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Neurology Flashcards

1
Q

What causes a stroke?

A
  • 85% due to ischaemia or infarction-> due to thrombus/emboli, atherosclerosis, shock or vasculitis
  • 15% due to intracranial haemorrhage
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2
Q

What is a transient ischaemic attack (TIA)?

A

Transient neurological dynsfunction secondary to ischaemia without infarction-> typically resolves within 24 hours and can precede stroke

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3
Q

What is a crescendo TIA?

A

When a patient has 2+ TIAs in a week

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4
Q

How can a stroke present (in general)?

A
  • FAST-> face, arm, speech, time
  • Weakess
  • Dysphasia-> speech problems
  • Visual or sensory loss
  • Sudden onset
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5
Q

What is the ROSIER tool used for?

A

Recognition of stroke in emergency room-> work out likelihood that clinical signs are due to a stroke

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6
Q

What are the risk factors for a stroke/TIA?

A

CVD, previous TIA/stroke, AF, carotid artery disease, HTN, diabetes, smoking, thrombophilia, COCP

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7
Q

Acute management of stroke?

A
  • Admission
  • Exclude hypoglycaemia (BMs)
  • Exclude haemorrhage (CT head)
  • Aspirin 300mg stat + continue for 2 weeks
  • Thrombolysis-> with alteplase/streptokinase within 4.5 hours of symptom onset
  • Thrombectomy-> mechanical removal within 6 hours (or 24 hours) of symptom onset
  • Be careful with BP-> don’t try lower as can risk hypoperfusion to brain
  • MDT + rehabilitation-> SALT, OT, physio etc
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8
Q

Treatment for TIA?

A

Aspirin 300mg daily + CVD secondary prevention

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9
Q

Investigations for stroke?

A
  • Blood glucose-> rule out hypoglycaemia
  • CT head-> rule out haemorrhage
  • Bloods-> lipids, PTT
  • ECG/CXR/TOE-> look for cardiac causes
  • Diffusion weighted MRI-> assess which vascular territory affected
  • Carotid US-> for stenosis + endartectomy/stent criteria
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10
Q

Secondary prevention of stroke?

A
  • Aspirin 300mg for 14 days + clopidogrel 75mg lifelong
  • Can use dipyramidole if clopidogrel CI’d
  • Consider atorvastatin 80mg OD + BP management
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11
Q

How does an anterior cerebral artery stroke present?

A

Lower limb weakness, loss of spontaneous speech, drowsy

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12
Q

How does a middle cerebral artery stroke present?

A

Upper limb weakness, face drop, aphasia, hemianopia

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13
Q

How does a posterior cerebral artery stroke present?

A

Visual field defects, visual agnosia, prosopagnosia

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14
Q

How does a brainstem stroke present?

A

Quadriplegia, locked in syndrome, retain awareness

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15
Q

How does a lacunar stroke present?

A

Motor +/- sensory deficit, dysarthria etc

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16
Q

What are the components of the Glasgow Coma Scale?

A
  • Eyes-> spontaneously open (4), to speech (3), to pain (2), don’t open (1)
  • Verbal response-> orientated (5), confused (4), inappropriate words (3), sounds (2), none (1)
  • Motor-> obeys commands (6), localises to pain (5), normal flexion (3), abnormal flexion (3), extends to pain (2), none (1)
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17
Q

What is an intracerebral bleed and where can this occur?

A
  • Bleed into brain tissue

- Lobar, deep, intraventricular, basal ganglia, cerebellar

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18
Q

What causes an intracranial bleed?

A

Spontaneous, ischaemia, tumours, aneurysm ruptures

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19
Q

What causes a subarachnoid haemorrhage?

A
  • Bleed between pia + arachnoid mater (where CSF located)

- Ruptured berry aneurysm

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20
Q

How does a subarachnoid haemorrhage typically present?

A
  • Thunderclap headache-> sudden, occipital, during strenuous activity
  • Neck stiffness, photophobia, vision loss, speech/weakness, LOC, seizures
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21
Q

What causes a subdural haemorrhage?

A
  • Bleed between the arachnoid and dura mater

- Rupture of bridging veins in outer meningeal layer

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22
Q

Who is most at risk of a subarachnoid haemorrhage?

A
  • More common in black patients, females and aged 45-70

- Associated with smoking, alcohol, cocaine, sickle cell disease and connective tissue disorders

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23
Q

Who is most at risk of subdural haemorrhage?

A

Often older and alcoholic-> more atrophy + more likely to rupture

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24
Q

What does a subdural haemorrhage look like on a CT head?

A
  • Crescent shape (thin line)

- Can cross cranial suture lines

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25
Q

What causes an extradural haemorrhage?

A
  • Bleed between the dura and skull
  • Middle meningeal artery rupture in temporo-parietal region
  • Can be due to temporal bone fracture
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26
Q

What does an extradural haemorrhage look like on a CT head?

A
  • Bi-convex (lemon) shape

- Can’t cross the cranial sutures

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27
Q

How does an extradural haemorrhage typically present?

A
  • Often young patient with a head injury
  • Ongoing headache
  • Period of improved neuro function then severe decline over a few hours (begins to compress)-> lucid interval
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28
Q

Investigations for subarachnoid haemorrhage?

A
  • CT head 1st line-> hyperattenuation
  • LP-> raised RBCs or xanthochromia (yellow + due to bilirubin breakdown)
  • Angiography (CT/MRI)-> locate source
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29
Q

Management of subarachnoid haemorrhage?

A
  • Coiling or clipping surgically
  • Nimodipine-> CCB used to prevent vasospasm (can cause ischaemia)
  • LP or shunt for hydrocephalus
  • Antiepiletics if seizures
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30
Q

How might a subdural haemorrhage present?

A
  • Often after deceleration injury <9 months ago
  • Latent period of 8-10 weeks
  • Fluctuating consciousness, headaches, personaliry change
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31
Q

How is subdural haemorrhage treated?

A

Surgical removal of clot then address cause

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32
Q

How is extradural haemorrhage treated?

A
  • Drainage + may ligate bleeding vessel

- Mannitol IV

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33
Q

What is multiple sclerosis?

A

Chronic and progressive demyelination of neurones in CNS due to immune activation against myelin

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34
Q

Who does multiple sclerosis typically affect?

A
  • Women under 50

- Often due to genes, low vitamin D, smoking, obesity, EBV

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35
Q

When do the symptoms of MS typically improve?

A

-During pregnancy and post-partum

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36
Q

What is the pathophysiology of MS?

A
  • Myelin covers axons in CNS-> from oligodendrocytes (CNS) + Schwann cells (PNS)
  • MS affects CNS-> inflammation around myelin + immune cell infiltration
  • Affects conduction of electrical signals of nerve
  • Usually multiple areas of demyelination during attacks (eg optic neuritis) but not all cause symptoms at same time
  • Re-myelinate in early disease but incomplete + permanent later
  • Lesions vary in location-> ‘disseminated in time and space’
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37
Q

How might MS present?

A
  • Optic neuritis
  • Eye movement abnormalities
  • Focal weaknesses
  • Focal sensory symptoms
  • Ataxia
  • Different disease patterns
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38
Q

What disease patterns of MS exist?

A
  • Clinically isolated syndrome
  • Relapsing-remitting
  • Primary progressive
  • Secondary progressive
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39
Q

How does optic neuritis typically present?

A
  • Unilateral loss of vision over hours-days
  • Central scotoma (enlarged blind spot)
  • Pain on eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect
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40
Q

What can cause optic neuritis?

A

MS, sarcoidosis, SLE, diabetes, syphilis, measles, mumps, Lyme disease

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41
Q

How is optic neuritis managed?

A
  • Ophthalmologist assessment
  • Steroids
  • Recover in 2-6 weeks
  • 50% get MS-> MRIs to predict
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42
Q

Other than optic neuritis, what eye symptoms can you get with MS?

A

Sixth cranial nerve palsy-> causes internuclear ophthalmoplegia + conjugate lateral gaze disorder

  • IO-> nerve + muscle issue
  • CLGD-> affected eye unable to abduct when looking laterally (ie stays in middle whilst other eye adducts) due to muscle dysfunction
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43
Q

What focal weaknesses can MS present with?

A

Bell’s palsy, Horner’s syndrome, limb paralysis, incontinence

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44
Q

What focal sensory symptoms can MS present with?

A

Trigeminal neuralgia, numbness, paraesthesia, Lhermitte’s sign

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45
Q

What is Lhermitte’s sign?

A
  • Present in MS
  • Electric shock down spine + limbs when flexing neck
  • Indicates disease (demyelination) in cervical spinal cord’s dorsal column
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46
Q

What types of ataxia can present in MS?

A
  • Sensory-> lose proprioception, positive Romberg’s test, psudoathetosis
  • Cerebellar-> lesions
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47
Q

What does the ‘clinically isolated syndrome’ disease pattern present as in MS?

A
  • The 1st episode of demyelination + neuro signs-> can’t diagnose based on this
  • If lesions are present on MRI are likely to develop MS
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48
Q

What does the ‘relapse-remitting’ disease pattern present as in MS?

A
  • Disease + symptoms then recovery
  • Active-> symptoms + lesions on MRI
  • Not active-> no symptoms
  • Can be worsening or not worsening over time
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49
Q

What does the ‘primary progressive’ disease pattern present as in MS?

A

Worsening disease from diagnosis, no relapse + remissions, active and/or progressive

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50
Q

What does the ‘secondary progressive’ disease pattern present as in MS?

A
  • Relapsing-remitting at first then progressive worsening + incomplete remissions
  • Symptoms become more permanent
  • Active and/or progressive
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51
Q

What does ‘active disease’ mean in MS?

A

New symptoms or MRI lesions

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52
Q

What does ‘progressing disease’ mean in MS?

A

Worsening over time regardless of relapse

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53
Q

Investigations and diagnosis for MRI?

A
  • Clinical
  • Disseminated in space and time
  • MRI lesions
  • LP-> oligoclonal bands in CSF
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54
Q

How are relapses treated in MS?

A
  • Methylprednisolone 500mg PO for 5 days

- If oral previously failed-> methylprednisolone IV 1g for 3-5 days

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55
Q

How is MS managed long-term?

A
  • Disease modifying drugs + biological therapies-> induce long term remission
  • Symptom control-> exercise, neuropathic meds, anti-depressants, oxynutynin/tolterodine (for urge incontinence), baclofen (spasticity)
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56
Q

What is motor neurone disease?

A

An umbrella term for conditions causing progressive decline of motor neurone function (doesn’t affect sensory nerves)

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57
Q

What are the different types of motor neurone disease?

A
  • Amyotrophic lateral sclerosis-> most common
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Primary lateral sclerosis
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58
Q

What is the pathophysiology of MND?

A
  • Degradation of upper + lower motor neurones

- Risk factors-> genetics, smoking, heavy metals, pesticides etc

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59
Q

What is the presentation of MND?

A
  • Insidious + progressive muscle weakness often starting in upper limbs-> progresses to trunk, face, speech, legs
  • Initial-> clumsy + drop things, dysarthria
  • LMN signs-> wasting, hypotonia, fasiculations, hyporeflexia
  • UMN signs-> hypertonia, spasticity, hyperreflexia, upgoing plantar responses
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60
Q

How in MND diagnosed?

A

Clinically + after ruling out other causes

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61
Q

Treatment options for MND?

A
  • None will stop/reverse disease
  • Riluzole-> slows progression
  • NIV-> for breathing support
  • Advance directives + end of life care planning
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62
Q

What is Parkinson’s disease?

A

Progressive reduction of dopamine in the basal ganglia (specifically the substantia nigra) causing movement disorders

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63
Q

What is the pathophysiology of Parkinson’s disease?

A
  • Basal ganglia structures help co-ordinate walking + voluntary movements + learning patterns
  • Substantia nigra-> produces dopamine (needed for BG functioning)
  • PD-> gradual fall in dopamine production
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64
Q

Presentation of Parkinson’s disease?

A

Typically triad of resting tremor + rigidity + bradykinesia (often in older male)

  • Resting tremor-> unilateral, pill rolling, improves with movement
  • Cogwheel rigidity-> tension in arm + gives way to movement in small increments
  • Bradykinesia-> small + slow movements eg small handwriting, shuffling gait, hard to initiate movements
  • Hypomimia-> reduced facial expressions
  • Depression + insomnia + cognitive impairment
  • Postural instability
  • Anosmia
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65
Q

What is benign essential tremor and how does it present?

A
  • Symmetrical essential tremor that improves at rest + after alcohol
  • Usually in hands, head, jaw
  • Worsened by fatigue, stress + caffiene
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66
Q

What are the ‘Parkinson’s plus’ syndromes?

A
  • Progressive supranuclear palsy
  • Corticobasal degeneration
  • Multiple system atrophy
  • Dementia with Lewy bodies
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67
Q

What is multiple system atrophy?

A

Neurones in multiple systems (including the basal ganglia) degenerate-> autonomic dysfunction, cerebellar and Parkinsonian symptoms

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68
Q

How does dementia with Lewy bodies typically present?

A
  • Parkinson features + progressive cognitive decline
  • Visual hallucinations (eg Lilliputian)
  • Delusions
  • REM sleep disorders
  • Fluctuating consciousness
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69
Q

How is Parkinson’s disease diagnosed?

A

Usually clinically-> can use the UK PD society brain bank clinical diagnostic criteria

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70
Q

Management options for Parkinson’s disease?

A
  • Co-beneldopa or co-careldopa (1st line)-> levodopa + peripheral decarboxylase inhibitors (to stop levodopa break down)
  • Dopamine agonists-> cabergoline, bromocriptine, ropinerole
  • Monoamine oxidase-B inhibitors-> selegiline or rasagiline
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71
Q

What are the potential side effects of dopaminergic drugs used in Parkinson’s?

A
  • Dystonias-> excess muscle contractions + abnormal movements
  • Chorea-> involuntary movements
  • Athetosis-> twisting/writhing of hands/feet
  • Levodopa can wear off quite quickly + can become ineffective after using for an extended period
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72
Q

Management of benign essential tremor?

A
  • Not usually needed
  • Propranolol
  • Primidone (anti-epileptic)
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73
Q

What is epilepsy?

A

An umbrella term for a tendency to have seizures

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74
Q

What is a seizure?

A

Transient episode of abnormal electrical activity in the brain

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75
Q

What are the investigations for a seizure/epilepsy?

A
  • Electroencephalogram (EEG)-> patterns in different forms
  • MRI brain-> structural problems
  • ECG-> cardiac causes eg syncope
  • BM-> rule out hypoglycaemia
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76
Q

How does a generalised tonic-clonic seizure typically present?

A
  • Not always a prodrome
  • LOC + tonic (tensing) then clonic (jerking)
  • Tongue biting, incontinence, groaning, irregular breathing
  • Post-ictal-> confused, drowsy, irritable, depression
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77
Q

How are generalised tonic-clonic seizures managed?

A

Sodium valproate or lamotrigine

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78
Q

How do focal seizures present?

A
  • Usually start in temporal lobe causing hearing, speech, memory and emotional symptoms
  • Hallucinations, deja vu, memory flashbacks, on auto-pilot etc
  • May be aware but one area of body has seizure
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79
Q

How are focal seizures managed?

A

Carbamazepine or lamotrigine

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80
Q

How do absence seizures usually present?

A
  • Usually in children

- Blank, stare into space, non-responsive, 10-20 seconds, return to normal abruptly

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81
Q

How are absence seizures treated?

A
  • Sodium valproate or ethosuximide

- 90% stop as get older

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82
Q

What are atonic seizures?

A
  • ‘Drop attacks’-> brief lapse in muscle tone for <3 minutes
  • Often start in kids
  • May indicate Lennox-Gastaut syndrome
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83
Q

What might atonic seizures indicate?

A

Lennox-Gastaut syndrome

84
Q

Treatment for atonic seizures?

A

Sodium valproate or lamotrigine

85
Q

What are myoclonic seizures?

A
  • Sudden brief muscle contractions + usually retain awareness
  • Can indicate juvenile myoclonic epilepsy
86
Q

What can myoclonic seizures in kids indicate?

A

Juvenile myoclonic epilepsy

87
Q

What is West syndrome?

A
  • Infantile spasms-> clusters of full body attacks
  • Usually start aged 6 months
  • Poor prognosis
88
Q

How is West syndrome (infantile spasms) treated?

A

Vigabatrin + prednisolone

89
Q

What is the prognosis of West syndrome (infantile spasms)?

A
  • 1/3 can be seizure free

- 1/3 die by age 25

90
Q

What is the mechanism of action of sodium valproate?

A

Increases GABA activity and relaxes the brain

91
Q

What are the side effects of sodium valproate?

A
  • Teratogenic-> not given to women + girls unless meet pregnancy prevention programme criteria
  • Liver damage, hepatitis, hair loss, tremor
92
Q

What are the side effects of carbamazepine?

A

Agranulocytosis, aplastic anaemia, P450 inducer

93
Q

What are the side effects of ethosuxamide?

A

Night terrors, rashes

94
Q

What are the side effects of phenytoin?

A

Folate deficiency, megaloblastic anaemia, vitamin D deficiency, osteomalacia, P450 inducer

95
Q

What are the side effects of lamotrigine?

A
  • Steven Johnson syndrome
  • Leukopaenia
  • DRESS syndrome-> drug rash with eosinophilia + systemic symptoms
96
Q

What is status epilepticus?

A

A seizure lasting >5 minutes (techically 30 minutes) or 3+ seizures in 1 hour

97
Q

How is status epilepticus managed?

A
  • ABCDE
  • IV lorazepam-> 4mg and repeat in 10 minutes if need to
  • IV phenytoin or phenobarbital

-If in the community-> buccal midazolam or rectal diazepam

98
Q

What causes neuropathic pain?

A

Abnormal functioning of the sensory nerves-> painful signals to brain

99
Q

What are some causes of neuropathic pain?

A
  • Nerve damage-> surgery, MS, diabetic foot
  • Trigeminal neuralgia
  • Post-herpatic neuralgia
  • Complex regional pain syndrome
100
Q

What is postherpatic neuralgia?

A

Neuropathic pain due to shingles-> usually on trunk + one dermatome

101
Q

What are the features of neuropathic pain?

A
  • Burning, tingling, pins + needles, electric shocks, loss of sensation
  • DN4 questionnaire-> score of 4+/10 may indicate
102
Q

How is neuropathic pain managed?

A

Amitriptyline, duloxetine, gabapentin, pregabalin, tramadol (for short-term flare), capsaicin, physio, psych

103
Q

How is trigeminal neuralgia treated?

A
  • Carbamazepine

- Decompression surgery

104
Q

What is complex regional pain syndrome (CRPS)?

A

Abnormal nerve function causes neuropathic pain + sensory issues

105
Q

How does complex regional pain syndrome (CRPS) present?

A
  • Painful, hypersensitivity, swelling, colour change, temperature change, abnormal sweating, hair growth
  • Usually in 1 limb after an injury
106
Q

How is complex regional pain syndrome (CRPS) treated?

A

Under a specialist with neuropathic pain medications

107
Q

What is the pathway of the facial nerve (CN VII)?

A

Exits brainstem at cerebellopontine angle-> through temporal bone-> through parotid gland-> splits to 5 branches (temporal, zygomatic, buccal, marginal manbibular, cervical)

108
Q

What are the different functions of the facial nerve (CN VII)?

A
  • Motor-> muscles of expression, stapedius (inner ear), some neck muscles
  • Sensory-> anterior 2/3 of the tongue
  • Parasympathetic-> submandibular, sublingual and lacrimal glands
109
Q

How does an upper motor neurone lesion present in facial nerve (CN VII) palsy and what might this indicate?

A
  • Forehead sparing + can move on affected side
  • Each side of the forehead has UMN innervation from both sides of the brain-> lesion on one side means will still be innervated from the other side
  • May indicate CVA or tumour-> more serious
110
Q

What might bilateral facial palsy indicate?

A

Bilateral UMN lesions-> MND or pseudobulbar palsy

111
Q

How does Bell’s palsy present?

A
  • Unilateral LMN palsy-> CN VII affected

- Recovery after few weeks but may get residual weakness for 12+ months

112
Q

What causes Bell’s palsy?

A

Idiopathic-> CN VII problem

113
Q

What is the treatment for Bell’s palsy?

A
  • Prednisolone 50mg for 10 days or reducing regime-> when present within 72 hours of symptoms
  • Lubricating eye drops or taping eye-> prevent damage + drying (exposure keratopathy)
114
Q

What is Ramsay-Hunt syndrome?

A

Facial nerve palsy due to varicella zoster virus (VZV)

115
Q

How does Ramsay-Hunt syndrome present?

A
  • Unilateral LMN palsy
  • Painful vesicular rash in ear canal + pinna + around ear
  • Can extend to tongue and hard palate
116
Q

How is Ramsay-Hunt syndrome treated?

A
  • Prednisolone + acyclovir

- Lubricating eye drops

117
Q

What can cause LMN facial nerve palsy?

A
  • Bell’s palsy
  • Ramsay-Hunt syndrome
  • Systemic-> DM, sarcoidosis, leukaemia, MS, GBS
  • Tumours-> acoustic neuroma, parotid tumour, cholestatomas
  • Trauma-> direct, damage from surgery, base of skull fracture
  • Otitis media infection
  • Malignant otitis externa
  • HIV
  • Lyme’s disease
118
Q

What are the symptoms and signs of raised intracranial pressure?

A
  • Headache-> constant, nocturnal, worse on waking or cough or strain or bend forward
  • Vomiting
  • Altered mental state
  • Visual field defect
  • Seizures
  • Unilateral pstosis
  • CN III + VI palsy
  • Papilloedema on fundoscopy
119
Q

Causes of raised intracranial pressure?

A

Tumours, haemorrhage, idiopathic intracranial hypertension, abscess, infection

120
Q

What are the red flag symptoms for a headache?

A

Constant, nocturnal, worse on waking or cough or strain or bend forward, weight loss, new neuro symptoms, vomiting

121
Q

What is the pathophysiology of papilloedema?

A
  • Swelling of optic disc secondary to raised ICP

- Sheath around optic nerve connected to subarachnoid space-> CSF flows into sheath when high pressure-> swells

122
Q

What does papilloedema look like on fundocscopy?

A

Blurred disc margin, curved retinal vessels over disc, loss of venous pulsation, engorged veins, haemorrhages, Paton’s lines

123
Q

What types of cancer commonly metastasise to the brain?

A

Lung, breast, renal cell, melanoma

124
Q

What is a glioma?

A

A tumour of the glial cells in the brain + spinal cord-> graded from 1 (benign) to malignant

125
Q

What are the different types of brain tumour?

A
  • Gliomas-> Astrocytoma, Oligodendroglioma, Ependymoma
  • Meningioma
  • Pituitary tumours
  • Acoustic neuroma
126
Q

What are the different types of gliomas?

A
  • Astrocytoma AKA glioblastoma multiforme-> most common + most malignant
  • Oligodendroglioma
  • Ependymoma (least malignant)
127
Q

What is a meningioma?

A

A benign tumour of the meninges-> can lead to raised ICP symptoms due to mass effect

128
Q

What is a meningioma?

A

A benign tumour of the meninges-> can lead to raised ICP symptoms

129
Q

What do pituitary tumours typically cause and why?

A
  • Bitemporal hemianopia (outer half of vision lost) due to pressing on the optic chiasm
  • Hormone deficiencies (hypopituitarism)
  • Hormone excess-> acromegaly, hyperprolactinaemia, Cushing’s, thyrotoxicosis
130
Q

What is an acoustic neuroma?

A
  • AKA vestibular schwannoma-> tumour of Schwann cells around auditory nerve (innervates inner ear)
  • Slow growing but can grow and produce symptoms
  • Usually unilateral
131
Q

In what condition can bilateral acoustic neuromas occur?

A

Neurofibromatosis type 2

132
Q

What are the symptoms of an acoustic neuroma?

A

Hearing loss, tinnitus, balance problems, CN VII palsy

133
Q

How are brain tumours treated?

A

Depends on type-> surgery, palliative care, chemo, radiotherapy

134
Q

How are pituitary tumours managed?

A
  • Transphenoidal surgery
  • Radiotherapy
  • Prolactin secreting-> bromocriptine
  • GH-secreting-> somatostatin analogues eg octreotide
135
Q

What is Huntington’s Chorea?

A

Autosomal dominant genetic condition in which the nervous system progressively deteriorates causing movement disorders

136
Q

What is the inheritance pattern of Huntington’s chorea?

A

Autosomal dominant

137
Q

What happens to the patient’s genes in Huntington’s chorea?

A
  • Trinucleotide repeat of HTT gene on chromosome 4

- Anticipation-> successive generations have more repeats so earlier onset + increased disease severity

138
Q

How does Huntington’s chorea present?

A
  • Insidious + progressive onset
  • Cognitive, behavioural + mood problems first
  • Movement-> involuntary (chorea), eye disorders, dysarthria, dysphagia
139
Q

How is Huntington’s chorea managed?

A
  • Genetic tests + counselling
  • No treatment stops or slows progression
  • Olanzapine or tetrabenzine can help with movement problems
140
Q

What commonly causes death in Huntington’s chorea?

A
  • Respiratory disease (more susceptible + less able to fight infection)
  • Suicide
141
Q

What is myasthenia gravis?

A

An autoimmune condition in which antibodies are made against acetylcholine receptors in the neuromuscular junction causing muscle weakness

142
Q

What is the pathophysiology of myasthenia gravis?

A
  • NMJs between motor nerves + muscles
  • Acetylcholine released by axons + bind to receptors on the posy-synaptic membrane to stimulate muscle contraction
  • These receptors used up more during activity-> less effective stimulation when increased
  • Antibodies in MG activate complement system in NMJ + damage cells at post-synaptic membrane
  • Antibodies in MG also destroy MuSK + LRP4 proteins in receptors
143
Q

How does myasthenia gravis present?

A
  • Diplopia, ptosis, weak facial movements, poor swallowing, jaw fatigue when chewing, slurred speech
  • Weakness worse with use, at the end of the day and when repeating movements
  • Minimal symptoms in the morning
  • Proximal + head/neck muscles
  • 20-40% of thymoma patients get
144
Q

Examination findings in myasthenia gravis?

A
  • Ptosis exaggerated by repetitive blinking or prolonged upward gaze
  • Repeated arm abduction causes weakness
  • Thymoma or scar from surgery
145
Q

How is myasthenia gravis diagnosed?

A
  • Ach-receptor antibodies (85%)
  • MuSK and LRP4 antibodies
  • CT/MRI of thymus-> thymoma
  • Edrophonium (neostigmine) test-> brief relief of symptoms when give to patient (stops Ach breakdown)
146
Q

Long-term treatment of myasthenia gravis?

A
  • Pyridostigmine or neostigmine-> reversible acetylcholinesterase inhibitors
  • Prednisolone or azathioprine
  • Thymectomy
  • Monoclonal antibodies eg rituximab
147
Q

What is myasthenia crisis?

A

Acute worsening of symptoms + respiratory failure-> often triggered by illness

148
Q

How is myasthenia crisis treated?

A
  • IV immunoglobiluns
  • Plasma exchange
  • May need BiPAP or intubation + ventilation
149
Q

What is Lambert-Eaton myasthenic syndrome and what is the pathophysiology?

A
  • Syndrome that occured in small cell lung cancer
  • Antibodies produced against voltage-gated calcium channels on small cell lung cancer cells
  • Antibodies damage calcium channels in NMJ presynaptic terminals-> less Ach released
150
Q

How does Lambert-Eaton myasthenic syndrome present?

A
  • Slower and less severe symptoms
  • Proximal leg muscle weakness, diplopia, ptosis, dysphagia
  • Autonomic dysfunction-> dry mouth, blurry vision, impotence, dizziness
  • Post-tetanic potentiation-> reduced reflexes normally but normal after strong muscle contraction
151
Q

How is Lambert-Eaton myasthenic syndrome managed

A
  • Consider investigations for small cell lung cancer
  • Amifampridine-> allows more Ach release in NMJ
  • Immunosuppression, IV Igs and plasmapheresis
152
Q

What is Charcot-Marie-Tooth syndrome?

A

An autosomal dominant inherited condition affecting peripheral motor and sensory nerves-> myelin or axonal dysfunction

153
Q

Presentation of Charcot-Marie-Tooth?

A
  • Reduced reflexes + tone
  • Peripheral sensory loss
  • Hand weakness
  • Distal muscle wasting-> inverted champagne bottle legs
  • Pes cavus-> high foot arch
154
Q

Management of Charcot-Marie-Tooth?

A

Mainly supportive with neuro, physios, OT, ortho surgeons

155
Q

Causes of peripheral neuropathy?

A

ABCDE

  • Alcohol
  • B12 deficiency
  • Cancer or CKD
  • Diabetes or Drugs (isonazid, amiodarone, cisplatin)
  • Every vasculitis
156
Q

What is Guillain-Barre syndrome?

A

An acute polyneuropathy than affects peripheral nerves usually triggered by an infection

157
Q

What infections commonly trigger Guillain-Barre syndrome?

A

Campylobacter jejuni, CMV, EBV

158
Q

How does Guillain-Barre syndrome present?

A
  • Acute symmetrical ascending sensory weakness
  • Reduced reflexes
  • Neuropathic pain
  • Can cause facial nerve weakness if progresses to cranial nerves
  • Symptoms within 4 weeks of infection-> peak in 2-4 weeks-> recover in months-years
159
Q

What is the pathophysiology of Guillain-Barre syndrome?

A

B-cells great antibodies against pathogen antigens but match proteins on nerve cells (myelin sheath or axon)

160
Q

How is Guillain-Barre syndrome diagnosed?

A
  • Clinically
  • Brighton criteria
  • Nerve conduction studies (reduced signal)
  • LP (CSF proteins raised)
161
Q

Treatment for Guillain-Barre syndrome?

A
  • IV immunoglobulins or plasma exchange
  • Supportive + VTE prophylaxis
  • Intubation if respiratory failure
162
Q

What is the prognosis of Guillain-Barre syndrome?

A
  • 80% fully recover
  • 15% get neuro disability
  • 5% die
163
Q

What is neurofibromatosis?

A

Genetic condition causing neuromas (benign nerve tumours) throughout the nervous system

164
Q

What is the diagnostic criteria for neurofibromatosis type 1?

A

2+ of classic features ie CRABBING

  • Cafe au lait spots-> 6+ measuring 5mm+ (kids) or 15mm+ (adults)
  • Relative with NF1
  • Axillary or inguinal freckles
  • Bony dysplasia (long bone bowing etc)
  • Iris hamartomas-> lisch nodules, 2+ yellow/brown spots on iris
  • Neurofibromas-> 2+ or 1 plexiform neurofibroma
  • Glioma of the optic nerve
165
Q

Investigations for neurofibromatosis type 1?

A
  • Clinical + CRABBING criteria
  • Genetic testing
  • X rays for bone lesions
  • CT or MRI for brain lesions
166
Q

Treatment for neurofibromatosis type 1?

A

None-> control symptoms + treat complications

167
Q

What are the complications of neurofibromatosis type 1?

A
  • Migraines
  • Epilepsy
  • LD + ADHD
  • Scoliosis
  • Vision loss due to optic nerve gliomas
  • Renal artery stenosis + HTN
  • Malignant peripheral nerve sheath tumours
  • GI stromal tumour (sarcoma)
  • Other cancers-> brain, spinal cord, leukaemia
168
Q

What is the genetic mutation behind neurofibromatosis type 1?

A

Autosomal dominant-> NF1 gene on chromosome 17-> neurofibromin code (tumour suppressor gene)

169
Q

What is the genetic mutation behind neurofibromatosis type 2?

A

Autosomal dominant-> gene on chromosome 22-> for merlin (tumour suppressor gene)

170
Q

How does neurofibromatosis type 2 present?

A

Bilateral acoustic neuromas (vestibular schwannomas)-> hearing loss, tinnitis, balance problems

171
Q

How is neurofibromatosis type 2 treated?

A

Surgery to resect tumours but risk of nerve damage

172
Q

What is tuberous sclerosis?

A

A genetic condition causing hamartomas (benign neoplastic tissue growth) to grow throughout the body

173
Q

What is the pathophysiology of tuberous sclerosis?

A

TSC1 gene on chromosome 9 (hamartin) or TSC2 on chromosome 16 (tuberin) mutations-> abnormal control of/unregulated size of cell growth

174
Q

What are the signs of tuberous sclerosis?

A

-Hamartomas-> benign lesions all over body (mostly eyes)
-Ash leaf spots-> depigmented areas
-Cafe-au-lait spots
-Shagreen patched-> thick + dimpled
-Angiofibromas-> papules over nose + cheeks
-Subungual fibromata-> on nail bed
Poliosis-> Isolated white hair patch
-Rhabdomyomas
-Gliomas
-Polycystic kidneys
-Neuro signs-> epilepsy, LD, development delay

175
Q

What is the stereotypical history for someone with tuberous sclerosis?

A

Child with epilepsy + skin features (hamartomas, cafe-au-lait spots, ash leaf spots etc)

176
Q

How is tuberous sclerosis managed?

A

Supportive + treat epilepsy

177
Q

What are some red flag symptoms and signs for serious neurological conditions?

A
  • Raised ICP signs (eg papilloedema, headache, vomiting)
  • Fever, photophobia, neck stiffness-> meningitis + encephalitis
  • New neurological symptoms-> haemorrhage, malignancy, stroke
  • Visual disturbance-> glaucoma, temporal arteritis
  • Dizziness-> stroke
  • Symptoms in pregnancy-> pre-eclampsia
178
Q

How does tension headache present?

A
  • Mild ache across the forehead, tight band, onset + resolves gradually
  • Triggered by stress, depression, alcohol, skipping meals, dehydration
179
Q

How is tension headache treated?

A

Reassurance, analgesia, relaxation, hot towels

180
Q

What are some of the triggers for tension headache?

A

Triggered by stress, depression, alcohol, skipping meals, dehydration

181
Q

What is a secondary headache?

A

Similar presentation to tension headache but with a clear cause-> infection, alcohol, head injury etc

182
Q

What is sinusitis?

A

Inflammation of the ethmoidal, maxillary, frontal and/or sphenoidal sinuses-> mostly viral

183
Q

How does sinusitis present?

A

Facial pain behind the nose, forehead and/or eyes with tenderness over sinuses

184
Q

How is sinusitis treated?

A
  • Usually resolves in 2-3 weeks
  • Nasal irrigation with saline
  • Steroid nasal spray if prolonged
185
Q

What is analgesia overuse headache?

A

Headache secondary to continuous use of analgesia-> presents similarly to tension

186
Q

How is analgesia overuse headache treated?

A

Withdrawal of analgesia

187
Q

What causes a hormonal headache?

A

Low oestrogen

188
Q

How does a hormonal headache present?

A
  • Starts 2 days before period and continues for first 3 days
  • Worsens around menopause and pregnancy (rule out pre-eclampsia)
189
Q

How is hormonal headache treated?

190
Q

What is cervical spondylosis?

A

Head and/or neck ache due to degenerative changes in the spine

191
Q

What are the symptoms of cervical spondylosis?

A

Neck pain worse on movement + headache

192
Q

How is cervical spondylosis treated?

A

-Exclude inflammation, malignancy, infection and nerve root/spinal cord lesions

193
Q

What is trigeminal neuralgia and what causes it?

A
  • Symptoms caused by irritation of the trigeminal nerve (CN V)
  • Can be any of the three branches (opthalmic, maxillary, mandibular)
  • Compression or MS
194
Q

How does trigeminal neuralgia present?

A
  • Intense facial pain
  • Comes on spontaneously
  • Lasts few seconds but can persist for hours
  • Electric shock sensation
  • Worsened over time
  • Triggers-> cold, spicy food, caffiene
195
Q

What causes a migraine?

A

Structural lesions, functional, chemical, vascular problems, inflammatory factors

196
Q

What are the different types of migraine?

A
  • With aura
  • Without aura
  • Silent-> aura + no headache
  • Hemiplegic
197
Q

How does a migraine present?

A
  • Headache-> moderate to severe, pounding/throbbing, unilateral normally, lasts 4-72 hours, comes in ‘attacks’
  • Aura-> visual changes eg sparks, blurring, lines
  • Photo/phonophobia, nausea and vomiting
198
Q

How does a hemiplegic migraine present?

A
  • Migraine type headache-> sudden or gradual onset
  • Hemiplegia-> unlateral limb weakness
  • Ataxia
  • Change in consciousness
199
Q

What can trigger a migraine?

A

Chocolate, cheese, OCP, caffiene, alcohol, anxiety, travel, exercise, bright lights, strong smells, dehydration, menstruation, abnormal sleep, trauma

200
Q

What are the five stages of migraine?

A

May only get 1-2 or all 5

  • Prodrome-> <3 days before, yawning, fatigue, mood changes
  • Aura-> <60 minutes
  • Headache-> 4-72 hours
  • Resolution-> fades usually after vomiting or sleeping
  • Postdromal/recovery
201
Q

Acute management of migraine?

A
  • Paracetamol + NSAIDs
  • Sumatriptan when starts
  • Antiemetics eg metoclopramide
  • Lying in dark room
202
Q

How does sumatriptan work in a migraine attack?

A

5HT receptor agonist-> acts on smooth muscle + vasoconstricts-> inhibits pain receptor activation + reduce CNS activity

203
Q

Prophylaxis of migraines?

A
  • Propanolol
  • Topiramate-> CI’d in pregnancy
  • Amitriptyline
  • Migraine diary + trigger avoidance
  • Acupuncture
  • Vitamin B2 (riboflavin) supplements
204
Q

Who is a typical patient with cluster headaches?

A

30-50 year old male smoker + triggered by alcohol, strong smells or exercise

205
Q

How do cluster headaches present?

A
  • Headache-> very severe, red/swollen/watery eye, ‘pacing the room’
  • Miosis, ptosis, nasal discharge, sweating
  • Attacks-> 15 mins to 3 hours, 3-4 times a day, for a few weeks-months, then remission for few years

Medicine (13 decks)

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