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Phase 3a - Arun&Erin > Neuro > Flashcards

Neuro Flashcards

1
Q

What is a tension headache?

A

Typically cause a mild ache or pressure in a band-like pattern around the head.

Develops and resolves gradually

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2
Q

What 5 things are tension headaches associated with?

A
  • Stress
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
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3
Q

What is the management of tension headaches?

A
  • Simple analgesia (ibuprofen/paracetamol)
  • Amitriptyline: 1st line for chronic/frequent tension headaches
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4
Q

What are 5 red flags associated with headache? (10)

A
  • Fever, photophobia, neck stiffness (meningitis, encephalitis)
  • New neurological symptoms (haemorrhage/tumours)
  • Visual disturbance (GCA, glaucoma, tumours)
  • Sudden onset occipital headache (SAH)
  • Worse on coughing or straining (raised intracranial pressure)
  • Postural, worse on standing, lying, bending over (raised IP)
  • Vomiting (raised IP, carbon monoxide poisoning)
  • Hx of trauma (intracranial haemorrhage)
  • Hx of cancer (brain metastasis)
  • Pregnancy (pre-eclampsia)
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5
Q

What is trigeminal neuralgia?

A

Causes sudden intense shooting facial pain along distribution of trigeminal nerve
May be triggered by touch, eating, talking, shaving, cold

  • ophthalmic
  • maxillary
  • mandibular
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6
Q

What is the management of trigeminal neuralgia?

A

Carbamazepine: 1st line

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7
Q

What is a cluster headache?

A

Severe unilateral headaches, usually orbital, that come in clusters of attacks then disappear for extended periods

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8
Q

Describe a typical patient who suffers from cluster headaches and their triggers

A

30-50 year old male smoker
Triggers: alcohol, strong smells, exercise

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9
Q

Name 5 symptoms of cluster headaches

A
  • Red, swollen, watering eye
  • Miosis (pupil constriction)
  • Ptosis (eyelid drooping)
  • Nasal discharge
  • Facial sweating

Typically unilateral

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10
Q

What is the management of an acute attack of cluster headaches?

A

Triptans (subcutaneous/intranasal sumatriptan)
High flow 100% oxygen

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11
Q

What is the prophylaxis management of cluster headaches?

A

Verapamil
Other options: Occipital nerve block, Prednisolone, Lithium

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12
Q

What is temporal arteritis?

A

Giant Cell Arteritis is a type of systemic vasculitis affecting medium and large arteries

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13
Q

What is the key complication of temporal arteritis?

A

Vision loss

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14
Q

Name 4 presenting symptoms of temporal arteritis

A
  • Unilateral headache: severe around temple/forehead
  • Scalp tenderness
  • Jaw claudication
  • Blurred/double vision (If left untreated - vision loss)
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15
Q

Name 3 associated features of temporal arteritis

A
  • Polymyalgia rheumatica Sx: shoulder/pelvic girdle pain & stiffness
  • Systemic Sx: wt loss, fatigue, fever
  • Carpel tunnel syndrome
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16
Q

Name 4 things a diagnosis of temporal arteritis is based on

A
  • Clinical presentation
  • Raised inflammatory markers (ESR)
  • Temporal artery biopsy (shows multinucleated giant cells)
  • Duplex ultrasound (shows hypoechoic ‘halo’ sign and stenosis of temporal artery)
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17
Q

What is the first line treatment of temporal arteritis?

A

Steroids started immediately to reduce the risk of vision loss:
* Prednisolone with no visual Sx or jaw claudication
* Methylprednisolone with visual Sx or jaw claudication

Once diagnosis confirmed, steroid dose is slowly weaned over 1-2 years

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18
Q

Name 3 other medications used to manage temporal arteritis

A
  • Aspirin: decreases vision loss/strokes
  • PPI (omeprazole): gastroprotection while on steroids
  • Bisphosphonates & calcium/vit D: bone protection while on steroids
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19
Q

What are the four main types of migraine?

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine
  • Hemiplegic migraine
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20
Q

What are the 5 stages of a migraine?

A
  1. Premonitory/Prodromal: can begin several days before the headache)
  2. Aura
  3. Headache
  4. Resolution
  5. Postdromal/Recovery
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21
Q

Name 8 typical features of a migraine headache

A
  • Usually unilateral, but can be bilateral
  • Moderate-severe intensity
  • Pounding/throbbing
  • Photophobia
  • Phonophobia
  • Osmophobia
  • Aura
  • N+V
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22
Q

What are the symptoms of an aura?

A

Can affect vision, sensation or language
* Visual Sx: sparks in vision, blurred, lines across vision, loss of visual fields
* Sensation: tingling, numbness
* Language: dysphasia

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23
Q

What are the main features of a hemiplegic migraine?

A
  • Hemiplegia (unilateral limb weakness)
  • Ataxia (loss of coordination)
  • Impaired consciousness

Can mimic a stroke/TIA, so must exclude these

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24
Q

Name 8 triggers of a migraine

A
  • Stress
  • Bright lights
  • Strong smells
  • Foods: chocolate, cheese, caffeine
  • Dehydration
  • Menstruation
  • Disrupted sleep
  • Trauma
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25
Q

Name 4 medications used to treat an acute attack of a migraine

A
  • NSAIDs (ibuprofen / naproxen)
  • Paracetamol
  • Triptans (sumatriptan)
  • Antiemetics for vomiting (metoclopramide / prochlorperazine)

Non-medical management: retreat to a dark, quiet room, sleeping

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26
Q

What is the role of triptans in the management of migraines?

A

Taken as soon as migraine headache starts, used to halt attack
If it doesn’t work, a second dose should not be taken for the same attack

They bind to & stimulate serotonin receptors to:
* inhibit transmission of pain signals
* inhibit release of inflammatory neuropeptides
* cause cranial vasoconstriction

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27
Q

Name 5 prophylactic medications used to treat a migraine?

A
  • Propanolol
  • Amitriptyline
  • Topiramate (teratogenic)
  • Pizotifen
  • Sodium valproate
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28
Q

What is the management of menstrual migraines?

A

Prophylactic triptans: e.g. zolmitriptan/frovatriptan

Sx tend to occur 2 days before until 3 days after start of menstruation

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29
Q

Name the 2 types of cerebrovascular accidents

A
  • Ischaemic stroke
  • Haemorrhagic stroke
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30
Q

Name 4 things that can disrupt the blood supply to the brain

A
  • Thrombus/embolus
  • Atherosclerosis
  • Shock
  • Vasculitis
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31
Q

What is a TIA?

A

Temporary (< 24hrs) neurological dysfunction caused by ischaemia without infarction

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32
Q

Name 6 symptoms of stroke

A
  • Limb weakness
  • Facial weakness
  • Dysphasia
  • Visual field defects
  • Sensory loss
  • Ataxia
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33
Q

Name 5 risk factors for stroke

A
  • Previous stroke or TIA
  • Atrial Fibrillation
  • Carotid artery stenosis
  • Hypertension
  • Diabetes
  • Raised cholesterol
  • Family Hx
  • Smoking
  • Obesity
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34
Q

What is the FAST tool for stroke?

A

Face
Arm
Speech
Time

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35
Q

Tx: What is the management of a TIA?

A
  • Aspirin 300mg daily
  • Referral for specialist assessment
  • Diffusion-weighted MRI scan
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36
Q

Tx: What is the immediate management of a stroke?

A
  • Immediate CT brain (to exclude haemorrhage)
  • Aspirin 300mg daily for 2 weeks
  • Admission to a specialist stroke centre
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37
Q

Tx: What management is considered once haemorrhage is excluded?

A

Thrombolysis with alteplase

  • Alteplase is a tissue plasminogen activator that rapidly breaks down clots
  • It may be given within 4.5hrs of symptom onset

Thrombectomy
* Considered in patients with a confirmed blockage of the proximal anterior/posterior circulation
* It may be considered within 24hrs of symptom onset and alongside IV thrombolysis

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38
Q

Ix: Name 2 things that are always investigated for in patients who have had a TIA or stroke

A
  • Carotid artery stenosis: carotid imaging
  • Atrial fibrillation: ECG

Anticoagulation is initiated for AF (after excluding haemorrhage and finishing 2 weeks of aspirin)
Surgical interventions are considered for significant CAS (carotid endarterectomy or angioplasty and stenting)

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39
Q

Tx: What is the secondary prevention of a stroke?

A
  • Clopidogrel 75mg once daily
  • Atorvastatin 20-80mg (not started immediately, usually delayed by at least 48hrs)
  • Blood pressure and diabetes control
  • Addressing modifiable risk factors (smoking, obesity, exercise)
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40
Q

What is a seizure?

A

Transient episodes of abnormal electrical activity in the brain

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41
Q

Name 5 types of seizures

A
  • Generalised tonic-clonic
  • Partial / focal
  • Myoclonic
  • Tonic
  • Atonic
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42
Q

What is a generalised tonic-clonic seizure?

A
  • Tonic - muscle tensing, followed by clonic - muscle jerking
  • Associated with a complete loss of consciousness
  • Before seizure pt may experience aura
  • May be tongue biting, incontinence, groaning and irregular breathing
  • After seizure: post-ictal period - pt is confused, tired, irritable, low
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43
Q

What is a partial/focal seizure?

A
  • Occurs in an isolated brain area, often in temporal lobes
  • Affect hearing, speech, memory, emotions
  • Pt remains awake
  • Simple: pt remains aware
  • Complex: pt loses awareness
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44
Q

Name 4 symptoms of a partial seizure

A
  • Deja vu
  • Strange smells/tastes/sight/sound sensations
  • Unusual emotions
  • Abnormal behaviours
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45
Q

How do myoclonic seizures present?

A
  • Sudden, brief muscle contractions
  • Pt remains awake
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46
Q

How do tonic seizures present?

A
  • Sudden onset of increased muscle tone - entire body stiffens
  • Only last a few seconds - a few minutes
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47
Q

How do atonic seizures present?

A
  • Cause ‘drop attacks’
  • Involve sudden loss of muscle tone, often resulting in a fall
  • Pts usually aware during episodes
  • Often begin in childhood
  • May be indicative of Lennox-Gastaut syndrome
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48
Q

How do absence seizures present?

A
  • Usually seen in children
  • Pt becomes blank, stares into space, then abruptly returns to normal
  • Unaware of surroundings and do not respond during episode
  • Typically last 10-20 secs
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49
Q

What is epilepsy?

A

Recurrent (2 or more) unprovoked epileptic seizures occuring > 24hrs apart

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50
Q

Name 2 main investigations and 4 additional investigations for epilepsy

A
  • EEG (electroencephalogram)
  • MRI brain: structural pathology

Additional Ix to exclude associated pathology:
* ECG
* Serum electrolytes (Na, K, Ca, Mg)
* Blood glucose (hypoglycaemia, diabetes)
* Blood & urine cultures, lumbar puncture (sepsis, encephalitis, meningitis)

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51
Q

What is the treatment for generalised tonic-clonic seizures?

A
  • Men/women who can’t have children: Sodium valproate
  • Women able to have children: Lamotrigine/ Levetiracetam
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52
Q

What is the treatment for partial/focal seizures?

A

Men/women who can’t have children: Lamotrigine/ Levetiracetam
Women able to have children: Lamotrigine/ Levetiracetam

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53
Q

What is the treatment for myoclonic seizures?

A

Men/women who can’t have children: Sodium valproate
Women able to have children: Levetiracetam

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54
Q

What is the treatment for tonic & atonic seizures?

A

Men/women who can’t have children: Sodium valproate
Women able to have children: Lamotrigine

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55
Q

What is the treatment for absence seizures?

A

Men/women who can’t have children: Ethosuximide
Women able to have children: Ethosuximide

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56
Q

How does sodium valproate work?

A

Increases activity of GABA: has a calming effect on the brain

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57
Q

Name 5 side effects of sodium valproate

A
  • Teratogenic
  • Liver damage / Hepatitis
  • Hair loss
  • Tremor
  • Reduced fertility
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58
Q

What is Status Epilepticus?

A

Either:
* A seizure lasting more than 5 minutes
* Multiple seizures without regaining consciousness in between

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59
Q

What is the management of status epilepticus?

A

ABCDE approach:
* Secure airway
* Give high-conc oxygen
* Check blood glucose levels
* Gain IV access (insert a cannula)

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60
Q

What is the medical treatment of status epilepticus?

A
  • 1st line: Benzodiazepine (repeated after 5-10 mins if seizure continues)
  • 2nd line (after 2 doses of benzos): IV levetiracetam, phenytoin or sodium valproate
  • 3rd line: phenobarbital or general anaesthesia
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61
Q

What is NEAD?

A

Non-epileptic attack disorder
* Seizures without a physical cause
* May be caused by brain dealing with overwhelming stress by ‘shutting down’
* Affects people with dissociative disorders

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62
Q

Name 4 features of a dissociative seizure (NEAD)?

A
  • Convulsions of arms/legs/head/body (uni- or bilateral)
  • Lose control of bladder/bowels
  • Bite your tongue
  • Go blank/stare
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63
Q

What is narcolepsy?

A

Condition where brain is unable to regulate sleeping and waking patterns normally

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64
Q

Name 5 features of narcolepsy

A
  • Excessive daytime sleepiness
  • Sleep attacks: falling asleep suddenly without warning
  • Cataplexy: temporary loss of muscle control resulting in weakness/possible collapse
  • Sleep paralysis: temporary inability to move/speak when waking up or falling asleep
  • Excessive dreaming / waking up in the night
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65
Q

What is the management of narcolepsy?

A
  • Improve sleeping habits
  • Take frequent, brief naps in the day
  • Keep to a strict bedtime routine
  • Inform DVLA and don’t drive
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66
Q

What is cataplexy?

A

A condition where strong emotion or laughter causes sudden brief muscle weakness, often resulting in collapse

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67
Q

What is the causative organism of shingles?

A

Varicella zoster virus (VZV)

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68
Q

What is the aetiology of shingles?

A
  • Primary infection with VZV manifests as chickenpox (varicella)
  • Following resolution, virus establishes latent infection within sensory nerve ganglions
  • Reactivation of these dormant viruses results in shingles (herpes zoster)
  • Virus spreads through affected sensory nerve, causing neuronal damage and causing a skin rash to develop in the corresponding dermatone
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69
Q

What are the signs of shingles?

A
  • Tingling/ pain in an area of skin
  • Headache/ feeling generally unwell
  • Rash appears a few days later anywhere on body
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70
Q

Describe the shingles rash

A
  • Blotches on skin, on one side of the body
  • Blotches become itchy blisters that ooze fluid - blisters dry out and scab a few days later
  • Rash may be around eye - ophthalmic division of trigeminal nerve
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71
Q

What is the treatment of shingles?

A

Mild rash - Tx not always needed
Antiviral tablets within 72 hours if:
* Weakened immune system
* Rash/pain is moderate/severe
* Rash is affecting other areas of your body apart from chest, tummy, back

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72
Q

Name an antiviral that can be used to treat shingles

A

Acyclovir

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73
Q

How long does shingles last?

A

Can take up to 4 weeks for rash to heal

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74
Q

What is Wernicke-Korsakoff syndrome?

A

Thiamine deficiency due to excessive alcohol consumption.
* thiamine is poorly absorbed in the presence of alcohol

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75
Q

What are the 2 stages of Wernicke-Korsakoff syndrome?

A
  • Wernicke’s encephalopathy: brain inflammation
  • Korsakoff’s syndrome: long-term condition due to untreated Wernicke’s encephalopathy
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76
Q

Name 3 symptoms of Wernicke’s encephalopathy

A
  • Confusion
  • opthalmoplegia
  • Ataxia: difficulty with coordinated movements
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77
Q

Name 3 symptoms of Korsakoff syndrome

A
  • Memory impairment: confabulation - invented memory
  • Difficulty understanding new info/ learning new skills
  • Personality changes: apathetic, very talkative etc..
  • Problems with concentration, planning, making decisions, solving problems
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78
Q

What is the treatment of Wernicke-Korsakoff syndrome?

A
  • IV thiamine
  • Stop drinking alcohol
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79
Q

What is Huntington’s disease?

A
  • Autosomal dominant condition that causes progressive neurological dysfunction
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80
Q

What is the genetic mutation in Huntington’s disease?

A
  • Trinucleotide repeat disorder
  • Genetic mutation in the HTT gene on chromosome 4 which codes for the Huntingtin (HTT) protein
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81
Q

What age do Huntington’s symptoms begin?

A

30 - 50 years old

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82
Q

Definition: Genetic anticipation

A

Successive generations have more repeats in the gene resulting in:
* Earlier age of onset
* Increased severity of disease

Feature of trinucleotide repeat disorders

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83
Q

What is the presentation of Huntington’s disease?

A

Cognitive/psychiatric/mood problems, followed by movement disorders:
* Chorea (involuntary random abnormal body movements)
* Dystonia (abnormal tone)
* Rigidity (increased resistance to passive joint movement)
* Eye movement disorders
* Dysarthria (speech difficulties)
* Dysphagia (swallowing difficulties)

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84
Q

How is a diagnosis of Huntinton’s disease made?

A

Genetic testing

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85
Q

What is the management of Huntington’s disease?

A

No cure
* Physio
* Speech & language therapy
* Tetrabenazine (for chorea Sx)
* Antidepressants
* End of life care
* Advanced directives

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86
Q

What is the prognosis of Huntington’s disease?

A
  • Life expectency is ~ 10-20 years after onset of Sx
  • As disease progresses, Pt becomes more frail/ susceptible to illnesses
  • Death often due to aspiration pneumonia or suicide
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87
Q

Definition: Parkinson’s disease

A

Condition where there is a progressive reduction in dopamine in the basal ganglia leading to disorders of movement

Sx are asymmetrical

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88
Q

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

A
  • Resting tremor: worse at rest
  • Rigidity: resisting passive movement
  • Bradykinesia: slow movement
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89
Q

Name 5 clinical features of Parkinson’s disease (8)

A
  • Pin-rolling tremor
  • Cogwheel rigidity
  • Bradykinesia: shuffling gait, micrographia, festinating gait, difficulty initiating movement, difficulty turning around, reduced facial movements/expressions
  • Depression
  • Insomnia
  • Anosmia
  • Postural instability
  • Cognitive impairment/ memory problems
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90
Q

Tx: What are the 4 treatment options for Parkinson’s disease?

A
  • Levodopa + peripheral decarboxylase inhibitor (e.g. carbidopa, benserazide)
  • COMT inhibitors
  • Dopamine agonists
  • Monoamine oxidase-B inhibitors
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91
Q

What is Levodopa?

A
  • Synthetic dopamine
  • Combined with a peripheral decarboxylase inhibitor which stops it from being metabolised before it reaches the brain
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92
Q

Name 2 combination drugs to treat Parkinson’s

A
  • Co-beneldopa (levodopa + benserazide)
  • Co-careldopa (levodopa + carbidopa)
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93
Q

What is the main SE of Levodopa and it’s Tx?

A

SE: Dyskinesia
Tx: Amantadine (glutamate antagonist)

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94
Q

Definition: Dyskinesia

A

Abnormal movements associated with excessive motor activity:

  • Dystonia: excessive muscle contraction leads to abnormal postures/exaggerated movements
  • Chorea: abnormal involuntary movements, jerking
  • Athetosis: involuntary twisting/writhing movements, usually in fingers/hands/feet
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95
Q

What are COMT inhibitors?

A

e.g. entacapone

  • Inhibits catechol-o-methyltransferase which metabolises levodopa
  • Taken with Levodopa to slow breakdown in the brain
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96
Q

What are dopamine agonists?

A
  • Mimic action of dopamine in the basal ganglia, stimulating dopamine receptors
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97
Q

Name 3 dopamine agonists

A
  • Bromocriptine
  • Cabergoline
  • Pergolide
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98
Q

What is the main SE of prolonged dopamine agonist use?

A

Pulmonary fibrosis

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99
Q

What are monoamine oxidase-B inhibitors?

A
  • Block the action of monoamine oxidase-B enzymes which break down the neurotransmitter dopamine

Monoamine oxidase enzymes break down other neurotransmitters such as serotonin and adrenaline, but monoamine oxidase-B is specific to dopamine

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100
Q

Name 2 examples of monoamine oxidase-B inhibitors

A
  • Selegiline
  • Rasagiline
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101
Q

What are the 4 types of dementias from most prevalent to least?

A
  • Alzheimer’s disease
  • Vascular dementia
  • Dementia with Lewy bodies (DLB)
  • Fronto-temporal dementia
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102
Q

Name 5 irreversible causes of dementia

A
  • Neurodegenerative: Alzheimer’s, F-T dementia, DLB, Parkinson’s, Huntington’s
  • Infections: HIV, encephalitis, syphilis
  • Toxins: alcohol, barbiturates, benzodiazepines
  • Vascular: vascular dementia, CVD
  • Head trauma
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103
Q

Name 3 reversible causes of dementia

A
  • Neurological: normal pressure hydrocephalus, intracranial tumours, CSH
  • Vitamin deficiencies: B12, folic acid, thiamine, nicotinic acid
  • Endocrine: Cushing’s, hypothyroidism
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104
Q

What is the pathophysiology of Alzheimer’s disease?

A
  • Degeneration of cholinergic neurons in the nucleus basalis of Meynert leading to acetylcholine deficiency due to accumulation of beta amyloid plaques
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105
Q

What are 2 microscopic physiological changes seen in Alzheimer’s disease?

A
  • Neurofibrillary tangles (intracellularly)
  • Beta-amyloid plaque formation (extracellularly)

These are pathological lesions progressively distributed around the brain

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106
Q

What are 3 macroscopic physiological changes seen in Alzheimer’s disease?

A
  • Cortical atrophy (commonly hippocampus)
  • Widened sulci
  • Enlarged ventricles
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107
Q

Name 7 risk factors for Alzheimer’s disease

A
  • Advancing age
  • Family Hx
  • Genetics
  • Down’s syndrome
  • Low IQ
  • CVD
  • Vascular RFs: stroke/MI, smoking, HTN, DM, high cholesterol
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108
Q

Clinical features: Name 3 symptoms in early stages of AD

A
  • Memory lapses
  • Difficulty finding words
  • Forgetting names of people/places
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109
Q

Clinical features: Name 4 symptoms during disease progression of AD

A
  • Apraxia
  • Agnosia
  • Confusion
  • Language problems
  • Impairment of executive functions
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110
Q

Clinical features: Name 7 symptoms in later stages of AD

A
  • Disorientation to time/place
  • Wandering
  • Apathy
  • Incontinence
  • Eating problems
  • Depression
  • Agitation
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111
Q

Aetiology: What is the cause of vascular dementia?

A

Cerebrovascular disease due to:
* stroke
* multi-infarcts
* chronic changes in small vessels (arteriosclerosis)

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112
Q

Name 6 clinical features of vascular dementia

A
  • Stepwise rather than continuous deterioration
  • Memory loss
  • Emotional and personality changes
  • Confusion
  • Neurological signs/Sx
  • On examination –> focal neurology (UMN signs) and signs of CVD
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113
Q

Ix: Name 10 investigations for dementia

A

Blood tests: FBC,CRP,U&E,calcium,LFT,glucose,vit B12 & folate,TFT

Non-routine Ix:
* Urine dipstick
* Chest Xray
* Syphilis serology & HIV testing
* CT/ MRI/ SPECT (to differentiate between AD, VascD and F-TD)
* ECG
* EEG
* Lumbar puncture
* Genetic tests
* Cognitive assessment

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114
Q

DDx: Name 5 differentials for dementia (9)

A
  • Normal ageing/ mild cognitive impairment
  • Delirium
  • Trauma: stroke, hypoxic, brain injury
  • Depression: poor concentration/impaired memory common in depression in the elderly
  • Late onset schizophrenia
  • Amnesic syndrome: severe disruption in memory with minimal deterioration in cognitive function
  • Learning disability
  • Substance misuse
  • Drug side effects: opiate, benzodiazepine
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115
Q

After a diagnosis of dementia, what are patients legally obliged to do?

A

Contact DVLA

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116
Q

Tx: What are 5 non-pharmacological managements of dementia?

A
  • Social support
  • Increasing assistance with day-to-day activities
  • Education
  • Community dementia teams & services
  • Home nursing and personal care
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117
Q

What are the aims of dementia treatment?

A
  • Promote independence
  • Maintain function
  • Treat symptoms
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118
Q

Tx: What is the pharmacological management of dementia?

A
  • Acetylcholinesterase inhibitors (mild/moderate AD)
  • N-methyl-D-aspartate receptor antagonist (moderate AD in those who are intolerant/contraindication to AChE inhibitors / severe AD)
  • Antipsychotic for challenging behaviour (risperidone)
  • Antidepressant for low mood (sertraline)
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119
Q

Tx: Name 3 AChE inhibitors

A
  • Donepezil
  • Galantamine
  • Rivastigmine
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120
Q

Tx: Name an NMDA receptor antagonist

A

Memantine

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121
Q

What is normal pressure hydrocephalus?

A

CSF (cerebrospinal fluid) building up abnormally within brain and spinal cord

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122
Q

What is the triad of symptoms in normal pressure hydrocephalus?

A
  • Dementia
  • Gait disturbance
  • Urinary incontinence
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123
Q

What are the 2 causes of hydrocephalus?

A
  • Over-production of CSF
  • Problem with draining/ absorbing CSF
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124
Q

What is normal CSF physiology?

A
  • Four ventricles: two lateral, 3rd ventricle, 4th ventricle
  • Ventricles contain CSF: provides cushion for brain tissue
  • CSF created in four choroid plexuses (one in each ventricle) and by walls of the ventricles
  • CSF absorbed into venous system by arachnoid granulations
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125
Q

What is the most common cause of hydrocephalus?

A

Aqueductal stenosis
* Cerebral aqueduct connecting 3rd + 4th ventricle is stenosed
* Blocks normal CSF flow
* CSF build up in lateral & 3rd ventricles
* Insufficient CSF drainage

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126
Q

Name 4 causes of hydrocephalus

A
  • Aqueductal stenosis
  • Arachnoid cysts: can block outflow of CSF
  • Arnold-Chiari malformation: cerebellum herniates down through foramen magnum, blocking outflow of CSF
  • Chromosomal abnormalities / congenital malformations
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127
Q

Name 5 signs of hydrocephalus in children

A
  • Enlarged head circumference: outward pressure on cranial bones (babies)
  • Bulging anterior fontanelle
  • Poor feeding & vomiting
  • Poor tone
  • Sleepiness
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128
Q

What is the treatment of hydrocephalus?

A

Ventriculoperitoneal Shunt
* Drains CSF from ventricles into peritoneal cavity (space & easily reabsorbed)
* Valve can regulate amount of CSF that is drained

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129
Q

Name 5 complications of a VP shunt

A
  • Infection
  • Blockage
  • Excessive drainage
  • Intraventricular haemorrhage during shunt related surgery
  • Outgrowing them (need replacing every 2 years as child grows)
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130
Q

Name 4 causes of increased pressure in the intracranial space

A
  • Brain tumours
  • Intracranial haemorrhage
  • Idiopathic intracranial hypertension
  • Abscess / infection
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131
Q

What concerning features indicate intracranial hypertension in patients with a headache?

A
  • Constant headache
  • Nocturnal
  • Worse on waking
  • Worse on coughing, straining, bending forward
  • Vomiting
  • Papilloedema on fundoscopy
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132
Q

What are 5 other presenting features of raised intracranial hypertension (not regarding headache)?

A
  • Altered mental state
  • Visual field defects
  • Seizures
  • Unilateral ptosis
  • 3rd & 6th nerve palsies
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133
Q

What are benign and malignant brain tumours called?

A
  • Benign - meningiomas
  • Malignant - glioblastomas
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134
Q

What is the presentation of brain tumours?

A

Progressive focal neurological Sx (depending on location of lesion)
Sx of raised ICP:
* Headache
* N+V
* Papilloedema
* Coma

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135
Q

What is papilloedema?

A

Swelling of the optic disc secondary to raised intracranial pressure

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136
Q

What are gliomas?

A

Tumours of the glial cells in the brain/spinal cord
* Glial cells surround neurones
* Include astrocytes, oligodendrocytes, ependymal cells

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137
Q

What are the 3 main types of glioma? (from most to least malignant)

A
  • Astrocytoma (most common form is glioblastoma)
  • Oligodendroglioma
  • Ependymoma
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138
Q

What are meningiomas?

A

Tumours growing from the cells of the meninges
* Usually benign, but take up space
* Mass effect can lead to raised intracranial pressure & neurological Sx

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139
Q

Name 4 cancers that metastasise to the brain

A
  • Lung
  • Breast
  • Renal cell carcinoma
  • Menaloma
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140
Q

What is the defect caused by pituitary tumours?

A

Can press on the optic chiasm causing bitemporal hemianopia (loss of outer half of visual fields in both eyes)

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141
Q

Name 4 hormone related diseases caused by pituitary tumours

A
  • Acromegaly (excessive GH)
  • Hyperprolactinaemia (excessive prolactin)
  • Cushing’s disease (excessive ACTH & cortisol)
  • Thyrotoxicosis (excessive TSH & thyroid hormone)
142
Q

What are 4 ways to manage pituitary tumours?

A
  • Trans-sphenoidal surgery
  • Radiotherapy
  • Bromocriptine (to block excess prolactin)
  • Somatostatin analogues (to block excess GH): e.g. octreotide
143
Q

What are acoustic neuromas?

A

Benign tumours of the Schwann cells that surround the auditory nerve
* Occur at the cerebellopontine angle
* Usually unilateral

144
Q

Name 5 symptoms of acoustic neuroma

Gradual onset

A
  • Unilateral sensorineural hearing loss
  • Unilateral tinnitus
  • Dizziness / imbalance
  • Sensation of fullness in ear
  • Facial nerve palsy
145
Q

What is the management of acoustic neuroma?

A
  • Conservative + monitoring
  • Surgery to remove tumour
  • Radiotherapy to reduce growth
146
Q

Name 2 investigations for brain tumours

A
  • MRI scan - 1st line
  • Biopsy - gives definitive histological diagnosis
147
Q

What are the 4 main options for treating a brain tumour?

A
  • Surgery
  • Chemotherapy
  • Radiotherapy
  • Palliative care
148
Q

What is multiple sclerosis?

A
  • Chronic, progressive autoimmune condition
  • Involves demyelination in CNS
  • Immune system attacks myelin sheath of the neurones
149
Q

Who typically presents with MS?

A
  • Younger adults
  • Women
150
Q

Describe the pathophysiology of MS

A
  • Inflammation and immune cell infiltration cause damage to the myelin
  • This affects the electrical signals moving along neurones
  • In early disease, re-myelination can occur = Sx resolve
  • In later stages, re-myelination is incomplete = Sx gradually become more permanent
151
Q

How must the lesions in MS present to be diagnosed with MS

A

Disseminated in time and space
* Vary in location = affected sites & Sx change over time

152
Q

Name 5 possible causes of MS

A
  • Genetics
  • EBV
  • Low vit D
  • Smoking
  • Obesity
153
Q

Describe the onset and duration of MS Sx

A
  • Sx progress over** > 24hrs**
  • Sx last days - weeks at first presentation then improve
154
Q

What is optic neuritis?

A
  • Most common presentation of MS
  • Demyelination of optic nerve
  • Presents with unilateral reduced vision developing over hours - days
155
Q

What are 4 key features of optic neuritis?

A
  • ** Central scotoma** - enlarged central blind spot
  • Pain with eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect - pupil in affected eye constricts more when shining a light in the contralateral eye
156
Q

Name 6 causes of optic neuritis other than MS

A
  • Sarcoidosis
  • SLE
  • Syphilis
  • Measles/mumps
  • Neuromyelitis optica
  • Lyme disease
157
Q

How is optic neuritis treated?

A
  • High dose steroids
  • Iv IG
158
Q

Name 3 ophthalmic Sx of MS

A
  • Optic neuritis
  • Nystagmus
  • Diplopia
159
Q

Name 4 Sx of focal weakness in MS

A
  • Incontinence
  • Horner syndrome
  • Facial nerve palsy
  • Limb paralysis
160
Q

Name 5 focal sensory Sx of MS

A
  • Trigeminal neuralgia
  • Numbness
  • Paraesthesia
  • Lhermitte’s sign - electric shock sensation travelling down spine when flexing neck
  • Sensory ataxia - due to loss of proprioception
161
Q

Name 4 cerebellar Sx of MS

A
  • Loss of balance / cerebellar ataxia
  • Diplopia
  • Dysarthria
  • Tremor
162
Q

What are the 4 main classifications of MS?

A
  1. Clinically Isolated Syndrome - unexplained first episode of neurological dysfunction
  2. Relapsing-remitting MS - unpredictable attacks of neurological dysfunction followed by recovery
  3. Secondary progressive MS - used to be RRMS but now there is progressive worsening of Sx with incomplete remissions
  4. Primary progressive MS - steady, progressive worsening of disease severity without remission
163
Q

How is a diagnosis of MS made?

A
  • Clinical picture & Sx
  • MRI scan - shows lesions
  • Lumbar puncture - detects oligoclonal bands in the CSF
164
Q

What is the treatment of an acute attack of MS?

A

High dose steroids - methylprednisolone

165
Q

What is the long term treatment of MS?

A
  • Disease-modifying agents - beta-IFN (decrease relapses)
  • Manage Sx: exercise, amitriptyline/gabapentin for neuropathic pain, SSRIs for depression etc..
166
Q

What is Guillain-Barre syndrome?

A

Acute paralytic polyneuropathy that affects the PNS. Causes acute, symmetrical ascending weakness (can cause sensory Sx)

167
Q

What organism are GBS particularly associated with?

A
  • Campylobacter jejuni
  • CMV (cytomegalovirus)
  • EBV (Epstein-Barr virus)
168
Q

What is the pathophysiology of GBS?

A

Molecular mimicry
* B cells create antibodies against the antigens on the triggering pathogen
* These antibodies also match proteins on the peripheral neurones
* May target proteins on myelin sheath or nerve axon itself

169
Q

Describe the symptom timeline and presentation of GBS

A
  • Sx start: within 4 weeks of triggering infection
  • Begin in feet and progress upward
  • Sx peak: 2-4 weeks
  • Recovery period: months to years
170
Q

Name 4 symptoms of GBS

A
  • Symmetrical ascending weakness
  • Reduced reflexes
  • Peripheral loss of sensation
  • Neuropathic pain

Autonomic dysfunction –> urinary retention, ileus, arrhythmias
May progress to cranial nerves –> facial weakness

171
Q

Name 2 investigations for GBS

A
  • Nerve conduction studies: reduced signal through nerves
  • Lumbar puncture: CSF shows raised protein & normal cell count
172
Q

What is the management of GBS?

A
  • Supportive care: IV fluids, HR control
  • VTE prophylaxis: PE leading cause of death
  • IV IG - 1st line
  • Plasmapheresis (plasma exchange)

Severe cases with resp failure: intubation/ventilation

173
Q

What is motor neuron disease?

A

Progressive neurodegenerative disease where motor neurones stop working
(sensory neurons aren’t affected = no sensory Sx)

174
Q

What are the 4 types of motor neuron disease?

A
  1. Amyotrophic lateral sclerosis- MC
  2. Progressive bulbar palsy
  3. Progressive muscular atrophy
  4. Primary lateral sclerosis
175
Q

What is the typical presentation of MND?

A
  • Progressive weakness of muscles throughout body: limbs, trunk, face, speech
  • Upper limb weakness noticed first: hand weakness/loss of dexterity
  • Increased fatigue when exercising
  • Clumsiness, tripping over, dropping things
  • Dysarthria: slurred speech
  • mix of LMN and UMN signs
176
Q

What are UMN signs? (5)

A
  • Hypertonia
  • Hyperreflexia
  • Spastic gait
  • Ankle clonus
  • Jaw clenching / exaggerated jaw jerk
  • +ve babinski sign**
177
Q

What are LMN signs? (4)

A
  • Hypotonia
  • Hyporeflexia
  • Fasciculations
  • Muscle atrophy –> weakness
  • negative babinski sign
178
Q

Name 2 investigations for MND

A
  • Nerve conduction studies
  • MRI
179
Q

What is the management of MND?

A

No cure!

  • Riluzole: slows disease progression
  • Non-invasive ventilation (NIV): when resp muscles weaken
  • End of life care
180
Q

What is the main cause of death in MND?

A

Respiratory failure (muscles of respiration affected)

181
Q

What is the prognosis of MND?

A

Survival of 3-5 years after Sx onset

182
Q

What is cerebral palsy?

A

Group of permanent, non-progressive conditions that affect movement & coordination resulting from damage to the brain around birth

183
Q

Name 2 antenatal causes of cerebral palsy?

A
  • Maternal infections
  • Trauma during pregnancy
184
Q

Name 2 perinatal causes of cerebral palsy?

A
  • Birth asphyxia / hypoxic-ischaemic injury
  • Pre-term birth
185
Q

Name 3 postnatal causes of cerebral palsy?

A
  • Meningitis
  • Head injury
  • Severe neonatal jaundice / Kernicterus
186
Q

What are the 4 types of cerebral palsy?

A
  • Spastic: UMN damage = hypertonia & reduced function
  • Dyskinetic basal ganglia damage = problems controlling muscle tone (hypertonia & hypotonia), athetoid movements, oro-motor problems
  • Ataxic: cerebellum damage = problems with coordinated movement
  • Mixed
187
Q

Name 6 signs of cerebral palsy

A
  • Failure to meet milestones
  • Increased/decreased tone (generally or in specific limbs)
  • Early development of hand preference
  • Problems with coordination, speech or walking
  • Feeding/swallowing problems
  • Learning difficulties
188
Q

What does a hemiplegic/ diplegic gait indicate?

A

UMN lesion

189
Q

What does a broad based/ ataxic gait indicate?

A

Cerebellar lesion

190
Q

What does a high stepping gait indicate?

A

Foot drop or LMN lesion

191
Q

What does a waddling gait indicate?

A

Pelvic muscle weakness due to myopathy

192
Q

What does an antalgic gait indicate?

A

limp = localised pain

193
Q

Name 4 symptoms of cerebral palsy

A
  • Hemiplegic/diplegic gait: increased muscle tone & spasticity in legs, extended leg & plantar flexion of feet/toes causes leg to swing around
  • UMN lesion signs (good muscle bulk, increased tone, brisk reflexes, slightly reduced power)
  • Athetoid movements: indicate extrapyramidal (basal ganglia) involvement
  • Coordination problems: cerebellar involvement
194
Q

What is the general management of cerebral palsy?

A

MDT approach
* Physio: prevent muscle contractures
* OT: help with ADLs
* SLT:

195
Q

What are possible medical treatments for cerebral palsy?

A
  • Baclofen: muscle relaxant to manage high muscle tone/spasticity
  • Botox: relieve spasticity by blocking nerve signals that cause muscle contraction - not permanent, wears off after 3-6 months
196
Q

Definition: Neurofibromatosis

A

Genetic condition that causes neuromas to develop throughout the NS

2 types: NF1 & NF2

197
Q

What is a neuroma?

A

Benign nerve tumour

198
Q

What chromosome is neurofibromatosis type 1 gene found on?

A

chromosome 17
* codes for a tumour suppressor protein called neurofibromin

199
Q

What is the genetic inheritance pattern of neurofibromatosis?

A

autosomal dominant

200
Q

What are the features of neurofibromatosis?

CRABBING

A
  • Cafe-au-lait spots
  • Relative with NF1
  • Axillary / inguinal freckling
  • Bony displaysia e.g. Bowing of a long bone / sphenoid wing dysplasia
  • Iris hamartomas (Lisch nodules)
  • Neurofibromas
  • Glioma of optic pathway
201
Q

What is a neurofibroma?

A
  • Skin-coloured
  • Raised nodules/papules
  • With smooth, regular surface

2 or more = significant

202
Q

What is a plexiform neurofibroma?

A

Larger, irregular, complex neurofibroma containing multiple cell types

a single plexiform neurofibroma is significant

203
Q

What is the management of NF1?

A

Treat complications

204
Q

What are some complications of NF1?

A
  • Malignant peripheral nerve sheath tumours (MPNST)
  • Gastrointestinal stromal tumour (GIST)
  • migraine
  • epilepsy
  • renal artery stenosis –> HTN
  • learning disability
  • scoliosis
  • vision loss (secondary to optic nerve glioma)
  • brain tumour
  • spinal cord tumour
205
Q

What chromosome is neurofibromatosis type 2 gene found on?

A

chromosome 22
* codes for tumour suppressor protein called merlin
* important in Schwann cells
* mutations lead to Schwannomas

206
Q

What is the main feature of NF2?

A

acoustic neuroma (tumour of the auditory nerve)

surgery can be used to resect the tumours - but risk of permanent nerve damage

207
Q

Definition: Meningitis

A

Inflammation of the meninges due to infection

208
Q

Where is CSF contained?

A

In the subarachnoid space within the meninges

209
Q

What are the 5 causes of bacterial meningitis?

A
  • Neisseria meningitidis (meningococcus)
  • Strep pneumoniae (pneumococcus)
  • H influenzae
  • Group B strep (particularly in neonates)
  • Listeria monocytogenes (particularly in neonates)
210
Q

What is meningococcal septicaemia?

A

when meningococcus bacterial infection is in the bloodstream
* can cause non-blanching rash

211
Q

What are the 3 most common causes of viral meningitis?

A
  • Enteroviruses e.g. coxsackievirus
  • Herpes simplex virus (HSV)
  • Varicella zoster virus (VZV)

  • Viral PCR testing can be done on a CSF sample
  • Aciclovir is used to treat HSV & VZV
212
Q

What are some symptoms of meningitis?

A
  • Fever
  • Neck stiffness
  • N+V
  • Headache
  • Photophobia
  • Altered consciousness
  • Seizures

Children: Non-blanching rash - meningococcal septicaemia

Neonates: Non-specific signs

213
Q

Name 2 special tests to look for meningeal irritation

A
  • Kernig’s
  • Brudzinski’s
214
Q

Describe Kernig’s test

A
  • Pt lies on back flexing one hip & knee to 90 degrees
  • Slowly straightens knee whilst keeping hip flexed
  • Creates stretch in meninges
  • If meningitis - spinal pain or resistance to movement
215
Q

Describe Brudzinski’s test

A
  • Pt lies on back
  • You gently lift their head & neck off bed, flexing chin to chest
  • If meningitis - this causes Pt to involuntarily flex hips & knees
216
Q

Describe the appearance of a CSF sample in meningitis

A
  • Bacterial - cloudy
  • Viral - clear
217
Q

Describe the protein of a CSF sample in meningitis

A

Bacterial - high
Viral - mildly raised/normal

218
Q

Describe the glucose of a CSF sample in meningitis

A

Bacterial - low
Viral - normal

219
Q

Describe the white cell count of a CSF sample in meningitis

A

Bacterial - high (neutrophils)
Viral - high (lymphocytes)

220
Q

Describe the bacterial culture of a CSF sample in meningitis

A

Bacterial - shows bacteria
Viral - negative

221
Q

What is the management of bacterial meningitis?

A

Medical emergency!!
* Children w/ suspected meningitis and non-blanching rash = urgent dose of benzylpenicillin
* Under 3 months - cefotaxime + amoxicillin
* Above 3 months - ceftriaxone
* Steroids - dexamethasone to reduce freq & severity of hearing loss/neurological complications

222
Q

What should be added if there is a risk of penicillin-resistant pneumococcal infection?

e.g. recent foreign travel / prolonged ABx exposure

A

Vancomycin

223
Q

What is the management of viral meningitis?

A

Acyclovir

(mainly HSV)

224
Q

What is the post-exposure prophylaxis for meningitis?

A

Ciprofloxacin - single dose

225
Q

Name 5 complications of meningitis

A
  • Hearing loss
  • Seizures & epilepsy
  • Cognitive impairment & LD
  • Memory loss
  • Focal neurological deficits - limb weakness / spasticity
226
Q

What is a brain abscess?

A

Intracerebreal collection of pus

227
Q

Name 3 causes of brain abscess

A
  • Cranial infections: mastoiditis, sinusitis, osteomyelitis
  • Penetrating head wounds
  • Haematogenous spread: bacterial endocarditis, IV drug use
228
Q

What are some symptoms of brain abscess?

A

Sx result from raised ICP, mass effect & focal brain injury
* Headache
* N+V
* Lethargy
* Seizures
* Personality changes
* Focal neurological deficits

229
Q

What investigation is done for a brain abscess?

A

Contrast-enhanced MRI with DWI

Contrast-enhanced CT if MRI unavailable

230
Q

What is the treatment of a brain abscess?

A
  • ABx: cefotaxime/ceftriaxone
  • CT-guided aspiration / surgical drainage
  • Corticosteroids for raised ICP Sx (dexamethasone)
231
Q

Definition: coma

A

State of unconsciousness where a person is unresponsive & cannot be woken

232
Q

What can cause a coma?

A
  • Severe head injury
  • Stroke
  • Severe alcohol poisoning
  • Encephalitis
  • Hypoglycaemia / Hyperglycaemia
233
Q

What is the management of someone in a coma?

A

Supporting body functions (breathing, BP etc) whilst treating underlying cause

234
Q

What is the Glasgow Coma Scale?

A

Used to assess the level of consciousness in a patient

235
Q

What is included in the Glasgow Coma Scale?

A

Eye opening
* Spontaneously - 4
* To sound - 3
* To pain - 2
* No response - 1

Verbal response
* Orientated - 5
* Confused conversation - 4
* Innapropriate words - 3
* Incomprehensible sounds - 2
* No response - 1

Motor response
* Obeys commands - 6
* Localises to pain - 5
* Withdraws to pain - 4
* Abnormal flexion response to pain - 3
* Abnormal extension response to pain - 2
* No response - 1

236
Q

Definition: Encephalitis

A

Inflammation of brain parenchyma associated w/ neurological dysfunction

237
Q

What are some features of encephalitis?

A
  • Altered mental state
  • Fever
  • Headache
  • Seizures
  • Focal neurological signs
238
Q

Name some investigations of encephalitis

A
  • Bloods
  • Lumbar puncture
  • CT scan
239
Q

What is the management of encephalitis?

A
  • Acyclovir - clears virus
  • Anti-inflammatory drugs - if fever/pain
  • Anticonvulsants - if seizures
240
Q

What is the triad of Horner syndrome?

A
  • Ptosis
  • Miosis
  • Anhidrosis
241
Q

What is the pathology of Horner syndrome?

A

Damage to sympathetic nervous system

242
Q

What are the causes of Horner syndrome?

4 Ss, 4 Ts, 4 Cs - Sentral, Torso, Cervical

A

Central lesions:
* Stroke
* Multiple Sclerosis
* Swelling (tumours)
* Syringomyelia (spinal cord cyst)

Pre-ganglionic lesions:
* Tumour (Pancoast tumour)
* Trauma
* Thyroidectomy
* Top rib (extra rib above clavicle)

Post-ganglionic lesions:
* Carotid aneurysm
* Carotid artery dissection
* Cavernous sinus thrombosis
* Cluster headache

243
Q

How do you test for Horner syndrome?

A

Cocaine eye drops
* stops noradrenalin re-uptake at neuromuscular junction
* causes normal eye to dilate (noradrenalin stimulates dilator muscles)
* In Horner, nerves aren’t releasing noradrenalin, so blocking re-uptake makes no difference = no pupil reaction

244
Q

What are the 5 branches of the facial nerve?

A
  1. Temporal
  2. Zygomatic
  3. Buccal
  4. Mandibular
  5. Cervical
245
Q

What is the motor function of the facial nerve?

A
  • Facial expression
  • Stapedius in the inner ear
  • Posterior digastric, stylohyoid and platysma muscles
246
Q

What is the sensory function of the facial nerve?

A

Taste from the anterior 2/3 of the tongue

247
Q

What is the difference between upper vs lower motor neurone facial nerve palsy?

A
  • UMN lesion: Forehead sparing
  • LMN lesion: patient cannot move their forehead on the affected side
248
Q

What are 2 causes of unilateral UMN lesions?

A
  • CVA (strokes)
  • Tumours
249
Q

What are 2 causes of bilateral UMN lesions?

These are rare

A
  • Pseudobulbar palsies
  • MND
250
Q

Definition: Bell’s Palsy

A

Unilateral, idiopathic LMN facial nerve palsy

251
Q

What are the clinical features of Bell’s Palsy?

A
  • Rapid onset < 72 hours
  • Unilateral facial weakness
  • Incomplete eye closure
  • Eyebrow, eyelid & mouth corner drooping
  • Loss of nasolabial fold
252
Q

What are some differentials for Bell’s Palsy?

A
  • Inner ear disease - otitis media, cholesteatoma
  • Parotid disease
  • GBS
  • Stroke
  • Tumours
  • Meningitis
  • MS
  • Sarcoidosis
253
Q

What is the management of Bell’s Palsy?

A
  • Generally supportive
  • Prednisolone - within 72 hours
  • Eye care - lubricating drops, eye taping at night
254
Q

Definition: Bulbar Palsy

A

LMN lesion of cranial nerves IX, X and XII

255
Q

Definition: Pseudobulbar palsy

A

UMN lesion of cranial nerves IX, X and XII

256
Q

What is the main difference in presentation between bulbar and pseudobulbar palsy?

A

Pseudonbulbar - Emotional lability
Bulbar - emotions not affected

257
Q

What are some causes of bulbar palsy?

A
  • Brainstem strokes & tumours
  • ALS (amyotrophic lateral sclerosis)
  • GBS
258
Q

What are some symptoms of bulbar palsy?

A
  • Dysphagia
  • Absent gag reflex
  • Tongue wasting
  • Slurred speech
  • Difficulty chewing
  • Aspiration of secretions
  • Emotions unaffected
259
Q

What is the management of bulbar palsy?

A

Symptom management
* Difficulty swallowing - feeding tube
* Speech & Language therapy

260
Q

Definition: Myasthenia Gravis

A

Autoimmune condition affecting neuromuscular junction
* causes muscle weakness

261
Q

What is the pattern of muscle weakness in myasthenia gravis?

A
  • Progressive worsening with activity
  • Improves with rest
262
Q

What ages does MG affect men and women?

A

Women - under 40 years
Men - over 60 years

263
Q

What is strongly linked to Myasthenia Gravis?

A

Thymomas

10-20% pts with MG

264
Q

What is the normal function of NMJ?

A

Motor neurones communicate with the muscles via NMJ
* Axons release Acetylcholine from presynaptic memb.
* Travels across synapse
* Attaches to receptors on post-synaptic memb.
* Stimulates muscle contraction

265
Q

What is the pathophysiology of myasthenia gravis?

A
  • Acetylcholine receptor antibodies (AchR) bind to post-synaptic ACh receptors = block them
  • Prevents stimulation by ACh
  • AChR antibodies also activate complement system within NMJ –> cell damage at post-synaptic memb.
  • MuSK & LRP4 antibodies cause ACh receptor destruction
266
Q

What antibodies are involved in myasthenia gravis?

A
  • Acetylcholine receptor antibodies (AChR)
  • Muscle-specific kinase antibodies (MuSK)
  • Low-density lipoprotein receptor-related protein 4 antibodies (LRP4)
267
Q

Describe how MG is worsened during activity and better during rest

A
  • The more the receptors are used during muscle activity = more they become blocked (i.e. less effective stimulation of muscle w/ increased activity)
  • With rest - receptors are cleared = Sx improve
268
Q

What muscles are mainly affected in myasthenia gravis?

A
  • Proximal muscles of limbs
  • Small muscles of head & neck
269
Q

What are some symptoms of myasthenia gravis?

A
  • Difficulty climbing stairs, standing from a seat, raising hands above head
  • Extraocular muscle weakness = diplopia
  • Eyelid weakness = ptosis
  • Facial movement weakness
  • Swallowing difficulty
  • Jaw fatigue when chewing
  • Slurred speech
270
Q

What investigations should you do for myasthenia gravis?

A
  • Antibody tests - AChR, MuSK, LRP4
  • CT/MRI of the thymus (look for thymoma)
  • Edrophonium test
271
Q

Describe the edrophonium test

A
  • Pt given IV edrophonium chloride (or neostigmine)
  • Normally - cholinesterase enzymes in NMJ break down ACh
  • Edrophonium blocks cholinesterase enzymes = reduces breakdown of ACh
  • Results = rise in ACh at NMJ = temporarily relieving weakness
272
Q

What is the management of myasthenia gravis?

A
  • Pyridostigmine = cholinesterase inhibitor (prolongs action of ACh - improves Sx)
  • Immunosuppression = prednisolone / azathioprine (suppresses production of antibodies)
  • Thymectomy = improves Sx (even w/o thymoma)
  • Rituximab if other Tx fails
273
Q

What is myasthenic crisis?

A
  • Acute worsening of Sx often triggered by another illness
  • Resp muscle weakness –> resp failure
  • May require non-invasive ventilation (BiPAP) or mechanical ventilation
274
Q

What is the treatment of myasthenic crisis?

A
  • IV immunoglobulins
  • Plasmapheresis
275
Q

Name some causes of mechanical back pain

A
  • Muscle/ ligament sprain
  • Sacroiliac joint dysfunction
  • Herniated disc
  • Scoliosis
  • Arthritis
276
Q

Name some red flag causes of back pain

A
  • Spinal fracture - major trauma
  • Cauda equina - saddle anaethesia, urinary retention, incontinence, bilateral sciatica
  • Spinal stenosis
  • Ankylosing spondylitis - < 40y, gradual onset, morning stiffness, night-time pain
  • Spinal infection - fever, Hx of IVDU
277
Q

Definition: Sciatica

A

Sx associated with irritation of sciatic nerve

278
Q

What is the route of the sciatic nerve?

A
  • L4 - S3 join together = sciatic nerve
  • Exits posterior part of pelvis through greater sciatic foramen
  • Travels down back of leg, at knee divides into tibial nerve and common peroneal nerve
279
Q

What is the function of the sciatic nerve?

A
  • Sensation to lateral lower leg & foot
  • Motor function to posterior thigh, lower leg & foot
280
Q

How does sciatica present?

A
  • Unilateral radiating pain: butt –> back of thigh –> below knee/foot
  • “electric / shooting”
  • Paraesthesia
  • Numbness
  • Motor weakness
281
Q

Name 3 causes of sciatica

A

Lumbosacral nerve root compression:
* Herniated disc
* Spinal stenosis
* Spondylolisthesis

282
Q

What investigation should you do for sciatica?

A

Sciatic stretch test
* Pt lies on back with leg straight
* You lift one leg from the ankle w/ knee extended until hip flexion limit (80-90 degrees)
* You dorsiflex pt’s ankle
* Sx improve w/ knee flexion

283
Q

What investigations should you do for back pain?

A
  • Spinal fractures: XR / CT
  • Cauda equina: Emergency MRI
  • Ankylosing spondylitis: CRP/ESR, XR spine (bamboo spine), MRI spine (bone marrow oedema)
284
Q

What is the management of lower back pain?

A
  • Analgesia - NSAIDs (alt: codeine), benzos for muscle spasm
  • Staying active
  • Physiotherapy & CBT (chronic back pain)
285
Q

What medications should be avoided in lower back pain? (5)

A
  • Opioids
  • Antidepressants
  • Amitriptyline
  • Gabapentin
  • Pregabalin
286
Q

What is the management of sciatica?

A

Mostly same as low back pain Tx
* DON’T USE: gabapentin, pregabalin, diazepam, corticosteroids, opioids
* DO USE: neuropathic meds = amitriptyline, duloxetine
* Specialist Mx: epidural corticosteroid injections, local anaesthetic injections, radiofrequency denervation, spinal decompression

287
Q

Definition: Spinal stenosis

A

Narrowing of part of the spinal canal = compression of spinal cord / nerve roots
* usually affects cervical or lumbar (MC) spine

288
Q

What are the 3 types of spinal stenosis?

A
  • Central (central spinal canal)
  • Lateral (nerve root canal)
  • Foramina (intervertebral foramina)
289
Q

What are some causes of spinal stenosis?

A
  • Congenital
  • Degenerative changes
  • Herniated discs
  • Spinal fractures
  • Tumours
290
Q

How does spinal stenosis present?

A
  • Gradual onset
  • Sx absent at rest, occur when walking/standing
  • Intermittent neurogenic claudication (pseudoclaudication)
  • lower back pain
  • butt & leg pain
  • leg weakness
291
Q

Definition: radiculopathy

A

Compression of the nerve roots as they exit the spinal cord and spinal column - leads to motor & sensory Sx

292
Q

What investigation should you do for spinal stenosis?

A

MRI
* exclude PAD (e.g. ABPI & CT angiogram) where intermittent claudication is present

293
Q

What is the management of spinal stenosis?

A
  • Exercise
  • Analgesia
  • Physio
  • Decompression surgery
  • Laminectomy
294
Q

Definition: Charcot-Marie-Tooth Disease

A

Inherited disease that causes motor & sensory neuropathy

295
Q

What is the epidemiology of CMT?

A
  • Autosomal dominant
  • Sx usually appear before 10 years old
296
Q

What are some features of CMT?

A
  • High foot arches (pes cavus)
  • Distal muscle wasting
  • Lower leg weakness - loss of ankle dorsiflexion = foot drop / high stepping gait
  • Hand weakness
  • Reduced tendon reflexes
  • Reduced muscle tone
  • Peripheral sensory loss
297
Q

Definition: stocking-glove distribution

A

Reduced sensory & motor function in peripheral nerves, typically affecting feet and hands

298
Q

What are 5 causes of peripheral neuropathy?

ABCDE

A
  • Alcohol
  • B12 deficiency
  • Cancer (e.g. myeloma) & CKD
  • Diabetes & Drugs
  • Every vasculitis
299
Q

Name 4 drugs that can cause peripheral neuropathy

A
  • Isoniazid
  • Amiodarone
  • Leflunomide
  • Cisplatin
300
Q

What is the management of CMT?

A

Supportive Mx with MDT
* Physios
* OTs
* Podiatrist

Analgesia for neuropathic pain - amitriptyline

301
Q

Definition: Mononeuropathy

A

Only affects a single nerve e.g. meralgia paraesthetica

302
Q

What is the cause of Subarachnoid Haemorrhage?

A

Ruptured cerebral aneurysm

303
Q

What are some risk factors for SAH?

A
  • Age 45 - 70
  • F > M
  • Black ethnic origin
  • HTN
  • Smoking
  • Excessive alcohol
  • Family Hx
  • Cocaine use
  • Sickle cell anaemia
  • Neurofibromatosis
304
Q

How does SAH present?

A
  • Thunderclap headache - sudden onset occipital headache
  • Neck stiffness
  • Photophobia
  • Vomiting
  • Neurological Sx
305
Q

What investigations should you do for SAH?

A
  • CT head (1st line): hyper-attenuation in subarachnoid space
  • Lumbar puncture if CT normal (at least 12 hours after Sx start): raised red cell count, xanthochromia (yelloow CSF due to bilirubin)
  • CT angiography - confirms location of bleed
306
Q

What is the management for SAH?

A
  • Surgical intervention - aneurysms (endovascular coiling/neurosurgical clipping)
  • Nimodipine = CCB to prevent vasospasm (usually results in brain ischaemia)
307
Q

What is a pseudo subarachnoid sign? And when do you see it?

A

SAH appearance on CT - due to loss of grey/white matter differentiation.
Due to severe hypoxic injury to the brain

308
Q

How do you treat hydrocephalus?

A
  • Lumbar puncture
  • External ventricular drain
  • VP shunt
309
Q

What is the triad caused by Cushing’s reflex?

A

Cushing’s reflex is a physiological response to raised ICP which attempts to improve perfusion. It leads to:
* HTN
* Bradycardia
* Irregular breathing pattern

310
Q

What is herniation in reference to the brain?

A

The movement of brain structures from one cranial compartment to another

311
Q

What is primary vs secondary brain injury?

A

Primary = initial injury
* skull fracture
* blood vessel injury
* haematoma

Secondary = indirect damage commonly caused by inadequate perfusion
* cerebral hypoxia
* acidosis
* hypoglycaemia
* cerebral oedema

312
Q

Where does a extradural haemorrhage occur?

A

Between the skull and dura mater

313
Q

Where does a subdural haemorrhage occur?

A

Between the dura mater and arachnoid mater

314
Q

What are the risk factors for intracranial bleeds?

A
  • Head injuries
  • HTN
  • Aneurysms
  • Brain tumours
  • Bleeding disorders
  • Anticoagulants (e.g. DOACs / warfarin)
315
Q

What is the cause of extradural haemorrhage?

A

Rupture of the middle meningeal artery in the temporoparietal region

316
Q

Extradural haemorrhage is associated with which fracture?

A

fracture of the temporal bone

317
Q

What are the characteristics of an extradural haemorrhage on a CT scan?

A
  • lentiform shape (lemon)
  • Limited by the cranial sutures
318
Q

What is the typical history for an extradural haemorrhage?

A
  • Young patient
  • Traumatic head injury
  • Ongoing headache
  • Period of improved neurological Sx & consciousness followed by rapid decline over hours as haematoma gets large enough to compress intracranial contents
319
Q

What is the cause of a subdural haemorrhage?

A

Rupture of bridging veins in outermost meningeal layer

320
Q

What are the characteristics of a subdural haemorrhage on a CT scan?

A
  • Crescent shape
  • NOT limited by the cranial sutures (they can cross over the sutures)
  • Instead limited by venous sinuses
321
Q

Who is most likely to get a subdural haemorrhage? And why?

A
  • Elderly
  • Alcoholics

Because they have more atrophy in their brains = vessels more prone to rupture

322
Q

What are the initial investigations you should do for an intracranial bleed?

A
  • Immediate CT head - to establish diagnosis
  • FBC (platelets) & coag screen
323
Q

What is the management of intracranial bleeds?

A
  • Correct any clotting abnormality - platelet transfusion or vit K for warfarin
  • Correct severe hypertension - avoid hypotension
  • Admit to specialist stroke centre
  • Small bleeds = managed conservatively (close monitoring & repeat imaging)
  • Consider surgery
324
Q

What are 2 surgical options for treating an extradural or subdural haematoma?

A
  • Craniotomy - open surgery, removing section of skull
  • Burr holes - small holes drilled into skull to drain blood
325
Q

What is anterior cord syndrome?

A

Front of the spinal cord is damaged, but posterior part is spared

326
Q

Which spinal tracts are affected in anterior cord syndrome?

A

Spinothalamic and Corticospinal

327
Q

What causes anterior cord syndrome?

A

Ischaemia within the anterior spinal artery
* Can cause damage to the anterior part of the spinal cord
* Analogous to a stroke within the spinal cord

Can also be caused by:
* External compression
* Flexion injuries

328
Q

What are the features of anterior cord syndrome?

A
  • Spinothalamic tracts: bilateral loss of pain & temperature
  • Corticospinal: bilateral spastic paralysis & UMN signs

Dorsal columns = posterior = won’t be affected: fine touch/proprioception/vibration will be preserved

329
Q

What is the management of anterior cord syndrome?

A
  • Immobilisation of neck/back - reducce further damage
  • Steroids - reduce inflammation/swelling
  • Surgery - decompress spinal cord / stabilise spine
  • Rehab - PT / OT
330
Q

What is cauda equina?

A

Surgical emergency where cauda equina nerve roots are compressed leading to neurological compromise

331
Q

What do the cauda equina nerves supply?

A
  • Sensation to the LL, perinuem, bladder & rectum
  • Motor innervation to the LL & anal/urethral sphincters
  • Parasympathetic innervation of bladder & rectum
332
Q

Name 5 causes of compression in cauda equina syndrome

A
  • Herniated disc (MC)
  • Tumours (metastasis)
  • Spondylolisthesis (anterior disaplacement of a vertebra out of line w/ one below
  • Abscess (infection)
  • Trauma
333
Q

What are the red flags to look out for in cauda equina syndrome?

A
  • Saddle anaesthesia
  • Loss of sensation in bladder/rectum
  • Urinary/faecal incontinence / retention
  • Bilateral sciatica
  • Bilateral / severe motor weakness in legs
  • Reduced anal tone
334
Q

What investigations should you do for cauda equina syndrome?

A
  • MRI lumbar spine
  • Straight leg raise (+ve)
335
Q

What is the management of cauda equina syndrome?

A

Lumbar decompression surgery
* laminectomy & discectomy

336
Q

What is a dermatome?

A

Area of skin supplied by a single spinal nerve

337
Q

What is a myotome?

A

Group of muscles innervated by a single spinal nerve

338
Q

What are myopathies?

A

Class of diseases that attack the skeletal muscles

339
Q

What are the types of myopathy?

A
  • Inflammatory
  • Steroids
  • Metabolic
  • Myotonic
  • Statin
  • Muscular dystrophy
  • Polio
340
Q

What are the symptoms of myopathy?

A
  • Muscle weakness
  • Muscle cramps / stiffness
  • Muscle spasms
  • Fatigue
341
Q

What is muscular dystrophy?

A

Group of conditions that affect the function of the muscles - cause progressive muscle weakness / degeneration

342
Q

What are the symptoms of myotonic dystrophy?

A
  • Weakness of smaller muscles first (face, jaw, neck)
  • muscle stiffness
  • Cataracts
  • dysphagia
  • slow, irregular heartbeat
343
Q

What is the management of muscular dystrophy?

A
  • No cure, so treat Sx & complications (e.g. PT, OT)
  • Steroids for Duchenne MD
344
Q

What is steroid myopathy?

A
  • Most common drug-induced myopathy, can be acute or chronic. Characterised by muscle weakness after starting steroids
  • Corticosteroid myopathy: after an endocrine cause e.g. cushings
345
Q

What investigation should you do for myopathy?

A

Muscle biopsy

346
Q

What can cause inflammatory myopathy?

A

Infections e.g. HIV, influenza, EBV

347
Q

What are metabolic myopathies?

A

Rare genetic diseases that affect metabolism and primarily affect muscle

348
Q

What is statin-induced myopathy?

A

Side effect of taking statins. Leads to muscle Sx e.g. weakness, stiffness, pain, fatigue

349
Q

What is poliomyelitis?

A

Viral infection causing nerve injury leading to paralysis

350
Q

What is bovine papular stomatitis?

A

Virus that can spread from cattle to farmers/vets. Causes skin lesions typically on hands/ forearms

351
Q

What is Uhthoff’s phenomenon?

A

Worsening of Sx on exercise/ in warm environment e.g. shower

Phase 3a - Arun&Erin (15 decks)

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