
Q

Abx in meningitis?

A
  • 2nd/3rd gen ceph (IV)
  • <3 months or >55 years - amoxicillin to cover listeria
  • Further abx directed by MC+S
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16
Q

Supporting therapy in meningitis?

A
  • Corticosteroids
  • Analgesics
  • Antipyretics
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17
Q

Management of viral meningitis?

A

Supportive therapy – analgesia, antipyretics, nutritional support, hydration

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18
Q

Vaccinations that protect against meningitis?

A

Vaccination against H. influenzae type b, meningococcus groups B and C and S. pneumoniae.

Quadrivalent vaccine (A, C, W, Y) for 17-18 year olds.

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19
Q

Pharmacological sedation?

A

Haloperidol 0.5mg PO, 1-2 hourly PRN – daily max = 5mg – avoid atypicals in elderly.

Can add lorazepam but try to avoid as tolerance and dependence may occurs (hangover effect)

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20
Q

Delirium screen investigations?

A
  • FBC, U&Es and creatinine, glucose, calcium, magnesium, LFTs, TFTs, cardiac enzymes, vitamin B12 levels
  • Syphilis serology, autoantibody screen
  • PSA, eGFR
  • Blood cultures/serology
  • ABG
  • CT head
  • Urine dipstick/MC+S,
  • ECG
  • Lumbar puncture
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21
Q

Risk factors for SAH?

A
  • Hypertension
  • Smoking
  • Cocaine use
  • Excessive alcohol intake
  • Family history (1st degree)
  • Genetic disorders (autosomal dominant adult polycystic disease, Ehlers-Danlos syndrome, neurofibromatosis, Marfan’s)
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22
Q

Signs in SAH?

A
  • Coma/depressed level of consciousness (direct effect of haemorrhage or mass effect)
  • Focal neurological signs (limb weakness, dysphagia)
  • Reactive hypertension III nerve palsy – indicates direct nerve damage from posterior communicating artery or basilar artery aneurysm
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23
Q

Imaging in SAH?

A
  • CT first line - hyperdense appearance in basal cisterns
    • If +ve –> angiography
    • If -ve –> MRI or lumbar puncture
  • Angiography determines the origin of the bleed - catheter angiography offers possibility of coiling the aneurysm.
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24
Q

ECG changes in SAH?

A
  • QT prolongation
  • Q waves
  • Dysrhythmias
  • ST elevation
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25
Q

Management of SAH?

A

GENERAL

  • Continuous observation, IV access, analgesia

PREVENTING ISCHAEMIA

  • Nimodipine (calcium antagonist)

DEFINITIVE

  • Surgical - clipping (11-14 days after) Antifibrinolytics reduce bleeding
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26
Q

Definition of status?

A

Seizure lasting for >30 minutes, or repeated seizures without intervening consciousness

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27
Q

Management of status?

A
  • Open and maintain airway
  • Recovery position
  • Oral/nasal airway
  • Oxygen
  • IV access if possible
  • Lorazepam
    • IV 2-4mg (2nd dose if no response in 10 min)
  • Phenytoin
    • 15-20mg/kg IVI at <50mg/min
    • Maintenance - 100mg/6-8h
    • OR Diazepam 100mg in 500mL of 5% glucose - infuse at 40mL/h
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28
Q

Pre hospital drugs for status?

A

Diazepam 10-20mg PR

Midazolam 10mg buccal

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29
Q

Causes of cranial nerve lesions?

A

Common = aneurysm, diabetes, MS, tumour, trauma/surgery, stroke

Rare = vasculitidies, sarcoidosis

Infection = Lyme disease, syphilis, HIV, Wernicke’s encephalopathy

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30
Q

Causes of altered visual fields?

A

glacucoma, retinitis pigmentosa, stoke, retinal occulsion, detached retina

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31
Q

Cause of enlarged blind spot?

A

Papilloedema

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32
Q

CN III - what does it innervate and what happens in palsy?

A
  • Medial, superior, and inferior recti, and inferior oblique muscles
  • Lateral rectus and superior oblique take over –> down and out.
  • Ptosis – due to ↓response of levator palpebrae superioris
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33
Q

CN IV - what does it innervate and what happens in palsy?

A
  • Superior oblique
  • Eye turns up and out, and elevates more as it moves medially
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34
Q

CN XI - what does it innervate and what happens in palsy?

A
  • Lateral Rectus
  • Eye medially deviated and movement lateral from midline is not possible
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35
Q

What happens in facial nerve palsy?

A
  • Inability to raise eyebrows, open eyes against resistance, do facial movements etc.
  • Forehead sparing in UMN lesion, not so in Bell’s palsy.
  • Lacrimation, salivation impaired (lesion proximal to geniculate ganglion)
  • Taste impaired (anterior 2/3 tongue – lesion above chorda tympani)
  • Hyperacusis (lesion above nerve to stapedius)
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36
Q

What does Weber’s test do?

A

Sensorineural deafness

  • Patient will report a quieter sound in the ear with the sensorineuronal hearing loss

Conductive hearing loss

  • Sound lateralises to affected ear - ear with the conductive hearing loss is only receiving input from the bone conduction and no air conduction, and the sound is perceived as louder in that ear
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37
Q

Glossopharyngeal taste distribution?

A

Posterior 1/3 of the tongue

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38
Q

Causes of acquired sensorineural deafness?

A

MINDMATT

  • Meniere’s
  • Infective
  • Neoplastic (acoustic neuroma)
  • Degenerative
  • Metabolic
  • Autoimmune
  • Toxic
  • Trauma
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39
Q

Features of median nerve palsy

A
  • Hand of benediction on trying to make a fist
  • Paraesthesiae in thumb, index and middle fingers – relieved by dangling hand over edge of bed and shaking it (‘wake and shake’)
  • Sensory loss and weakness of abductor pollicics brevis +/- wasting of thenar eminence
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40
Q

Management of median nerve pasly?

A

Splinting; local steroid injection +/- decompression surgery.

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41
Q

Cause of ulnar nerve palsy?

A

Trauma

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42
Q

Cause of median nerve palsy?

A

(C6-T1)

Swelling/compression in tunnel myxoedema, prolonged flexion (Colle’s splint), acromegaly, myeloma, local tumours (lipoma, ganglion), RA, amyloidosis, pregnancy, sarcoidosis.

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43
Q

Signs of ulnar nerve palsy?

A

(C7-T1)

  • Weakness/wasting of medial (ulnar) wrist flexors, interossei and medial two lumbricals
  • Cannot cross fingers in good luck sign/claw hand
  • Hypothenar eminence wasting, weak 5th digit abduction, 4th/5th DIP joint flexion
  • Sensory loss over medial 1½ fingers and ulnar side of hand
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44
Q

What does radial nerve innervate?

A

C5-T1

  • Opens the fist
  • muscles involved = BEAST –> brachioradialis, extensors, abductor pollicis longus, supinator & triceps.
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45
Q

Cause of radial nerve palsy?

A

Compression against humerus

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46
Q

Signs of radial nerve palsy?

A

Wrist/finger drop with elbow flexed and arm pronated

Sensory loss variable – anatomical snuff box mostly

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47
Q

Main 2 signs of brachial plexus injury?

A

Klumpke’s palsy (lower) and Erb’s palsy (upper)

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48
Q

Signs of Phrenic nerve palsy?

A

(C3-5)

Orthopnoea & raised hemidiaphragm on CXR

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49
Q

Signs of common peroneal nerve palsy?

A

(L4-S1)

  • Foot drop, weak ankle dorsiflexion/eversion
  • Sensory loss over dorsal foot.
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50
Q

Signs of tibial nerve palsy?

A

(L4-S3)

Inability to stand on tiptoe (plantarflexion), invert the foot, or flex the toes, with sensory loss over the sole.

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51
Q

Features of sensory neuropathy?

A
  • Numbness; pins and needles/paraesthesiae; ‘glove and stocking’ distribution,
  • Difficulty handling small objects like buttons
  • Signs of trauma (finger burns) or joint deformation may indicate sensory loss
  • Diabetic and alcoholic neuropathies are typically painful
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52
Q

Causes of peripheral neuropathy?

A

A = alcohol

B = B12/folate deciciency

C = Cancer/Connective Tissue/Collagen

D = Diabetes

E = Endocrine e.g. hypothyroid

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53
Q

Features of motor neuropathy?

A

Guillain-Barré, Lead Poisoning, Charcot-Marie-Tooth

  • Often progressive (may be rapid)
  • Weak or clumsy hands; difficulty in walking (falls, stumbling)
  • Difficulty in breathing (↓vital capacity)
  • Signs = LMN lesion - wasting/weakness in distal muscles of hands/feet – reflexes are reduced/absent
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54
Q

Features of autonomic neuropathy?

A

DM, amyloidosis, Guillain Barré, Sjogren’s Syndrome, HIV, Leprosy, SLE

  • Postural hypotension, decreased sweating, ejaculatory failure, Horner’s syndrome
  • Constipation, nocturnal diarrhoea, urinary retention, erectile dysfunction
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55
Q

Investigations to do in peripheral neuropathy?

A
  • Bloods
    • FBC, ESR, glucose, U+E, LFT, TSH, B12, electrophoresis, ANA, ANCA
  • Urinalysis
  • Imaging
    • CXR
  • Other
    • LP +/- specific genetic tests; nerve conduction studies
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56
Q

Management in peripheral neuropathy?

A
  • Treat cause; involve physio and OT.
  • Foot care and shoe choice [Symbol] minimise trauma.
  • Splinting
  • IV immunoglobulin in Guillain-Barré and demyelinating polyradiculoneuropathy
  • Steroids/immunosuppressants may help in vasculitic causes
  • Neuropathic pain –> amitriptyline, duloxetine, gabapentin and pregabalin
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57
Q

What vessels rupture in subdural?

A
  • Cortical bridging veins
  • Connect the venous system of the brain to the large intradural venous sinuses and lie relatively unprotected in the subdural space
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58
Q

Risk factors for subdural?

A
  • Any factor that stretches bridging veins –> cerebral atrophy, low CSF pressure after shunting
  • Alcoholism
  • Coagulation disorder/anticoagulation
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59
Q

Signs in subdural?

A
  • Fluctuating conscious level
    • History of gradual onset headahces, memory loss, personality change, dementia, confusion, drowsiness
    • Symptoms vary from day to day with intervening lucid periods
  • Focal neurological signs
    • Often hemiparesis on the side ipsilateral to the lesion (false localising sign)
  • Aphasia
    • If lesion on the left side
60
Q

CT/MRI findings in subdural?

A

Shows clot +/- midline shift.

Crescent-shaped collection of blood (increased density) over 1 hemisphere.

61
Q

Management of subdural?

A

Irrigation/evacuation (via burr twist drill and burr hole craniostomy) = 1st line

Craniotomy = 2nd line

62
Q

Artery that ruptures in extradural?

A

Middle meningeal - typically after trauma to temple

63
Q

Extradural signs?

A
  • Hemiparesis +/- brisk reflexes and upgoing plantars
  • Ipsilateral pupil dilates –> coma deepens –> bilateral limb weakness
  • Breathing becomes deep and irregular (brainstem compression)
  • Bradycardia and raised BP (Cushing’s response) are late signs
64
Q

CT findings in extradural?

A

Haematoma (biconvex/lens-shaped are of increased density); blood forms more rounded shape (dural attachments to skull keep it more localised.

65
Q

Drug you can give to decrease ICP? (e.g. in Extradural etc)

A

Mannitol

66
Q

Types of MS?

A
67
Q

Definition of MS?

A

Presence of multiple neurological deficits which are separated in time and space.

68
Q

Features of MS?

A
  • Optic neuritis – usually unilateral
  • Transverse myelitis - acute episode of bilateral weakness of legs, with loss of control of bowels and bladder.
  • Neurogenic bladder dysfunction – urgency +/- incontinence and frequency
  • Impotence
  • Sensory deficits – tingling in restricted distribution, trigeminal neuralgia, Lhermitte’s phenomenon (electricity sensation down spine on neck flexion)
  • UMN deficit – spastic weakness of legs
  • Cerebellar damage – ataxia, dysarthria, nystagmus
  • Vertigo
  • Dementia in later stage
69
Q

Investigations in MS?

A
  • Bloods
    • FBC, CRP, ESR, U&Es, LFTs, TFTs, glucose, HIV, calcium and B12 levels
  • MRI
    • 95% have periventricular lesions
    • 90% discrete white matter abnormalities
    • Focal demyelination – plaques in optic nerve, brainstem and spinal cord
    • Gadolinium enhancement improves sensitivity
  • CSF
    • Oligoclonal bands of IgG on electrophoresis that are not present in serum suggest CNS inflammation.
  • Visual Evoked Potentials
    • Show conduction changes consistent with demyelination – increased latency in patients with optic neuritis.
70
Q

3 categories of treatment in MS?

A
  1. Steroids
  2. Disease-modifying
  3. Symptomatic
71
Q

Steroids in MS?

A

Methylprednisolone – shortens acute relapses (use sparingly) – doesn’t alter overall prognosis.

72
Q

Disease-modifying therapy in MS?

A

Interferons (IFN-1β and IFN-1α)

  • ↓Relapses 30% and ↓lesion accumulation on MRI. Modest role in delaying disability.

MABs

  • Alemtuzumab/Natalizumab – better than interferons.

Non-immunosuppressive

  • Glatiramer, mioxantrone

Others

  • Azathioprine is good for relapsing remitting.
73
Q

Symptomatic treatment in MS?

A

Spasticity

  • Baclofen, diazepam, dantrolene, tizanidine.

Tremor

  • Botulinum toxin A

Urgency/Frequency

  • Intermittent self-catheterisation/tolterodine
74
Q

Triad of features in Parkinson’s Disease?

A
  1. Tremor
    • ​​Worse at rest; often ‘pill rolling’
  2. Rigidity/↑Tone
    • ​​‘Cogwheel ridigity’ - jerky resistance to passive movement- felt by rapid pronation/supination
    • ‘Lead pipe rigidity’ - sustained resistance to passive movement throughout the whole range of motion, with no fluctuations
  3. Bradykinesia/Hypokinesis​
    • Slow to initiate movement and slow, low amplitude repetitive actions (low blink rate, monotonous hypophonic speech, migrographia).
    • Gait: ↓arm swing, festinance, freezing at obstacles or doors
    • Expressionless face (hypomimesis)
75
Q

Non-motor features of Parkinson’s disease?

A
  • Sense of smell reduced
  • Constipation
  • Visual hallucinations
  • Frequency/urgency
  • Dribbling of saliva
  • Depression and dementia
76
Q

Investigations in Parkinson’s Disease?

A

Usually clinical diagnosis

SPECT scan

77
Q

Medical management of Parkinson’s Disease?

A

Levodopa

  • Co-beneldopa/Co-careldopa (combined with dopa-decarboxylase inhibitor)
  • Variable response (unpredictable freezing) and reduced end of dose response.
  • Key decision = when to start. Cons = ↓efficacy over time, dopamine-induced dyskinesias (5-10 years), psychosis, visual hallucinations, N+V (domperidone)

Dopamine Agonists

  • Ropinirole/pramipexole (transdermal).
  • Drowsiness, nausea, hallucinations, compulsive behaviour
  • Apomorphine = potent DA (continuous SC infusion) – evens out end-of-dose effects

Anticholinergics, MAO-B inhibitors, COMT inhibitors

78
Q

Neuropsychiatric and surgical management of Parkinon’s Disease?

A

Neuropsychiatric

  • Deep brain stimulation

Surgical

  • Surgical ablation of overactive basal ganglia circuits (subthalamic nuclei)
79
Q

Definition of…

  1. Prodrome
  2. Aura
  3. Partial (focal)
  4. Primary generalised
  5. Simple
  6. Complex
  7. Secondary Generalised
A
  1. Prodrome = Change in mood/ behaviour (hrs -days)
  2. Aura = Simple partial seizure (temporal) which may precede
  3. Partial (focal) = Features referable to part of one hemisphere
  4. Primary generalised = No warning/aura. Discharge throughout cortex w/o localising features
  5. Simple = awareness unimpaired
  6. Complex = awareness impaired
  7. Secondary generalised = focal seziure –> generalised (e.g. aura –> ton-clon)
80
Q

Causes of epilepsy/seizures?

A

2/3 are idiopathic (often familial)

  • Congenital
    • NF, tuberous sclerosis, TORCH, perinatal anoxia
  • Acquired
    • Vascular (CVA), cortical scarring (trauma, infection), SOL, SLE, PAN, MS, sarcoidosis
  • Non-Epileptic Seizures
    • Withdrawal (EtOH, opiates, benzos), metabolic (glucose, Na, Ca, urea, NH3), ↑ICP, infection, eclampsia, pseudoseizures
81
Q

Features of simple partial seizures?

A

Focal motor, sensory, autonomic or psychic symptoms

82
Q

Features of compex partial seizures?

A

5 As (usually from temporal lobe)

  • Aura
  • Autonomic (skin colour change, temperature, palpitations)
  • Awareness lost (motor arrest, motionless state)
  • Automatisms (lip-smacking, fumbling, chewing, swallowing)
  • Amnesia
83
Q

Features of Absence seizures?

A

ABSCENCES

  • ABrupt onset/offset
  • Short (<10s)
  • Eyes (glazed, blank stare)
  • Normal (intelligence, examination, brain scan)
  • Clonus (or automatisms)
  • EEG (3Hz spike and wave)
  • Stimulated by hyperventilation and photics
84
Q

Features of tonic-clonic seizures?

A
  • LoC
  • Tonic = limbs stiffen; Clonic = rhythmic jerking of limbs
  • Cyanosis; incontinence; tongue biting (lateral)
  • Post-ictal confusion and drowsiness
85
Q
A
86
Q

Features of myoclonic seizures?

A

Sudden jerk of limb, face or trunk

87
Q

Features of atonic seizures?

A

Sudden loss of muscle tone à fall (no LoC)

88
Q

What is West Syndrome?

A

Clusters of head nodding and arm jerks (EEG shows hypasarrhythmia)

89
Q

Investigations in seizures/epilepsy?

A
  • Bloods – FBC, U+E, LFT, calcium, glucose
  • Urine toxicology
  • ECG
  • Imaging – MRI (focal onset, adult epilepsy, seizures in spite of treatment)
  • EEG – to support diagnosis and help classification
90
Q

General advice for epileptics/potential epileptics?

A

Advise against driving, swimming, bathing alone until Dx is established

Diagnosis –> no driving until seizure free for 1 year (HGV 10 years seizure and medication free)

91
Q

Drugs for different types of epilepsy?

A
92
Q

Women and AEDs?

A
  • Avoid valproate (lamotrigine or CBZ instead)
  • 5mg folic acid daily if child-bearing age
  • CBZ and phenytoin are inducers and ↓efficacy of OCP
93
Q

Enzyme effects of AEDs?

A

INDUCERS (reduce concentration)

  • Carbamezapine
  • Phenytoin
  • Barbituates

INHIBITORS (increase concentration)

  • Valproate
94
Q

Side effects of lamotrigine?

A
  • Skin rash
  • Rash
  • Diplopia/blurred vision
  • Levels affected by inducers/inhibitors
95
Q

Side effects of carbamazepine?

A
  • Leukopenia
  • Skin reactions
  • Diplopia/blurred vision
  • SIADH –> hyponatraemia
96
Q

Side effects of valproate?

A

ALPROAT3E

  • Appetite↑
  • Liver failure
  • Pancreatitis
  • Reversible hair loss
  • Oedema
  • Ataxia
  • Teratogenicity, Tremor, Thrombocytopenia
  • Encephalopathy (due to ammonia)
97
Q

Side effects of phenytoin?

A
  • Gingival hypertrophy
  • Hirsutism
  • Cerebellar signs (ataxia, nystagmus, dysarthria)
  • Peripheral sensory neuropathy
  • Diplopia
  • Tremor
98
Q

+ve and -ve features of tension headahce?

A

Bilateral - may have photophobia and phonophobia

No nausea/vomiting or significant systemic upset/neurological deficit

99
Q

Lifestyle changes in management of tension headahce?

A
  • Avoid overwork/stress, excess alcohol, lack of exercise. Strategies to counteract stress.
  • Treat clinical depression.
  • Avoid analgesic abuse – max 12 doses per week.
  • Headache diary
  • Reassurance
100
Q

Drug therapy/alternative therapies for tension headache?

A

If <2 days a week – OTC analgesics.

  • Paracetamol – not great
  • NSAID or aspirin
  • Avoid codeine

If frequent/chronic –> aim for long term remission (prophylaxis)

  • Low dose amitriptyline
  • 3 week course of naproxen BD

Alternative = acupuncture

101
Q

Definition of migraine? Two theories of aetiology?

A

Syndrome characterised by periodic headaches with complete resolution between attacks.

  • Vascular theory = aura due to vasoconstriction, headache due to vasodilation
  • Neuronal theory = aura associated with spreading neuronal inhibition
102
Q

Who gets migraines? When in life? Which type is most common?

A

25% prevalence in women, 8% in men

Usually first attack before age 30

Migraine without aura 3x more common than migraine without aura

103
Q

Diagnostic criteria for common migraine (without aura)?

A

At least 5 attacks, all fulfilling following criteria

  • Frontotemporal headahce lasting 4-72 hours with at least 2 of the following characteristics
    • Unilateral location
    • Pulsating/throbbing quality
    • Moderate to severe pain intensity
    • Causing problems/avoidance of routine physical activity
  • With at least one of
    • N+V
    • Photophobia/phonophobia
    • Not attributable to another disorder
104
Q

Onset of simple migraine?

A

Usually gradual - peak after 2-12 hours, gradually subsiding.

Often begin in morning, possibly waking them from sleep

105
Q
A
106
Q

Non-obvious symptoms/signs of simple migraine?

A
  • Symptoms
    • Anorexia, blurred vision, impaired concentration, nasal stuffiness, hunger, tenesmus, diarrhoea, abdominal pain, polyuria, pallor, sweating, and sensations of heat or cold
  • Signs
    • Localized oedema of the scalp, face, or under the eyes; scalp tenderness; prominence of temporal blood vessels; or neck stiffness and tenderness
107
Q

Diagnosis of classical migraine (with aura)?

A

Diagnosis = at least 2 attacks. Aura has at least one of the following characteristics (but no motor weakness)

  • Fully reversible visual symptoms (flickering lights, spots or lines, loss of vision)
  • Fully reversible sensory symptoms (paraesthesiae, numbness)
    • Less common –> usually starts in the hand, migrates up the arm, then involves the face, lips, and tongue. Numbness may follow the paraesthesia.
    • Sensory auras rarely occur alone, and usually follow visual auras
108
Q

When does headahce occur in classical migraine?

A

During the aura or follows the aura within 60 mins

109
Q

Complications of migraine?

A
  1. ↑Risk of ischaemic stroke (RR = 2.16)
    • More so in migraine with aura – OCP + migraine with aura = NO (8x risk)
  2. ↑Risk of depression, BAD, anxiety, panic disorder
  3. Status migranosus – debilitating migraine that lasts more than 72 hours
  4. Migrainous infarction – cerebral infarction occurring during course of typical attack of migraine with aura.
110
Q

Differentials for migraine?

A
  1. Primary headache - tension, cluster
  2. Secondary - intracranial tumour
  3. Others = depression, sinusitis, dental caries, epilepsy, TIA, arteriovenous malformations, phaeochromocytoma
111
Q

Acute management of migraine?

A

Pharmacological

  • Combination Therapy
    • Oral triptan (5HT agonist - rizatriptan, sumatriptan) + NSAID or paracetamol
    • Antiemetics (metoclopramide) – relieves nausea and enhances efficacy of analgesics

General

  • Identify and avoid trigger factors
  • Regular sleep and dietary measures
112
Q

In whom are triptans contraindicated?

A
  • IHD
  • Coronary spasm
  • Uncontrolled BP
  • Recent lithium
  • SSRIs
113
Q

How do triptans work?

A

5HT agonists

Constrict cranial arteries and inhibit release of substance P/pro-inflammatory neuropeptides –> block transmission from trigeminal nerve.

114
Q

Prevention of migraines?

A

General

  • Identify and avoid trigger factors = most important.
  • If migraine recurring 4 or more times per month –> treat prophylactically

1st Line

  • Topiramate or Propranolol
  • Amitriptyline

2nd Line

  • Pizotifen (can cause weight gain) - triptan
  • Gabapentin, pregabalin
  • Valproate
115
Q

Problems with topiramate?

A

Can cause foetal malformations and impair effectiveness of hormonal contraceptives

116
Q

Combined motor and senory disorders?

A
117
Q

What is Brown Sequard?

A
  1. Ipsilateral upper motor neurone signs (weakness)
  2. Contralateral spinothalamic signs (no pain/temp)
  3. ipsilateral dorsal column signs (no vibration/proprioception)

Results from an injury to one side of the spinal cord resulting in hemisection of the cord - damage to corticospinal tract, spinothalamic tract and dorsal columns

118
Q

What is Anterior cord syndrome?

A
119
Q

What is posterior cord syndrome?

A
120
Q

What is central cord syndrome?

A
121
Q

Risk factors for fibromyalgia?

A

female sex, middle age, low income household, divorced, low educational status

122
Q

Features of fibromyalgia?

A
  1. Pain – chronic (>3 months) and widespread (involves left and right sides, above and below the waist, and the axial skeleton.
    • Allodynia = pain in response to non-painful stimulus.
    • Hyperaesthesia = exaggerated perception of pain in respon=se to a mildly painful stimulus.
  2. Profound fatigue – unrefreshing sleep, significant fatigue and pain with small increases in physical exertion.
  3. Additional Features – morning stiffness, paraesthesiae (without underlying cause), headaches (migraine and tension), poor concentration, low mood, sleep disturbance.

All investigations normal.

123
Q

What is Myasthenia Gravis? What is it associated with?

A

Autoimmune disease mediated by antibodies to nicotinic acetylcholine receptors on post-synaptic membrane of neuromuscular junction.

Associated with AI disease (RA, SLE)

124
Q

Symptoms of Myasthenia Gravis?

A

Slowly increasing or relapsing muscular fatigue. Muscle groups affected (in order):

  • Extraocular
  • bulbar (swallowing, chewing)
  • face
  • neck
  • limb girdle
  • trunk

Symptoms exacerbated by:

  • Pregnancy, hypokalaemia, infection, over-treatment, change of climate, emotion, exercise, gentamicin, opiates, tetracycline, quinine, beta-blockers
125
Q

Signs of myasthenia gravis?

A
  • Ptosis; diplopia;
  • Myasthenic snarl on smiling;
  • ‘Peek sign’ or orbicularis fatigability (eyelids begin to separate after manual opposition to sustained closure)
  • On couning to 50, the voice fades
  • Tendon reflexes normal
126
Q

Tests for myasthenia?

A

Anti-AChR antibodies (90%)

Ptosis improves by >2mm after ice application to eyelid for >2 min

127
Q

How is myasthenia treated?

A

Treated with anticholinesterases, immunosuppression (steroids, azathioprine, ciclosporin)

128
Q

Causes of hydrocephalus?

A
  • Post-meningitis
  • SAH
  • Trauma
  • Neoplastic
  • Dural sinus thrombosis
129
Q

Presentation of adult hydrocephalus?

A
  • Features of raised ICP
  • Impaired upward gaze
  • Mental impairment
  • Gait apraxia; up going plantars, tendon jerks exaggerated
  • Urinary incontinence due to sphincter dysfunction
  • Hypopituitarism due to enlargement of 3rd ventricle into posterior fossa.
130
Q

Presentation of infantile hydrocephalus?

A
  • Macrocephaly – anterior fontanelle enlarged and tense
  • Scalp veins are prominent
  • Irritability
  • Poor feeding/FTT
  • Developmental delay
  • Convulsions/mental impairment
  • Setting sun appearance - lids retracted, eyes depressed forwards and downwards, upward gaze is impaired
131
Q

Management of hydrocephalus?

A
  • Treat cause
  • Ventriculoperitoneal shunt – burr hole à silicone tube in lateral ventricle –> drains CSF subcutaneously into peritoneum.
132
Q

Most common type of MND? What is its pathophysiology?

A

Amyotrophic Lateral Sclerosis (ALS)

  • Selective loss of neurons in motor cortex, cranial nerve nuclei and anterior horn cells
  • Combined UMN and LMN signs - no sensory loss or sphincter disturbance - different from MS/polyneuropathies
  • Never affects eye movements - different from Myasthenia
  • Closely linked with FTD
133
Q

Symptoms of MND?

A
  • >40 yrs
  • Stumbling spastic gait
  • Foot drop +/- proximal myopathy
  • Weak grip (door-handles don’t turn) and shoulder abduction (hair washing is hard)
134
Q

Signs of MND?

A

UMN

  • Spasticity, brisk reflexes, ↑plantars

LMN

  • Wasting, fasciculation of tongue, abdomen, back, thigh.
  • Speech and swallowing sometimes affected (bulbar signs)
135
Q

Causes of encephalitis?

A
  • Usually viral = HSV1/2, CMV, EBV, VZV, arboviruses, HIV
  • Non-viral = any bacterial meningitis, TB, malaria, Lyme disease
136
Q

Presentation of encephalitis?

A
  • Infectious prodrome à fever, rash, LNs, cold sores, conjunctivitis, meningeal signs
  • Bizarre behaviour or personality change
  • Confusion, ↓GCS –> coma
  • Fever, headache
  • Focal neurology –> seizures
  • Hx of travel or animal bite
137
Q

Cerebellar Signs?

A

Lesions cause ipsilateral signs

DANISH

  • Dysdiadochokinesis, Dysmetria (past-pointing)
  • Ataxia (limb, truncal)
  • Nystagmus
  • Intention tremor
  • Slurred speech, Scanning dysarthria
  • Hypotonia
138
Q

Causes of cerebellar signs?

A

PASTRIES

  • Posterior fossa tumours
  • Alcohol
  • Stroke
  • Trauma
  • Rare (paraneoplastic syndromes)
  • Inherited (Freidrich’s ataxia)
  • Epilepsy drugs (phenytoin)
  • Sclerosis (multiple)
139
Q

Name some primary brain tumours?

General presentation of tumours?

A

Astrocytoma, Glioblastoma, Oligodendrocytoma, Ependyoma, Meningioma

  • Signs of raised ICP
  • Seizures
  • Evolving focal neurology (localising signs)
  • Personality change
140
Q

What is this and what does it indicate?

A

Peek sign - Myasthenia Gravis

141
Q

Investigations/management of encephalitis?

A
  • Bloods – cultures, viral PCR, malaria film
  • Contrast CT – focal bilateral temporal involvement = HSV
  • LP - ↑protein, lymphocytes, PCR

Treat with IV Aciclovir; supportive management in HDU/ICU.

142
Q

Stroke mimics?

A
  • With abnormal scans
    • Tumours – fluctuating gradual onset
    • Abscess – fever, fluctuating onset
    • Haematomas – subdural, extradural
  • With normal scans
    • Todd’s paresis – focal weakness in a part of the body after a seizure. This weakness typically affects appendages and is localized to either the left or right side of the body. It usually subsides completely within 48 hour
    • Migraine
    • Neuroglyopenia (low blood sugars)

Seizures, spreading depolarisation, subdural, sugars, sepsis

143
Q

Stroke management?

A
  • Aspirin 300mg PO (600mg PR) 14 days à switch to clopidogrel 75mg afterwards
  • Admit to stroke unit care
  • Monitor BP <150/90
  • O2 >93%
  • Early SALT assessment
  • 40-80mg atorvastatin
    • If anterior circulation – carotid endarterectomy (doppler à if 50% stenosed within 2 weeks, or >70% stenosed within 12 weeks, consider surgery).
144
Q

Anticoagulation in AF/stroke?

A
  • Not until TWO WEEKS AFTER – consider if AF.
  • Warfarin, DOACs
  • CHADVASc in AF/HASBLED
    • Relative risk reduction in stroke is 2/3
    • Questions about lifestyle and other drugs and liver disease
    • Counsel on lifestyle!! – 5 a day, fishy oils, less salt, cut down on booze, cut out the fags.
    • Vocational stuff – can you return to work? Driving?
145
Q

Things to mention in bad stokes?

A
  1. Problems after stroke
    • Immobility
      • Pressure sores
      • Contractures – physio, botulinum, baclofen
      • PE/DVT – compression stockings
      • UTI/aspiration pneumonitis
  2. Prognosis
    • Haemorrhage = poor prognosis (long term disability if survive)
    • Ischaemic = if dense, poor (50% mortality at 30 days, long term disability) if smaller, is better (lower recurrence)
  3. Difficult decisions
    • Long term feeding (NG, PEG etc)
    • EOL care – palliation, second opinions, withholding/withdrawing care
146
Q
A

- FINALS (24 decks)

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