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C TO REVISE - PHASE 3A > NEURO > Flashcards

NEURO Flashcards

1
Q

STROKE
What are the causes of ischaemic strokes?

A

small vessel occlusion by thrombus
atherothromboembolism (e.g. from carotid artery)
cardioembolism (post MI, valve disease, IE)
hyper viscosity
hypoperfusion
vasculitis
fat emboli from a long bone fracture
venous sinus thrombosis

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2
Q

STROKE
What are the causes of haemorrhagic stroke?

A

Bleeding from the brain vasculature

  1. Hypertension - stiff and brittle vessels, prone to rupture
  2. Secondary to ischaemic stroke - bleeding after reperfusion
  3. Head trauma
  4. Arteriovenous malformations
  5. Vasculitis
  6. Vascular tumours
  7. Carotid artery dissection
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3
Q

STROKE
What are some important differentials of stroke?

A
  • Metabolic (hypo or hyperglycaemia, electrolytes)
  • Intracranial tumours, hemiplegic migraine
  • Infection (meningitis)
  • Head injury, seizure (focal > Todd’s paralysis)
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4
Q

STROKE
What other investigations may you do in stroke?

A
  • ECG 72h tape to look for paroxysmal AF, MI.
  • ECHO to check for endocarditis or CHD
  • CTA/MRA or carotid doppler USS to look for dissection or carotid stenosis
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5
Q

STROKE
What are some contraindications to treatment with alteplase?

A
  • Haemorrhagic stroke
  • Recent surgery
  • GI bleeding
  • Pregnancy
  • Hx of intracranial haemorrhage
  • Active cancer
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6
Q

STROKE
What medication and general management may be given in stroke prevention?

A
  • Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
  • Anticoagulation if have AF but wait 2w post-stroke
  • Manage co-morbidities (HTN, DM)
  • Cholesterol >3.5mmol/L diet + 80mg atorvastatin
  • VTE assessment + monitor for infection
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7
Q

STROKE
What is the CHA2DS2-VaSc score

A
  • Congestive heart failure
  • HTN
  • Age 65-74 (1), ≥75 (2)
  • Diabetes
  • Prev stroke/TIA (2)
  • Vascular disease
  • Sex female
  • 1 = consider anticoagulation, ≥2 = anticoagulate
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8
Q

STROKE
What is the HAS-BLED score?

A
  • HTN >160mmHg
  • Abnormal liver/renal function
  • Stroke
  • Bleeding Hx or predisposition
  • Labile INR
  • Elderly >65y
  • Drug/alcohol use
  • ≥3 = high risk of bleeding
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9
Q

SAH
What is the pathophysiology of a subarachnoid haemorrhage (SAH)?

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
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10
Q

SAH
What is the management of SAH?

A
  • NIMOPIDINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
  • surgery = endovascular coiling
  • IV fluids - maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
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11
Q

EDH
What are some differentials for EDH?

A
  • Epilepsy,
  • CO poisoning,
  • carotid dissection
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12
Q

EDH
What is the management for EDH?

A

STABILISE PATIENT

URGENT SURGERY

clot evacuation
ligation of bleeding vessel
IV MANNITOL
- to reduce ICP

airway care
- intubation and ventilation

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13
Q

SDH
What is the pathophysiology of a SDH?

A
  1. bleeding from bridging veins into the subdural space forms a haematoma
  2. then bleeding stops
  3. weeks/months later the haematoma starts to autolyse - massive increase in oncotic and osmotic pressure. Water is sucked in and haematoma enlarges
  4. gradual rise in ICP over weeks
  5. midline structures shift away from side of clot - causes tentorial herniation and coning
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14
Q

SDH
What is the management of SDH?

A

SURGERY
1* = irrigation via burr-hole craniostomy
2* = craniotomy

IV MANNITOL - to reduce ICP

address cause of trauma

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15
Q

EPILEPSY
Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

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16
Q

EPILEPSY
what is the treatment for absence (petit mal) epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Ethosuximide to females of childbearing potential

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17
Q

STATUS EPILEPTICUS
What are some causes of status epilepticus?

A
  • Poor adherence #1
  • Infections (meningitis, encephalitis)
  • Worsening of primary cause of epilepsy (e.g. brain tumour growing)
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18
Q

LOC
What are the potential causes of LOC?

A

CRASH
- Cardiogenic (more alarming)
- Reflex (neurally mediated)
- Arterial
- Systemic
- Head

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19
Q

PARKINSON’S DISEASE
What are 4 differential diagnoses to consider in Parkinson’s disease?

A

Parkinson’s plus syndromes –
- Progressive supranuclear palsy
- Multiple system atrophy
- Lewy Body dementia
- Corticobasal degeneration

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20
Q

PARKINSON’S DISEASE
What is progressive supranuclear palsy?

A
  • Early falls, cognitive decline or both sides being equally affected
  • Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
  • Impaired vertical gaze (down worse = issues reading or descending stairs)
  • Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes
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21
Q

PARKINSON’S DISEASE
What is multiple system atrophy?

A
  • Neurones in multiple systems in the brain degenerate
  • Degeneration in basal ganglia > Parkinsonism
  • Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction
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22
Q

PARKINSON’S DISEASE
What is corticobasal degeneration?

A
  • Early myoclonic jerks, gait apraxia, agnosia + alien limb
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23
Q

PARKINSON’S DISEASE
What investigations would you do in Parkinson’s disease?

A

DaTscan

Functional neuroimaging - PET

Can confirm by reaction to levodopa

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24
Q

PARKINSON’S DISEASE
What is the management of Parkinson’s disease?

A
  • Lifestyle: education, exercise, physio, MDT

young onset + fit
- Dopamine agonist (ropinirole)
- MAO-B inhibitor (rasagiline)
- L-DOPA (co-careldopa)

frail + co-morbidities
- L-DOPA (co-careldopa)
- MAO-B inhibitor (rasagiline)

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25
Q

HUNTINGTON’S DISEASE
What is the pathophysiology of Huntington’s disease?

A
  • Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
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26
Q

HUNTINGTON’S DISEASE
How does Huntington’s disease present?

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety

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27
Q

HUNTINGTON’S DISEASE
What investigations would you do for Huntington’s disease?

A
  • GENETIC TESTING - with pre- + post-test counselling (cannot give to children have to be old enough to decide themselves), high risk of suicide with diagnosis
  • MRI HEAD - shows atrophy of striatum
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28
Q

HEADACHES
What is the management of acute glaucoma?

A
  • Immediate expert help + IV acetazolamide (carbonic anhydrase inhibitor)
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29
Q

TRIGEMINAL NEURALGIA
What is the pathophysiology of trigeminal neuralgia?
What is affected?

A
  • Compression of trigeminal nerve results in demyelination + excitation of the nerve resulting in erratic pain signalling
  • Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly
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30
Q

TRIGEMINAL NEURALGIA
What are the causes of trigeminal neuralgia?

A

Compression of trigeminal nerve by a loop of vein or artery
Aneurysms
Meningeal inflammation
Tumours

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31
Q

MIGRAINE
What are the triggers of migraines?

A

CHOCOLATE –
- Chocolate
- Hangovers
- Orgasms
- Cheese/caffeine
- Oral contraceptives
- Lie-ins
- Alcohol
- Travel
- Exercise

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32
Q

MND
What are the 4 types of MND?
Best and worse prognosis?

A
  • Amyotrophic lateral sclerosis (ALS)
  • Progressive bulbar palsy (worst prognosis)
  • Progressive muscular atrophy (best prognosis)
  • Primary lateral sclerosis
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33
Q

MND
What is progressive bulbar palsy?
What does it affect?
What does it need to be differentiated from?

A
  • Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
  • Primarily affects muscles of talking, chewing, tongue palsy + swallowing
  • Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations
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34
Q

MND
What is…

i) progressive muscular atrophy?
ii) primary lateral sclerosis?

A

i) Anterior horn cells affected so LMN signs only, distal > proximal
ii) Loss of cells in motor cortex so UMN signs only

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35
Q

MND
What is the general clinical presentation of MND?

A
  • Insidious + progressive muscle weakness affecting limbs, trunk, face + speech
  • Often first noticed in upper limbs, may be fatigue when exercising
  • May have stumbling spastic gait, weak grip + clumsiness
  • Dysarthria, dysphagia, emotional lability in pseudobulbar palsy
  • NO SENSORY SYMPTOMS
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36
Q

MND
What are UMN signs?

A

Hypertonia or spasticity,
brisk reflexes
upgoing plantars,
muscle wasting

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37
Q

MND
What are some important differentials of MND and how can they be differentiated?

A
  • Cervical spine lesion as may present with UMN signs
  • Myasthenia gravis but MND NEVER affects eye movements
  • Multiple sclerosis but MND NEVER affects sphincters or sensation
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38
Q

MND
What are some investigations for MND?

A

Head/spine MRI
Blood tests = muscle enzymes, autoantibodies
Nerve conduction studies
EMG
Lumbar Puncture

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39
Q

MND
What medication may be given in MND?

A
  • RILUZOLE – Na+ blocker inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
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40
Q

MULTIPLE SCLEROSIS
What are some classic sites for MS?

A
  • Periventricular white matter lesions
  • Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles
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41
Q

MULTIPLE SCLEROSIS
What is the diagnostic criteria for MS?

A

McDonald criteria –
- Multiple CNS lesions (≥2)
- Sx that last >24h
- Disseminated in space (Clinically or on MRI) and time (>1m apart)

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42
Q

MULTIPLE SCLEROSIS
What are the symptoms of MS?

A

DEMYELINATION –
- Diplopia (CN VI)
- Eye movement pain (optic neuritis, v common)
- Motor weakness
- nYstagmus
- Elevated temp worsens
- Lhermitte’s sign
- Intention tremor
- Neuropathic pain
- Ataxia
- Talking slurred (dysarthria)
- Impotence
- Overactive bladder
- Numbness

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43
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is the pattern of motor weakness?

A

i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower

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44
Q

MULTIPLE SCLEROSIS
What are some signs of MS?

A
  • UMN = spastic paraparesis, brisk reflexes, hypertonia
  • Sensory = loss of sensation, cerebellar signs
  • Relative afferent pupillary defect
  • Internuclear ophthalmoplegia
  • Optic atrophy (pale optic disc) in chronic MS
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45
Q

MULTIPLE SCLEROSIS
What is relative afferent pupillary defect?

A
  • Seen on swinging light test (retina or optic nerve lesion –afferent issue)
  • The affected and normal eye appears to dilate when light is shone on the affected eye
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46
Q

MULTIPLE SCLEROSIS
What is internuclear ophthalmoplegia?

A
  • CN VI/medial longitudinal fasciculus lesion
  • Disorder of conjugate lateral gaze with;
    – Decreased adduction of ipsilateral eye
    – Nystagmus on abduction of contralateral eye
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47
Q

MULTIPLE SCLEROSIS
What is the management of MS remissions?

A
  • First line = beta-interferons (1b) to decrease # relapses + lesions on MRI but SEs = depression, flu Sx + miscarriage
  • 2nd line = DMARDs (monoclonal antibody) - natalizumab, dimethyl fumarate
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48
Q

MULTIPLE SCLEROSIS
What is the general symptomatic management for MS?

A

Spasticity
- BACLOFEN (GABA analogue, reduces Ca2+ influx)
- TIZANIDINE (alpha-2 agonist)
- BOTOX INJECTION (reduces ACh in neuromuscular junction)

urinary incontinence = catheterisation

incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs

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49
Q

MENINGITIS
What are the bacterial causes of meningitis?

A

N. meningitidis
S. pneumoniae
H. influenzae

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50
Q

MENINGITIS
What are the viral causes of meningitis?

A

Enterovirus (most common viral)
HSV
CMV
Varicella zoster virus

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51
Q

MENINGITIS
What is the management of bacterial meningitis

A
  • IV cefotaxime
    • amoxicillin to cover listeria (potential contraction in birth) in <3m
  • Dexamethasone to reduce frequency + severity of neurological sequelae
  • Adjust treatment according to sensitivities
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52
Q

ENCEPHALITIS
What investigations would you do for encephalitis?

A
  • Blood culture + CSF serology for viral PCR
    MRI - shows areas of inflammation, may be midline shifting
    EEG - periodic sharp and slow wave complexes
    lumbar puncture
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53
Q

BRAIN ABSCESS
What are the most common causative organisms?

A
  • Staph. aureus + strep. pnuemoniae
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54
Q

BRAIN ABSCESS
What is the management of brain abscess?

A
  • CT guided aspiration via burr hole or craniotomy + abscess cavity debridement
  • Craniotomy usually if no response to aspiration or if reoccurs
  • Abx with IV ceftriaxone + metronidazole, ICP Mx with dexamethasone
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55
Q

BRAIN DEATH + COMA
What are lateralising signs?
Give an example of one

A
  • Signs that occur from one hemisphere of the brain but not the other, helps to localise pathology
  • Fixed dilated pupil (CN3 palsy)
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56
Q

BRAIN DEATH + COMA
What is the main differential of a third nerve palsy?
How can they be differentiated?

A
  • Blind eye
  • Blind eye will not give contralateral responsiveness but other causes will + if you shine light in good eye then dilated pupil will restrict
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57
Q

BRAIN DEATH + COMA
What are the components of ‘eyes’ in GCS?

A

E4 = opens spontaneously
E3 = opens to verbal command
E2 = opens to pain
E1 = no response

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58
Q

BRAIN DEATH + COMA
What are the components of ‘verbal’ in GCS?

A

V5 = orientated in TPP, answers appropriately
V4 = confused conversation, odd answers
V3 = inappropriate words (random, abusive)
V2 = incomprehensible sounds (groans)
V1 = no response

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59
Q

BRAIN DEATH + COMA
What are the components of ‘motor’ in GCS?

A

M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = flexion to pain
M2 = extension to pain
M1 = no response

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60
Q

MYASTHENIA GRAVIS
What will patients with myasthenia gravis struggle with?

A
  • Hairs, chairs + stairs (proximal muscle weakness)
  • Speech, mastication, face + neck weakness
  • Resp muscles (breathing difficulty + dysphagia dangerous features which indicates advancing disease)
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61
Q

MYASTHENIA GRAVIS
What are the signs of myasthenia gravis?

A
  • Ptosis, diplopia (extra-ocular muscle weakness)
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62
Q

MYASTHENIA GRAVIS
What are some clinical signs of myasthenia gravis?

A
  • Repeated blinking = ptosis
  • Repeated abduction of one arm 20x + compare to other side
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63
Q

MYASTHENIA GRAVIS
What investigations would you do for myasthenia gravis?

A

mostly clinical examination
positive tensilon test
anti-AChR antibodies
TFTs
EMG
CT of thymus
crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis

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64
Q

MYASTHENIA GRAVIS
What is the management of myasthenia gravis?

A
  • Acetylcholinesterase inhibitors like pyridostigmine or rivastigmine
  • Immunosuppression with prednisolone (acute) or azathioprine to suppress antibody production
  • Thymectomy if thymoma or anti-AChR +ve disease
  • Plasmapheresis for severe relapsing cases
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65
Q

GUILLAIN-BARRE
What is the pathophysiology of GBS?

A
  • B cells produce antibodies against the antigens on the pathogen causing the preceding infection and these antibodies also match proteins on the nerve cells leading to demyelination and potentially axonal degeneration
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66
Q

GUILLAIN-BARRE
What are the causes of GBS?

A
  • Often triggered by preceding illness 4w before symptoms

Bacteria
- Camplylobacter jejuni
- Mycoplasma pneumoniae

Viruses
- CMV
- EBV
- HIV
- Herpes zoster

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67
Q

GUILLAIN-BARRE
What are the investigations for GBS?

A

Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
bloods - FBC, U&E, LFT, TFT
Spirometry = respiratory involvement
ECG

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68
Q

GUILLAIN-BARRE
What is the main treatment for GBS?

A
  • IVIg reduces duration + severity of paralysis but C/I if IgA deficiency as would cause anaphylaxis
  • Plasma exchange
  • Intubation, ventilation + ICU admission in severe cases in resp failure
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69
Q

BRAIN TUMOURS
What investigations would you perform for brain tumours?

A
  • CT/MRI head (MRI gold standard)
  • LP C/I if Sx of raised ICP until after imaging
  • Audiogram + gadolinium enhanced MRI head for acoustic neuroma
  • MR angiography may be useful to define site or blood supply of mass
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70
Q

NEUROPATHY
What is the pathophysiology of mononeuritis multiplex?

A
  • Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit
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71
Q

NEUROPATHY
What are the causes of peripheral neuropathy?

A

ABCDE –
- Alcohol
- B12 deficiency
- Cancer + CKD
- Diabetes + drugs (isoniazid, amiodarone)
- Every vasculitis

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72
Q

NEUROPATHY
In terms of peripheral neuropathy, what conditions show a…

i) mostly motor loss?
ii) mostly sensory loss?

A

i) GBS, chronic inflammatory demyelination polyneuropathy (chronic GBS), Charcot-Marie-Tooth disease
ii) DM, CKD, deficiencies

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73
Q

NEUROPATHY
What is Charcot-Marie-Tooth disease?

A
  • Autosomal dominant condition.
  • Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
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74
Q

NEUROPATHY
What muscles does the median nerve innervate?

A

LLOAF –
- Lateral lumbricals x2
- Opponens pollicis
- Abductor pollicis brevis
- Flexor pollicis brevis

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75
Q

NEUROPATHY
What is the clinical presentation of carpal tunnel syndrome?

A
  • Aching pain in hand + arm (especially at night)
  • Paraesthesia in radial 3.5 digits relieved by dangling hand over edge of bed + shaking (wake + shake)
  • Difficulty with precision grip
  • Sensory loss (radial 3.5 digits palmar + fingertips dorsally)
  • Wasting of thenar eminence (APB, FPB + OP)
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76
Q

NEUROPATHY
In terms of the optic nerve, what does a…

i) L optic nerve lesion
ii) Optic chiasma lesion
iii) L optic tract lesion
iv) L Baum’s loop lesion
v) L Meyer’s loop lesion

cause?

A

i) No vision through L eye
ii) Bitemporal hemianopia
iii) Contralateral (R) homonymous hemianopia
iv) Inferior R homonymous quadrantanopia
v) Superior R homonymous quadrantanopia

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77
Q

NEUROPATHY
Where is Baum’s loop located?
Where is Meyer’s loop located?
How can you remember which is superior/inferior?

A
  • Parietal lobe
  • Temporal lobe
  • PITS – Parietal Inferior Temporal Superior
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78
Q

NEUROPATHY
What does a CN7 lesion cause?

A

Face, ear, taste, tear –
- Muscles of expression
- Stapedius
- Anterior 2/3rd tongue
- Parasympathetic fibres to lacrimal + salivary glands

79
Q

NEUROPATHY
What does a CN9/10 lesion cause?

A
  • Swallow, gag + cough issues
  • Uvula deviated away from side of lesion
80
Q

NEUROPATHY
What are the investigations used in neuropathy?

A
  • Neuropathy screen (symmetrical) = FBC, CRP/ESR, U+E, glucose, TFT, B12 + folate
  • Vasculitis screen (asymmetrical) = first 3 + ANA, ANCA, anti-dsDNA, RhF, complement
  • EMG + nerve conduction studies
81
Q

CORD COMPRESSION
What are the signs of spinal cord compression?

A
  • Motor, reflex + sensory level = normal ABOVE lesion
  • LMN signs = AT level
  • UMN signs = BELOW level
  • Tone + reflexes usually reduced in acute cord compression
  • ?Sign of infection like tender spine, pyrexia
82
Q

CORD COMPRESSION
How does degenerative cervical myelopathy present?

A
  • Pain, loss of motor or sensory function affecting neck, upper or lower limbs
  • Loss of autonomic function
  • Hoffman’s sign +ve
83
Q

SPINAL CORD INJURY
What is Brown-Sequard syndrome?

A
  • Lateral hemisection of spinal cord
  • Ipsilateral weakness below the lesion (lateral corticospinal)
  • Ipsilateral loss of fine touch, proprioception + vibration (DCML)
  • Contralateral loss of pain + temp (lateral spinothalamic)
84
Q

ANTERIOR CORD SYNDROME
What is anterior cord syndrome?

A
  • Anterior spinal artery occlusion or compression
  • Bilateral spastic paresis (lateral corticospinal)
  • Bilateral loss of pain + temp (lateral spinothalamic)
85
Q

SPINAL CORD INJURY
What is posterior cord syndrome?

A
  • Trauma or posterior spinal artery occlusion
  • Loss of fine touch, proprioception + vibration (DCML)
86
Q

MYOPATHY
What are the investigations for myopathies?

A
  • CRP/ESR, creatinine kinase elevated
  • Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy
87
Q

HYDROCEPHALUS
What is the purpose of CSF?

A
  • Protects brain from damage
  • Removes waste products from the brain
  • Provides brain with nutrients to function properly
88
Q

HYDROCEPHALUS
What is the usual flow of CSF in the brain?

A
  • Lateral ventricles
  • Foramen of Munro
  • 3rd ventricle
  • Cerebral aqueduct
  • 4th ventricle
  • Subarachnoid space (Medially by foramen of Magendie, Laterally by Luschka)
  • Dural sinus via arachnoid granulations
89
Q

HYDROCEPHALUS
What are the investigations for hydrocephalus?

A
  • CT head = enlarged ventricles
  • MRI head if suspected underlying lesion
  • LP is both diagnostic + therapeutic (caution in obstructive as difference in cranial/spinal pressures can cause brain herniation)
90
Q

HYDROCEPHALUS
What is the management of hydrocephalus?

A
  • An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside
  • Ventriculoperitoneal shunt = surgically implanted into brain to drain excess fluid (may become blocked or infected)
  • Endoscopic third ventriculostomy = hole made in floor of 3rd ventricle to allow trapped CSF to escape to be reabsorbed
91
Q

NEURO PHARMACOLOGY
Give some examples of anti-epileptic drugs (AEDs).
What is their mechanism of action?

A
  • Carbamazepine, valproate, lamotrigine, levetiracetam, phenytoin, ethosuximide.
  • Inhibit voltage-gated Na+ channels which prevents excitability of neurones > reduced firing > stops seizure, some promote GABA release
92
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) carbamazepine?
ii) valproate?
iii) lamotrigine

A

i) Blurred vision, headache, drowsiness – agranulocytosis, aplastic anaemia, P450 inducer
ii) Teratogenic, hepatitis, hair loss, tremor, weight gain – some interactions with antidepressants
iii) Blurred vision, headache, drowsiness – Steven-Johnson syndrome + risk of leukopenia

93
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) phenytoin?
ii) levetiracetam?
iii) ethosuximide?

A

i) Megaloblastic anaemia (folate), osteomalacia, teratogenic, P450 interactions – Steven-Johnson syndrome
ii) Headache, drowsiness – some interactions with antidepressants
iii) Night terrors, rashes

94
Q

NEURO PHARMACOLOGY
What are the side effects of Levodopa?

A
  • Postural hypotension
  • Confusion
  • Dyskinesias (abnormal movements)
  • Effectiveness decreases with time (even with dose increase)
  • On-off effect
  • Psychosis
95
Q

NEURO PHARMACOLOGY
Give some examples of dopamine receptor agonists.
What is the mechanism of action?
What are some side effects?
What monitoring is required?

A
  • Bromocriptine, cabergoline, ropinirole
  • Increases amount of dopamine in CNS
  • Hallucinations (more than levodopa), postural hypotension
  • ECHO, ESR, creatinine + CXR prior to Rx
96
Q

NEURO PHARMACOLOGY
What are some adverse effects of dopamine receptor agonists?

A
  • Pulmonary retroperitoneal + cardiac fibrosis
  • Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)
97
Q

NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?

A
  • Catechol-o-methyltransferase (COMT) inhibitor = entacapone
  • Monoamine oxidase-B (MAO-B) inhibitor = selegiline
  • Inhibit enzymatic breakdown of dopamine
98
Q

NEURO PHARMACOLOGY
Why are dopamine receptor agonists + COMT/MAO-B inhibitors used in Parkinson’s disease?

A
  • Delay use of levodopa + then used in combination to reduce levodopa dose as levodopa is most effective treatment
99
Q

NEURO PHARMACOLOGY
What are some SEs + C/Is of triptans?

A
  • Dizziness, dry mouth, sleepy, nausea
  • C/I in CVD
100
Q

MENIERE’S DISEASE
What is Ménières disease?

A
  • Increased pressure in endolymphatic system due to increased volume of inner ear.
101
Q

STROKE
what is the mechanism of action for alteplase / streptokinase (thrombolysis drugs for ischaemic stroke)?

A
  • Converts plasminogen > plasmin so promotes breakdown of fibrin clot
  • Alteplase (tPA) or can use streptokinase
102
Q

EDH
Which vessels most commonly are affected in extradural haematomas?
which other vessels can be affected?

A
  • Middle meningeal artery
  • 25% venous if fracture disrupts the venous sinuses
103
Q

SDH
what are the risk factors of SDH?

A
  • Elderly - brain atrophy, dementia
  • Frequent falls - epileptics, alcoholics
  • Anticoagulants
  • babies - traumatic injury (“shaking baby syndrome”)bridging veins stretched so more likely to rupture,
104
Q

EPILEPSY
Define seizure

A

Paroxysmal event in which changes of behaviour, sensation, cognition + consciousness caused by excessive, hypersynchronous neurological discharges in the brain

105
Q

PARKINSON’S DISEASE
what can exacerbate parkinson’s disease?

A

Anticholinergics can precipitate confusion

106
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Lhermitte’s sign?

A

Neck flexion causes electric shock sensation down spine

107
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Uhthoff’s phenomenon?

A

symptoms worsening in heat e.g. in the shower/exercise

108
Q

ENCEPHALITIS
What are the non-viral causes of encephalitis?

A

Bacterial meningitis
TB
Malaria
Lyme’s disease

109
Q

MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?

A

Abx, CCBs, beta-blockers, lithium + statins

110
Q

NEUROPATHY
What can cause mononeuritis multiplex?

A

Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis

111
Q

RADICULOPATHY
What is radiculopathy?

A

Sx caused by pinching of a nerve root as they exit the spinal cord

112
Q

MENIERE’S DISEASE
What causes it?

A

Idiopathic, trauma, endo

113
Q

MENIERE’S DISEASE
How is it managed?

A

Bed rest, reassurance

114
Q

SHINGLES
what are the risk factors for shingles?

A
  • increasing age
  • immunocompromised
  • HIV, hodgkins lymphoma, bone marrow transplants
115
Q

NEUROFIBROMATOSIS
what are the clinical signs of NF1?

A
  • cafe-au-lait spots on the skin
  • pea-sized lumps under skin
  • skeletal abnormalities
  • tumour on optic nerve
116
Q

NEUROFIBROMATOSIS
what are the clincial signs of NF2?

A
  • acoustic neuromas
  • family history
  • meningioma, schwannoma, juvenile cortical cataracts or glioma
117
Q

NARCOLEPSY
what is the management?

A

1st line = sleep hygiene + lifestyle changes
can also consider pharmacotherapy
- modafinil
- pitolisant
- sodium oxybate

118
Q

RADICULOPATHY
what are the causes?

A
  • intervertebral disc prolapse
  • degenerative diseases of the spine
  • fracture (trauma or pathological)
  • malignancy (metastatic)
  • infection (extradural abscesses, osteomyelitis)
119
Q

WERNICKE-KORSAKOFF SYNDROME
what are the clinical signs?

A
  • mental confusion/amnesia
  • vision problems
  • coma
  • tremor
  • ataxia
  • hypothermia
  • low blood pressure
120
Q

CATAPLEXY
what is it?

A

sudden muscle weakness triggered by strong emotions such as laughter, anger and surprise

121
Q

CATAPLEXY
what happens during an attack?

A
  • slurred speech
  • impaired eyesight (double vision, unable to focus)
  • hearing and awareness are undisturbed (remain conscious)
122
Q

CATAPLEXY
what is the management?

A

sodium oxybate
tricyclic antidepressants (clomipramine)
SSRIs

123
Q

EDH
what is the appearance of EDH on non-contrast head CT?

A

lens shaped haematoma = LEMON SHAPE
doesn’t cross suture lines
shows midline shift

124
Q

SDH
what is the appearance of SDH on non-contrast head CT?

A

crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time)
unilateral
shows midline shift

125
Q

EPILEPSY
what is the treatment for generalised myoclonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Levetiracetam/Topiramate to females of childbearing potential

126
Q

PARKINSON’S DISEASE
Give 2 histopathological signs of Parkinson’s disease

A
  1. Loss of dopaminergic neurones in the substantia nigra
  2. Lewy bodies
127
Q

HUNTINGTON’S DISEASE
what are the signs of Huntington’s disease?

A

Abnormal eye movements
Dysarthria
Dysphagia
Rigidity
Ataxia

128
Q

MND
Does MND cause sensory loss or sphincter disturbance?

A

No (clinical feature of MS)

129
Q

MND
What are LMN signs?

A

Hypotonia + muscle wasting,
reduced reflexes,
fasciculations (particularly tongue)

130
Q

MND
What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes

131
Q

MULTIPLE SCLEROSIS
What are the differential diagnosis’s of MS

A

SLE
Sjogren’s
AIDS
Syphilis

132
Q

MENINGITIS
Give 4 potential adverse effect of a lumbar puncture

A

Headache
Paraesthesia
CSF leak
Damage to spinal cord

133
Q

ENCEPHALITIS
Name the main triad of symptoms of encephalitis

A

Fever + headache + altered mental state

134
Q

MYASTHENIA GRAVIS
What can weakness due to myasthenia gravis be worsened by?

A

Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs

135
Q

NEUROPATHY
What is the generic clinical presentation of mononeuritis multiplex?

A

Subacute presentation (months rather than years), painful, asymmetrical sensory + motor neuropathy

136
Q

ANTERIOR CORD SYNDROME
what are the causes?

A
  • iatrogenic - thoracic and thoracoabdominal AA repair
  • aortic dissection
  • atherothrombotic disease
  • emboli
  • vasculitis
137
Q

ANTERIOR CORD SYNDROME
what are the symptoms?

A
  • acute motor dysfunction
  • loss of pain and temperature sensation below level of infarction
  • autonomic dysfunction - neurogenic bowel/bladder
  • acute onset back pain
138
Q

ANTERIOR CORD SYNDROME
what are the investigations?

A

MRI - ‘owls eyes’ hyperintensities in anterior horns

lumbar puncture, CSF testing, blood and urine to rule out other causes

139
Q

ANTERIOR CORD SYNDROME
what is the treatment?

A
  • IV fluids to increase intravascular volume
  • vasopressor medications to increase systemic vascular resistance
  • lumbar drain to remove CSF

symptomatic management
- mechanical ventilation
- catheterisation

140
Q

HORNER’S SYNDROME
what is the pathophysiology of horner’s syndrome?

A

unilateral damage to the sympathetic chain

141
Q

HORNER’S SYNDROME
what are the causes of 1st order horner’s syndrome?

A

stroke, tumours of hypothalamus, spinal cord lesions

142
Q

HORNER’S SYNDROME
what are the causes of 2nd order horner’s syndrome?

A

tumours of upper chest cavity, trauma to the neck

143
Q

HORNER’S SYNDROME
what are the causes of 3rd order horner’s syndrome?

A

lesions to carotid artery, middle ear infections, injury to base of the skull

144
Q

HORNER’S SYNDROME
what are the clinical features of horner’s syndrome?

A

MAPLE

Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)

145
Q

HORNER’S SYNDROME
what are the investigations for horner’s syndrome?

A

clinical examination

MRI - detect lesions

146
Q

BULBAR PALSY
what are the symptoms?

A
  • dysphagia
  • reduced/absent gag reflex
  • slurred speech
  • aspiration of secretions
  • dysphonia
  • dysarthria
  • drooling
  • difficulty chewing
  • nasal regurgitation
  • atrophic tongue
    weak jaw/facial muscles
147
Q

BULBAR PALSY
what are the investigations?

A

MRI
lumbar puncture

148
Q

STRABISMUS
what is it?

A

where there is misalignment of the visual axes of the eyes; it may be latent or manifest and, if manifest, it may be constant or intermittent

149
Q

STRABISMUS
what are the causes?

A
  • congenital
  • graves (restricted eye movement)
  • myasthenia gravis
  • intra-cranial process (mass, raised ICP, CNS infarction, inflammation of CNS)
150
Q

STRABISMUS
what are the symptoms?

A
  • diplopia
  • eye misalignment
  • amblyopia (decreased vision in an anatomically normal eye)
  • abnormal eye movements
  • visual confusion
  • asthenopia (ocular discomfort)
151
Q

STRABISMUS
what are the risk factors?

A

FHx of strabismus
prematurity
low birth weight
maternal smoking during pregnancy

152
Q

STRABISMUS
what are the investigations?

A
  • cover test
  • simultaneous prism and cover test (SPCT)
  • uncover test (UCT)
  • alternate prism cover test (APCT)
  • Hirschberg test
  • Krimsky test
153
Q

STRABISMUS
what is the management?

A

definitive treatment = extraocular muscle surgery

correction of refractive errors

treatment of amblyopia - eye patch

treatment for diplopia - patch, prisms, high prescription, orthoptic exercises

154
Q

SCIATICA
what are the risk factors?

A
  • previous injury
  • overweight
  • lack of core strength
  • physically demanding job
  • diabetes
  • osteoarthritis
  • inactivity
  • smoking
155
Q

SCIATICA
what are the causes?

A
  • herniated/slipped disc - puts pressure on nerve root
  • degenerative disc disease
  • spinal stenosis
  • spondylolisthesis
  • osteoarthritis
  • trauma
  • cauda equina syndrome
156
Q

MYOPATHY
what is myotonic dystrophy?

A

autosomal dominant genetic condition causing progressive muscle weakness
most common form of muscular dystrophy to occur in adults

157
Q

MYOPATHY
what are the causes of myotonic dystrophy type 1 and 2?

A

type 1 - DMPK gene mutation on chromosome 19

type 2 = ZNF9 gene on chromosome 3

158
Q

TIA
What are the causes of a transient ischaemia attack (TIA)?

A
  • Artherothromboembolism of the carotid - main cause (can hear carotid bruit)
  • Cardioembolism - in AF, after MI, valve disease/prosthetic valve
  • Hyperviscosity - polycythaemia, sickle cell, high WBCC
  • hypoperfusion - postural hypotension, decreased flow
159
Q

TIA
what are the differential diagnosis’s for a TIA

A

Migraine aura
Epilepsy
Hypoglycaemia
Hyperventilation
retinal bleed
syncope - due to arrhythmia

160
Q

TIA
what is the ABCD2 score?

A

Assesses risk of stoke in the next 7 days for those who have had a TIA

age
BP
clinical features - unilateral weakness, speech disturbance
duration of TIA
presence of diabetes mellitus

161
Q

HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?

A

excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue

  • injury
  • bleeding
  • infection
  • brain tumour
  • brain surgery
162
Q

CHRONIC FATIGUE SYNDROME
what is it?

A

It is a disorder characterized by extreme fatigue or tiredness that doesn’t go away with rest and can’t be explained by an underlying medical condition.

163
Q

CHRONIC FATIGUE SYNDROME
What are the causes?

A

unknown - could be:
- viruses (EBV, rubella, RRV)
- a weakened immune system
- stress
- hormonal imbalances

164
Q

CHRONIC FATIGUE SYNDROME
what are the risk factors?

A
  • sex (female)
  • genetic predisposition
  • allergies
  • stress
  • environmental factors
165
Q

CHRONIC FATIGUE SYNDROME
what are the symptoms?

A
  • severe fatigue that interferes with daily life for >6 months
  • sleep problems
    • feeling unrefreshed after night’s sleep
    • chronic insomnia
  • memory loss
  • reduced concentration
  • orthostatic intolerance
  • muscle pain
  • frequent headaches
  • multi-joint pain without redness or swelling
  • frequent sore throat
166
Q

CHRONIC FATIGUE SYNDROME
what are the differentials?

A

mononucleosis
lyme disease
MS
SLE
hypothyroidism
fibromyalgia
depression
sleep disorders

167
Q

CHRONIC FATIGUE SYNDROME
what is the management?

A

no cure
- pacing activities
- reduce caffeine, nicotine and alcohol
- create sleep routine
- antidepressant medications
- complementary/alternative medicines

168
Q

MENIERE’S DISEASE
what is the classical triad of symptoms?

A

vertigo
hearing loss - worse during attacks
tinnitus

169
Q

SAH
give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
170
Q

EPILEPSY
how do lamotrigine and carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

171
Q

EPILEPSY
how does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

172
Q

EPLILEPSY
give 4 potential side effects of anti-epileptic drugs (AEDs)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
173
Q

PARKINSONS DISEASE
what is the pathway for dopamine production?

A

Tyrosine –> L-dopa –> Dopamine

174
Q

HYDROCEPHALUS
What are some causes of non-obstructive hydrocephalus?

A
  • Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage)
  • increased CSF production (choroid plexus tumour) but very rare
175
Q

DIABETIC NEUROPATHY
what is the management for gastroparesis?

A

metoclopramide, domperidone or erythromycin

176
Q

STROKE
What vessels can be affected in total anterior circulation syndrome (TACS)?

A
  • ACA, MCA, carotid
177
Q

STROKE
What vessels can be affected in a partial anterior circulation syndrome (PACS)?

A
  • ACA, MCA, carotid (same vessels as TACS)
178
Q

STROKE
What vessels can be affected in a posterior circulation syndrome (POCS)?

A
  • PCA, vertebrobasilar artery or branches
179
Q

STROKE
What vessels can be affected in lacunar syndrome (LACS) and what does that mean?

A
  • Perforating arteries so no higher cortical dysfunction or visual field abnormality, subcortical stroke
180
Q

STROKE
How would lateral medullary/Wallenberg’s syndrome present?
What vessel is implicated?

A
  • Cerebellar: ataxia, nystagmus
  • Ipsi: dysphagia, facial numbness + CN palsy
  • Contra: limb sensory loss
  • Posterior inferior cerebellar artery
181
Q

STROKE
How would lateral pontine syndrome present?
What vessel is implicated?

A
  • Similar to Wallenberg’s but ipsilateral facial paralysis + deafness
  • Anterior inferior cerebellar artery
182
Q

STROKE
What criteria must be met for a total anterior circulation syndrome (TACS)?

A

All three Hs –
- Hemiplegia (unilateral ± sensory deficit of face, arm leg)
- Homonymous hemianopia
- Higher cerebral dysfunction (dysphasia, visuospatial disturbance)

183
Q

STROKE
What criteria must be met for a partial anterior circulation syndrome (PACS)?

A
  • 2/3 of the criteria for TACS:
  • Hemiplegia (unilateral ± sensory deficit of face, arm leg)
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disturbance)
184
Q

STROKE
What criteria must be met for a posterior circulation syndrome (POCS)?

A

One of the following –
- Cranial nerve palsy + contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder (e.g. gaze palsy)
- Cerebellar dysfunction (ataxia, nystagmus, vertigo)
- Isolated homonymous hemianopia + cortical blindness

185
Q

STROKE
What criteria must be met for a lacunar syndrome (LACS)?

A

One of following –
- Pure sensory stroke (thalamus)
- Pure motor stroke (posterior limb of internal capsule)
- Sensori-motor stroke
- Ataxic hemiparesis

186
Q

STROKE
What areas can be affected in lacunar syndrome (LACS)?

A
  • Thalamus, basal ganglia, internal capsule
187
Q

NEUROPATHY
Roots of the ulnar nerve?
What causes ulnar neuropathy?

A
  • C7–T1
  • Elbow trauma or fracture, elbow arthritis
188
Q

NEUROPATHY
What are the motor signs of ulnar neuropathy?

A

Weakness/wasting of –
- Interossei (can’t do good luck sign)
- Medial lumbricals (claw hand)
- Hypothenar eminence
- +ve Froment’s sign when grip paper between thumb + index finger

189
Q

NEUROPATHY
What are the sensory signs of ulnar neuropathy?

A
  • Sensory loss 1.5 fingers ulnar side on dorsal + palmar aspects
190
Q

NEUROPATHY
Roots of the radial nerve?
What causes radial neuropathy?

A
  • C5-T1
  • Compression against humerus
191
Q

NEUROPATHY
What are the motor signs of radial neuropathy?
What are the sensory signs?

A
  • Wrist + finger drop (weak extension), can’t open first
  • Below fingertips on radial 3.5 fingers dorsally, part of thenar eminence
192
Q

NEUROPATHY
Roots of sciatic nerve?
Causes of neuropathy?
Presentation?

A
  • L4–S3
  • Pelvic tumours or pelvic/femoral #
  • M = foot drop, S = loss below the knee laterally
193
Q

NEUROPATHY
Roots of common peroneal nerve?
Causes of neuropathy?
Presentation?

A
  • L4–S1
  • Damaged as winds round fibular head by trauma or sitting cross-legged (classic after night out)
  • M = foot drop, weak ankle dorsiflexion + eversion with high steppage gait, S = loss over dorsal foot

C TO REVISE - PHASE 3A (11 decks)

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