Nervous System Flashcards

1
Q

Anatomy of dorsal columns Mode: Cell body: Decussation:

A

Anatomy of dorsal columns

Mode: fine touch, vibration, proprioception

Cell body: dorsal root ganglion

Decussation: in medulla, via medial lemniscus

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2
Q

Anatomy of lateral spinothalamic tract Mode: Cell body: Decussation:

A

Anatomy of lateral spinothalamic tract Mode: pain, temperature Cell body: dorsal root ganglion Decussation: in cord, at entry level

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3
Q

Anatomy of lateral corticospinal tract Mode: Cell body: Decussation:

A

Anatomy of lateral corticospinal tract Mode: motor (body) Cell body: primary motor cortex Decussation: ventral medulla (pyramidal)

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4
Q

Which cranial nerve nuclei (3-12) lie in each brainstem structure? Midbrain: Pons: Medulla:

A

Which cranial nerve nuclei (3-12) lie in each brainstem structure? Midbrain: 3, 4, (5) Pons: 5, 6, 7, 8 Medulla: (5), 9, 10, 11, 12

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5
Q

Cerebellar Syndrome Effects:

A

DDANISH

Dysdiadochokinesia

Dysmetria

Ataxia

Nystagmus (horizontal = ipsilateral hemisphere)

Intention tremor

Speech (slurred, stoccato, scanning dysarthria)

Hypotonia

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6
Q

Cerebellar Syndrome Causes:

A

PASTRIES

Paraneoplastic

Alcohol (B1/B12 deficiency)

Sclerosis (MS)

Tumour

Rare (Multiple System Atrophy, Friedrich’s Ataxia, Ataxia Telangiectasia)

Iatrogenic (phenytoin)

Endocrine (hypothyroidism)

Stroke (vertebrobasilar)

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7
Q

Lateral Medullary Syndrome Cause: Features:

A

Cause: occlusion of one vertebral artery or posterior inferior cerebellar artery (PICA)

Features: DANVAH

  • Dysphagia
  • Ataxia (ipsilateral)
  • Nystagmus (ipsilateral)
  • Vertigo
  • Anaesthesia (ipsilateral trigeminal, contralateral pain)
  • Horner’s Syndrome (ipsilateral)
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8
Q

6th + 7th CN palsy, contralateral hemiplegia Where is the lesion? What is the eponymous syndrome?

A

Pons

Millard-Gubler Syndrome

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9
Q

Pt aware, cognitively intact, paralysed except for eye muscles Where is the lesion? What is the syndrome? Give 2 causes

A

Ventral pons

Locked-In Syndrome

1) ventral pontine infarction (basilar artery) 2) central pontine myelinolysis (rapid correction of hyponatraemia)

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10
Q

Ipsilateral CN 5, 6, 7, 8 palsies + cerebellar signs Where is the lesion? What is the syndrome? Give 4 causes

A

Cerebellopontine angle

Cerebellopontine Angle Syndrome

1) acoustic neuroma 2) meningioma 3) cerebellar astrocytoma 4) metastasis (eg breast)

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11
Q

Anterior Spinal Artery (Beck’s) Syndrome Definition: Causes: Effects:

A

Definition: infarction of spinal cord in distribution of anterior spinal artery (ventral 2/3rds)

Causes: aortic aneurysm dissection or repair

Effects: para-/quadri-paresis, impaired pain + temperature sensation, intact touch + proprioception

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12
Q

DDx: muscle weakness

A
  • CEREBRUM / BRAINSTEM:
    • Vascular - infarct, haemorrhage
    • Inflammation - MS S.O.L
    • Infection - encephalitis, abscess
  • CORD:
    • Vascular - ant spinal artery infarct
    • Inflammation - MS
    • Trauma
  • ANTERIOR HORN: motor neuron disease, polio
  • ROOTS: spondylosis, cauda equina syndrome, carcinoma
  • MOTOR NERVES:
    • Mononeuropathy - compression, trauma
    • Polyneuropathy - GBS, CMT
  • NMJ: myasthenia gravis, Lambert-Eaton, botulism
  • MUSCLE:
    • AI - polymyositis, dermatomyositis
    • Toxins - steroids Inherited - muscular dystrophy (D/B)
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13
Q

DDx (motor): gait disturbance

A

1) Where is it. 2) Is it UMN, LMN, parkinsonian or mixed

BILATERAL

  • Parkinsonian: PD, parkinsonism (multiple system atrophy, dementia w Lewy bodies, progressive supranuclear palsy, corticobasal degeneration)
  • UMN:
    • Brain - CP, MS
    • Cord - compression, trauma, syringomyelia, transverse myelitis, hereditary spastic paraparesis
  • LMN:
    • Corda equina syndrome (emergency)
    • Polyneuropathy - CMT, GBS, DM
  • Mixed
    • MAST = MND, Ataxia (Friedrichs), Subacute combined degen of cord, Taboparesis

UNILATERAL

  • UMN :
    • Brain - MS, SOL, CVS
    • Cord - MS, tumour P
  • LMN:
    • Ant horn - polio
    • Radicular - L5 root lesion
    • Peripheral - sciatic, common peroneal nerve trauma
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14
Q

DDx (sensory): gait disturbance

A

VESTIBULAR (Romberg’s +ve): Meniere’s, viral labyrinthitis, brainstem lesion

CEREBELLAR (ataxic): EtOH, infarct

PROPRIOCEPTIVE (Romberg’s +ve): Dorsal columns - B12 deficiency Peripheral neuropathy - DM, EtOH, uraemia

VISUAL LOSS

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15
Q

Causes: blackouts

A

CARDIAC:

  • reflexes: vasovagal
  • rhythm - brady - heart block, sick sinus, longQT tachy - SVT, VT
  • structural - AS, HOCM, PE, LVF, tamponade

NEUROLOGICAL:

  • Epilepsy, drop attacks
  • CVA

SYSTEMIC: hypoglycaemia, hypoxia, hypercapnoea (anxiety)

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16
Q

Causes: vertigo

A

‘IMBALANCE’

INFECTION/INJURY: labyrinthitis, Ramsay Hunt, trauma

MENIERE’S: recurrent +/- n/v, tinnitis

BPPV

AMINOGLYCOSIDES / frusemide

LYMPH: fistula between inner and middle ears

ARTERIAL: migraine, CVA

NERVE: acoustic neuroma, vestiibular swannoma

CENTRAL: demyelination, infarct, tumour

EPILEPSY: complex partial

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17
Q

Causes: hearing loss (conductive)

A

Conductive: WIDENING

  • Wax
  • Infection (otitis media)
  • Drum perforation
  • Extra (trauma)
  • Neoplasia
  • INjury (barotrauma)
  • Granulomatous (GwP, sarcoid)
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18
Q

Causes: action / postural tremor

A

‘BEATS’

Benign essential tremor

Endocrine - thyrotoxicosis, hypoglycaemia, phaeo

Alcohol withdrawal

Toxins - beta agonists, theophylline, valproate

Sympathetic - physiological, enhanced in anxiety

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19
Q

Causes: acute confusional state

A

‘PINCH ME(^5)’

Pain

Infection (often UTI in elderly)

Neurological (stroke, subdural)

Constipation

Hydration insufficient

Medications (opioids, sedatives, L-DOPA)

Electrolytes (hyponatraemia, hyper/hypocalcaemia, uraemia)

Endocrine (hyper/hypothyroid, hypoglycaemia)

EToH

Encephelopathy (B12/folate deficiency)

Environment

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20
Q

DDx: acute headache

A

VASCULAR - haemorrhage, infarction, sinus venous thrombosis

INFECTION/INFLAMMATION - meningitis, encephalitis, abscess

RAISED ICP - tumour, glaucoma

REDUCED ICP - spontaneous intracranial hypotension (dural CSF leak)

SYSTEMIC - sinusitis, tonsillitis, HTN, toxins

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21
Q

DDx: chronic headache

A

‘MCD TINGS’

MIGRAINE

CLUSTER

DRUGS - analgesics, caffeine, vasodilators

TENSION

ICP - up (tumour aneurysm, AVM, benign intracranial HTN), down (spontanoeus intracranial hypotension)

NEURALGIA - trigeminal

GIANT CELL ARTERITIS

SYSTEMIC - HTN, uraemia

(AS)

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22
Q

Red Flags: headache

A

SNOOP’

  • SYSTEMIC - fever, wt loss
  • NEUROLOGICAL - confusion, impaired consciousness/speech/sensation/power
  • ONSET - sudden
  • OLDER PT - new onset, progressive (?giant cell arteritis)
  • PMH - worse than usual, unilateral eye pain

(AS)

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23
Q

Mx: migraine

A

Acute episode: 1st: paracetamol + metoclopramide

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24
Q

TIA: score for subsequent stroke risk

A

ABCD2

Age >=60

BP >=140/90

Clinical: unilateral weakness (2), speech disturbance (1)

Duration: 10-60 min (1), >60 min (2)

DM hx

Score: 0-2: outpt mx 3+: consider admission

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25
Q

Migraine w/o aura: diagnostic criteria (International Headaches Society)

A

Criteria

A: At least 5 attacks fulfilling criteria B-D

B: Headache attacks lasting 4-72 hours* (untreated or unsuccessfully treated)

C: Headache has 2+ of:

    1. unilateral location
    1. pulsating quality (i.e., varying with the heartbeat)
    1. moderate or severe pain intensity
    1. aggravation by or causing avoidance of routine physical activity

D: During headache 1+ of:

    1. N/V
    1. photophobia and phonophobia

E: no alternative diagnosis is suggested in hx or O/E

(Passmedicine)

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26
Q

Generalised tonic-clonic seizures: Long-term mx (1st line, 2nd line)

A

1st line: sodium valproate

2nd line: lamotrigine, carbemazepine

Started after second seizure, or first if neurological deficit, abnormal imaging, epileptiform EEG, pt request.

(**NICE)

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27
Q

Partial seizures: Long term mx (1st line, 2nd line)

A

1st line: lamotrigine or carbemazepine

2nd line: sodium valproate

Started after second seizure, or first if neurological deficit, abnormal imaging, epileptiform EEG, pt request.

(NICE)

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28
Q

Absence seizures: Long term mx (1st line)

A

1st line: sodium valproate or ethosuximide

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29
Q

Myoclonic seizures: Long term mx (1st line, 2nd line)

A

1st line: sodium valproate

2nd line: lamotrigine, carbemazepine

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30
Q

III nerve palsy: causes

A
  • Medical: pupil-sparing
    • HTN
    • DM
  • Surgical: SOL, posterior communicating artery aneurysm (compression), trauma
    • pupil dilates early as parasympathetic fibres on outside more vulnerable

(Mirza)

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31
Q

Partial ptosis: causes

A
  • Unilateral
    • Horner’s (small pupil)
    • IIIrd nerve palsy (big pupil)
  • Bilateral
    • Myasthenia gravis
    • Bilateral Horner’s
    • Myotonic dystrophy (type 1)

(Mirza)

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32
Q

VI nerve palsy: causes

A
  • Medical
    • T2DM
    • HTN
    • Raised ICP
    • MS

(Mirza)​

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33
Q

Raised intracranial pressure: signs (including characteristic triad)

A
  • Cushing’s triad: hypertension, bradycardia, abnormal breathing
  • Fundoscopy signs
    • Loss of retinal vein pulsation (early)
    • Papilloedema (late)
  • Focal neurology (inc III and VI nerve palsies)
  • Headache, reduced GCS, N/V

(Mirza)

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34
Q

Spastic parapresis: causes

A
  • Emergency: spinal cord compression
  • Non-emergency
    • CVA
    • MS
    • MND
    • Cervical spondylosis

(Mirza)

35
Q

Muscle wasting of the hands: causes

A
  • Unilateral
    • Global: ‘PBC’
      • Pancoast’s
      • Brachial plexus injury
      • Cervical rib
    • Myotomal
      • Thenar: carpal tunnel
      • Radial/ulnar/median nerve lesion
  • Bilateral
    • RA
    • MND
    • Charcot-Marie-Tooth (early sign)
    • Cervical spondylosis

(Mirza)

36
Q

Neurofibromatosis Type 1: triad

A
  • Neurofibromas
  • Cafe au lait spots (>6 of >15mm)
  • Lisch spots on iris (hamartomas of iris visible using slit lamp)

(Mirza, BMJ)

37
Q

What is the inheritance pattern of NF1 and NF2

A

Both autosomal dominant

38
Q

NF1: incidence

A

1 / 3000

(UpToDate)

39
Q

Recognise the presenting symptoms of neurofibromatosis

A

NF1 triad: cafe au lait spots + neurofibromas + iris Lisch nodules

+ axilliary freckling (= Crowe’s sign)

+ learning difficulties, seizures

40
Q

NF1: complications

A
  • ‘HTML’:
    • HTN (increased risk of phaeochromocytoma and renal artery stenosis)
    • Thoracic kyphosis –> respiratory compromise
    • Malignant change (in 10%)
    • Learning difficulties / behvioural problems

(Mirza)

41
Q

NF1: management

A
  • Pt education (screening family members, including genetic testing in pregnancy)
  • MDT approach
    • Paediatric neurologist
    • Geneticist
    • Opthalmolgist
  • Screen for complications (eg monitor BP, resp function, signs of malignancy)
42
Q

PACES: you suspect dx of Bell’s palsy and have examined VII nerve, what other things should you examine for?

A
  • localise lesion: examine CNs VI (pons lesion), V&VIII (cerebropontine angle lesion)
  • examine for Ramsay Hunt: look for vesicular rash in ears (herpes zoster from geniculate ganglion of VII)
  • ask about hyperacusis (stapedius palsy) and changes in taste
  • examine parotids (rule out parotid tumour)
  • (Mirza)*
43
Q

Define Bell’s palsy

A

Diagnosis of exclusion: acute unilateral peripheral facial nerve palsy, evolving over 72h and affecting all facial zones.

(BMJ, OHCM)

44
Q

Summarise the prognosis for patients with Bell’s palsy

A

Morbidity - complete recovery 70%, minor impairment 13%, major impairment 19%

(BMJ)

45
Q

Explain the aetiology / risk factors of Bell’s palsy

A

Idiopathic

Ramsay Hunt (+ other infective eg TB, Lyme disease)

Brainstem lesion (CVA, tumour)

Parotid tumour

Trauma

(OHCM)

46
Q

Identify appropriate investigations for Bell’s palsy

A

Bloods: VZV Abs, BM, ESR, Borrelia Abs (if ?Lyme disease)

Imaging: MRI (if ? SOL)

Nerve conduction studies

(OHCM)

47
Q

Generate a management plan for Bell’s palsy

A

Conservative - tailored facial exercises to optimise motor function (poorly evidenced)

Medical

  • steroids (prednisolone), esp if present within 72h
  • protect eye if evidence of drying (eg dark glasses)

Surgical

  • to resolve poor eye closure (eg lid loading procedure, lateral tarsorrhaphy)
  • augment facial symmetry (Botox)
  • (OHCM)*
48
Q

Identify the possible complications of Bell’s palsy

A
  • recurrence (7%)
  • eye drying and abrasion –> corneal damage –> blindness
  • deformity –> psychological sequelae
49
Q

O/E and UMN picture in the lower limbs and LMN picture in the upper limbs should make you think of what diagnosis?

A

Amyotrophic lateral sclerosis

50
Q

Causes: hearing loss (sensorineural)

A

Sensorineural: DIVINITY

  • Developmental (Alport’s, perinatal anoxia/infection)
  • Infection (mumps)
  • Vascular (stroke, eg in internal auditory artery)
  • INflammation (sarcoid, vasculitides)
  • Injury (inc noise)
  • Toxins (gentamicin, frusemide, aspirin)
  • lYmph (Meniere’s, ruptured round window)

(AS)

51
Q

Generate a management plan for trigeminal neuralgia

A

Medical

  • 1st line: carbemazepine (100mg PO BD, titrate up until remission then lowest possible maintenance dose)
  • If ineffective, refer to pain/neurology

(NICE)

52
Q

Explain the aetiology of subarachnoid haemorrhage

A
  • Berry anuerysm rupture (80%): RFs Ehlers-Danlos, Marfans, PCKD
  • AV malformation
  • Trauma
  • Tumours

(passmedicine)

53
Q

Generate a management plan for ischaemic stroke

A
  • Immediate
    • CT head: exlude haemorrhagic stroke
    • Aspirin 300mg: start ASAP (w/i 24h, continue for 2w then start long-term anticoagulation)
        • PPI if dyspepsia hx
    • <4.5h from onset: thrombolysis (alteplase)
    • maintain glucose, O2, BP w/i normal limits
  • Secondary prevention Anticoagulation (lifelong)
    • 1st: Clopidogrel
    • 2nd: Aspirin + dipyridamole (if clopidogrel CI)
    • 3rd: Dipyridamole (if aspirin CI)
  • RF modification:
    • statin: if cholesterol >3.5 mmol/L. Start >48h after stroke (reduce risk of haemorrhagic infarct)
    • Carotid endarterectomy: if carotid stenosis >70% (european criteria)

(NICE)

54
Q

What are the contraindications to thrombolysis in ?stroke (absolute and relative)

A

Contraindications to thrombolysis:

  • Absolute
    • Bleeding risk: ?haemorrhagic stroke, ?SAH, oesophageal varices, intracranial neoplasm, active bleeding
    • Previous: intracranial haemorrhage, GI bleed (previous 3w), stroke / head trauma (previous 3w), lumpar puncture (previous 1w)
    • Seizure at onset of stroke
    • Pregnancy
    • Uncontrolled hypertension >200/120mmHg
  • Relative
    • ?intracardiac thrombus
    • INR >1.7
    • Active diabetic haemorrhagic retinopathy
    • Major surgery / trauma in preceding 2 weeks

(Passmedicine)

55
Q

Explain the aetiology of Horner’s syndrome

A

Causes:

central (symp chain): brainstem strokes eg lateral medullary infarct (Horner’s + impaired eye movements + ipsilateral ataxia), MS, SOL, syringomyelia

pre-ganglionic: Pancoast’s, surgery/trauma, thoracic outlet obstruction

post-ganglionic: carotid artery aneurysm / surgery

= cervical ganglion

(UpToDate)

56
Q

What is Refsum’s disease?

A

AutoR neurological disorder

Peroxisomal disorder –> accumulation of phytanic acid

Retinitis pigmentosa + cerebellar ataxia + peripheral neuropathy + increased CSF protein

(AS Adam)

57
Q

Identify appropriate investigations for Refsum’s Disease

A

1) serum phytanic acid: raised
2) peripheral nerve biopsy: hypertrophic onion bulb formation
* (AS Adam)*

58
Q

Generate a management plan for Refsum’s Disease

A
  • Conservative: dietary restriction of phytanic acid (fats + fish)
  • Medical: plasmaphoresis

(AS Adam)

59
Q

Identify appropriate investigations for subarachnoid haemorrhage

A
  • CT: negative in 5%
  • lumbar puncture: done after 12 hrs if CT scan -ve (allowing time for xanthochromia to develop)
  • regular neuro obs: pupils, GCS, BP

(AS)

60
Q

Generate a management plan for subarachnoid haemorrhage

A
  • Neurosurgical opinion
  • Medical
    • Regular neuro obs: pupils, BP, GCS
    • Intubate/ventilate: if GCS <8
    • Nimodipine: brain-specific CCB, reduces vasospasm to reduce risk of stroke/rebleeding. 3w course while risk of complications.
    • IV fluids: keep sBP >160

(Meeran, AS, passmedicine)

61
Q

Identify the possible complications of subarachnoid haemorrhage

A

BBSS: bleed, blockage, stroke, siadh

  • rebleeding (in 30%) - peaks day 10
  • obstructive hydrocephalus (due to blood in ventricles)
  • cerebral ischaemia (due to vasospasm) - risk at days 5-14
  • SIADH –> hyponatraemia

(AS, Meeran)

62
Q

Summarise the prognosis for patients with subarachnoid haemorrhage

A

Mortality: 25% dead at 6m

Morbidity: 50% survivors severely disabled at 6m

(BMJ)

63
Q

Generate a management plan for subdural haematoma

A

1st line: irrigation / evacuation via burr-hole craniotomy

2nd line: craniotomy

address causes of trauma

(AS)

64
Q

Generate a management plan for Parkinson’s disease

A
  • Conservative: encourage physical activity (reduces progression), Parkinson’s UK, walking aids, PT/OT, depression screening
  • Medical
    • Dopaminergics:
      • L-DOPA (postpone for as long as possible in young pts, due to tolerance): eg levodopa, carbidopa
      • MAO-B Is: eg rasagiline
      • Da agonists (mainly in young pts)
        • domperidone (to reduce DA-induced nausea)
    • Rescue pen: apomorphine (DA agonist) for sudden freezing
    • Atypical antipsychotics: for psychosis
    • SSRIs: for depression
  • Surgical
    • Deep brain stimulation

(AS)

65
Q

L-DOPA: side effects

A

‘DOPAMINE’

  • Dyskinesia
  • On-off motor performance fluctuations
  • Psychosis
  • Arterial BP drop
  • Mouth dryness
  • Insomnia
  • N/V
  • Excessive daytime sleepiness

(AS)

66
Q

Identify appropriate investigations for multiple sclerosis

A
  • Confirm diagnosis
    • MRI head + neck (T2): ring enhancing lesions show active inflammation
    • LP: oligoclonal bands IgG (on electrophoresis)
    • Bloods: anti-myelin basic protein Ab

(path, AS)

67
Q

Generate a management plan for multiple sclerosis

A
  • Conservative: regular exercise, sleep hygiene, mindfullness, reduce stress
  • Medical
    • Acute - induce remission
      • High-dose steroids (methylpred 1g/24h IV/PO for 3d)
    • Long-term
      • Maintain remission (specialist)
        • IFN-beta (or PEG-IFN-beta)
        • Biologicals: alemtuzumab, natalizumab
      • Supportive (FED UP)
        • Fatigue: modafinil
        • Erectile dysfunction: sildenafil
        • Depression: SSRI
        • Urgency / frequency: oxybutynin
        • Pain: TCAs, gapapentin

(AS, BMJ)

68
Q

Identify the possible complications of multiple sclerosis

A
  • Progression
  • Steroid complications: cushing’s, osteoperosis, UTI
  • FED UP
    • Fatigue
    • Eye-problems
    • Depression
    • Urgency /frequency
    • Pain

(BMJ, AS)

69
Q

Summarise the prognosis for patients with multiple sclerosis

A

Extremely variable

Multiple relapses, motor + cerebellar involvement associated with worse prognosis

(BMJ)

70
Q

What are the characteristics of an Argyll Robertson Pupil?

Where is the lesion?

One common cause

A

Accomodates, but does not react

Pretectal region

Tertiary syphilis (ie neurosyphilis)

71
Q

What are the characteristics of a Holmes-Addie pupil?

Where is the lesion?

One common cause

A

Myotonic cause: dilated at rest, contracts slowly to light, keeps contracting after light, dilates slowly

+ ipsilateral reduced LL refexes

Lesion in parasympathetic fibres of IIIrd nerve

Post-infective (viral or bacterial)

(meeran)

72
Q

What is a Marcus Gunn Pupil

Where is the lesion?

One common cause

A

Relative afferent pupillary defect

Optic nerve

Multiple sclerosis

(Meeran)

73
Q

What red flags with parkinsonism may suggest Parkinson’s Plus Syndrome

A

‘VIVAA’

  • Vertical gaze palsy: progressive supranuclear palsy
    • +/- speech/swallow problems, truncal rigidity, early postural instability
  • Impotence / incontinence: multiple system atrophy
    • +/- autonomic features, postural hypotension, nystagmus (lateral), cerebellar / pyramidal signs
  • Visual hallucinations: Lew-body dementia
    • +/- fluctuating cognition, early dementia
  • Akinetic rigidity one limb, astereognosis (can’t identify object by feeling it), apraxia: Corticobasal degeneration
  • Ataxia or pyramidal signs: Vascular Parkinsonism

(OHCM)

74
Q

Define status epilepticus

A

Status epilepticus = >30 mins continusous seizure, or repeated seizures for 30 mins without intervening consciousness

(OHCM)

75
Q

Generate a management plan for status epilepticus

A
  • ABCDE
    • Airway: speech (suggests pseudoseizure), check for evidence of vomiting, consider airway adjunct
    • Breathing: auscultate chest for evidence of aspiration, do ABG, do pulse oximetry, give high flow O2
    • Circulation: get IV access, check HR, BP, cap refill, ECG
    • Disability: assess GCS!
    • Exposure: check GLUCOSE, check for evidence of PE, check temperature, if Hx of ETOH abuse then check thiamine
  • Immediate: call for help, warn anaesthetists
    • 1st line – IV lorazepam / rectal diazepam (repeat at 10 mins if no improv)
    • 2nd line – IV phenytoin/phenobarbitone (repeat half dose if no improve)
    • 3rd line – IV phenobarbitone
    • 4th line – Get anaesthetist. IV propofol/midazolam/sodium thiopentone

(Y3 notes)

76
Q

Identify appropriate investigations for epilepsy

A
  • EEG – All pts with suspected seizure should have EEG, though not necessarily diagnostic. Usually shows spikes during seizure (generalised, myoclonic, atonic).
    • Grand-Mal seizures will show bilateral synchrony in the epileptiform activity
    • Absence seizures show activity at 3Hz.
  • MRI – important for diagnosis of epilepsy syndromes

(Y3 notes)

77
Q

Identify possible complications of status epilepticus

A
  • Focal neurology
  • Cognitive dysfunction: esp memory problems

Both improve with time

(BMJ)

78
Q

Identify risk factors for stroke

A

RFs:

  • Modifiable
    • HTN: #1
    • AF (5% risk. If anticoagulated, 1% risk)
    • T2DM
    • hyperlipidaemia
    • smoking
  • Unmodifiable
    • Age
    • Male
    • FHx
    • ethnicity: Asian, black

(500SBAs, INTERSTOKE study)

79
Q

Give potential causes of spinal cord compression

A
  • Trauma: vertebral #
  • Infection: epidural abscess, TB
  • Malignancy: mets from breast / thyroid / bronchus / kidney / prostate
  • Disc prolapse: above L1/2

(AS)

80
Q

What are the clinical features of spinal cord compression?

A
  • Pain: local, deep + radicular
  • Weakness: LMN @ level, UMN below level
  • Sensory level
  • Sphincter disturbance

(AS)

81
Q

Identify appropriate investigations for spinal cord compression

A
  • Confirm dx: MRI definitive
  • Assess cause
    • Look for primaries: CXR, CT head abdo pelvis
    • Bloods: FBC, CRP, ESR, B12, UEs, LFTs, PSA

(AS, OHCM)

82
Q

Generate a management plan for spinal cord compression

A

Emergency

  • Malignancy:
    • dexamethasone IV
    • consider chemo / radio +/- decompressive laminectomy
  • Abscess: surgical decompression, IV Abx

(AS, OHCM)

83
Q

Identify the possible complications of spinal cord compression

A
  • Autonomic dysfunction (incontinence, bradycardia, posutural hypotension, erectile dysfunction)
  • Sensorimotor dysfunction (–> spastic paraparesis, pressure ulcers)
  • Surgical complications (infection, bleeding, DVT, PE)

(BMJ)