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Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is stroke also called?

A

Cerebrovasculat accident (CVA)

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2
Q

Label the following:

A
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3
Q

What causes CVAs?

A

Ischaemia / infarction = inadequate blood supply

Intracranial haemorrhage

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4
Q

What can distrupt blood to the brain?

A

Thrombus formation / embolus e.g. in patients with AF

Atherosclerosis

Shock

Vasculitis

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5
Q

What is a TIA?

A

Transient ischaemic attack

Fomerly symptoms of stroke which resolved in 24 hours

Updated definition = transient neurological dysfunction secondary to ischaemia without infarction

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6
Q

What does a TIA often precede?

A

Full stroke (crescendo TIA = 2 or more per week)

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7
Q

What are the symptoms of a stroke?

A

Sudden:

  • Limb weakness
  • Facial weakness
  • Dysphagia (speech disturbance)
  • Visual or sensory loss
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8
Q

What are the risk factors of a stroke?

A

CVD e.g. angina, myocardial infarction, PVD

Previous stroke or TIA

Atrial fibrillation

Carotid artery disease

HTN

Diabetes

Smoking

Vasculitis

Thrombophilia

COCP

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9
Q

What is the FAST tool for identifying stroke in the community?

A

Face

Arm

Speech

Time (call 999)

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10
Q

What is the ROSIER tool?

A

Clinical scoring tool based on clinical features and duration (stroke is likely if anything above 0)

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11
Q

What is the management of a patient with a stroke?

A

Admit to specialist stroke centre

Exclude hypoglycaemia

Immediate CT brain to exclude primary intracerebral haemorrhage

Aspirin 300mg stat (after CT) continued for 2 weeks

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12
Q

How should thrombolysis be performed (after CT brain has excluded intracranial haemorrhage)

A

Alteplase (a tissue plasminogen activator) that rapidly breaks down clots and can reverse the effect of the stroke (given within a defined window of opportunity e.g. 4.5 hours)

Need monitoring for post thrombolysis complication e.g. intracranial / systemic haemorrhage (repeated CT scans of brain)

Thrombectomy (not used after 24 hours since onset of symptoms)

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13
Q

Why should blood pressure not be lowered during a stroke?

A

Risks reducing perfusion to the brain

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14
Q

What is the management of TIA?

A

Aspirin 300mg daily

Secondary prevention measures for CVD

Referred and seen within 24 hours by stroke specialist

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15
Q

What specialist imaging can be use to find area affected by stroke?

A

Diffusion-weighted MRI - gold standard technique (CT = alternative)

Carotid ultrasound (assess for carotid stenosis)

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16
Q

What is the treatment for carotid stenosis?

A

Endarterectomy (to remove plaque or carotid stenting)

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17
Q

What treatment is given for secondary prevention of stroke?

A

Clopidogrel 75mg once daily (alternatively dipyridamole 200mg twice daily)

Atorvastatin 80mg (started by not immediately)

Carotid endarterectomy or stenting in patients with carotid artery disease

Treat modifiable risk factors e.g. HTN and diabetes

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18
Q

Who is involved in stroke rehabilitation?

A

Nurses

Speech and language (SALT)

Nutrition and dietetics

Physiotherapy

Occupational therapy

Social services

Optometry and opthalmology

Psychology

Orthotics

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19
Q

What percentage of strokes are caused by intracranial bleeds?

A

10-20%

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20
Q

Label the following:

A
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21
Q

What are some risk factors for intracranial bleeds?

A

Head injury

Hypertension

Aneurysms

Ischaemic stroke can progress to haemorrhage

Brain tumours

Anticoagulants e.g. warfarin

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22
Q

How do intracranial bleeds present?

A

Seizures

Weakness

Vomiting

Reduced consciousness

Other sudden onset neurological symptoms

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23
Q

How to calculate the glasgow coma score?

A

Eyes

  • Spontaneous = 4
  • Speech = 3
  • Pain = 2
  • None = 1

Verbal response

  • Orientated = 5
  • Confused conversation = 4
  • Inappropriate words = 3
  • Incomprehensible sounds = 2
  • None = 1

Motor response

  • Obeys commands = 6
  • Localises pain = 5
  • Normal flexion = 4
  • Abnormal flexion = 3
  • Extends = 2
  • None = 1
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24
Q

What glasgow score indicates that airways need securing?

A

8/15 or below

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25
Q

What is a subdural haemorrhage caused by?

A

Rupture of the bridging veins in the outermost meningeal layer (in between dura mater and arachnoid mater)

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26
Q

How do subdural haemorrhages appear on a CT scan?

A

Crescent shape and not limited by cranial sutures

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27
Q

Who do subdural haemorrhages occur more often in?

A

Elderly or alcoholic patients (have more atrophy in brains making rupture of vessels more likely)

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28
Q

What are extradural haemorrhages usually caused by?

A

Rupture of the middle meningeal artery in the temporo-parietal region (can be associated with fracture of the temporal bone)

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29
Q

Where does an extradural haemorrhage occur?

A

Between skull and dura mater

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30
Q

How does an extradural haemorrhage appear on a CT scan?

A

Bi-convex shape and limited by the cranial sutures

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31
Q

What is the typical history of a patient with extradural haemorrhage?

A

Young patient with traumatic head injury with ongoing headache (period of improvement in symptoms followed by rapid decline as haematoma compresses intracranial contents)

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32
Q

Where can intracerebral haemorrhages occur?

A

Lobar intracerebral haemorrhage

Deep intracerebral haemorrhage

Intraventricular haemorrhage

Basal ganglia haemorrhage

Cerebellar haemorrhage

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33
Q

How does an intracerebral haemorrhage present?

A

Similarly to a stroke (occur spontaneously / bleeding into ischaemic infarct / tumour / rupture of aneurysm)

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34
Q

Where is the bleeding in subarachnoid haemorrhage?

A

Into subarachnoid space where CSF is located (between pia mater and the arachnoid membrane)

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35
Q

What normally causes a subarachnoid haemorrhage?

A

Cerebral aneurysm

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36
Q

What is the typical history of a subarachnoid haemorrhage?

A

Occurs during strenuous activity e.g. weight lifting / sex (occuring so suddenly it’s known as a thunderclap headache)

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37
Q

What are subarachnoid haemorrhages associated with?

A

Cocaine and sickle cell anaemia

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38
Q

What is the management of intracranial bleeds?

A

Immediate CT head

Check FBC and clotting

Admit to specialist stroke unit

Discuss surgery with neurosurgical centre

Consider intubation and ventilation

Correct any clotting abnormalities

Correct severe hypertension but avoid hypotension

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39
Q

What is a subarachnoid haemorrhage usually the result of?

A

Ruptured cerebral aneurysm

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40
Q

Are subarachnoid haemorrhages dangerous?

A

Very high mortality and morbidity

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41
Q

What are the features of a subarachnoid haemorrhage?

A

Thunderclap headache

Neck stiffness

Photophobia

Vision changes

Neuro symptoms e.g. speech changes, weakness, seizures and loss of consciousness

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42
Q

What are some risk factors for subarachnoid haemorrhages?

A

Hypertension

Smoking

Excessive alcohol consumption

Cocaine use

FH

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43
Q

Who is subarachnoid haemorrhage most common in?

A

Black patients

Female patients

Age 45 - 70

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44
Q

What conditions are subarachnoid haemorrhages associated with?

A

Sickle cell anaemia

Connective tissue disorders (e.g. Marfan or Ehlers-Danlos)

Neurofibromatosis

ADPKD

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45
Q

What is the first line investigation for subarachnoid haemorrhage?

A

CT head (blood causes hyperattenuation in the subarachnoid space)

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46
Q

What further investigations are there for subarachnoid haemorrhage?

A

Lumbar puncture to collect sample of CSF if CT head is negative:

  • Red cell count will be raised (if RCC is decreasing in number over samples, could be due to traumatic lumbar puncture)
  • Xanthochromia (yellow colour of CSF caused by bilirubin)

Angiography (CT / MRI) can be used once subarachnoid haemorrhage is confirmed to locate bleeding

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47
Q

What is the managament of a subarachnoid haemorrhage?

A

In a specialist neurosurgical unit

  • Reduced consciousness = intubation and ventilation
  • Surgical intervention to treat aneurysms (coiling - inserting catheter into arterial system “endovascular approach”, alternative is clipping - cranial surgery and clipping aneurysm to seal it)
  • Nimodipine - CCB to prevent vasospasm (common complication that can result in brain ischaemia)
  • Lumbar puncture or insertion of a shunt may be required to treat hydrocephalus
  • Antiepileptic medication can be used for seizures
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48
Q

What is multiple sclerosis?

A

Chronic and progressive condition

Involves demyelination of the myelinated neurones in the central nervous system caused by inflammatory process involving the activation of the immune cells against the myelin

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49
Q

When does MS present?

A

Younger adults (under 50) - more common in women - symptoms improve in pregnancy and in postpartum period

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50
Q

What is myelin and where does it come from?

A

Myelin covers axons of neurones in the CNS - helps electrical impulses move faster along the axon

Myelin is provided by cells that wrap around axons:

  • Schwann cells in peripheral nervous system
  • Oligodendrocytes in central nervous system
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51
Q

Where does MS typically affect?

A

Central nervous system (oligodendrocytes) - affects way electrical signals travel along nerve

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52
Q

Why do symptoms resolve in early disease of MS?

A

Re-myelination can occur (in later stages re-myelination is incomplete and symptoms become more permanent)

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53
Q

How do MS lesions change?

A

Disseminated in time and space

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54
Q

What are the causes of MS?

A

Multiple genes

EBV

Low vitamin D

Smoking

Obesity

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55
Q

What are the signs and symptoms of MS?

A

Optic neuritis

Eve movement abnormalities

Focal weakness

Focal sensory symptoms

Ataxia

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56
Q

How does optic neuritis present?

A

Unilateral reduced vision

Central scotoma (enlarged blind spot)

Pain on eye movement

Impaired colour vision

Relative afferent pupullary defect

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57
Q

What are the causes other than MS of optic neuritis?

A

Sarcoidosis

SLE

Diabetes

Syphilis

Measles

Mumps

Lyme disease

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58
Q

What is the management of patients presenting with acute loss of vision?

A

Seen by opthalmologist

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59
Q

What is the treatment of optic neuritis?

A

Steroids and recovery takes 2-6 weeks (changes on MRI can help predict which patients will go on to develop MS)

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60
Q

Why may patients with MS present with double vision?

A

Lesion in sixth cranial nerve (abducens)

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61
Q

What do unilateral lesions in the sixth nerve cause?

A

Internuclear ophthalmoplegia

Internuclear = never fibres which connect between cranial nerve nuclei that controls eye movements (3rd, 4th and 6th cranial nerve nuclei) - these nerve fibres coordinate eye movements

Ophthalmoplegia = problems with muscles around eyes

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62
Q

What issues with gaze does a lesion in 6th cranial nerve cause?

A

Conjugate lateral gaze disorder

Conjugate = connected

Lateral gaze = both eyes move together to look laterally to left or right

When looking laterally in direction of affected eye, the affected eye will not move

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63
Q

What focal weakness does MS cause?

A

Bells palsy

Horners syndrome

Limb paralysis

Incontinence

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64
Q

What focal sensory symptoms does MS cause?

A

Trigeminal neuralgia

Numbness

Paraesthesia (pins and needles)

Lhermitte’s sign - electric shock sensation travels down spine and into limbs when flexing neck - indicates disease in the cervical spinal cord in the dorsal column - caused by stretching the demyelinated dorsal column

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65
Q

What are the different forms of ataxia (problems with coordinated movement)?

A

Sensory = loss of proprioceptive sense (ability to sense position of the joint - causes positive Romberg’s test and can cause pseusoathetosis)

Cerebellar = problems with cerebellum coordinating movement (suggests cerebellar lesions)

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66
Q

What is the disease course of MS?

A

Highly variable, some relapsing-remitting for life whereas others are primary progressive

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67
Q

Can a diagnosis of MS be made from a clinically isolated syndrome?

A

Not one one episode - must be disseminated in time and space - may never have another episode / develop MS (if lesions are seen then more likely to develop)

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68
Q

What is secondary progressive MS?

A

Disease was relapsing-remitting but now progressive worsening of symptoms with incomplete remission

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69
Q

How is a diagnosis of MS made?

A

By neurologist based on clinical picture and symptoms (symptoms have to be progressive for a period of 1 year to diagnose primary progressive MS)

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70
Q

What investigations can support a diagnosis of MS?

A

MRI scans can demonstrate typical lesions

Lumbar puncture can detect “oligoclonal bands” in the CSF

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71
Q

Who is involved in MS MDT?

A

Neurologists

Specialist nurses

Physiotherapy

Occupational therapy

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72
Q

What is the treatment of MS?

A

Disease modifying drugs and biologic therapy (aim of treatment is to induce long term remission with no evidence of disease activity)

Drugs target interleukins, cytokines and various immune cells

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73
Q

How are relapses of MS treated?

A

Steroids - methylprednisolone

500mg orally daily for 5 days (1g IV for 3-5 days where oral treatment has failed / relapses are severe)

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74
Q

How to treat symptoms in MS?

A

Exercise to maintain activity and strength

Neuropathic pain managed with meds e.g. amitriptyline or gabapentin

Depression - SSRIs

Urge incontinence - anticholinergic medications e.g. tolterodine or oxybutynin (can worsen cognitive impairment)

Spacsticity can be managed with baclofen, gabapentin and physio

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75
Q

What is motor neurone disease (MND)?

A

Umbrella term for diagnoses of progressive, fatal condition where motor neurones stop functioning

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76
Q

Name some common MNDs?

A

Amylotropic lateral sclerosis (AML) - stephen hawking had this

Progressive bulbar palsy - primarly affects talking and swallowing muscles

Progressive muscular atrophy

Primary lateral sclerosis

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77
Q

What are the risk factors for MND?

A

Genetic component (take good FH)

Smoking, exposure to heavy metals and certain pesticides also increase the risk

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78
Q

Which neurones are affected in MND?

A

Upper and lower motor

Sensory neurones are spared

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79
Q

How does MND present?

A

Late, middle aged man possibly with affected relative

Insidious, progressive weakness of muscles affecting limbs (upper first), trunk, face and speech

Increased fatigue when exercising

Clumsiness, dropping things, falling over

Dysarthria (slurred speech)

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80
Q

What are signs of lower motor neurone disease?

A

Muscle wasting

Reduced tone

Fasciculations (twitching in muscles)

Reduced reflexes

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81
Q

What are some signs of upper motor neurone disease?

A

Increased tone or spasticity

Brisk relexes

Upgoing plantar responses

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82
Q

How is MND diagnosed?

A

Clinical presentation (excluding other conditions)

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83
Q

What is the management of MND?

A

No effective treatment for halting / reversing disease

Riluzole - slows progression of disease and extends survival by a few months in AML (licensed in UK and initiated by specialist)

Edaravone (used in US but not UK, potential to slow disease)

Non-invasive ventilation (NIV) used at home to support breathing at night

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84
Q

What else form part of the management plan for MND?

A

Effectively breaking bad news

Involving MDT in supporting and maintaining quality of life

Advanced directives to document patients wishes as disease progresses

End of life care planning

Patients usually die of resp failure or pneumonia

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85
Q

What is Parkinson’s disease?

A

Disease of progressive reduction of dopamine in the basal ganglia of brain leading to disorders of movement (classically asymmetrical)

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86
Q

What is the classic triad of features in Parkinson’s disease?

A

Resting tremor (not needed for diagnosis)

Rigidity

Bradykinesia

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87
Q

What is the basal ganglia?

A

Group of structures in the middle of the brain responsible for coordinating habitual movements e.g. walking, looking around, learning movement patterns

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88
Q

What part of the basal ganglia produces dopamine (essential for its functioning)?

A

Substantia nigra

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89
Q

At what age do patients with parkinson present?

A

Older (around 70)

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90
Q

Describe the unilateral tremor in Parkinsons?

A

Frequency of 4-6 Hz (occurs 4-6 times a second - pill rolling tremor)

More pronounced when resting or if distracted (ask pt to mime painting a fence with the other hand)

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91
Q

Describe the cogwheel rigidity in Parkinsons?

A

Rigidity = resistance to passive movement of a joint (flex and extend arm at elbow = tension that gives way in small increments - cogwheel)

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92
Q

How does bradykinesia present in Parkinson’s?

A

Handwriting gets smaller

Small steps (shuffling gait)

Difficulty initiating movement (e.g. from standing still to walking)

Difficulty in turning around when standing (take lots of little steps)

Reduced facial movements / expressions (hypomimia)

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93
Q

What are the other features affecting patients with Parkinsons?

A

Depression

Sleep disturbance and insomnia

Loss of sense of smell (anosmia)

Postural instability

Cognitive impairment / memory problems

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94
Q

How to distinguish a benign essential tremor from a Parkinson’s tremor?

A

Parkinson’s = asymmetrical, 4-6 hertz, worse at rest, improves with intentional movement, no change with alcohol

Benign = symmetrical 5-8 hertz, improves at rest, worse with intentional movement, improves with alcohol

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95
Q

What is multiple system atrophy?

A

Neurones of multiple systems in brain degenerate affecting the basal ganglia as well as multiple other areas causing parkinson’s presentation as well as autonomic dysfunction (postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia)

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96
Q

What is dementia with lewy bodies?

A

Type of demential associated with features of Parkinsonism causing progressive cognitive decline (associated symptoms = visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness)

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97
Q

What are the other parkinson’s plus syndromes?

A
  • Progressive supranuclear palsy
  • Corticobasal degeneration
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98
Q

How should Parkinson’s be diagnosed?

A

Clinically based on symptoms and examination by specialist

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99
Q

When do patients with Parkinson’s describe themselves as “on”?

A

Medications are acting and moving freely (“off” when medications wear out)

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100
Q

What medications are given for Parkinson’s?

A

Levodopa

COMT inhibitor

Dopamine agonist

Monoamine oxidase-B inhibitor

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101
Q

What is Levodopa? What is it usually given with?

A

Synthetic dopamine (given orally)

Drug to stop levodopa being broken down in body before it enters the brain (peripheral decarboxylase inhibitors e.g. carbidopa and benserazide)

Co-benyldopa (levodopa and benserazide)

Co-careldopa (levodopa and carbidopa)

Levodopa is most effective treamtnet but becomes less over time - often reserved for when other treatments are not managing symptoms

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102
Q

What is the main side effect of dopamine?

A

Dose is too high = dyskinesias (abnormal movements associated with excessive motor activity):

  • Dystonia (excessive contraction = abnormal posture / exaggerated movement)
  • Chorea (abnormal involuntary movements can be jerking and random)
  • Athetosis (involuntary twisting / writing usually in fingers, hands or feet)
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103
Q

What are COMT inhibitors?

Give an example?

How do they work?

A

Inhibit catechol-o-methyltransferase (COMT) - this enzyme metabolises levodopa in both the brain and body

Taken with levodopa and decarboxylase inhibitor to slow breakdown of levodopa

Entacapone

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104
Q

How do dopamine agonists work?

What is a side effect?

Give some examples?

A

Mimic dopamine in the basal ganglia and stimulate the dopamine receptors (less effective than levodopa - used to delay levadopas use, then used in combination)

Pulmonary fibrosis

  • Bromocryptine
  • Pergolide
  • Carbergoline
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105
Q

How do monoamine oxidase-B inhibitors work?

A

Monoamine oxidase enzymes break down neurotransmitters e.g. dopamine, serotonin and adrenaline (monoamine oxidase-B enzyme is more specific to dopamine)

Used to delay the use of levodopa and then in combination with levodopa to reduce required dose

  • Selegiline
  • Rasagiline
106
Q

What is benign essential tremor?

A

Common condition associated with older age - characterised by a fine tremor affecting all voluntary muscles (most noticable in hands, can also affect head, jaw and voice)

107
Q

What are the features of a benign essential tremor?

A

Fine tremor

Symmetrical

More prominent on voluntary side

Worse when tires, stressed or after caffeine

Improved by alcohol

Absent during sleep

108
Q

What are the other causes of a tremor?

A

Parkinson’s

MS

Huntington’s Chorea

Hyperthyroidism

Fever

Medications (e.g. antipsychotics)

109
Q

What medications can be tried to improve symptoms of benign essential tremor?

A

Propanolol (non-selective beta blocker)

Primidone (barbiturate anti-epileptic medication)

110
Q

What is epilepsy?

A

Umbrella term for condition where tendency towards seizures (transient episodes of abnormal electrical acitivity in the brain)

111
Q

What investigations are there for epilepsy?

A

Electroencephalogram (EEG) can show typical patterns

MRI brain to diagnose structural problems that may be associated with seizures

ECG can be used to exclude problems with the heart

112
Q

What are generalised tonic-clonic seizures?

A

Loss of consciousness and tonic (muscle tensing - typically comes first) and clonic (muscle jerking) episodes

Associated with:

  • Tongue biting
  • Incontinence
  • Groaning
  • Irregular breathing
113
Q

What happens after a tonic-clonic seizure?

A

Prolonged post-ictal phase (confused, drowsy and feels irritable or depressed)

114
Q

What is the management of tonic-clonic seizures?

A

First line: sodium valporate

Second line: lamotrigine or carbamazepine

115
Q

What are focal seizures? How do they present?

A

Seizure starts in temporal lobe affecting hearing, speech, memory and emotions

  • Hallucinations
  • Memory flashbacks
  • Deja vu
  • Doing strange things on autopilot
116
Q

What is the treatment of focal seizures?

A

Reverse of tonic-clonic:

  • First line: carbamazepine or lamotrigine
  • Second line: sodium valporate or levetiracetam
117
Q

What are absence seizures?

What is the treatment of absence seizures?

A

Typically happen in children - patient becomes blank, stares into space and then abruptly returns to normal (last 10-20 seconds) most patients stop having seizures as get older

First line = sodium valporate or ethosuximide

118
Q

What are atonic seizures?

What may they be suggestive of?

What is the treatment of atonic seizures?

A

Aka “drop attacks” - brief lapses in muscle tone (lasting no longer than 3 minutes - begin in childhood)

May indicate Lennox-Gastaut syndrome

First line = sodium valporate

Second line = lamotrigine

119
Q

What are myoclonic seizures?

What is the treatment?

A

Sudden brief muscle contraction like a “jump” - patient usually remains awake - can occur in any epilepsy but typically occur in juvenile myoclonic epilepsy

First line = sodium valporate

Second line = lamotrigine, levetiracetam or topiramate

120
Q

What are infantile spasms?

What are they also known as?

A

Rare disorder starting at 6 months- characterised byclustersoffull body spasms, poor prognosis:

1/3 die by age 25, 1/3 are seizure free

Also known as West syndrome

Treatment = prednisolone, vigabatrin

121
Q

How does sodium valporate work?

A

Increases activity of GABA (has a relaxing effect on the brain) used first line in most epilepsy (except focal seizures)

Side effects:

  • Teratogenic - need contraception (must be avoided in girls / women unless no suitable alternative)
  • Liver damage and hepatitis
  • Hair loss
  • Tremor
122
Q

What medication is first line for focal seizures? What are some side effects?

A

Carbamazepine

  • Agranulocytosis
  • Aplastic anaemia
  • Induces the P450 system so many drug interactions
123
Q

What are some notable side effects of phenytoin?

A

Folate and vitamin D deficiency

Megaloblastic anaemia (folate deficiency)

Osteomalacia (vitamin D deficiency)

124
Q

What are some notable side effects of ethosuzimide?

A

Night terrors

Rashes

125
Q

What are some notable side effects of lamotrigine?

A

Stevens-Johnson syndrome

DRESS syndrome (life threatening rashes)

Leukopenia

126
Q

What is statis epilepticus?

A

Seizure lasting more than 5 minutes

More than 3 seizures in one hour

127
Q

What is the management of status epileptics in the hospital?

A

ABCDE approach

Secure airway

Give high-concentration oxygen

Assess cardiac and respiratory function

Check blood glucose levels

IV access

IV lorazepam 4mg, repeated after 10 minutes if seizure continues

If seizures persist: IV phenobarbital or phenytoin

128
Q

What are some medical options for status epilepticus in the community?

A

Buccal midazolam

Rectal diazepam

129
Q

What is neuropathic pain?

A

Abnormal functioning of sensory nerves delivering abnormal painful signals to the brain

130
Q

What can cause neuropathic pain?

A

Postherpetic neuralgia from shingles is in the distribution of a dermatome and usually on the trunk

Nerve damage from surgery

Multiple sclerosis

Diabetic neuralgia (on feet)

Trigeminal neuralgia

Complex regional pain syndrome (CRPS)

131
Q

What are the features of neuropathic pain?

A

Burning

Tingling

Pins and needles

Electric shock

Loss of sensation to touch of affected area

132
Q

What questionnaire is used to assess neuropathic pain?

A

DN4 questionnaire (scored out of 10 for pain)

4 or more indicates neuropathic pain

133
Q

What are the four first line treatments for neuropathic pain?

A

Amitriptyline - TCA

Duloxetine - SNRI

Gabapentin is an anticonvulsant

Pregabalin is an anticonvulsant

134
Q

What are the other options for neuropathic pain?

A

Tramadol only as rescue for flares

Capsaicin cream (chilli pepper cream) for localised areas of pain

Physiotherapy to maintain strength

Psychological input to help with understanding and coping

135
Q

What medication is used first line for trigeminal neuralgia?

A

Carbamazepine (if doesnt work then referral to specialist)

136
Q

What is complex regional pain syndrome?

A

Abnormal nerve functioning can cause neuropathic pain and abnormal sensations - usually isolated to one limb often triggered by injury to the area

Area can be become hypersensitive even to wearing clothing (intermittently swells, changes colour, temperature, flushes with blood and sweat abnormally)

Treatment guided by pain specialist

137
Q

Where does the facial nerve exit the brainstem? What does it pass through?

A

Exits at cerebellopontine angle passing through temporal bone and parotid gland

138
Q

What are the five branches of the facial nerve?

A

Temporal

Zygomatic

Buccal

Marginal mandibular

Cervical

139
Q

What are the motor, sensory and parasympathetic functions of the facial nerve?

A

Motor: muscles of facial expression, stapedius in middle ear, posterior digastric, stylohyoid and platysma muscles in the neck

Sensory: taste from anterior 2/3 of tongue

Parasympathetic: supplt to submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production)

140
Q

What is the management of upper motor neurone facial nerve palsy vs lower?

A

Upper = referred urgently with a suspected stroke

Lower = reassured and managed in community

141
Q

How to distinguish between upper motor neurone lesion and lower motor neurone lesion?

A

Each side of the forehead has upper motor neurone innervation by both sides of the brain but only lower motor neurone innervation from one side of the brain

  • UMNL = forehead spared
  • LMNL = forehead not spared
142
Q

How does a lower motor neurone facial palsy present?

A

Forehead affected

Drooping of eyelid, exposing of eye

Loss of nasolabial fold

143
Q

What causes a unilateral upper motor lesion?

A

CVA (stroke)

Tumour

144
Q

What may cause bilateral motor neurone lesion (rare)?

A

Pseudobulbar palsy

MND

145
Q

What causes bell’s palsy?

A

Common idiopathic condition causing unilateral lower motor neurone facial nerve palsy (majority of patients recover over several weeks but some recovery may take up to 12 months)

146
Q

What treatment is recommended for Bell’s palsy?

A

Prednisolone:

  • 50mg for 10 days
  • 60mg for 5 days followed by 5 day regime of reducing 10mg a day

(antiviral PLUS steroid MAY offer small benefit)

147
Q

What additional managament is there for Bell’s palsy?

A

Lubricating eye drops to prevent eye on affected side drying out

If eye pain = ophthalmology review for exposure keratopathy

Tape can be used to keep eye shut at night

148
Q

What is Ramsay-Hunt syndrome and how does it present?

A

Caused by herpes zoster virus - presents as unilateral lower motor neurone facial palsy

  • Painful and tender vesicular rash in the ear canal, pinna and around the ear
  • Rash can extend to anterior 2/3 of the tongue and hard palate
149
Q

What is the treatment of Ramsay-Hunt syndrome?

A

Prednisolone

Aciclovir

May also require lubricating eye drops

150
Q

What are some other causes of lower motor neurone facial palsy?

A

Infection: otitis media, malignant otitis externa, HIV, lyme’s disease

Systemic disease: diabetes, sarcoidosis, leukaemia, MS, Guillain-Barre syndrome

Tumours: acoustic neuroma, parotid tumours, cholesteatomas

Trauma: direct nerve damage, damage during surgery, base of skull fractures

151
Q

Give an example of a benign brain tumour and a highly malignant?

A

Benign = meningioma

Highly malignant = glioblastoma

152
Q

How do brain tumours present?

A

Focal neurological symptoms depending on location of lesion (e.g. frontal lobe personality changes)

Raised intracranial pressure symptoms

153
Q

What causes raised intracranial pressure?

A

Brain tumours

Intracranial haemorrhage

Idiopathic intracranial hypertension

Abscesses or infection

154
Q

How does the headache of raised intracranial pressure present?

A

Constant

Nocturnal

Worse on waking

Worse on coughing, straining or bending forwards

Vomiting

155
Q

What are the other presenting features of raised intracranial pressure?

A

Altered mental state

Visual field defects

Seizures (particularly focal)

Unilateral ptosis

Third and sixth nerve palsies

Papilloedema (on fundoscopy)

156
Q

What is papilloedema?

A

Swelling of the optic disc secondary to raised intracranial pressure (papill = small rounded raised area)

Sheath around optic nerve is connected with subarachnoid space - CSF under high pressure can flow into optic nerve sheath increasing pressure around optic nerve

Can be seen on fundoscopy

157
Q

What are the fundoscopic changes in papilloedema?

A

Blurring of optic disc margin

Elevated optic disc (look at way retinal vessels flow across disc)

Loss of venous pulsation

Engorged retinal veins

Haemorrhages around optic disc

Paton’s lines = creases in retina around optic disc

158
Q

Which cancers commonly metastasis to the brain?

A

Lung

Breast

RCC

Melanoma

159
Q

What are gliomas? Give 3 examples (from most - least malignant)

A

Tumours of the glial cells in the brain or spinal cord

  • Astrocytoma (glioblastoma multiforme is most common)
  • Oligodendroglioma
  • Ependymoma
160
Q

How are gliomas graded?

A

1-4 (1 = most benign, 4 = most malignant)

161
Q

What are meningiomas?

A

Tumours growing from cells of the meninges in the brain and spinal cord - usually benign (take up space and mass effect leads to raised intracranial pressure and neuro symptoms)

162
Q

How may a pituitary tumour present if it grows large enough?

A

Presses on optic chiasm causing a bitemporal hemianopia (loss of outer half of visual fields)

163
Q

How else may pituitary tumours present?

A

Hypopituitarism or excess hormone release:

  • Acromegaly
  • Hyperprolactinaemia
  • Cushing’s disease
  • Thyrotoxicosis
164
Q

What are acoustic neuromas? AKA vestibular schwannomas?

A

Tumours of the Schwann cells surrounding auditory nerve that innervates the inner ear

Occur around the “cerebellopontine angle” (aka cerebellopontine angle tumours)

Slow growing

Usually unilateral (bilateral acoustic neuromas are associated with neurofibromatosis type 2

165
Q

What are the classic symptoms of an acoustic neuroma?

A

Hearing loss

Tinnitus

Balance problems

(also associated with facial nerve palsy)

166
Q

What are the management options for brain tumours?

A

Palliative care

Chemo

Radiotherapy

Surgery

167
Q

How are pituitary tumours treated?

A

Trans-sphenoidal surgery

RT

Bronocriptine to block prolactin-secreting tumours

Somatostatin analogues (e.g. ocreotide) to block growth hormone-secreting tumours

168
Q

What is Huntington’s chorea?

A

Autosomal dominant genetic condition which causes a progressive deterioration in the nervous system (usually asymptomatic until symptoms begin aged 30-50)

169
Q

What is the genetic mutation in Huntington’s chorea?

A

‘trinucleotide repeat disorder involving a genetic mutation in the HTT gene on chromosome 4

170
Q

Huntington’s chorea displays ‘anticipation’, what is this?

A

Feature of trinucleotide repeat disorder where successive generations have more repeats in the gene causing earlier age of onset and increased severity of disease

171
Q

How does Huntington’s chorea present?

A

Begins with cognitive, psychiatric or mood problems followed by:

  • Chorea (involuntary, abnormal movements)
  • Eye movement disorders
  • Speech difficulties (dysarthria)
  • Swallowing difficulties (dysphagia)
172
Q

How is Huntington’s chorea diagnosed?

A

Genetic testing for the faulty gene (pre-test and post-test counselling regarding implications for result)

173
Q

What is the management of Huntington’s chorea?

A

No treatment options for slowing / stopping progression

  • Effectively breaking bad news
  • Involvement of MDT in supporting their QoL
  • Speech and language therapy for speech / swallowing difficulties
  • Genetic counselling regarding relatives, pregnancy and children
  • Advanced directives to document patients wishes
  • End of life care planning
174
Q

Which medications can help with disordered movement?

A

Antipsychotics (e.g. olanzapine)

Benzodiazepines (e.g. diazepam)

Dopamine-depleting agents (e.g. tetrabenazine)

175
Q

What is the prognosis of Huntington’s chorea?

A

Progressive condition - life expectancy around 15-20 years after onset of symptoms

As disease progresses patient becomes more susceptible and less able to fight off illnesses

Death is often due to respiratory disease (e.g. pneumonia)

Suicide is more common than in gen pop

176
Q

What is myasthenia gravis?

A

Autoimmune condition, causing muscle weakness, worse with activity, improves with rest

Affects women under 40 and men over 60

177
Q

Which disease is linked with myasthenia gravis?

A

Thymoma (tumour of the thymus gland)

178
Q

What happens across a normal synapse?

A

Motor nerves communicate with muscles at neuromuscular junctions - axonsof motor nerves are situated across asynapsefrompost-synaptic membraneon themuscle cell- these axons releaseneurotransmitter(acetylcholine) which leads tomuscle contraction

179
Q

What antibody is produced by patients with myasthenia gravis?

A

Acetylcholine receptor antibodies (85%) - bind to postsynaptic neuromuscular junction receptors - blocking acetylcholine from binding and activating the complement system causing damage to cells at post synaptic membrane

180
Q

Which other antibodies are produced in myathenia gravis?

A

Against muscle-specific kinase (MuSK) and antibodies against low-density lipiprotein receptor-related protein 4 (LRP4)

MuSK and LRP4 are important proteins for creation of acetylcholine receptors

181
Q

How does myasthenia gravis present?

A

Weakness worse with muscle use and improves with rest

Minimal in morning and worse at end of day

Affects proximal muscles and those of head and neck

  • Diplopia (extraocular muscle weakness)
  • Ptosis (eyelid weakness)
  • Weakness in facial muscle
  • Difficulty with swallowing
  • Fatigue in jaw when chewing
  • Slurred speech
182
Q

How to examine for myasthnia gravis?

A

Repeated blinking exacerbates ptosis

Prolonged upward gazing exacerbates diplopia on further eye movement testing

Repeated abduction of arm 20 times will cause unilateral weakness when comparing both sides

Check for thymectomy scar

Test forced vital capacity (FVC)

183
Q

How is myasthenia gravis diagnosed?

A

Testing for antibodies:

  • Acetylcholine receptor (ACh-R) antibodies
  • Muscle-specific kinase (MuSK) antibodies
  • LRP4 (low density lipoprotein receptor-related protein 4) antibodies

CT or MRI of thymus gland to look for thymoma

Edrophonium test can be useful if doubt about diagnosis

184
Q

How is the edrophonium test performed?

A

Given IV dose of edrophonium chloride (or neostigmine)

Edrophonium blocks cholinesterase enzymes breaking down acetylcholine - providing brief relief from weakness

185
Q

What are the treatment options for myasthenia gravis?

A

Reversible acetylcholinesteras inhibitors (usually pyridostigmine or neostigmine) increasing amount of acetylcholine

Immunosuppression (prednisolone or azathioprine) suppressing production of antibodies

Thymectomy can improve symptoms even in patients without a thymoma

Monoclonal antibodies (e.g. rituximab - targets B cells reducing antibodies OR eculizumab - targets completment protein C5)

186
Q

What is a myasthenic crisis?

What is the treatment?

A

Acute worsening of symptoms often triggered by another illness e.g. respiratory tract infection - patients may require non-invasive ventilation with BiPAP or full intubation and ventilation

Treat with:

  • IV immunoglobulins
  • Plasma exchange
187
Q

What is Lambert-Eaton myasthenic syndrome similar to?

A

Myasthenia gravis (progressive muscle weakness with increased use)

188
Q

What does Lambert-Eaton syndrome usually occur in conjunction with? Why?

A

Small-cell lung cancer - antibodies produced by immune system against voltage-gated calcium channels in small cell lung cancer (SCLC) also attach channels in presynaptic terminals of neuromuscular junction (so acetylcholine cannot be released)

189
Q

How does Lambert-Eaton syndrome present?

A

Slowly - proximal muscles are mostly affected

Affects intraocular muscles causing double vision (diplopia)

Levator muscles in eyelids cause drooping (ptosis)

Oropharyngeal muscles causing slurred speech and swallowing problems (dysphagia)

Autonomic dysfunction:

  • Dry mouth
  • Blurred vision
  • Impotence
  • Dizziness
190
Q

What is found on examination of a patient with Lambert-Eaton syndrome?

A

Reduced tendon reflexes

Post-tetanic potentiation - reflexes are temporarily normal following strong muscle contraction e.g. after max quadricep contraction

191
Q

What is the treatment of Lambert-Eaton syndrome?

A

Consider investigation for small cell lung cancer

Amifampridine allows more acetylcholine to be released in neuromuscular junction synapses by blocking voltage-gated potassium channels in presynaptic cells prolonging depolorisation of cell membrane

Other options:

  • Immunosuppressants (e.g. prednisolone or azathioprine)
  • IV immunoglobulins
  • Plasmapheresis
192
Q

What is Charcot-Marie-Tooth disease?

A

Inherited disease affecting peripheral motor and sensory neurones causing dysfunction in the myelin or axons (usually autosomal dominant inheritance)

Symptoms usually appear before 10 years old (can be 40 or later)

193
Q

What are the classical features of Charcot-Marie-Tooth?

A

High foot arches (pes cavus)

Distal muscle wasting = “inverted champagne bottle legs”

Weakness in lower legs - particularly loss of ankle dorsiflexion

Weakness in hands

Reduced tendon reflexes

Reduced muscle tone

Peripheral sensory loss

194
Q

What are some causes of peripheral neuropathy?

A

Alcohol

B12 deficiency

Cancer and Chronic kidney disease

Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin)

Every vasculitis

195
Q

What is the managament of Charcot-Marie Tooth?

A

Purely supportive

  • Neurologists to make diagnosis
  • Physiotherapists to maintain muscle strength & ROM
  • Occupational therapists to assist with AoDL
  • Podiatrists
  • Orthopaedic surgeons to correct disabling joint deformities
196
Q

What is Guillain-Barré syndrome?

A

Acute paralytic polyneuropathy affecting the peripheral nervous system causing acute, symmetrical, ascending weakness

Usually triggered by infection (campylobacter jejuni, cytomegalovirus, EBV)

197
Q

What is thought to cause Guillain-Barre syndrome?

A

Molecular mimicry - B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection - antibodies also match proteins on nerve cells (either on myelin sheath or on nerve axon)

198
Q

How does Guillain-Barre syndrome present?

A

Symmetrical ascending weakness (starting at feet)

Reduced reflexes

Peripheral loss of sensation or neuropathic pain

May progress to cranial nerves and cause facial nerve weakness

199
Q

What is the course of Guillain-Barré syndrome?

A

Usually starts within 4 weeks of preceding infection - starting at feet and progress upwards

Recovery can take months to years

200
Q

How is Guillain-Barré diagnosed? What criteria can help with diagnosis?

A

Clinically diagnosed - Brighton criteria

201
Q

What investigations can support diagnosis of Guillain-Barré?

A

Nerve conduction studies (reduced signal through nerves)

Lumbar puncture for CSF (raised protein with a normal cell count and glucose)

202
Q

What is the management of Guillain-Barré syndrome?

A

IV immunoglobulins

Plasma exchange (alternative to IV IG)

Supportive care

VTE prophylaxis (pulmonary embolism is a leading cause of death)

Intubation and ventilation if respiratory failure

203
Q

What is the prognosis of Guillain-Barré syndrome?

A

80% fully recover

15% left with neuro disability

5% die

204
Q

What is neurofibromatosis?

A

Genetic condtion causing benign nerve tumours (neuromas) to develop throughout the nervous system

Two types:

  • Neurofibromatosis type 1 (more common)
  • Neurofibromatosis type 2
205
Q

What is the genetic mutation is NF1?

A

Found on chromosome 17 - codes for a protein called neurofibromin - tumour suppressor protein (inheritance is autosomal dominant)

206
Q

What is the diagnostic criteria for NF1?

A

CRABBING (must be at least 2)

  • Cafe au lait spots (6 or more) >5mm in children or 15mm in adults
  • Relative with NF1
  • Axillary or inguinal freckles
  • Bony dysplasia such as bowing of long bone or sphenoid wing dysplasia
  • Iris hamartomas (Lisch nodules) (2 or more) - yellow brown spots on the iris
  • Neurofibromas (2 / more) or 1 plexiform neurofibroma
  • Glioma of the optic nerve
207
Q

What investigations can be performed when there is diagnostic doubt?

A

Genetic testing

X-rays to investigate bone pain / lesions

CT and MRI to investigate lesions in brain, spinal cord and elsewhere

208
Q

What is the management of NF1?

A

Control symptoms, treat complications

209
Q

What are the complications of NF1?

A

Migraines

Epilepsy

Renal artery stenosis causign hypertension

Learning and behavioural problems (e.g. ADHD)

Scoliosis of the spine

Vision loss (secondary to optic nerve gliomas)

Malignant peripheral nerve sheath tumours

GI stromal tumour (type of sarcoma)

Brain tumour

Spinal cord tumour (paraplegia)

Increased risk of cancer (e.g. breast)

Leukaemia

210
Q

What is the genetic mutation in NF2?

A

Mutation in chromosome 22 which codes for protein called merlin (tumour suppressor protein - important for Schwann cells)

Causes schwannomas - inherited in autosomal dominant pattern

211
Q

What is NF2 mostly associated with?

A

Acoustic neuromas - tumours of the auditory nerve innervating inner ear - symptoms:

  • Hearing loss
  • Tinnitus
  • Balance problems
212
Q

What do bilateral acoustic neuromas indicate?

213
Q

How do schwannomas present? How can they be treated?

A

Symptoms based on location of lesion

Surgery can resect tumours although risk of permanent nerve damage

214
Q

What is tuberous sclerosis?

A

Genetic condition - characteristically causing hamartomas (benign neoplastic growths of the originating tissue)

215
Q

Where do hamartomas typically affect?

A

Skin

Brain

Lungs

Heart

Kidneys

Eyes

216
Q

What does is the genetic mutation in tuberous sclerosis?

A

TSC1 gene on chromosome 9 which codes for hamartin

TSC2 gene on chromosome 16 which codes for tuberin

217
Q

What do hamartin and tuberin do?

A

Interact with each other to control size and growth of cells (abnormalities in one of these causes abnormal cell size and growth)

218
Q

What are the skin signs of tuberous sclerosis?

A

Ash leaf spots - depigmented aread of skin shaped like ash leaf

Shagreen patches - thickened, dimpled, pigmented patches of skin

Angiofibromas - small skin coloured / pigmented papules occuring over nose and cheeks

Subungual fibromata - fibromas under nail bed - usually circular painless lumps that displace the nail

Cafe-au-lait spots - light brown coloured flat pigmented lesions on skin

Poliosis - isolated patch of which hair on head, eyebrows, eyelashes or beard

219
Q

What are the neurological features of tuberous sclerosis?

A

Epilepsy

Learning disability and developmental delay

220
Q

What are the other features of tuberous sclerosis?

A

Rhabdomyomas in the heart

Gliomas (tumours of the brain and spinal cord)

Polycystic kidneys

Lymphangioleiomyomatosis (abnormal growth in smooth muscle cells, often affecting lungs)

Retinal hamartomas

221
Q

How does tuberous sclerosis present?

A

Child with epilepsy and skin features of tuberous sclerosis

222
Q

What is the management of tuberous sclerosis?

A

Supportive with monitoring and treating of complications such as epilepsy (no treatment for underlying gene defect)

223
Q

What are the differential diagnoses of headaches?

A

Tension headaches

Migraines

Cluster headaches

Secondary headaches

Sinusitis

Giant cell arthritis

Glaucoma

Intracranial haemorrhage

Subarachnoid haemorrhage

Analgesic headache

Hormonal headache

Cervical spondylosis

Trigeminal neuralgia

Raised ICP

Meningitis

Encephalitis

224
Q

What are some red flags for headache?

A

Fever, photophobia or neck stiffness (meningitis or encephalitis)

New neurological symptoms (haemorrhage, malignancy or stroke)

Dizziness (stroke)

Visual disturbance (temporal arteritis or glaucoma)

Sudden onset occipital headache (subarachnoid haemorrhage)

Worse on coughing or straining (raised intracranial pressure)

Postural, worse on standing, lying or bending over (raised intracranial pressure)

Severe enough to wake the patient from sleep

Vomiting (raised intracranial pressure or carbon monoxide poisoning)

History of trauma (intracranial haemorrhage)

Pregnancy (pre-eclampsia)

225
Q

What should be in the examination of a patient with a headache?

A

Fundoscopy (look for papilloedema)

Indicates raised ICP (due to brain tumour, benign intracranial hypertension and intracranial bleed)

226
Q

How do tension headaches present?

A

Mild ache across forehead in band like pattern (ache in frontalis, temporalis or occipital muscles)

No visual changes

227
Q

What are tension headaches associated with?

A

Stress

Depression

Alcohol

Skipping meals

Dehydration

228
Q

What is the treatment of tension headaches?

A

Reassurance

Basic analgesia

Relaxation techniques

Hot towels to local area

229
Q

How do secondary headaches present?

A

Similar to tension headache but clear cause

230
Q

What can cause secondary headaches?

A

Underlying medical conditions e.g. infection, obstructive sleep apnoea, or pre-eclampsia

Alcohol

Head injury

Carbon monoxide poisoning

231
Q

What is sinusitis?

A

Headache associated with inflammation, in ethmoidal, maxillary, frontal or sphenoidal sinuses

Causes facial pain behind nose, forehead and eyes

Tenderness over affected sinus

232
Q

When does sinusitus usually resolve?

A

Within 2-3 weeks (mostly viral) nasal irrigation with saline can be helpful

Prolonged = steroid nasal spray (abx occasionally required)

233
Q

What is an analgesic headache?

A

Headache caused by long term analgesia use

Withdrawal of analgesia is important in treating headache

234
Q

What are hormonal headaches?

A

Related to low levels of oestrogen (produce generic, non-specific, tension like headache)

Appear:

  • 2 days before and first 3 days of menstrual period
  • Around menopause
  • Pregnancy (worse in first few weeks, improves in last 6 months - if in the 2nd half then investigate for pre-eclampsia)

Oral contraceptive pill can improve hormonal headaches

235
Q

What is cervical spondylosis?

A

Condition caused by degenerative changes in the cervical spine causing neck pain, usually worse on movement (can also cause headache)

Must exclude other causes e.g. inflammation, malignancy, infection, spinal cord lesions

236
Q

What are the branches of the trigeminal nerve?

A

Opthalmic V1

Maxillary V2

Mandibular V3

237
Q

What causes trigeminal neuralgia?

A

Unclear (thought to be compression of nerve)

Most cases are unilateral

5-10% of patients with MS have trigeminal neuralgia

238
Q

How does trigeminal neuralgia present?

A

Facial pain comes on spontanously lasting few seconds to few hours (electricity like shooting pain)

239
Q

What can trigger pain in trigeminal neuralgia?

A

Cold weather

Spicy food

Caffeine

Citrus fruits

240
Q

What medication is first line for trigeminal neuralgia?

A

Carbamazepine (surgery to decompress / damage nerve is an option)

241
Q

What are the different types of migraine?

A

Migraine without aura

Migraine with aura

Silent migraine

Hemiplegic migraine

242
Q

What are the features of a migraine?

A

Last between 4 - 72 hours:

  • pounding / throbbing in nature
  • usually unilateral
  • Photophobia
  • Phonophobia (loud noises)
  • With / without aura
  • N&V
243
Q

What is an aura?

A

Term to describe visual changes associated with migraines:

  • Sparks in vision
  • Blurring vision
  • Lines across vision
  • Loss of different visual fields
244
Q

How does a hemiplegic stroke present?

A

Mimics stroke:

  • Typical migraine symptoms
  • Sudden / gradual onset
  • Hemiplegia (unilateral weakness of limbs)
  • Ataxia
  • Changes in consciousness
245
Q

What are some potential triggers of a migraine?

A

Stress

Bright lights

Strong smells

Certain foods (e.g. chocolate, cheese, caffeine)

Dehydration

Menstruation

Abnormal sleep patterns

Trauma

246
Q

What are the 5 stages of a migraine?

A

Premonitory or prodromal stage (begin 3 days before headache e.g. yawning, fatigue or mood changes)

Aura (lasting up to 60 mins)

Headache (lasting 4-72 hours)

Resolution (fades away / relieved by vomiting / sleeping)

Postdromal or recovery phase

247
Q

What are the options for acute medical management for migraine?

A

Paracetamol

Triptans (e.g. sumatriptan 50mg as the migraine starts)

NSAIDs (e.g. ibuprofen or naproxen)

Antiemetics if vomiting occurs (e.g. metoclopramide)

248
Q

What are triptans? How are they hypothesised to work?

A

5HT receptors agonists (serotonin receptor agonists)

Act on:

  • Smooth muscles in arteries to cause vasoconstriction
  • Peripheral pain receptors to inhibit activation of pain receptors
  • Reduce neuronal activity in the CNS
249
Q

What medications can be used as migraine prophylaxis?

A

Propranolol

Topiramate (teratogenic and causes cleft lip / palate - DONT GET PREGNANT)

Amitriptyline

250
Q

What else can help with migraines?

A

Acupuncture (reported to be as effective as prophylactic medication)

Supplementation with B2 (riboflavin) may reduce frequency and severity

If specifically triggered around menstruation then prophylaxis with NSAIDs (e.g. mefanamic acid) or triptans (frovatriptan or zolmitriptan)

251
Q

What is the prognosis of migraines?

A

Better over time and go into remission

252
Q

What are cluster headaches?

Who do they typically affect?

What are the triggers?

A

Severe headaches usually around eye

Clusters = 3-4 attacks a day for weeks / months followed by pain free period for 1-2 years (attacks = 15mins - 3 hours)

30-50 year old male smoker

Triggers = alcohol, strong smells and exercise

253
Q

What are the symptoms of cluster headaches?

A

Suicide headaches:

  • Red, swollen, watering eye
  • Pupil contriction (miosis)
  • Eyelid drooping (ptosis)
  • Nasal discharge
  • Facial swelling
254
Q

What are the acute and prophylactic treatment of cluster headaches?

A

Acute = triptans (e.g. sumatriptan 6mg injected subcut) and high flow 100% oxygen for 15-20 mins

Prophylaxis = verapamil, lithium, prednisolone (short course 2-3 weeks to break cycle during clusters)

255
Q

How does damage to median nerve present?

A

Motor and sensory to lateral half of hand

256
Q

What does the sciatic nerve form?

What can damage to these nerves cause?

A

Tibial

Common perineal nerves = damage - foot drop

257
Q

What are the risk factors for raised ICP?

A

Female

Obesity

Drugs (tetracycline, steroids, COCP, vitamin A, lithium)

Pregnancy

258
Q

What are the features of idiopathic intracranial hypertension?

A

Headache

Blurred vision

Papilloedema

Enlarged blind spot

259
Q

What is the management of idiopathic intracranial hypertension?

A

Weight loss

Diuretics (e.g. acetazolamide)

Repeated LP

260
Q

What is Uhthoff’s phenomenon?

A

Worsening of MS symptoms after a hot shower

Medicine (12 decks)

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