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Neuro Diseases Flashcards

1
Q

What is the epidemiology of MS?

A

Females
Presentation between 20-40
White populations

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2
Q

What is the aetiology/ risk factors for MS?

A 
Not understood
Exposure to EBV in childhood
Living far from equator and low vit D 
White populations
Female
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3
Q

Briefly explain the pathophysiology of MS

A

Autoimmune mediated demyelination of olgiodendrocytes.
T cells activate B cells to produce autoantibodies against myelin. Myelin does regenerate but new myelin is less efficient and is temp dependent. Repeated demyelination leads to axonal loss and incomplete recovery= Relapsing and remitting symptoms
There is also sclerosis which further blocks conduction

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4
Q

What are the types of MS?

A

Relapsing and remitting (80%)
Secondary progressive
Primary progressive (10-15%)

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5
Q

What is the most common type of MS?

A

Relapsing and remitting

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6
Q

Where does demyelination normally occur in MS?

A

Optic nerves, around ventricles, corpus callosum, brainstem and cerebellar connections, cervical cord

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7
Q

How is MS treated?

A 
Advise to live a stress free life
Give Vitamin D
Acute relapse= IV methyprenisolone 
Frequent relapse= SC interferon 1B or 1A= Antinflammatory cytokines 
Monoclonal antibodies= IV alemtuzumab
IV natalizumab and dimethyl fumarate
Symptomatic treatments= Physiotherapy, bac lofen, botox
Stem cell treatments
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8
Q

What are the clinical features of MS?

A 
Usually presents aged 20-40
Symptoms worsen with heat
Pain in one eye upon eye movement
Reduced central vision
Lhermitte's sign= Tingling into limbs on flex of neck
Leg weakness
Dysphagia 
Numbness 
Trigeminal neuralgia
Cerebellar symptoms 
Urinary incontinance
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9
Q

How is MS diagnosed?

A

MRI scan= 95% have periventricular lesions, white matter abnormalities
Bloods to rule out others= FBC, U&Es, HIV test, glucose, inflammatory markers
Must have 2+ attacks affecting different parts of of CNS
Lumbar puncture= IgG bands
Electrophysiology

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10
Q

What is the aetiology of meningitis?

A
  • Normally= N. Meningitdes (Droplets), strep. pneumoniae, haemophilius influenza
  • Pregnancy= Listeria monocytogenes
  • Neonates= E. coli, group B haemolytic strep
  • Viral= Enterovirus, herpes simplex virus
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11
Q

What are the risk factors of meningitis?

A
  • Intrathecal drugs
  • IV drug abuse
  • Immunocompromised
  • Elderly
  • Pregnant
  • Crowding
  • Diabetes
  • Malignancy
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12
Q

What is the clinical presentation of bacterial meningitis?

A
  • Headache, fever and neck stiffness
  • Sudden onset
  • Papilloedema
  • Malaise, rigors, photophobia, vomitting, irritability
  • Positive Kernig’s and Brudzinskis signs
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13
Q

What is the clinical presentation of septicaemia?

A

Non blanching petechial (glass test) and purpuric skin rash, seizures

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14
Q

What is the clinical presentation of viral meningitis?

A
  • Benign self limiting condition (4-10 days)

- Headaches for months following

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15
Q

What is the clinical presentation of chronic meningitis?

A
  • Long history of vague symptoms of headache, anorexia, vomitting
  • Triad (Headache, neck stiffness, fever) is often absent of late
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16
Q

What is the lumbar puncture result of bacterial meningitis?

A
  • Cells= Polymorphs
  • Protein= Raised
  • Glucose= Low
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17
Q

What is the lumbar puncture result of chronic (TB) meningitis?

A
  • Cells= Lymphocytes
  • Protein= Raised
  • Glucose= Low/ Normal
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18
Q

What is the lumbar puncture result of viral meningitis?

A
  • Cells= Lymphocytes
  • Protein= Normal
  • Glucose= Normal
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19
Q

How is meningitis diagnosed?

A
  • Blood cultures before lumbar
  • Lumbar puncture at L4
  • Blood tests= FBC, U&E, CRP
  • CT of head for tumour
  • Throat swabs
  • Don’t perform lumbar if septicaemia is suspected
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20
Q

How is meningitis treated?

A
  • Bacterial= IV Cefotaxime or IV Ceftriaxone
  • IV chloramphenicol if CI with penicilins
  • If immunocompromised, add IV amoxicillin to cover listeria
  • Consider steroids e.g. dexamethasone to reduced cerebral oedema
  • Prophylaxis for contacts
  • Viral meningitis= aciclovir
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21
Q

What is the cause of extradural haemorrhage?

A
  • Most commonly due to a traumatic head injury resulting in fracture of the temporal or parietal bone causing laceration of the middle meningeal artery, typically after temple trauma
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22
Q

What are the risk factors for extradural haemorrhage?

A

Usually occurs in young adults

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23
Q

What are the clinical features of extradural haemorrhage?

A
  • Severe headache, nausea and vomitting, confusion and seizures, weakness and brisk reflexes
  • Rapid rise in ICP
  • Ipsilateral pupil dilates, coma, bilateral limb weakness, deep and irregular breathing
  • Coning
  • Death due to respiratory arrest
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24
Q

How is extradural haemorrhage treated?

A
  • ABCDE emergency management= asses and stabilise patient
  • Give IV mannitol if increased ICP
  • Refer to neurosurgery
  • Maintain airway
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25
Q

How is extradural haemorrhage diagnosed?

A
  • CT of head (gold standard)= shows hyperdense haematoma that is biconcave/lemon shaped
  • Skull x ray= May be normal or show fracture lines crossing the course of the middle meningeal artery
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26
Q

What is the commonest primary headache?

A

Tension headache

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27
Q

What are the causes of tension headache?

A
  • Stress
  • Sleep deprivation
  • Bad posture
  • Hunger
  • Eye strain
  • Anxiety
  • Noise
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28
Q

What is the clinical presentation of tension headache?

A
  • Usually has 1 of the following= Bilateral, pressing/tight non-pulsatile, mild/moderate intensity, scalp muscle tenderness
  • Band-like tight sensation
  • Pressure behind eyes
  • Can last 30mins-7days
  • Episodic (<15days/month) or chronic (>15days/month)
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29
Q

How is tension headache diagnosed?

A

Clinical diagnosis from history

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30
Q

How is tension headache treated?

A
  • Lifestyle advice
  • Stress relief e.g. massage, accupuncture
  • Symptomatic treatment= aspirin, paracetamol, NSAIDS (but don’t use too much, to prevent a medication overuse headache)
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31
Q

What is the epidemiology of cluster headache?

A
  • Rarer than migraine
  • More common in males
  • Affects adults= 20-40yrs
  • Commoner in smokers
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32
Q

What are the risk factors for cluster headache?

A
  • Smoker
  • Male
  • Autosomal dominant gene has a role
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33
Q

What are the clinical features of a cluster headache?

A
  • Rapid onset of excrutiating pain around one eye, temple or forehead
  • Ipsilateral cranial autonomic features= Facial flushing, eye may become watery and bloodshot, blocked nose, miosis +/- ptosis
  • Rises to crescendo over minutes and lasts 15-160 mins, once or twice a day, usually at same time
  • Episodic clusters last 4-12 weeks and are followed by pain free periods of months or even yrs between clusters
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34
Q

How are cluster headaches diagnosed?

A

Clinical diagnosis= At least 5 headache attacks fulfilling the above criteria

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35
Q

How are cluster headaches treated?

A
  • Acute attack: analgesics are unhelpful. Give oxygen for 15 mins
  • Triptan = serotonin receptor antagonists- reduces vascular inflammation
  • Calcium channel blocker is first line prevention
  • Avoid alcohol during cluster period
  • Corticosteroids may help during cluster
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36
Q

What is the epidemiology of trigeminal neuralgia?

A
  • Peak incidence between 50-60yrs
  • More common in females
  • Prevalence increases with age
  • May be due to genetic predisposition
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37
Q

What are the risk factors for trigeminal neuralgia?

A
  • Hypertension

- Triggers= Washing affected area, shaving, eating, talking, dental work

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38
Q

Briefly explain the pathophysiology of trigeminal neuralgia

A

Compression of the trigeminal nerve by a loop of vein or artery resulting in local demyelination, or due to local pathology (tumours, infarction, MS) resulting in erratic pain signalling

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39
Q

What are the clinical features of trigeminal neuralgia?

A
  • Almost always unilateral
  • At least three attacks of unilateral facial pain
  • Occurs in 1 or more distributions of the trigeminal nerve, with no radiation beyond the trigeminal distribution
  • Pain has at least 3 of the following- reoccurring, severe intensity, shooting stabbing or electric pain, precipitated by innocuous stimuli
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40
Q

How is trigeminal neuralgia treated?

A
  • Typical analgesics and opioids do not work
  • Anticonvulsants can suppress attacks
  • Other options include phenytoin, gabepentin, lamotrigine
  • May spontaneously remit after 6-12 months
  • Surgery may be necessary; microvascular decompression, gamma knife surgery
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41
Q

How is trigeminal neuralgia diagnosed?

A
  • At least 3 attacks with unilateral facial pain

- MRI to exclude secondary causes

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42
Q

What is the epidemiology of Herpes Zoster infection?

A
  • 90% of 16 yr olds have been exposed (chickenpox)

- Shingles can affect all ages but is seen as a disease of the elderly

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43
Q

What are the risk factors for shingles?

A

Increasing age

Immunocompromised

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44
Q

Briefly explain the pathophysiology of shingles

A
  • Latent varicella zoster virus is reactivated in the dorsal root ganglia and travels down the affected nerve via the sensory root in dermatomal distribution
  • Results in perineural and intrameural inflammation
  • Most commonly occurs in thoracic nerve, and then the ophthalmic division of the trigeminal nerve
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45
Q

What are the clinical features of shingles?

A
  • Pain and paraesthesia in dermatomal distribution
  • Malaise, myalgia, headache and fever
  • Can be over a week before eruption occurs
  • Rash- consists of papules and vesicles, causes neuritic pain, crust formation and drying occurs.
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46
Q

How is shingles diagnosed?

A
  • Clinical diagnosis

- Eruption of rash is virtually diagnostic

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47
Q

How is shingles treated?

A
  • Oral antiviral therapy begun with 72 hrs of rash onset (Oral aciclovir, oral valiciclovir, oral famcliclovir )
  • Topical antibiotic treatment
  • Analgesia
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48
Q

What are some possible complications of shingles?

A
  • Opthalmic branch of trigeminal nerve (will affect site)

- Post herpetic neuralgia= burning, intractable pain lasting for over four months, responds poorly to analgesics

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49
Q

Briefly explain the pathophysiology of encephalitis?

A
  • Disease which mostly affects frontal and temporal lobes resulting in decreased consciousness, confusion and focal signs
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50
Q

What is the aetiology of encephalitis?

A
  • Mainly viral= Herpes simplex, EBV, cytomegalovirus, varicella zoster, HIV
  • Non viral= Bacterial meningitis, malaria, TB
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51
Q

What are the clinical features of encephalitis?

A
  • Whole brain infected= Problems in higher functioning and consciousness
  • Triad= fever, headache, altered mental status
  • Begins with features of viral infection= triad, myalgia, fatigue, nausea
  • Progresses to: personality and behavioral changes, coma, drowsiness, seizures
  • Focal neurological deficit=hemiparesis and dysphagia
  • Raised ICP and midline shift
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52
Q

How is encephalitis diagnosed?

A
  • MRI: shows area of inflammation and swelling, generally in the temporal lobes in HSV encephalitis. May be midline shifting due to raised ICP
  • Electroencephalography (EEG): shows periodic sharp and slow wave complexes
  • Blood and CSF serology
  • Lumbar puncture shows increased lymphocytes, viral detection by CSF PCR
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53
Q

How is encephalitis treated?

A
  • If viral immediate treatment with anti-viral e.g. IV aciclovir- even before the investigation results are available
  • Early treatment can reduce mortality and long neuro damage
  • Anti seizure medication e.g. primadone
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54
Q

What is the epidemiology of subdural haemorrhage?

A
  • Most common in patients with small brain (Babies, elderly and alcoholics)
  • Majority of SDHs are from trauma, but can be minor/long ago
  • Chronic/ apparently spontaneous SDH is common in elderly
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55
Q

What are the causes of subdural haemorrhage?

A
  • Trauma causing bleeding from bridging veins between the cortex and venous sinuses, causing a haematoma between dura and arachnoid mata
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56
Q

What are the clinical features of subdural haemorrhage?

A
  • Interval between injury and symptoms can be days-months
  • Fluctuating levels of consciousness with insidious physical or intellectual slowing
  • Personality change
  • Unsteadyness
  • Signs of raised intercranial pressure= headache, vomitting, nausea, seizure, raised BP
  • Focal neurology (hemiparesis, sensory loss)
  • Stupor, coma and coning
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57
Q

How is a subdural haemorrhage diagnosed?

A

CT of head to show diffuse spreading, hyperdense, crescent shaped collection of blood over one hemisphere

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58
Q

How is subdural haemorrhage treated?

A
  • Stabilise patient
  • Refer to neurosurgeons: Irrigation/ evacuation via burr twist drill and burr hole craniotomy
  • Address cause of trauma
  • IV mannitol to reduce ICP
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59
Q

What are the commonest neoplasms to metastasise to the CNS?

A
  • Non-small cell ling
  • Small cell lung
  • Breast
  • Melanoma
  • Renal cell
  • GI
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60
Q

What are the risk factors for primary brain tumours?

A
  • More common in affluent groups
  • Ionising radiation
  • Vinyl chloride
  • Immunosuppression
  • Family history= genetics
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61
Q

What are the most common primary brain tumours?

A
  • Gliomas= Astrocytomas or oligodendromas

- Meningiomas

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62
Q

What is the most common primary brain tumour?

A

Astrocytoma

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63
Q

What are the clinical features of brain tumours?

A
  • Progressive focal neurological deficit
  • Raised ICP= Headaches, drowsiness, vomitting
  • Epilepsy= Focal or generalised
  • General cancer symptoms= Weight loss, malaise, anaemia
  • Papilloedema
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64
Q

How are brain tumours diagnosed?

A
  • CT or MRI to determine size and location of lesions
  • Blood tests
  • Biopsy via skull Burr Hole
  • Positron Emission Tomography
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65
Q

How are brain tumours treated ?

A
  • Surgery if less than 75
  • Radiotherapy
  • Medical treatment of symptoms
  • Palliative care
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66
Q

What are the two types of stroke?

A

Ischaemic and haemorrhagic

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67
Q

What is the epidemiology of ischaemic stroke?

A
  • Accounts for 80% of all strokes
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68
Q

What causes ischaemic stroke?

A
  • Small vessel occlusion/ thrombosis in situ
  • Cardiac emboli from AF, MI or infective endocarditis
  • Large artery stenosis
  • Artherothromboembolism
  • Hypoperfusion, vasculitis, hyperviscocity
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69
Q

Briefly explain the pathophysiology of ischaemic stroke

A

Arterial disease and atherosclerosis causes thrombosis to occur which blocks a vessel leading to ischaemia

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70
Q

What are the clinical features of ischaemic stroke?

A
  • Cerebral hemisphere: signs contralateral to the affected side, hemiplegia, hemisensory loss, upper motor neurone facial weakness and hemianopia
  • Brainstem: Complex, depends on location
  • Multi infarct: Multiple steps progressing to dementia
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71
Q

What are the causes of CNS bleeds?

A
  • Trauma
  • Aneurysm rupture
  • Anticoagulation
  • Thrombolysis
  • Carotid artery dissection
  • Subarachnoid haemorrhage
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72
Q

What is the epidemiology of haemorrhagic stroke?

A
  • Accounts for 17% of strokes
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73
Q

What are the clinical features of haemorrhagic stroke?

A
  • Severe headache= like being hit in the head
  • Nausea/ vomitting
  • Sudden loss of conscious
  • Classic stroke symptoms= signs contralateral to affected. Hemiplegia, hemisensory loss, upper motor neurone facial weakness and hemianopia
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74
Q

Briefly explain the pathophysiology of haemorrhagic stroke

A
  • Hypertension resulting in micro aneurysm rupture
  • Cerebral amyloid angiopathy: Deposition of amyloid B on the walls of small and medium sized arteries in normotensive patients
  • Space occupying lesion e.g. tumour
  • Young adults: Carotid/vetebral artery dissection
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75
Q

What are the risk factors for haemorrhagic stroke?

A

Hypertension, excess alcohol, smoking and age

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76
Q

How is ischaemic stroke treated?

A

Aspirin, IV alteplase in at least 4.5 hours (thrombolytic; IV tissue plasminogen activator), antiplatelet (aspirin -> lifelong clopidogrel), maintain glucose, NBM

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77
Q

How is ischaemic stroke treated?

A

Stop anticoagulants.

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78
Q

What is the epidemiology of cauda equina syndrome?

A
  • Rare, occuring mainly in adults but can occur at any age

- Occurs in around 2% of herniated discs

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79
Q

What is the aetiology of cauda equina syndrome?

A
  • Herniation of lumbar disc= most commonly at L4/5 or L5/S1
  • Tumours/ metastasis
  • Trauma
  • Infection
  • Spondylolisthesis
  • Post op haematoma
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80
Q

What are the clinical features of cauda equina syndrome?

A
  • Sciatica= pain, numbness and a tingling sensation that radiates from lower back and travels down one leg to the foot
  • Saddle anaesthesia
  • Bladder/ bowel dysfunction
  • Erectile dysfunction
  • Variable leg weakness that is flaccid and areflexic (LMN signs)
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81
Q

Briefly explain the pathophysiology of cauda equina syndrome

A
  • Nerve root compression caudal to the termination of the spinal cord at L1/2
  • Usually large central disc herniations at L4/5 or L5/S1 levels
  • Generally S1-S5 nerve root compression
82
Q

How is cauda equina syndrome diagnosed?

A
  • MRI to localise lesions
  • Knee flexion- test L5-S1
  • Ankle plantar flexion- test S1-S2
  • Straight leg raising- L5/S1 root problem
  • Femoral stretch test
83
Q

How is cauda equina syndrome treated?

A
  • Refer to neurosurgeon ASAP to relieve pressure
  • Microdiscectomy- removal of part of the disc
  • Epidural steroid injection
  • Surgical spine fixation
  • Spinal fusion= reduces pain
84
Q

What causes CN4 palsy?

A
  • Trauma to orbit (rare)
85
Q

What causes CN6 palsy?

A
  • MS, Wernike’s encephalopathy, pontine stroke
86
Q

What causes CN8 palsy?

A
  • Skull fracture, toxic drug effects, ear infections
87
Q

What causes CN9 palsy?

A
  • Jugular foreman lesion
88
Q

What causes CN3 palsy?

A
  • Raised ICP, Diabetes, hypertension, giant cell arteritis
89
Q

What causes CN5 palsy?

A
  • Trigeminal neuralgia, herpes zoster, nasopharyngeal cancer
90
Q

What causes CN7 palsy?

A
  • Bells palsy, fractures of petrous bone, middle ear infections, inflammation of parotid
91
Q

What are the symptoms of CN4 palsy?

A
  • Head tilt

- Diplopia on looking down

92
Q

What are the symptoms of CN6 palsy?

A
  • Adducts eye
93
Q

What are the symptoms of CN8 palsy?

A
  • Hearing impairment

- Vertigo and lack of balance

94
Q

What are the symptoms of CN9 palsy?

A
  • Gag reflex issues, swallowing issues, vocal issues
95
Q

What are the symptoms of CN3 palsy?

A
  • Ptosis
  • Fixed, dilated pupils
  • Eyes down and out
96
Q

What are the symptoms of CN5 palsy?

A
  • Jaw deviates to side of lesion, loss of corneal reflex
97
Q

What are the symptoms of CN7 palsy?

A
  • Facial droop and weakness
98
Q

What is a TIA?

A
  • Transient ischaemic attack

- Rapid onset of neurological dysfunction due to temporary focal cerebral ischaemia without infarct (24 hrs)

99
Q

What is the epidemiology of TIAs?

A
  • 15% of first strokes are preceded by TIA
  • More common in males than females
  • Black ethnicity are at greater risk
100
Q

What are the clinical features of TIAs?

A
  • Sudden loss of function, usually only for minutes, with complete recovery
  • 90% are carotid= Amaurosis fugax (Sudden loss of vision in eye), aphasia, hemiparesis, hemisensory loss, hemianopic visual loss
  • 10% are vertebrobasilar= Diplopia, vertigo, vomitting, choking, dysarthria, ataxia, hemisensory lsos, hemianopia, tetraparesis, loss of consciousness
101
Q

What are the risk factors for TIA?

A
  • Age
  • Hypertension
  • Smoking
  • Diabetes
  • Heart disease
  • Excess alcohol
  • Hyperlipidaemia
  • Raised packed cell vol
  • Combined oral contraceptive
  • Clotting disorders
102
Q

What is the ABCD2 score?

A

The risk of having a stroke after a TIA

103
Q

How is the ABCD2 score calculated?

A
  • Age>60= 1
  • BP >140/90= 1
  • Unilateral weakness= 2 or Speech disturbance with out weakness= 1
  • Symptoms for over an hour= 2 or Symptoms for 10-59 mins= 1
  • Diabetes= 1
104
Q

How is TIA diagnosed?

A 
- Bloods
= FBC for polycythaemia 
= ESR raised in vasculitis
= Glucose for hypoglycaemia
= Creatinine, electrolytes, cholesterol
- ECG for AF or MI
- Carotid artery doppler Ultrasound to look for stenosis/ atheroma
- MR/CT angiography if stenosis to determine extent
105
Q

What is the epidemiology of subarachnoid haemorrhage?

A
  • Typical age 35-65
106
Q

What are the risk factors for subarachnoid haemorrhage?

A
  • Hypertension
  • Family history
  • Diseases that predispose; PKD, Ehlers-Danlos, coarctation of aorta
  • Smoking, bleeding disorders, post-menopausal decreased oestrogen
107
Q

What is the aetiology of subarachnoid haemorrhage?

A
  • No cause found= 10%
  • Rupture of saccular aneurysm e.g. berry aneurysms= 80%
  • Atrioventricular malformations= 10%
108
Q

What are the clinical features of subarachnoid haemorrhage?

A
  • Sudden onset severe occipital headache= Thunder clap
  • Vomitting, collapse, seizures often follow
  • Depressed levels of consciousness
  • Neck stiffness, retinal and vitreous bleed
  • Kernig’s sign and Brudzinski’s sign
  • Papilloedema
  • Focal neurology
  • Marked increase in BP as a reflex
  • Sentinel headache in 6%
109
Q

What is a migraine?

A
  • Recurrent throbbing headache for 4-72 hrs
110
Q

What are the types of migraine?

A
  • Aura= Characteristically unilateral. Visual disturbance, photosensitivty, nausea,
  • Without aura= Characteristically unilateral, no eyesight disturbances
  • Variant= Unilateral motor or sensory symptoms resembling a stroke
111
Q

What are the general migraine clinical features?

A

At least 2 of; unilateral pain, throbbing-type pain, moderate-severe intensity, motion sensitivity
At least 1 of; nausea/ vomitting, photophobia, normal examination

112
Q

Briefly explain the pathophysiology of migraines?

A
  • Changes in brainstem blood flow cases an unstable trigeminal nerve nucleus
  • Release of vasoactive neuropeptides causes neurogenic inflammation
113
Q

What things trigger migraine?

A

CHOCOLATE

  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese
  • Oral contraceptive
  • Lie ins
  • Alcohol
  • Tumult
  • Exercise
114
Q

How are migraines diagnosed?

A
  • Clinical features
  • Neuroimaging; rule out mass lesions
  • Lumbar puncture if worried for SAH
115
Q

How are migraines treated?

A
  • Reduce triggers
  • Passes in sleep
  • Painkillers
  • Triptans e.g. sumatriptan
  • Can use tricyclic antidepressants, anti convulsants or beta blockers
116
Q

What is giant cell arteritis?

A

Systemic immune mediated vasculitis affecting medium- large arteries of the aorta

117
Q

What are the risk factors for giant cell arteritis?

A
  • Genetic

- Age- incidence increases with age

118
Q

What is the epidemiology of giant cell arteritis?

A
  • Primarily in those over 50
  • Most common in caucasians
  • More common in females
119
Q

Briefly explain the pathophysiology of giant cell arteritis

A
  • Granulomatous arteritis of unknown aetiology affecting in particular the extradural arteries and the large cerebral arteries
  • Arteries become inflamed, thickened and can obstruct blood flow
120
Q

What are the clinical features of giant cell arteritis?

A
  • Severe headache
  • Tenderness of scalp or temple, claudication of the jaw when eating
  • Tenderness and swelling of one or more artery
  • Sudden painless vision loss
  • Malaise, lethargy, fever, associated symptoms of PMR
  • Dyspnoea, morning stiffness and unequal or weak pulses
121
Q

How is giant cell arteritis diagnosed?

A
  • Diagnostic criteria; 3 or more of= over 50, new headache, temporal artery tenderness, ESR raised, abnormal artery biopsy
122
Q

How is giant cell arteritis treated?

A
  • High dose corticosteroids rapidly e.g. oral prednisolone to stop vision loss
123
Q

What is a possible complication of giant cell arteritis?

A

Polymyalgia rheumatica in 50%

124
Q

What is carpal tunnel syndrome?

A

The most common mononeuropathy. Results from pressure and compression on the median nerve as it passes through the carpal tunnel

125
Q

What is the epidemiology of carpal tunnel syndrome?

A

More common in females as women have narrower wrists but similar sized tendons

126
Q

What is the aetiology of carpal tunnel syndrome?

A
  • Usually idiopathic

- Usually in over 30s

127
Q

What are the clinical features of carpal tunnel syndrome?

A
  • Symptoms are intermittent
  • Aching pain in hand and arm
  • Paraesthesiae in median nerve distribution
  • Relieved by dangling hand over side of bed = Wake and shake
  • Wasting of thenar eminence
  • Light touch, 2 pt discrimination and sweating
128
Q

How is carpal tunnel syndrome diagnosed?

A
  • Electromyography; See slowing of conduction velocity in the median sensory nerves across the carpal tunnel
  • Phalens test= patient can only maximally flex wrist for 1 min
  • Tinels test= Tapping on nerve at wrist induces tingling
129
Q

How is carpal tunnel syndrome treated?

A
  • Wrist splint at night
  • Local steroid injection
  • Decompression surgery
130
Q

What is a cerebrovascular accident?

A

Syndrome of rapid onset neurological deficit caused by focal, cerebral, spinal or retinal infarct. Lasts more than 24 hrs

131
Q

What is the epidemiology of cerebrovascular accident?

A
  • 3rd most common cause of death in high income countries
  • Leading cause of adult disability worldwide
  • Rates are higher in Asian and black African populations
  • Uncommon in those under 40
  • More common in men
132
Q

What are the risk factors for cerebrovascular accident?

A
  • Male
  • Black or Asian
  • Hypertension
  • Past TIA
  • Smoking
  • Diabetes
  • Increasing age
  • Heart disease
  • Alcohol
  • Polycythaemia, thrombophilia
  • AF
  • Hypercholesterolaemia
  • Combined pill
  • Vasculitis
  • Infective endocarditis
133
Q

How are cerebrovascular accidents diagnosed?

A
  • Urgent CT of head= Infarction is seen as a low density lesion, subtle changes evident within 3 hrs
  • ECG, BP monitoring= Look for AF
  • FBC to look for thrombocytopenia and polycythaemia
  • Blood glucose to rule out hypoglycaemia
134
Q

How are cerebrovascular accidents treated?

A
  • Maximise reversible ischaemic tissue; ensure hydration and o2 stats
  • Thrombolysis= Tissue plasminogen activator e.g. IV alteplase, then antiplatelet therapy e.g. clopidogrel 24 hrs later
135
Q

What are the clinical features of peripheral neuropathies?

A
  • Can be asymptomatic
  • Diabetes; long history of paresthesia, pain, weakness, wasting, incontinence, sexual dysfunction
  • Foot ulcer
136
Q

What are the 6 mechanisms that cause peripheral neuropathies?

A
  1. Demyelination
  2. Axonal degeneration
  3. Compression
  4. Infarction
  5. Infiltration
  6. Wallerian degeneration
137
Q

What is the aetiology of peripheral neuropathies?

A
  • Guillain Barre syndrome
  • Diabetes
  • Alcohol
138
Q

How are peripheral neuropathies diagnosed?

A
  • Nerve conduction studies
  • FBC
  • Diabetes screen
139
Q

How are peripheral neuropathies treated?

A

Diabetic control, Amitriptyline for neuropathic pain

140
Q

What is Guillain-Barre syndrome?

A

An acute inflammatory demyelinating ascending polyneuropathy affecting the peripheral nervous system following an upper resp tract or GI infection

141
Q

What are the clinical feature of Guillain-Barre syndrome?

A
  • 1-3 weeks post infection, a symmetrical ascending muscle weakness starts
  • Lost reflexes
  • Some paraesthesia
  • Little to no muscle wasting
142
Q

What are the risk factors for Guillain-Barre syndrome?

A
  • History of resp or GI infections, 1-3 weeks prior to onset
  • Vaccinations have been implicated
  • Post pregnancy
143
Q

What causes Guillain-Barre syndrome?

A
  • Antibodies to an infection in GI or resp tract attacks the peripheral nerves
  • Usually caused by C. jejuni or CMV
144
Q

How is Guillain-Barre syndrome diagnosed?

A
  • Clinical
  • Antibody screen
  • Nerve conduction studies
  • CSF at L4: Raised proteins with normal WCC
  • Monitor FVC
145
Q

How is Guillain-Barre syndrome treated?

A
  • IV immunoglobulins for 4 days
  • Plasma exchange possible
  • Ventilate if needed
  • Low molecular weight heparin e.g. SC enoxaparin, and compression stockings to reduce thrombotic risk
146
Q

What is myasthenia gravis?

A

Autoimmune disease against nicotinic acetyl choline receptors in neuromuscular junction

147
Q

What are the clinical features of myasthenia gravis?

A
  • Weakness, fatigability of ocular, bulbar and proximal limbs
  • Improves after rest
  • Look for ptosis, diplopia and myasthenic snarl on smiling
  • Resp difficulties
148
Q

Briefly explain the pathophysiology of myasthenia gravis

A

Autoantibodies to nicotinic acetylcholine receptors or MuSK at the post-synaptic membrane of the neuromuscular junction, causing receptor blockade/loss

149
Q

What are the causes of myasthenia gravis?

A
  • Under 50= Associated with other autoimmune diseases

- Over 50= Thymic hyperplasia or thymic tumour

150
Q

What is the epidemiology of myasthenia gravis?

A
  • Women more than men
  • Peak age of incidence at 30 in women
  • Peak age of incidence at 60 in men
151
Q

How is myasthenia gravis diagnosed?

A
  • Anti-AChR antibodies in serum (incerased in 90%)
  • Electromyography or nerve stimulation tests
  • Ice test; improvement of ptosis with ice
  • CT of thymus to look for hyperplasia, tumour etc
152
Q

How is myasthenia gravis treated?

A
  • Anticholinesterases; pyridostigmine
  • Immunosuppressants if anticholinesterases don’t work; prednisolone or azathioprine
  • Thymectomy
153
Q

What is a myasthenia crisis?

A

Weakness of the respiratory muscles. Treat with plasmapheresis and IV immunoglobulins

154
Q

What is Huntington’s disease?

A

Autosomal dominant neurogenerative, loss of GABA and Ach, but dopamine spared.

155
Q

What is Chorea?

A

A continuous flow of jerky, semi purposeful movements. May interfere with voluntary movements but cease during sleep

156
Q

What are the clinical features of Huntington’s disease?

A
  • Relentlessly progressive
  • Chorea
  • Personality changes
  • Dysarthria, dysphagia and abnormal eye movements
  • Associated with seizures
  • Later, dementia
  • Behavioural symptoms
157
Q

Briefly explain the pathophysiology of Huntington’s disease?

A

Presence of mutant huntingtin protein leads to loss of neurones in the caudate nucleus and putamen of the basal ganglia. This leads to depletion of GABA and ACh

158
Q

What is the epidemiology of Huntington’s disease?

A
  • Usually onset in middle age
  • Autosomal dominant condition with full penetrance
  • Very rare
159
Q

What is the aetiology of Huntington’s disease?

A
  • Autosomal dominant

- CAG repeats in Huntingtin protein gene on chromosome 4

160
Q

How is Huntington’s disease diagnosed?

A
  • Genetic testing

- CT/MRI= Shows caudate nucleus atrophy and increased size of the frontal horns of lateral ventricles

161
Q

How is Huntington’s disease treated?

A
  • Treat chorea symptoms= Benzodiazepine, anticonvulsants, muscle relaxant, sodium valproate
  • Genetic counselling
  • Antidepressants such as SSRIs
  • Antipsychotic agents
  • Risperidone for aggression
162
Q

What are the risk factors for Huntington’s disease?

A

Family history

163
Q

What is epilepsy?

A

The recurrent tendancy to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures/

164
Q

What are the types of epilepsy?

A
  • Generalised tonic clonic (Grand mals)
  • Absence (Petite mals)
  • Myoclonic, tonic and akinetic
  • Partial
165
Q

What are the risk factors for epilepsy?

A
  • Family history
  • Premature born babies
  • Abnormal vessels in brain
  • Alzheimer’s or dementia
  • Use of drugs e.g. cocaine
  • Stroke/ brain tumour/ infection
166
Q

Briefly explain the pathophysiology of epilepsy

A

Uncontrolled electrical activity in the brain. Innervation of muscle fibres can cause physical movements and sensory disturbance

167
Q

What is generalised tonic clonic epilepsy?

A
  • Sudden onset of rigid tonic phase, followed by convulsion (clonic) phase/
  • Tongue biting, incontinence of urine, drowsiness/ coma
168
Q

What is absense epilepsy?

A
  • Usually in childhood

- Caese activity, stares and pales

169
Q

What is myoclonic, tonic and akinetic epilepsy?

A
  • Muscle jerking (myoclonic), intense stiffening (Tonic) or cessation of movement
  • Falling and loss of consciousness (Akinetic)
170
Q

How is epilepsy diagnosed?

A
  • To make a clinical diagnosis, there needs to be at least 2 unprovoked seizures >24 hrs apart
  • Short term video EEG
  • CT, MRI
171
Q

How is generalised tonic clonic epilepsy treated?

A
  • AED: Sodium valproate
  • Lamotrigine
  • Carbamazepine
  • Diazepam for seizure control
172
Q

How is absence epilepsy treated?

A
  • AED: Sodium valproate
  • Lamotrigine
  • Ethosuximide
173
Q

What is the first line treatment for partial epilepsy?

A
  • AED: Lamotrigine or carbamazepine
174
Q

What are the types of motor neurone disease?

A
  • Amyotrophic lateral sclerosis (most common)= UMN + LMN
  • Primary lateral sclerosis= UMN
  • Progressive muscular atrophy= LMN
  • Progressive bulbar palsy= UMN+ LMN of the lower cranial nerves
175
Q

What are the clinical features of motor neurone disease?

A
  • Depends on type
  • Upper limbs; Reduced dexterity, stiffness, wasting of intrinsic muscles of the hands
  • Lower limbs; Tripping, stumbling gait, foot drop
  • Bulbar; Slurred speech, hoarsness, dysphagia
  • Muscular atrophy and spasticity
  • Never affects eye movements or sensory
176
Q

What causes motor neurone disease?

A
  • Unknown

- Family history= Mutations in free radical scavenging enzyme copper/zinc superoxide dismutase

177
Q

What is the epidemiology motor neurone disease?

A
  • Relatively uncommon
  • Middle age
  • More common in men
178
Q

How is motor neurone disease diagnosed?

A
  • Clinical= 3 or more LMN+UMN signs
  • EMG: Muscle degeneration
  • Brain/ cord MRI= Helps to exclude structural causes
  • Lumbar puncture to exclude inflammatory causes
179
Q

How is motor neurone disease treated?

A
  • Sodium channel blocker; Riluzole
  • Symptomatic treatment=
    Spasms; Baclofen
    Drooling; Propantheline
    Analgesia; NSAIDs such as diclofenac
180
Q

What is Parkinson’s disease?

A

Degeneration movement disorder caused by reduction in dopamine in the substantia nigra

181
Q

What is the epidemiology of Parkinson’s disease?

A
  • Increasing prevelance with age
  • Peak age of onset at 35-65 yrs
  • More common in males
182
Q

What causes Parkinson’s disease?

A
  • Genetic links

- Some environmental link; less common in smokers

183
Q

What are the clinical features of Parkinson’s disease?

A
  • Gradual onset of symptoms= asymmetrical
  • Starts with impaired dexterity or unilateral foot drop
  • Anosmia, depression, aches, REM sleep disorders, urinary urgency, hypotension
  • Rigidity, bradykinesia, and resting tremor
  • Pill rolling tremor
  • Speech becomes quiet, indestinct and flat
  • Drooling
184
Q

Briefly describe the pathophysiology of Parkinson’s disease

A

Progressive loss of dopamine secreting cells from the substantia nigra causes an alteration in neural circuits in the basal ganglia. Thought to be due to abnormal accumulation of alpha-synuclein bound to ubequitin= lewy bodys in the cytoplasm

185
Q

How is Parkinson’s disease diagnosed?

A
  • Clinical
  • Can confirm with response to levodopa
  • MRI = intially normal, but will show atrophy of substantia nigra
186
Q

How is Parkinson’s disease treated?

A
  • Gold standard= Levodopa alongside a decarboxylase inhibitor e.g. co-careldopa
  • Dopamine agonist
  • MAO-B inhibitors; selegiline
  • Deep brain stimulation
187
Q

What is the most common cause of acute compression of the spinal cord?

A

Vertebral body neoplasms (commonly from lung, breast, kidney, prostate or thyroid)

188
Q

How are spinal cord compressions diagnosed?

A
  • MRI (Gold standard)

- Biopsy/ surgical exploration may be required

189
Q

What is the epidemiology of Alzheimer’s Disease?

A

Onset may be as early as 40 yrs (and even earlier if patient has Down’s syndrome)

190
Q

What are the causes of Alzheimer’s Disease?

A
  • Environmental and genetic
  • Accumulation of beta-amyloid peptide
  • Defective clearance of beta-amyloid plaques
191
Q

What are the risk factors for Alzheimer’s Disease?

A
  • 1st degree relative
  • Down’s syndrome
  • Homozygous for apolipiprotein e
  • Hypertension, diabetes, hyperlipidaemia, AF
  • Decreased activity
  • Depression and loneliness
192
Q

What are the clinical features of Alzheimer’s Disease?

A
  • General features of dementia
  • Insidious onset with steady progression
  • Short term memory loss, disintergreation of personality
  • Decline in language, visuospatial skills and agnosia
193
Q

How is Alzheimer’s Disease treated?

A
  • Acetylcholinesterase inhibitors e.g. rivastagmine
  • Antiglutamatergic treatment= Memantine
  • Folic acid and B vitamins
194
Q

What are the types of dementia?

A
  • Alzheimers (50%)
  • Vascular (25%)
  • Lewy-body (15%)
  • Fronto-temporal
  • Parkinsons
  • Mixed
195
Q

What are the risk factors for dementia?

A

Family history, age, Down’s syndrome, alcohol use, obesity, high blood pressure, diabetes, hypercholesterolaemia, atherosclerosis, depression, high oestrogen

196
Q

What are the clinical features of vascular dementia?

A

Stepwise deterioration with declines followed by short periods of stability. History of TIA or strokes.

197
Q

Briefly explain the pathophysiology of vascular dementia

A

Brain damage due to cerebrovascular disease; either a major stroke, multiple smaller unrecognised strokes or chronic changes in smaller vessels

198
Q

Briefly explain the pathophysiology of Lewy-body dementia

A

Deposition of abnormal protein within neurons in the brain stem and neocortex

199
Q

What are the clinical features of Lewy-body dementia?

A
  • Fluctuating cognition with pronounced variation in attention and alertness
  • Memory loss in later stages
  • Impairment in attention, visuospatial ability is prominent
  • Depression and sleep disorders
  • Parkinson’s
200
Q

How is dementia diagnosed?

A
  • History; assess cognitive functions
  • Mini mental state exam (24 or less is impairment in cognition)
  • Exclude rarer causes of dementia (B12 deficiency, thyroid fucnction tests, HIV)
  • MRI to see extent of atrophy
201
Q

How is dementia prevented?

A
  • Healthy behaviours
  • Smoking cessation
  • Good diet
  • Physical activity
  • Mental activities
  • Leisure activities
  • Education

Phase 2a (31 decks)

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