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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a stroke?

A

A cerebrovascular accident - hypoperfusion to the brain causing ischaemia and infarction of brain tissue.

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2
Q

What causes a stroke?

A

Ischaemic (clots) or haemorrhagic (bleeds).

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3
Q

What is a transient ischaemic attack?

A

Sudden onset transient neurological dysfunction secondary to ischaemia without infarction which lasts under 24 hours (usually 5-15 minutes).

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4
Q

Why is a TIA significant?

A

Often precedes a stroke.

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5
Q

What is a crescendo TIA?

A

Two or more TIAs in one week which makes it high risk of a stroke.

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6
Q

How is a TIA and stroke differentiated?

A

After recovery:
-TIA - Symptoms resolve in minutes, always less than 24h and no infarct.
-Stroke - Symptoms last at least 24h with infarction.

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7
Q

What causes a TIA?

A

Thrombo-emboli in the carotid artery/major brain vessel.

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8
Q

What are the risk factors for stroke?

A

Same as CVD:
Smoking, obesity, T2DM, hypertension, AF, hypercholesterolaemia, previous TIA.

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9
Q

How is a stroke diagnosed?

A

Identifying a stroke - FAST (face, arms, speech, time).
-Non-contrast head CT/diffusion weighted MRI:
TIA/ischaemic - Mostly normal.
Haemorrhagic - Hyperdense blood.

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10
Q

How is a TIA managed?

A

Start daily aspirin and secondary prevention with statins and clopidogrel.

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11
Q

How is a haemorrhagic stroke managed?

A

Referral to neurosurgery for evacuation of blood.
IV mannitol to reduce ICP.

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12
Q

How is an ischaemic stroke managed?

A

Within 4h - thrombolysis with alteplase.
If large - thrombectomy.

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13
Q

What is the secondary prevention of stroke?

A

Modify risk factors and start stroke rehab.
-Daily clopidogrel and statin.

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14
Q

What percentage of strokes are ischaemic?

A

85%.

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15
Q

What percentage of strokes are haemorrhagic?

A

15%.

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16
Q

What are six risk factors for intercranial bleeds?

A

Head trauma, hypertension, aneurysms, brain tumours, anticoagulants, connective tissue disorders.

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17
Q

How do intercranial bleeds present?

A

Sudden onset headache with seizures, vomiting, reduced GCS and other sudden onset neurological symptoms.
-Signs of raised ICP:
Cushing triad - bradycardia, increased PP, irregular breathing.

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18
Q

What is amaurosis fugax?

A

Transient loss of vision due to decreased blood flow to retina (retinal/ophthalmic artery occlusion).

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19
Q

How are intercranial bleeds diagnosed?

A

CT/MRI of head and referral to neurosurgery for removal.

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20
Q

What is the Glasgow coma scale (GCS)?

A

An assessment tool for assessing the level of consciousness based on eyes, verbal and motor response.

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21
Q

Explain the GCS.

A

-Eye opening response ranked 1-4 (none, to pain, to speech, spontaneous).
-Speech response ranked 1-5 (none, sounds, bad words, confused conversation, orientated).
-Motor response ranked 1-6 (none, extends, abnormal flexion, flexion, localises pain, obeys).

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22
Q

What are the main four locations of intercranial bleeds?

A

Subarachnoid, subdural, extradural and intercranial.

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23
Q

Explain an intracerebral haemorrhage.

A

Bleeding into brain tissue, can be located anywhere in brain tissue.

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24
Q

What is a subarachnoid haemorrhage?

A

Bleeding into subarachnoid space where CSF is located, between pia and arachnoid matter.

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25
Q

What is the main cause of subarachnoid haemorrhages?

A

Ruptured cerebral aneurysms.

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26
Q

How does a subarachnoid haemorrhage present?

A

Thunderclap headache.

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27
Q

What is a subdural haemorrhage?

A

Bleeds between the dura and arachnoid matter.

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28
Q

What causes a subdural haemorrhage?

A

Rupture of bridging veins of outer meningeal layers.

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29
Q

How does a subdural haemorrhage appear on CT scan?

A

Crescent/banana shaped not limited by cranial structures.

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30
Q

What is an extradural haemorrhage?

A

Bleed between the skull and dura.

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31
Q

What causes an extradural haemorrhage?

A

Rupture of middle meningeal artery.

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32
Q

How does an extradural haemorrhage appear on CT scan?

A

Bi-convex shaped limited by cranial strictures.

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33
Q

What are the main two CNS infections?

A

Meningitis and encephalitis.

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34
Q

What is meningitis?

A

Inflammation of the meninges which line the brain and spinal cord.

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35
Q

What causes meningitis?

A

Viral or bacterial infection.

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36
Q

What is meningococcal meningitis?

A

When bacteria are infecting meninges and CSF around the brain and spinal cord.

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37
Q

What is meningococcal septicaemia?

A

When the the meningococcal bacterial infection is in the bloodstream. This is the cause of the non-blanching rash caused by DIC.

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38
Q

What is the most common cause of meningitis?

A

Viral is more common than bacterial.

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39
Q

Explain viral meningitis and it’s causes.

A

More common and less severe.
-Mostly caused by HSV, VZV and enteroviruses (coxsackie).

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40
Q

What is the management for viral meningitis?

A

Usually only supportive.
If confirmed HSV meningitis - aciclovir.

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41
Q

What are the most common causes of bacterial meningitis in adults?

A

N. meningitidis and S. pneumoniae.

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42
Q

What is the most common cause of bacterial meningitis in neonates? Why?

A

Group B strep - lives harmlessly on vagina.

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43
Q

What is a cause of bacterial meningitis in the very young and very old?

A

Listeria.

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44
Q

Describe N. meningitidis.

A

Gram negative diplococcus.
-Vaccines available - MenB/C, ACWY.

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45
Q

Describe S. pneumoniae.

A

Gram positive diplococcus in chains.-Vaccine available - PCV.

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46
Q

What are the four risk factors for meningitis?

A

Extremes of ages, immunocompromised, crowded environment, not vaccinated.

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47
Q

What are seven main symptoms of meningitis?

A

Fever, neck stiffness, photophobia, vomiting, headache, altered consciousness and seizures.

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48
Q

How does meningococcal septicaemia present?

A

Non-blanching rash.

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49
Q

How does meningitis present in neonates?

A

Non-specific: fever, poor feeding and lethargy.
-Lumbar puncture in neonates with fever and lethargy.

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50
Q

What are two tests to test for meningeal irritation?

A

Kernig’s test - Can’t extend knee when the hip is flexed without pain due to meninges stretching and being irritated.
Brudzinski’s test - When the neck is flexed, the knees and hips involuntarily flex.

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51
Q

How is meningitis investigated?

A

Lumbar puncture at L4 and CSF analysis.-CSF sample also sent for viral PCR testing.

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52
Q

What are CSF results in viral meningitis?

A

Clear, normal or raised protein, normal glucose, high WCC (lymphocytes) and negative bacterial culture.

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53
Q

What are the CSF results in bacterial meningitis?

A

Cloudy, high protein, low glucose, high WCC (neutrophils) and positive bacterial culture.

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54
Q

How is bacterial meningitis and meningococcal septicaemia treated in the community?

A

IM benzylpenicillin and hospital referral.

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55
Q

How is bacterial meningitis and meningococcal septicaemia treated in hospital for neonates aged 1-3 months?

A

IM cefotaxime and amoxicllin.

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56
Q

How is bacterial meningitis and meningococcal septicaemia treated in hospital for people aged above 3 months?

A

Ceftriaxone.

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57
Q

How is bacterial meningitis and meningococcal septicaemia treated in hospital if there’s a risk of MRSA?

A

Vancomycin.

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58
Q

What is the supportive treatment in hospital for bacterial meningitis?

A

Dexamethasone - reduces the frequency of hearing loss and neurological deficit.

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59
Q

What are five complications of meningitis?

A

Hearing loss, seizures/epilepsy, cognitive impairment/memory loss, focal neuro symptoms.

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60
Q

What is the post exposure prophylaxis treatment to meningitis?

A

Single dose of ciprofloxacin.

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61
Q

What is encephalitis?

A

Inflammation of the brain.

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62
Q

What are the causes of encephalitis?

A

Infective and non infective.

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63
Q

What are the infective causes of encephalitis?

A

Viral, bacterial is very rare in the UK.
-Mostly HSV-1.
-Others include HSV-2, CMV, EBV, VZV and HIV.

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64
Q

What are the two risk factors for encephalitis?

A

Extremes of age, immunocompromised.

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65
Q

How does encephalitis present?

A

With fever, headache, altered consciousness, altered cognition and unusual behaviour.
-Acute onset focal neuro symptoms and acute onset focal seizures.

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66
Q

How is encephalitis diagnosed?

A

Lumbar puncture and send CSF off for viral PCR testing.
-CT/MRI.

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67
Q

How is encephalitis treated?

A

IV antivirals according to cause:
-Aciclovir for HSV and VZV.
-Ganciclovir for CMV.

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68
Q

What are the complications of encephalitis?

A

Fatigue, personality changes, cognitive changes, learning disability, headaches, movement disorders, seizures.

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69
Q

What is multiple sclerosis?

A

An autoimmune, chronic and progressive condition that involved demyelination of the myelinated neurones of the CNS.

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70
Q

When does MS usually present and who is it most common in?

A

Usually presents in young adults under 50 and is more common in women.

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71
Q

When do symptoms improve in MS?

A

When pregnant or in postpartum period.

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72
Q

What are the five main causes of MS?

A

EBV, genes, low vitamin D, smoking and obesity.

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73
Q

What are seven risk factors for MS?

A

Females, 20-40y, autoimmune disease, family history, EBV, smoking, obesity.

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74
Q

What is the key term in MS used to describe the way MS lesions change over time in different locations?

A

Disseminated in time and space.

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75
Q

What are the different disease patterns in MS?

A

-Relapse-remitting (mc) - episodes of disease followed by recovery.
-Primary progressive - Gradual deterioration without recovery.
-Secondary progressive - Relapse-remitting but now primary progressive.

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76
Q

What is usually the first presenting symptom in MS?

A

Optic neuritis - loss of vision in one eye due to myelinated and inflamed optic nerve.

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77
Q

How does MS present?

A

Paresthesia, blurred vision, numbness with Lhermitte’s sign (when neck is flexed - electric shock sensation) that is worsened by heat.
-Bell’s palsy, limb weakness, incontinence.
-6th CN lesion - internuclear ophthalmoplegia and conjugated lateral gaze disorder.

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78
Q

What are the two main investigations for MS?

A

MRI of brain and spinal cord showing lesions.
Lumbar puncture which shows oligoclonal bands in CSF.

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79
Q

Which criteria has to be satisified for a diagnosis of MS?

A

McDonald criteria - 2+ attacks, separate events that affect different parts of the CNS (disseminated in time and space).

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80
Q

How are acute relapses of MS treated?

A

IV methylprednisolone.

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81
Q

How is MS prophylactically treated to modify the disease?

A

DMARDs and biologics.

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82
Q

What is Guillian-Barre syndrome?

A

An acute paralytic polyneuropathy that affects the peripheral nervous system.

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83
Q

Who does Guillian-Barre syndrome affect?

A

Males aged 15-30 and 50-70.

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84
Q

What causes Guillian-Barre syndrome?

A

Triggered by an infection:
-C. jejuni (mc), CMV and EBV.

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85
Q

Describe the pathophysiology of Guillian-Barre syndrome.

A

Molecular mimicry - Plasma cells make antibodies against antigens on the pathogen of preceding infection. These antibodies also match the proteins on Schwann cells and attack those.
-Causing demyelination of PNS and polyneuropathy.

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86
Q

Describe the clinical course of Guillian-Barre syndrome.

A

4 weeks before - Gastroenteritis/infection.
Symptoms start.
2-4 weeks - Peak symptoms.
Months-years - Recovery period.

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87
Q

Describe the prognosis of Guillian-Barre syndrome.

A

80% fully recover.
15% left with neurological disability.
5% will die.

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88
Q

How does Guillian Barre syndrome present?

A

Symmetrical ascending weakness and paralysis (feet up).
Reduced reflexes, peripheral loss of sensation.
Respiratory failure in 35%.

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89
Q

How is Guillian-Barre syndrome diagnosed?

A

Nerve conduction studies.
Lumbar puncture - raised protein, normal WCC and glucose (inflammation with no infection).

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90
Q

What is the treatment for Guillian-Barre syndrome?

A

IV Ig for 5 days or plasma exchange.
Supportive care and VTE prophylaxis (PE is a cause of death).
In respiratory failure - intubation, ventilation and ICU admission.

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91
Q

What is Parkinson’s disease?

A

Progressive reduction of dopamine in the basal ganglia of the brain which leads to movement disorders which causes problems like shaking and stiffness that get worse over time.

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92
Q

Describe the pathophysiology of Parkinson’s disease.

A

Loss of dopaminergic neurones from substantia nigra. -Presence of Lewy bodies.

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93
Q

What are the two most common neurodegenerative disorders?

A
  1. Dementia.
  2. Parkinson’s.
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94
Q

What is the typical Parkinson’s patient?

A

Old man around 70y.

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95
Q

What are three risk factors for Parkinson’s disease?

A

Family history, males, higher age.

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96
Q

What are the main triad of symptoms in Parkinson’s disease?

A

Resting tremor, rigidity, bradykinesia.-Usually unilateral.

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97
Q

Describe the presenting symptoms of Parkinson’s disease.

A

-Unilateral tremor - pill rolling tremor 4-6 times a second.
-Cogwheel rigidity.
-Bradykinesia - movements get slower and smaller.

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98
Q

Describe the bradykinesia in Parkinson’s disease.

A

Slowness of movement:
-Smaller handwriting, shuffling gait, difficulty initiating movement, difficulty turning when stood up, reduced facial movement/expression.

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99
Q

What are five other symptoms of Parkinson’s disease?

A

Insomnia, anosmia, postural instability, depression, cognitive impairment.

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100
Q

How is Parkinson’s diagnosed?

A

Diagnosed clinically based on presentation and examination - bradykinesia, tremor, rigidity.

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101
Q

What is the treatment for Parkinson’s disease?

A

Levodopa and decarboxylase inhibitors (carbidopa) to stop levodopa from being broken down.
-Others:
Monoamine oxidase B inhibitors.
Dopamine agonists (cabergoline/bromocriptine).

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102
Q

How successful is the treatment for Parkinson’s disease?

A

Works very well initially but the body soon becomes resistant.

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103
Q

What is a key differential diagnosis for Parkinson’s disease?

A

Benign essential tremor.

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104
Q

What is benign essential tremor?

A

Common tremor associated with older age. Mostly in the hands.

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105
Q

Compare and contrast benign essential tremor and Parkinson’s.

A

Parkinson’s - Asymmetrical.
BET - Symmetrical.

Parkinson’s - 4-6Hz.
BET - 5-8Hz.

Parkinson’s - Worse at rest.
BET - Improves with rest.

Parkinson’s - Improves with intentional movement.
BET - Worse with intentional movement.

Parkinson’s - Other Parkinson’s features.
BET - No other Parkinson’s features.

Parkinson’s - No change with alcohol.
BET - Improves with alcohol.

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106
Q

What is Huntington’s disease?

A

An autosomal dominant genetic condition with full penetrance that causes progressive deterioration within the nervous system.

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107
Q

What is Huntington’s disease caused by?

A

Trinucleotide (CAG) repeat disorder in HTT gene on chromosome 4.

108
Q

What does Huntington’s disease display?

A

Anticipation - successive generations have more repeats in the gene which leads to earlier age of onset and increased severity of the disease.

109
Q

What is the life expectancy of Huntington’s disease?

A

15-20 years after symptoms start.

110
Q

When does Huntington’s disease usually begin to present?

A

Asymptomatic until ages 30-50.

111
Q

Describe the number of trinucleotide repeats and their effects in Huntington’s.

A

<35 - No Huntington’s.
35-55 - Huntington’s.
>60 - Severe Huntington’s.

112
Q

What causes symptoms in Huntington’s disease? (pathophysiology).

A
  1. Caudate nucleus atrophies.
  2. Inhibitory neurones in the corpus striatum degenerate.
  3. Levels of GABA decrease.
  4. Excessive nigrostriatal pathway.
113
Q

How does Huntington’s disease present?

A

Chorea - excessive limb jerking.
Dementia, psychiatric issues, depression.
Eye movement disorders, dysarthria, dysphagia.

114
Q

How is Huntington’s disease diagnosed?

A

Family history of earlier and more severe Huntington’s.
Genetic test - 35 CAG repeats on chromosome 4.

115
Q

What is the management of Huntington’s disease?

A

Extensive counselling and breaking bad news.
Speech and language therapy.
End of life care planning.
-Medications:
Antipsychotics, benzodiazepines, dopamine antagonists.
-SSRIs for depression.

116
Q

What is dementia?

A

Irreversible, progressive decline and impairment of higher brain function (memory, judgement, language, personality).

117
Q

Does dementia occur with consciousness changes?

A

No, occurs without impairment of consciousness.

118
Q

What are the main four types of dementia and how prevalent are they?

A

Alzheimer’s - 60%.
Vascular - 20%.
Lewy body - 10%.
Frontotemporal - 5%.

119
Q

What is the biggest risk factor for dementia?

A

Increasing age.

120
Q

Describe Alzheimer’s disease and it’s pathophysiology.

A

Most common cause of dementia due to beta amyloid plaques due to breakdown of PPA and tall neurofibrillary tangles (tau proteins) in cerebral cortex.
-This results in the death of brain cells.

121
Q

What is the pattern of cognitive decline in dementia?

A

Steady decline in cognitive function.

122
Q

What are two risk factors for Alzheimer’s disease?

A

Down’s syndrome, ApoE4 mutation.

123
Q

Describe the presentation of Alzheimer’s.

A

Usually after 60, affects all of brain.
Main presenting symptom is memory loss.
-Agnosia, apraxia and aphasia.

124
Q

What is vascular dementia? Who is it more common in?

A

Dementia due to cerebrovascular damage (stroke, TIA).More common in men with previous stroke.

125
Q

What is the pattern of cognitive decline in people with vascular dementia?

A

Stepwise fashion.

126
Q

How does vascular dementia present?

A

Cognitive impairment with mood disturbances and psychiatric issues.

127
Q

What is Lewy body dementia?

A

Dementia due to spherical Lewy body proteins deposited in the brain.

128
Q

Describe the link between Lewy body dementia and Parkinson’s disease.

A

Lewy body proteins are present in both, they are more widespread in Lewy body dementia and concentrated in the substantia nigra in Parkinson’s.
-Parkinson’s before - Parkinson dementia.
-LBD before - Lewy body dementia with Parkinsonism.

129
Q

Describe the presentation of Lewy body dementia.

A

Often presents with visual hallucinations, Parkinson’s symptoms and cognitive decline.

130
Q

What is Frontotemporal dementia?

A

Neuron damage and death in the frontal and temporal lobes due to deposition of tau proteins.

131
Q

How does Frontotemporal dementia present?

A

Speech and language - temporal.
Thinking and memory - frontal.

132
Q

How is dementia diagnosed?

A

MMSE and brain MRI.

133
Q

Describe the MMSE.

A

Tool to assess mental status and screen for cognitive impairment.
-Out of 30:
>25 is normal.
18-25 is impaired.
<17 is severely impaired.

134
Q

What is the conservative management of dementia?

A

Social stimulation and exercise.

135
Q

What is the treatment for Alzheimer’s disease?

A

Acetylcholinesterase inhibitor - donepezil.

136
Q

What is the treatment for vascular dementia?

A

Antihypertensives - ACEi (ramipril).

137
Q

How can headaches be divided?

A

Into primary and secondary.

138
Q

What are primary headaches?

A

Those with no pathology - more common.

139
Q

What are secondary headaches?

A

Secondary to pathology.

140
Q

What are the four most common types of primary headaches?

A

Tension, migraine, cluster, drug induced (medication overuse).

141
Q

What are five causes of secondary headaches?

A

GCA, infection, subarachnoid haemorrhage, cerebrovascular disease, eye/ear/sinus pathology.

142
Q

What are seven red flags for headaches?

A

Fever, photophobia, neck stiffness, new neurological symptoms, dizziness, visual disturbance and vomiting.

143
Q

What are tension headaches?

A

Most common primary headache with a mild ache across the forehead due to muscle aches.

144
Q

What are tension headaches associated and not associated with?

A

Associated with stress, depression, alcohol, hunger and dehydration.
NOT associated with visual changes or N+V.

145
Q

What is the treatment of tension headaches?

A

Simple analgesia (aspirin and paracetamol).

146
Q

Describe the site, character and severity of tension headaches.

A

Site - Bilateral.
Character - Pressing/tightening.
Severity - Mild/moderate, non disabling.

147
Q

What are cluster headaches?

A

A rare, disabling unilateral, excruciating stabbing pain headache.

148
Q

How long do each type of primary headache usually last?

A

Tension - 30m to 7 days.
Cluster - 15m to 3 hours.
Migraine - 4h to 3 days.

149
Q

What are migraines?

A

Complex neurological condition that causes headaches and associated symptoms. They occur in attacks that follow a typical pattern.

150
Q

What are the types of migraine?

A

-With aura (visual phenomena - sparks, blurred, lines, blind spots).
-Without aura.
-Silent migraine (with aura, without headache).
-Hemiplegic migraine.

151
Q

What are the triggers of migraines?

A

CHOCOLATE:-Chocolate, hangovers, orgasms, cheese, oral contraceptives, lie ins, alcohol, tumult (loud noise), exercise.

152
Q

Explain the five stages of migraine.

A

Prodromal - mood changes, days before.
Aura - visual changes, minutes before.
Headache - throbbing/pounding up to 3 days.
Resolution - headache fades or relieved by vomiting.
Recovery - headache is gone.

153
Q

What is a hemiplegic migraine?

A

Mimic strokes - migraines with unilateral weakness.

154
Q

How do migraines typically present?

A

Unilateral pounding/throbbing headache at moderate to severe intensity.
-Can be bilateral.
-Photophobia, phonophobia, N+V.

155
Q

How are migraines diagnosed?

A

Clinical unless other pathology is suspected.
-Normal neuro exam.

156
Q

What are the acute management of migraines?

A

Paracetamol, aspirin, NSAIDs, triptans.
Triptans (5HT agonists) abort migraines when they start.
If N+V - Use anti-emetics such as metoclopramide.

157
Q

What is migraine prophylaxis?

A

Propranolol, topiramate, amitriptyline.

158
Q

Describe the prognosis of migraines.

A

They tend to get better over time and people go into remission.

159
Q

What are four indicators of secondary headaches?

A

Thunderclap headaches, focal neurological deficit, associated systemic features, patients over 50.

160
Q

What is epilepsy? What is the criteria?

A

Idiopathic cause of seizures. 2 or more episodes more than 24h apart.

161
Q

What are two risk factors for epilepsy?

A

Familial inherited and dementia.

162
Q

What are seizures?

A

Transient episodes of abnormal electrical activity in the brain.

163
Q

What are the causes of seizures?

A

VITAMINDE:
Vascular, infection, trauma, autoimmune, metabolic, idiopathic, neoplasms, dementia/drugs, eclampsia.

164
Q

Describe the pathophysiology of seizures.

A

The normal balance between GABA and glutamate shifts towards glutamate.
-More excitatory with increased glutamate stimulation and increased GABA inhibition.

165
Q

Describe the stages of epileptic seizures.

A

Usually last less than 2 minutes:

-Prodrome - Mood changes, days before.
-Aura - Deja vu and automatisms minutes before.
-Ictal seizure.
-Post-ictal period - Confusion, headache, decreased GCS, dysphasia, sore tongue and Todd’s paralysis.

166
Q

What are the nine types of seizures?

A

Tonic clonic, absence, tonic, clonic, myoclonic, atonic, simple focal, complex focal, status epilepticus.

167
Q

Describe tonic-clonic seizures.

A

Grand mal - tonic (rigidity and fall) and clonic (jerking of limbs).

168
Q

Describe absence seizures.

A

Petit mal - childhood seizures of staring blankly into space. Last up to 15s.

169
Q

Describe myoclonic seizures.

A

Jerking of limbs, only last a few seconds.

170
Q

Describe clonic seizures and tonic seizures.

A

Clonic - Shaking and jerking of limbs (may lose consciousness).
Tonic - Muscles become stiff (may fall).

171
Q

Describe atonic seizures.

A

All muscles relax and you may fall to the ground.

172
Q

Describe simple focal seizures.

A

Remain awake and aware - strange feeling, unusual tastes and smells, tingling, intense emotion, stiffness/twitching in part of body.

173
Q

Describe complex focal seizures.

A

Random body movements - lose awareness and have no memory of it.
-Smacking lips, rubbing hands, noises, moving arms, chewing/swallowing.

174
Q

Describe status epilepticus.

A

Any seizure that lasts for more than 5m, or a seizure back to back or 3 seizures in one hour.

175
Q

What are the investigations of epilepsy/seizures?

A

EEG to show electrical patterns.
MRI to show underlying pathology of brain.
ECG to exclude heart problems.

176
Q

What is the management of epilepsy?

A

Sodium valproate - most forms.
Carbamazepine - focal seizures.
Status epilepticus - benzodiazepines.

177
Q

What is motor neurone disease?

A

Umbrella term that describes neurodegenerative disorders progressively affecting motor neurones but not sensory neurones.

178
Q

What is the most common type of MND?

A

Amyotrophic lateral sclerosis (ALS).

179
Q

What are three less common types of MND?

A

Progressive bulbar palsy, primary lateral sclerosis, progressive muscular atrophy.

180
Q

Describe the pathophysiology of MND.

A

Affects both UMN and LMN causing both UMN and LMN signs.
-The sensory neurones are spared.

181
Q

What are five risk factors for MND?

A

Family history, male, smoking, heavy metals, pesticides.

182
Q

What is a typical MND patient?

A

Older man with affected relative, with mixed UMN and LMN signs.
-No eye signs or sensory signs.

183
Q

What are UMN signs in MND?

A

Increased muscle tone and spasticity, fast reflexes, upgoing plantar responses (Babinski sign).

184
Q

What are LMN signs in MND?

A

Muscle wasting, reduced tone, twitching, reduced reflexes.

185
Q

How is MND diagnosed?

A

Clinical - excluding other conditions.

186
Q

What is the management of MND?

A

No treatments to stop or reverse disease.
-Riluzole slows progression of the disease.
-Break bad news, end of life care.

187
Q

What are three complications of MND?

A

Respiratory failure, aspiration pneumonia, swallowing failure.

188
Q

How do patients with MND usually die?

A

Of pneumonia or respiratory failure.

189
Q

What is myasthenia gravis?

A

Autoimmune condition against neuromuscular junction post synaptic receptors.

190
Q

Who is affected by myasthenia gravis?

A

Affects males and females equally bur at different ages:
-Females at 40.
-Males at 60.

191
Q

What is myasthenia gravis linked to?

A

Thymus gland cancer - thymoma.
-15% of myasthenia gravis have a thymoma.
-30% of patients with a thymoma develop myasthenia gravis.

192
Q

Describe the pathophysiology of myasthenia gravis.

A

Autoantibodies:
85% Anti Ach-R - Bind to post synaptic receptor and inhibits. More binding during exercise so less effective stimulation of muscle with increased activity, improves at rest.
15% Anti MuSK - MuSK helps synthesise Ach-R resulting in decreased Ach-R expression of post-synaptic membrane.

193
Q

How does myasthenia gravis present? What are 6 signs?

A

Muscle weakness that is worse with exertion and better with rest which starts at the the head/neck and progresses to lower body.

-Diplopia, ptosis, myasthenia snarl, fatiguability, swallowing difficulties, slurred speech.

194
Q

What are the investigations for myasthenia gravis?

A

Serology - Anti Ach-R, anti MuSK.
CT/MRI thymus or thymectomy scar.
Edrophonium test - IV edrophonium test.

195
Q

Explain the edrophonium test in myasthenia gravis.

A

Give IV edrophonium (reversible ACHase inhibitor).
-Normally ACHase in nmj breaks down Ach but edrophonium blocks these and stops the breakdown of Ach. Ach levels increase temporarily and relives the weakness.
This confirms a diagnosis of myasthenia gravis.

196
Q

What is the management of myasthenia gravis?

A

1st line - ACHase inhibitors (neostigmine, pyridostigmine).
2nd line - Immunosuppression with steroids.
-Thymectomy.

197
Q

What is a serious complication of myasthenia gravis?

A

Myasthenic crisis - acute symptoms worsening with severe respiratory weakness.

198
Q

How is myasthenic crisis treated?

A

Plasma exchange or IV Ig.
Ventilation.

199
Q

What is giant cell arteritis?

A

Large vessel vasculitis.

200
Q

How does a CNI lesion present?

A

With anosmia (loss of smell).

201
Q

How does a CNII lesion present?

A

Vision loss.

202
Q

How does a CNIII lesion present?

A

Ptosis, down and out eye, fixed dilated pupil.

203
Q

How does a CNIV lesion present?

A

Diplopia looking down.

204
Q

How does a CNVI lesion present?

A

Adducted eye.

205
Q

How does a CNV lesion present?

A

Jaw deviates towards affected side, loss of corneal reflex, trigeminal neuralgia.

206
Q

How does a CNVII lesion present?

A

Facial drop with no forehead sparing.

207
Q

What causes a CNVII lesion?

A

Bell’s palsy, parotid inflammation.

208
Q

How does a CNVIII lesion present and what causes it?

A

Hearing loss and loss of balance.
Due to skull changes and compression.

209
Q

How do both CNIX and CNX lesions present?

A

Impaired gag reflex, swallowing, respiratory and vocal issues.

210
Q

How does a CNXI lesion present?

A

Unable to shrug shoulders.

211
Q

How does a CNXII lesion present?

A

Tongue deviation towards side of lesion.

212
Q

What is peripheral neuropathy?

A

Nerve pathology of the peripheral nerves outside of the CNS.

213
Q

What is carpal tunnel syndrome?

A

Pressure of the median nerve (C6-T1) passing through the carpal tunnel.

214
Q

How does carpal tunnel syndrome present?

A

Gradual onset weakness of grip with an aching hand/forearm, paresthesia of hand and wasting of thenar eminence.

215
Q

How is carpal tunnel syndrome investigated?

A

Phalen test - flexing fist for 1 minute which will cause paresthesia and pain.
Tinel test - tapping wrist causes tingling.
Durkan’s test - Pressing on carpal tunnel for 30s, paresthesia and pain is positive.

216
Q

What is the management of carpal tunnel syndrome?

A

1st line - Splint and pain relief.
2nd line - Corticosteroids.
3rd line - Surgical decompression.

217
Q

Describe the epidemiology of carpal tunnel syndrome.

A

Affects females more than males, affects 5-10% of population.

218
Q

What are six risk factors for carpal tunnel syndrome?

A

Pregnancy, hypothyroidism, RA, obesity, overuse of wrist (tennis, rowing), diabetes.

219
Q

What is radial nerve palsy? How does it present?

A

C5-T1 - Presents with wrist drop.

220
Q

What is ulnar nerve palsy? How does it present?

A

C8-T1 - Presents with claw hand.

221
Q

What is sciatica?

A

Symptoms due to irritation of the sciatic nerve.

222
Q

What causes sciatica?

A

L5/L1 lesion due to spinal causes (disc herniation/prolapse) or non-spinal (tumours, pregnancy).

223
Q

How does sciatica present?

A

Pain from buttock down lateral leg to pinky toe.

224
Q

How is sciatica investigated?

A

Can’t raise leg straight without pain.
Sciatic stretch test - raise legs to point of discomfort, dorsiflex foot, pain = positive.
MRI of spinal cord to investigate intervertebral discs.

225
Q

How is sciatica treated?

A

Analgesia and physiotherapy.
Neurosurgery for disc herniation/prolapse.

226
Q

What are the main causes of peripheral neuropathy?

A

DAVID:
Diabetes, alcoholism, vitamin B12 deficiency, infective/inherited, drugs.

227
Q

Where does the spinal cord run from?

A

C1-L1.

228
Q

How does spinal cord compression present?

A

Spastic paraparesis, radicular pain at level of compression and sensory loss below level of compression.

229
Q

What are four causes of spinal cord compression?

A

TB, degenerative disc and vertebral lesions, vertebral neoplasms.

230
Q

What are the investigations and management of spinal cord compression?

A

Spinal cord MRI/CT.
-Neurosurgery.

231
Q

What is cauda equina syndrome?

A

Compression below the conus medullaris (L1 - End of spinal cord).

232
Q

What causes cauda equina syndrome?

A

Commonly lumbar disc herniation.

233
Q

How does cauda equina syndrome present?

A

Leg weakness with LMN signs, saddle anaesthesia and bowel/bladder dysfunction.

234
Q

What is Charcot-Marie-Tooth syndrome?

A

Usually an autosomal dominant inherited disease that affects the peripheral motor and sensory nerves, which cases dysfunction in myelin or axons.

235
Q

How does Charcot-Marie-Tooth syndrome usually present?

A

Pes cavus (high arched feet), distal muscle wasting (inverted champagne bottle legs), weakness in lower legs (loss of ankle dorsiflexion).
Other - hand weakness, reduced tendon reflexes, reduced muscle tone, peripheral sensory loss.

236
Q

What is shingles?

A

Reactivation of VZV virus after chickenpox. Peripheral nerves attacked via sensory dorsal root.

237
Q

How does shingles present and how is it treated?

A

Painful rash confined to a dermatome.
Treated with oral aciclovir.

238
Q

What is Duchenne muscular dystrophy?

A

X-linked recessive mutated dystrophin gene - affects only boys where muscles are replaced with adipose tissue.

239
Q

What is Lambert Eaton syndrome?

A

Disease with similar features to myasthenia gravis - causes progressive muscle weakness with increased use as a result of damage to nmj.

240
Q

Who does Lambert Eaton syndrome occur in?

A

Typically in those with SCLC - antibodies against calcium channels in SCLC which also target calcium channels in presynaptic terminals in nmj’s - no Ach released.

241
Q

Are primary or secondary brain tumours more common?

A

Secondary brain tumours are much more common than primary.

242
Q

Which five cancers most commonly spread to the brain?

A

Lung (SCLC, NSCLC), breast, melanoma, kidney, gastric.

243
Q

What are four types of primary brain tumour?

A

Astrocytoma, oligodendrocytoma, meningioma, schwannoma.

244
Q

How are astrocytomas graded?

A

From 1-4.
1 being benign and 4 is glioblastoma.

245
Q

How do brain tumours present?

A

Increased ICP, focal neurology, headache, seizures, weight loss and lethargy.

246
Q

How are brain tumours investigated and managed?

A

MRI/CT of head.
-Surgery, chemo, radio and steroids.

247
Q

What is syncope?

A

Term used to describe the event of temporarily losing consciousness due to disruption of blood flow to the brain often leading to a fall.

248
Q

What are four causes of primary syncope?

A

Dehydration, hunger, extended standing in warm environment, vasovagal response to stimuli (blood, pain).

249
Q

What are secondary causes of syncope?

A

Hypoglycaemia, anaemia, infection, anaphylaxis, arrhythmias, heart disease.

250
Q

How does syncope present?

A

Hot/clammy, sweaty, heavy, dizzy/lightheaded, vision going blurry/dark, headache.

251
Q

What investigations are used for syncope?

A

ECG for arrhythmia (24h if paroxysmal suspected), ECHO for suspected structural heart disease.
Bloods - FBC, U+E and glucose (anaemia, arrhythmias, diabetes).

252
Q

How is syncope managed?

A

Avoid triggers in primary, management of underlying pathology.

253
Q

Which brain haemorrhagic events are strokes and which ones aren’t?

A

Intracerebral haemorrhage and subarachnoid haemorrhage - STROKES.
Subdural and extradural haematomas - NOT STROKES.

254
Q

How does an ischaemic stroke affecting the ACA present?

A

Contralateral weakness and sensory loss of lower limb.

255
Q

How does an ischaemic stroke affecting the MCA present?

A

Contralateral motor weakness and sensory loss.
Speech issues due to Wernicke’s and Broca’s areas being affected.

256
Q

How do different intercranial bleeds appear on CT scans?

A

Extradural - Bi-convex shape (lemon).
Subdural - Crescent shape (banana).
Subarachnoid - Star shaped lesion.

257
Q

What are the three main types of seizures?

A

Primary generalised.
Partial focal.
Partial seizure with secondary generlisation.

258
Q

Compare generalised and focal seizures.

A

Generalised - Bilateral, affects all brain.
Focal - Confined to one region.

259
Q

How do focal temporal seizures present?

A

Dysphasia, memory and emotion is affected.

260
Q

How do focal frontal seizures present?

A

Motor disturbances, Todd’s palsy (temporary paralysis), Jacksonian march (tingling/twitching in an area of the body that gets larger).

261
Q

How do focal parietal seizures present?

A

Paresthesia.

262
Q

How do focal occipital seizures present?

A

Visual phenomena - spots, lines, flashes.

263
Q

What medication is used when sodium valproate is contraindicated?

A

Lamotrigine.

264
Q

What is the first line treatment for trigeminal neuralgia?

A

Carbamazepine.

265
Q

When is lamotrigine used instead of sodium valproate?

A

Children and pregnant women.

Phase 2a (15 decks)

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