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Phase 3a > Neurology PTS > Flashcards

Neurology PTS Flashcards

1
Q

What are the features of an ataxic gait?

A
  • Wide based
  • Falls
  • Cannot walk heel-to-toe
  • Often worse in the dark or with eyes closed
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2
Q

What are the 2 main causes of an ataxic gait?

A
  • Cerebellar problem
  • Issue with proprioception
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3
Q

What are the cerebellar causes of an ataxic gait?

A
  • MS
  • Posterior fossa tumour
  • Alcohol
  • Phenytoin toxicity
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4
Q

If they are ataxic on the right, which side of cerebellum is the problem?

A

Right

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5
Q

What is the feature of cerebellar syndrome?

A

Ataxia plus nystagmus

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6
Q

What are the proprioceptive causes of an ataxic gait?

A
  • Sensory neuropathies (low b12)
  • Inner ear problem (affecting the vestibular system)
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7
Q

What tyest helps you distinguish between proprioceptive and cerebellar causes of ataxic gait?

A
  • If they can walk normally with their eyes open and the problem starts when they close their eyes (proprioceptive cause)
  • If the problem is there all the time (cerebellar cause)
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8
Q

What are the features and causes of a circumduction (spastic) gait?

A

Features - stiff gait, circumduction of the legs, +/- scuffing of the toe of the shoes
Cause - stroke (hemiplegia)

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9
Q

What are the features and causes of a shuffling (extra-pyramidal) gait?

A

Features - flexed posture, shuffling feet, postural instability, slow to start (struggle with the initiation of movements)
Caused by - Parkinson’s disease, PDP+ syndromes and other causes of Parkinsonism such as use of antipsychotic medications

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10
Q

What are the causes of an antalgic gait?

A

Aka limping
Generally caused by a painful limb - MSK problem is the most likely differential

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11
Q

What are the features and causes of a high stepping gait?

A

Features - trip over often as they struggle with dorsiflexion of the foot, lift feet high whilst walking to avoid tripping over
Cause - foot drop (common peroneal nerve palsy)

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12
Q

What are the features and causes of Trendelenberg gait?

A

Features - unstable hip, ‘sound side sags’ on Trendelenberg test
Causes - congenital hip dislocation, DDH, gluteus medius muscle weakness, superior gluteal nerve damage

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13
Q

What are the features and causes of an apraxic gait?

A

Features - pathognomonic ‘gluing to the floor’ on attempting walking, wide based unsteady gait with a tendency to fall (‘novice on ice’)
Causes - normal pressure hydrocephalus, multi-infarct states, Alzheimer’s disease

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14
Q

How should an abnormal gait be investigated?

A

History - duration/onset of symptoms (rapid onset of gait abnormality is likely to be an acute event such as a stroke, slower onset could be something like parkinson’s)
Examination - rigidity, pain, facsiculations
Tests - CT, MRI, blood tests (all the usual plus B12 - deficiency causes nerve problems)

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15
Q

Define neuropathy

A

Dysfunction or disease of the nerves typically causing weakness or numbness

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16
Q

How does the onset of an episode of weakness help you assess the cause of it?

A

Sudden onset - likely to be a vascular event
Medium onset - likely to be related to demyelination
Insidious onset - think of things such as slow-growing tumours

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17
Q

What is the cause of proximal weakness?

A

muscle problem (hair, chairs, stairs)
Struggle to do things close to their trunk

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18
Q

What is the cause of distal weakness?

A

Nerve problem
Neuropathy starts distally and works its way up - glove and stocking pattern

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19
Q

What is the cause of symmetrical weakness?

A

Genetic or metabolic causes
DM, muscular dystrophy

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20
Q

What is the cause of asymetrical weakness?

A

Vasculitis or inflammatory

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21
Q

What is the cause on mononeuropathic weakness?

A

Entrapment e.b. carpal or ulnar tunnel

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22
Q

What is the cause of polyneuropathic weakness?

A

Likely something systemic such as DM

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23
Q

What does variability of muscle weakness tell you about the possible diagnosis?

A

Fatigueability - NMJ issue - myasthenia gravis
Relapsing/remitting pattern - inflammatory - MS/ CNS disease

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24
Q

What are some peripheral nerve causes of muscle weakness?

A

Polyneuropathy
Mononeuropathy
Mononeuritis multiplex - lots of nerves affected all over the place randomly
Common causes - DM, idiopathic
Other - B12 deficiency, alcohol/drugs,, metabolic abnormalities, paraneoplastic syndromes
Guillian Barre syndrome

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25
Q

What are the features of peripheral neuropathy?

A
  • Chronic and slowly progressive
  • Starts in the legs and longer nerves first
  • Sensory, motor or both
  • Glove and stocking distribution
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26
Q

How does mononeuritis multiplex present and what are some causes?

A
  • Individually nerves picked off randomly
  • Subacute presentation
  • Inflmmatory/ immune mediated
  • Causes - inflammation of the vasa nervorum can block off the blood supply to the nerve causing sudden deficit
  • Vasculitis, sarcoidosis
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27
Q

How does mononeuropathy present and what are some causes?

A
  • Individual nerve deficits in isolaion
  • Upper limb nerves mostly affected at compression points
  • Median nerve entrapment most common (carpal tunnel)
  • Ulnar nerve entrapment at elbow (previous elbow fractures or arthritis)
  • Radial nerve in axilla
  • Common peroneal nerve in the leg
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28
Q

What are the features of a myasthenic crisis?

A
  • severe muscle weakness including respiratory muscles
  • High risk of death
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29
Q

What causes a myasthenic crisis?

A
  • Infection
  • Natural part of the disease
  • Under dosing or overdosing of medication
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30
Q

How should a myasthenia crisis be treated?

A
  • Urgent review by neurologists
  • Serial FVC measurements - monitor breathing
  • Anaesthetist review
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31
Q

How does muscular dystrophy present and what clinical test can be done to demonstrate it?

A
  • Presents in childhood with a proximal pattern of muscle weakness
  • Often he can have a very bulky muscles at first - pseudohypertrophy
  • Then muscle wasting occurs later on
  • Scoliosis is prominent later on
  • Gower test positive
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32
Q

What are some common muscle disorders seen in neurology?

A
  • Steroid myopathy
  • Statin myopathy
  • Metabolic and endocrine myopathies
  • Myotonic dystrophy
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33
Q

What are some rarer muscle disorders seen in neurology?

A
  • Most muscular dystrophies (Duchenne and Becker, facioscapularhumeral muscular dystrophy, limb gurdle muscular dystrophy)
  • Inflammatory muscle disease (polymyositis dermatomyositis)
  • Mitochondrial disorders
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34
Q

How should neuropathy be investigated?

A
  • History and examination
  • Neuropathy screen (if symmetrical presentation) - FBC, ESR, U&E, CRP, ANA, ANCA, anti-dsDNA, RhF, complement
  • EMG, nerve conduction studies
  • CSF sample (if MS suspected)
  • Nerve biopsy
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35
Q

How is myopathy investigated?

A
  • Creatinine kinase - released when muscle is broken down
  • EMG
  • ESR, CRP
  • +/- genetics (DMD, Becker)
  • +/- biopsy
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36
Q

How is neuropathy treated?

A
  • 20% are idiopathic so no reatment other than symptom relief (neuropathic analgesia e.g. gabapentin, pregabalin, amitriptyline)
  • Treat underlying cause (e.g. DM)
  • Inflammatory neuropathies (prednisolone plus steroid-sparing agents e.g. azathioprine)
  • Vasculitic neuropathy e.g. Wegner’s - treat these quickly with prednisolone and cyclophosphamide to avoid irreversible damage
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37
Q

How are muscle disorders treated?

A
  • Removal of causative agent (steroids or statins)
  • Immunosupress if inflammatory

Supportive therapy
- OT - adaptations to help live with condition
- Physio - prevent contractures
- Back - scoliosis therapy and back care
- Renal protection - myoglobin can cause kidney damage
- Diet - need to keep a low BMI and good nutrition

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38
Q

What is the definition of coma/brain death?

A

Unarousable unresponsiveness

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39
Q

What are the 3 domains used in the assessing Glasgow Coma Scale?

A

Best eye opening response
Best verbal response
Best pain response

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40
Q

What are the 4 levels of best eye opening response?

A
  1. Spontaneously
  2. To speech
  3. To pain
  4. None
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41
Q

What are the 5 levels to best verbal response?

A
  1. Orientated in time/place/person
  2. Confused
  3. Inappropriate words
  4. Incomprehensible sounds
  5. none
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42
Q

What are the 6 levels of best pain response?

A
  1. Obeys commands
  2. Localises pain
  3. Normal flexion to pain
  4. Abnormal flexion o pain
  5. Extends to pain
  6. None
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43
Q

What are lateralising signs in neurology?

A

Signs that occur from one hemisphere of the brain but not the other
They will present quie obviously - the appearance will be difficult in one side of the body

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44
Q

What causes a fixed dilated pupil?

A
  • 3rd nerve palsy

-3rd nerve comes out of the brain stem and goes over the apex of the petrous part of the temporal bone as it goes through the cavernous sinus to supply the eye
- This means it’s susceptible to being damaged when the brain is swollen, bleeding, trauma, etc
- Parasympathetic fibres (job is to constrict the pupil) so when they are damaged the pupil is fixed in the dilated position

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45
Q

What is a differential for a fixed dilated pupil?

A
  • 3rd nerve palsy
  • Blind eye (other eye should still respond to light)
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46
Q

What are some metabolic causes of coma?

A
  • Drugs, poisoning, acohol
  • Hypoglycaemia
  • Hyperglycaemia (Ketoacidotic)
  • Hypoxia
  • CO2 narcosis (COPD)
  • Speticaemia, hypothermia, myxoedema, Addisonian crisis, hepatic/uraemia encephalopathy due to kidney or liver failure
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47
Q

What are some neurological causes of coma?

A
  • Trauma
  • Infection (meningitis, encephalitis, HSV)
  • Vascular (stroke, subdural, subarachnoid, hypertensive encephalopathy)
  • Epilepsy (non convulsive status epilepticus, post-ictal state)
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48
Q

How is the unconscious patient managed?

A
  • ABC - life support
  • IV access
  • Stabilise cervical spine
  • Control any seizures - phenytoin loading
  • Treat potential causes - IV glucose, thiamine, nalaxone if pupils small
  • Brief collateral history and examination
  • Vital signs and pupils checked often
  • Investigations - bloods, cultures, CXR, CT head
  • Continually re-assess and plan investigations
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49
Q

What important factor of the history must you establish in someone presenting with dizziness?

A

What the patient actually means when they say dizzy and whether or not it represents vertigo

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50
Q

What is the definition of vertigo?

A
  • an illusion of movement, often rotary, of the patient of their surroundings
  • spinning/tilting/veering sideways feeling
  • as if being push and pulled
  • always worse with movement
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51
Q

What are the causes of vertigo?

A
  • motion sickness
  • alcohol intoxication
  • benign positional vertigo
  • acute labyrinthitis
  • meniere’s disease
  • ototoxicity
  • acoustic neuroma
  • traumatic damage
  • herpes zoster
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52
Q

How does vertigo present?

A
  • pushing/pulling/spinning/veering feeling
  • worsened by movement
  • relief on lying/sitting still
  • difficulty walking or standing
  • nausea
  • vomiting
  • pallor
  • sweating
  • if there is associated hearing loss or tinnitus - labyrinthitis or CN VIII involvement
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53
Q

What are some features in the history which would point you away from a diagnosis of vertigo?

A
  • faintness
  • light headedness
  • loss of awareness during attacks
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54
Q

How would you investigate vertigo?

A

History
Tilt table test
MRI scan if suspect acoustic neuroma or other brain issue

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55
Q

How is vertigo managed?

A
  • Symptomatic treatment for dizziness in acute labyrinthitis prochlorperazine (stemil)
  • Antihistamines can help with dizziness (cinnarizine)
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56
Q

What are the 3 types of primary headaches?

A

Tension headaches
Migraine
Cluster headache

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57
Q

What are some examples of secondary headaches?

A
  • Sinusitis related headache
  • Medication overuse headache
  • Space occupying lesions
  • Meningitis
  • Subarachnoid haemorrhage
  • Post traumatic headache
  • Post-dural puncture headache (after LP or epidural)
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58
Q

What is the most common cause of headache?

A

tension headache

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59
Q

What are the causes of headaches that cause meningism and what signs would you see?

A
  • Meningitis - fever, photophobia, stiff neck, purpuric rash, coma
  • Encephalitis - fever, odd behaviour, fits, decreased consciousness
  • Subarachnoid haemorrhage - sudden onset, thunderclap, worst headache ever, stiff neck, focal signs
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60
Q

What type of headache is seen with head injury?

A
  • Present at the site of trauma mainly, but may also be more generalised
  • last about 2 weeks, resistant to analgesia
  • Exclude extradural haematoma if drowsiness +/- lucid interval and/pr focal signs
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61
Q

How does a headache due to venous sinus thrombosis present?

A
  • subacute or sudden headache
  • papilloedema - check eyes!
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62
Q

Which tropical disease can cause headache?

A
  • malaria
  • these will have a travel history and associated flu-like illness
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63
Q

What are the symptoms of a sinusitis headache?

A
  • Dull, constant ache over frontal/maxillary sinuses, may also be felt right in the middle of the nose/forehead
  • Tenderness
  • Post-nasal drip
  • pain worse when leaning forwards
  • common with coryza (cold, hay-fever)
  • pain lasts 1-2 weeks
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64
Q

How does acute glaucoma present?

A
  • elderly, long-sighted people
  • constant aching pain develops rapidly around one eye, radiating to the forehead
  • symptoms - markedly reduced vision, visual halos, n&v
  • signs - red, congested eye, cloudy cornea, dilated non-responsive pupil (may be oval shaped), decreased acuity
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65
Q

What sort of things can precipitate acute glaucoma?

A
  • Dilating eye-drops
  • emotional upset
  • sitting in the dark
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66
Q

How do you treat acute glaucoma?

A
  • immediate expert help
  • IV acetazolamide (a corbonic anhydrase inhibitor)
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67
Q

What are the features of migraine?

A
  • recurrent acute attacks
  • vomiting
  • photophobia
  • may be unilateral
  • may have aura
  • may notice particular triggers
  • family history
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68
Q

How are migraines treated?

A
  • acute - triptan + NSAID or triptan + paracetamol
  • prophylaxis - topiramate or propranolol
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69
Q

What are the features of cluster headaches?

A
  • another recurrent acute attack of headache disorder
  • most disabling primary headache
  • rapid onset excrutiating pain around one eye
  • eye may become blood shot, have lid swelling, miosis, ptosis, lacrimation etc.
  • unilateral pain
  • once or twice a day, often nocturnal
  • alarm clock headaches - may wake the person at night
  • can last a few weeks, go away and come back years later
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70
Q

How are cluster headaches treated?

A
  • for an acute attack - 100% oxygen for 15 mins plus sumatriptan
  • prophylaxis - verapamil
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71
Q

What are the clinical features of trigeminal neuralgia?

A
  • typical patient - asian male >50 years
  • paroxysms of intense stabbing pain, lasting secounds, in the trigeminal nerve distribution
  • unilateral
  • face screw up with pain
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72
Q

What are some triggers for trigeminal neuralgia?

A
  • washing the area
  • shaving
  • eating
  • talking
  • dental prosthesis
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73
Q

How is trigeminal neuralgia treated?

A

carbamazepine (anti-epileptic)

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74
Q

What are some causes of recurrernt aseptic meningitis?

A
  • HSV 2, SLE, sarcoidosis
  • skull fracture - could be leaving access to subarachnoid space
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75
Q

What are the clinical features and treatment of giant cell arteritis?

A
  • exclude in all >50 with headache lasting a few weeks
  • tender, thickened, pulseless temporal arteries
  • jaw claudication
  • ESR >40mm/h
  • treatment - stat high dose methylprednisolone
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76
Q

What are the clinical features of tension headaches?

A
  • bilateral non-pulsatile headache
  • +/- scalp tenderness
  • no vomiting or sensitivity to head movement
  • stress relief may be helpful - massage, antidepressants, simple analgesia but warn the, not to use it too much (do not use any simple analgesia for >15 days each month or any complex analgesia for more than >10 days)
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77
Q

What are the clinical features of a headache due to raised ICP?

A
  • worse when - lying down, waking, bending forward, coughing
  • associated signs - vomiting, papilloedema, seizures, false localising signs, odd behaviour
  • causes - SOL, idiopathic intracranial hypertension
  • LP contraindicated until after imaging
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78
Q

What are the 2 broad categories in which movement disorders can be split into?

A
  1. akinetic rigid syndromes (decreased movements) - PD and PD+ syndromes
  2. Disorders of increased movements - tics, jerks, dystonia, ballismus, tardive syndromes
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79
Q

What are the main signs of Parkinson’s disease?

A
  1. Bradykinesia
  2. Rigidity
  3. Pill-rolling tremor
  4. Shuffling gait
  5. Loss of postural reflexes
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80
Q

What are some red flag symptoms which may lead you to believe its not PD and instead a PD+ syndrome?

A
  • early falls
  • early cognitive decline
  • early bladder and bowel dysfunction
  • both sides affected equally
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81
Q

What are the 4 PD+ syndromes?

A
  1. Progressive supra-nuclear palsy (PSP)
  2. Cortico-basal degeneration
  3. Multi-system atrophy
  4. Lewy body dementia
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82
Q

What are the features of PSP?

A
  • early falls
  • early cognitive impairment
  • occurs above the nuclei of CN3, 4 and 6
  • difficulty moving the eyes
  • ocular cephalic reflex will be present (caused by a supra-nuclear issue) they tilt/turn their head to look at things rather than moving their eyes
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83
Q

What are the features of multi-system atrophy?

A
  • early bladder and bowel dysfunction
  • autonomic involvement - i.e. causing postural hypotension and falls
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84
Q

What are the features of Lewy body dementia

A
  • early visual hallucinations
  • clouding of consciousness
  • sleep behaviour disorder
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85
Q

What are the extra features of cortico-basal degeneration?

A
  • early myoclonic jerks
  • apraxia
  • agnosia (inability to appreciate sensory input even though the end organ is not dysfunctional)
  • alien limb
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86
Q

What are the 3 types of tremor and what can cause them?

A
  1. Intention - cerebellar issue
  2. Resting - Parkinson’s Disease
  3. Postural - anxiety, increased adrenaline, salbutamol, valproate, lithium, benign essential tremor
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87
Q

What are the 3 types of jerks and what causes them?

A
  1. Tic - e.g. Tourettes, affects top half of body, can be suppressed for a short while, can be treated with antipsychotics
  2. Chorea - involuntary, semi-purposeful movements, anywhere in the body. Huntington’s disease, treat with haloperidol (dopamine blockade). Can also occur if you over treat parkinson’s disease
  3. Myoclonic jerk - sudden, non-purposeful. CJD, epilepsy, cortical myoclonic jerks (can be triggered by touching the affected part)
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88
Q

What is dystonia and what causes it?

A
  • very slow, not postural movements (happen in an abnormal/strange position), can affect any part of the body, can be task specific (i.e. only during writing)
  • writers cramp
  • torticlonus (neck)
  • involuntary, slow
  • basal ganglia issue - can be genetic, can start in childhood
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89
Q

How can dystonia be treated?

A
  • paralyse overactive muscles with botox
  • anti-cholinergics (such as oxybutynin)
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90
Q

What is ballismus and what causes it?

A
  • much more bigger and obvious that chorea but the same kind of movement
  • caused by - vascular issue with the subthalamic nucleus (i.e. thalamic stroke)
  • if hemi - only affects one side (hemi ballismus, hemi chorea)
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91
Q

What are tardive syndromes and what causes them?

A
  • tardive = delayed onset, occurs due to chronic exposure to dopamine antagonists (antipsychotics, anti-emetics)
  • may be permanent - even once the causative medication has been stopped
  • tardive dyskinesia - chewing and primacing movements involving the face, mouth and tongue. Common in schizophrenics or have been on long-term typical anti-psychotics
  • tardive dystonia - twisting/turning of the limbs and back
  • tardive myoclonic, tourettism and tremor can also occur
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92
Q

Which anti-psychotics are less likely to cause tardive symptoms?

A
  • Quetiapine
  • Olanzipine
  • Clozipine
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93
Q

What investigations would you do in someone presenting with a movement disorder?

A
  • History
  • Examination
  • MRI brain - PD, HD, Lewy body, vascular insult
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94
Q

How do you manage movement disorders?

A

Treat underlying cause:
- PD - Levodopa, selegiline
- Huntington’s - Haloperidol, physiotherapy
- Myoclonic jerks associated with epilepsy - AED such as valproate

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95
Q

What are some neurological causes of altered sensation?

A
  • Could mean absolutely anything depending on where the loss of sensation is
  • If in doubt - MS
  • Peripheral neuropathy due to diabetes etc.
  • GBS - ascending paralysis and numbness
  • Spinal cord compression - legs, saddle paraesthesia
  • NEVER MND
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96
Q

What are the important questions to ask in a history for loss of consciousness/blackouts?

A

Establish exactly what is meant by blackout – LOC, falling without LOC, cloudy/double vision, vertigo
WITNESS ACCOUNT
Head banging
Tongue biting
Before/during/after – how they felt (any warning signs or anything)
Incontinence
Previous episodes
Sleepy or muscle aches afterwards

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97
Q

What are some causes of blackouts/LOC?

A

Vasovagal (neurocardiogenic) syncope – fainting
Situation syncope – coughing, effort (on exercise – often cardiac in origin – aortic stenosis or HCM, micturition (men, at night)
Carotid sinus syncope – hypersensitive baroreceptors cause excessive reflex bradycardia on minimal stimulation (head turning, shaving)
Epilepsy
NEA
Drop attacks – cataplexy (emotions), hydrocephalus
Hypoglycaemia
Orthostatic hypertension (POTS – Postural Orthostatic Tachycardia)
Anxiety – hyperventilation
Facticious blackouts
Choking

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98
Q

What investigations/examinations would you like to do on someone with LOC/blackouts?

A

Vital signs
Cardiovascular examination
Neurological examination
Lying and standing BP
Glucose
U&E, FBC
EEG
24 hour ECG
Echo
CT/MRI if necessary

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99
Q

How are blackouts/LOC managed?

A

Until the cause is known – no driving (until blackout free for 1 year)

Treat underlying cause – e.g. anti-epileptics, avoiding triggers for fainting

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100
Q

What are the vascular causes of unilateral loss of vision?

A

Amaurosis fugax/central retinal artery occlusion (branch of the opthalmic artery which supplies the whole retina)
Central retinal vein occlusion
Anterior ischaemic optic neuropathy (ischaemia of posterior choroidal/ciliary artery that supplies the head of the optic nerve) – can be arteritic – think GCA – or non artertic
Stroke affecting the occipital lobe of the brain
GCA
Vitreous haemorrhage – when blood leaks into the vitreous humor between the lens and retina (assoc. w/ diabetic retinopathy, CRVO, macular degeneration

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101
Q

What are some non-vascular causes of unilateral loss of vision?

A

Optic neuritis (main one to know for the exams because of MS) – inflammation of the optic nerve. Can occur by itself or with MS

Retinal detachment – flashes/floaters with decrease in vision

Acute angle closure glaucoma – painful red eye, nausea and vomiting

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102
Q

What factors in the clinical presentation of unilateral loss of vision help you to identify the cause?

A

Character – cloudy vision (MS type picture), “like pulling a curtain over my eyes” – amarousis fugax
Onset – sudden = vascular, subacute = MS or other
If they’ve ever had it or anything similar before
Exacerbating and relieving factors – important as certain things (hot bath) will exacerbate symptoms caused by MS
Impact on function – very important to determine

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103
Q

What investigations would you do in someone presenting with unilateral loss of vision?

A

Full eye examination (movements, acuity, fundoscopy)
MRI
VEP (visual evoked potential) –shine light into eye and time how long it takes to reach the back of the eye? – helps diagnose optic neuritis
Fluorescecin angiography – central retinal vein occlusion
Tonometry – measures intra-ocular pressure (glaucoma)
USS – ocular USS to look for vitreous haemorrhage/retinal detachment
LP – shows oligoclonal bands in MS

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104
Q

How should unilateral loss of vision be treated?

A

Treat underlying cause

If in doubt give steroids – if it’s a cause such as MS or GCA then steroids will help

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105
Q

How does spinal cord compression generally present?

A

Weak legs

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106
Q

What questions are essential to ask someone presenting with weak legs?

A

Onset – sudden or progressive onset weakness is an EMERGENCY
Flaccid or spastic?
Sensory loss? – sensory level usually means spinal cord disease
Loss of sphincter control
Signs of infection? – e.g. extradural abscess (tender spine, pyrexia, raised WCC and inflammatory markers)
SADDLE PARASTHESIA

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107
Q

Cord compression causes leg weakness. What are the causes of cord compression?

A

Malignancy (primary or secondary – usually secondary)
Infection (epidural abscess)
Disc prolapse
Haematoma (if on warfarin)
Myeloma – rule out in anyone >50 w/ back pain

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108
Q

Secondary malignancy is the most common cause of cord compression. What are the 5 cancers which spread to bone?

A

Breast
Thyroid
Prostate
Kidney
Lung

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109
Q

What are some other causes of leg weakness?

A

Unilateral foot drop – DM, common peroneal nerve palsy, stroke, MS, prolapsed disc
Weak legs with no sensory loss – MND, polio, parasagittal meningioma
Hereditary spastic paraplegia (more chronic picture)
Parasites - schistosomiasis – look for eosinophils
Peripheral neuropathy
Myopathy (rare, arms also involved)

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110
Q

What are the symptoms of spinal cord compression?

A

Spinal or root pain – may precede weakness and sensory loss
Leg weakness
Numbness/tingling
Arm weakness – cervical cord lesion
Bladder and anal sphincter involvement – later manifestation (hesitancy, frequency, painless retention)

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111
Q

What are the signs of cord compression?

A

Motor, reflex and sensory level – normal findings ABOVE the lesion, LMN signs at the level, UMN signs below the level

Tone and reflexes usually reduced in acute cord compression

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112
Q

What is cauda equina syndrome?

A

Cord compression below the level of termination of the spinal cord

Spinal cord ends at L1/L2 vertebral level

Cauda equina = MEDICAL EMERGENCY

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113
Q

What are the causes of cauda equina syndrome?

A

Same as for spinal cord compression in general

Most commonly = malignancy
Disc prolapse/trauma
Infection

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114
Q

What are the signs and symptoms of cauda equina syndrome?

A

Mixed UMN/LMN leg weakness
Early urinary retention and constipation
Back pain
Sacral sensory disturbance
Erectile dysfunction
Pain down the legs
“saddle paraesthesia” - ask them if it feels strange sitting/wiping
Asymmetrical paralysis of the legs – trouble walking
Decreased sphincter tone – DO PR

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115
Q

What are some differentials for cord compression?

A

Transverse myelitis
MS
Trauma
Dissecting aneurysm
GBS – although this is not a cord pathology (if affects the roots and nerves)

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116
Q

What investigations should be done for someone presenting with leg weakness/suspected cord compression?

A

Imaging – ASK QUICKLY AS POSSIBLE (speed of imaging should match the rate of progression of symptoms)
MRI – gold standard
PR
If there’s a mass – biopsy or surgical exploration may be needed
Screening blood tests – FBC, ESR, B12, LFT, U&E, syphilis serology

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117
Q

How should cord compression be managed?

A

If malignancy – give dexamethasone stat and consider chemo/radio/surgery

Epidural abscess – surgical decompression and antibiotics

Cauda equina – surgery (asap)

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118
Q

Define dysphasia

A

Impairment of language caused by brain damage

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119
Q

Define dysarthria

A

Difficulty with articulation of speech due to incoordination or weakness of the speech-related musculature

Slurred speech
Language is normal

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120
Q

Define dysphonia

A

Difficulty with speech volume due to weakness of respiratory muscles or vocal cords (MG, GBS)

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121
Q

What are the causes of dysphasia/aphasia?

A

STROKE

To a particular part of the brain – causing either an expressive or receptive dysphasia

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122
Q

Which area of the brain is affected by a stroke which causes expressive dysphasia?

A

Broca’s area

Dominant hemisphere (usually the left side, regardless of handedness)

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123
Q

In which area of the brain would a stroke cause receptive dysphasia?

A

Wernicke’s area

Dominant hemisphere

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124
Q

The way to remember which way round:

A

Expressive – Broca’s

Receptive – Wernicke’s

E and B come first in the alphabet so they go together
R and W come last in the alphabet, so they go together

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125
Q

What causes dysarthria?

A

Cerebellar disease
Extrapyramidal disease – i.e. stroke
Pseudobulbar palsy – MND, severe MS
Bulbar palsy – facial nerve palsy, GBS, MND

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126
Q

What is the difference between bulbar and pseudobulbar palsy?

A

PSEUDO – affects the upper motor neurones

BULBAR – affects the lower motor neurones (of CN 9,10,11,12)

Pseudobulbar dysarthria – slow, nasal, effortful ‘hot potato’ voice
Bulbar dysarthria – nasal speech due to paralysis of the palate

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127
Q

What causes dysphonia?

A

Myasthenia gravis

Guillian Barre Syndrome

Parkinson’s disease (causes mixed picture of dysphonia and dysarthria)

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128
Q

How does Broca’s (expressive) dysphasia present?

A

Non-fluent speech produced with effort and frustration

Malformed words e.g. spoot for spoon

Reading and writing are impaired but comprehension is intact - patients understand questions and attempt to convey meaningful answers

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129
Q

How does Wernicke’s (receptive) dysphasia present?

A

Empty, fluent speech – saying words that sound right or are in the correct semantic field (flush for brush, comb for brush) – the words are coming out easily but aren’t correct

May be mistaken for psychotic speech
Patient oblivious to errors
CANNOT RESPOND TO REQUESTS – reading, writing and comprehension are impaired, replies are inappropriate

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130
Q

How would you decipher whether someone had expressive or receptive dysphasia?

A

Ask them to follow a command, i.e. blink, squeeze my hand

Expressive – they are able to follow the command

Receptive – they aren’t able to follow the command

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131
Q

What is nominal dysphasia?

A

They cannot name objects

But other aspects of speech are normal

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132
Q

How do you screen for dysarthria in a neurological examination?

A

Ask them to say “baby hippopotamus” or “British constitution”

If they have cerebellar disease – they will slur this as if drunk (due to ataxia of the speech muscles)

And then speech will be irregular in volume and staccato in quality (each word/part of the speech is separate and distinguished from each other – does not flow)

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133
Q

How do you investigate speech problems?

A

Have a conversation with the patient
Ask questions that test fluency, reception, understanding and articulation – e.g. how did you travel here today?
Assess dysphasia by asking – what is this? (e.g. pen) – if nominal they won’t be able to answer
British constitution
Ask the patient to follow one, 2 and 3 step commands

134
Q

How are speech problems managed?

A

Speech and language therapy team – single most important way to help speech problems

Speech therapy may not help but is still important

135
Q

Define dysphagia

A

Difficulty swallowing

136
Q

What are some neurological disorders that can cause difficulty swallowing?

A

Myasthenia gravis
Neurological bulbar palsy
Pseudobulbar palsy
Syringobulbia (fluid filled cavities in the brain stem, affect function)
Bulbar poliomyelitis
Wilson’s disease
Parkinson’s disease
stroke

137
Q

What are some non-neurological conditions which cause swallowing difficulty?

A

Cancer
Benign strictures
Pharyngeal pouch
Achalasia
Oesophageal spasm
Systemic sclerosis (scleroderma)

138
Q

What are some important questions to ask in a history for swallowing difficulty?

A

Difficulty swallowing both solids and liquids from the start?
Yes – motility disorder (achalasia, CNS)
No – if solids then liquids, suspect stricture (benign or cancerous)
Is it difficult to make the swallowing movement? – if yes, suspect bulbar palsy, espeically if the patient coughs on swallowing
If swallowing painful? (odonophagia) – if yes, suspect cancer, ulcer or spasm
Intermittent, constant, getting worse?
Intermittent – oesophageal spasm
Constant and worsening – malignant stricture
Does the neck bulge/gurgle on drinking – if yes, suspect pharyngeal pouch

139
Q

What investigations would you do for someone presenting with dysphagia?

A

FBC – anaemia (cancer)
U&E – dehydration (unable to take on adequate fluids)
CXR
Barium swallow
Upper GI endoscopy

140
Q

How should neurological swallowing problems be managed?

A

Swallow assessment
Speech and language therapy

Depending on severity – NG feeding/PEG

Rehabilitation and physiotherapy – particular if had stroke

141
Q

What are some neurological conditions which cause breathing difficulty and how should this be managed?

A

Guillian-Barre Syndrome
Motor neurone disease (respiratory depression common cause of death)
Duchenne Muscular Dystrophy
Myasthenia Gravis

Monitor FVC closely – esp. in GBS (can cause rapid death)

Treatment – ventilation if necessary, monitor regularly

142
Q

Define incontinence

A

The involuntary leakage of urine/faeces

At a time which is not socially acceptable to pass urine/faeces

143
Q

What are some neurological causes of incontinence?

A

MS
Stroke
Parkinson’s disease
Spinal trauma
Cord compression and cauda equina
Brain tumour
Diabetes
Guillian Barre?
Normal pressure hydrocephalus

144
Q

What are some important associated symptoms to ask about in someone presenting with incontinence?

A

Back pain and saddle paraesthesia – cauda equina?
Back pain and a motor/sensory level of defecit – spinal cord compression?
Behaviour changes and headaches/symptoms of raised ICP - brain tumour?
Do they have diabetes? How well is it controlled?
Have they had another isolated neurological complaint such as blurry vision – MS?
What is their age, are they shuffling when waling – Parkinson’s?

145
Q

How would you investigate someone with an acute onset of incontinence that you suspect could be due to a neurological cause?

A

MRI scan if suspect – cord compression, MS, PD

Urine dip stick and cultures – check for infections (if they person has Alzheimer’s etc., a new onset infection may cause them to suddenly become incontinent)

146
Q

How is urinary incontinence managed?

A

Conservative measures– pads, intermittent self-catheterisation, indwelling catheter

Treat underlying cause
Surgery an option if severe
If spinal cord damage/paralysis – permanent catheter

147
Q

What is urinary retention?

A

Inability to empty the bladder due to obstruction or decreased detrusor power

148
Q

What are some causes of acute urinary retention?

A

Prostatic obstruction due to BPH (most common cause in men)
Urethral strictures
Anticholinergics (e.g. oxybutynin)
‘Holding’
Alcohol
Drug use – ecstasy
Constipation
Post-operative (pain, inflammation, anaesthetics)
Infection
Neurological – cauda equina syndrome
Carcinoma

149
Q

What are some causes of chronic urinary retention?

A

Prostatic enlargement
Pelvic malignancy
Rectal surgery – causing nerve damage
Diabetes mellitus
CNS disease – transverse myelitis, MS, zoster

150
Q

How does acute urinary retention present?

A

Unable to pass urine

Bladder is tender on abdominal examination

Contains ~600ml urine

151
Q

How does chronic urinary retention present?

A

More insidious onset
Often painless
Bladder capacity may be >1.5 L

Presents with – overflow incontinence, acute on chronic retention, lower abdominal mass, UTI, renal failure

152
Q

How would you investigate someone presenting with urinary retention?

A

Examination – abdominal examination particularly palpation and percussion of the bladder to assess extent of retention, DRE (feel for enlarged prostate, check tone if suspect cauda equina), perineal sensation

MSU

U&E, FBC, PSA (could be prostate)

153
Q

What are some conservative measures to help manage urinary retention?

A

Tricks to aid voiding:
Analgesia
Privacy on the ward/side room
Walk around
Stand to void
Sound of running water
Hot bath

154
Q

What are some other measures to manage urinary retention (if those tricks fail)?

A

Catheterise

Alpha-blocker – Tamsulosin – relaxes the muscle in the bladder neck, making it easier to urinate (also has an effect on the prostate if this is the cause of the retention)

Intermitted self-catheterisation sometimes required – can do at home if needed

155
Q

What is optic neuritis?

A

Inflammation of the optic nerve

Often associated with a MS (often the first manifestation)

Can occur as a clinically isolate syndrome

156
Q

What are the causes of optic neuritis?

A

MS
Infection (lyme, syphillis, HIV)
B12 deficiency
Arteritis – can cause optic neuritis (e.g. GCA)
Lots of things – inflammatory in origin

157
Q

How does optic neuritis present?

A

Reduced visual acuity over a few days
Pain on moving eye
Exacerbated by heat or on exercise
Relative afferent pupillary defect
Dyschromatopsia (abnormal perception of colours)
Recovery of vision usually occurs (6 weeks)

158
Q

What investigations would you do for someone presenting with suspect optic neuritis/unilateral loss of vision?

A

Full eye examination – movements, acuity, fundoscopy
Visual evoked potentials
Inflammatory markers – ESR, CRP
If suspect MS – MRI scan (looking for oval shaped lesions) and LP (looking for oligoclonal bands)

159
Q

How is optic neuritis treated?

A

Steroids – reduce pain and hasten recovery (e.g. prednisolone) – high dose 500mg oral steroids for 5 weeks

When giving steroids – also give PPI for gastric protection

Zoledronate if starting long-term steroids (bone protection)

160
Q

What is the definition of Multiple sclerosis?

A

A chronic inflammatory condition in which there is demyelination of the central nervous system giving rise to a multitude of different symptoms

161
Q

What are the criteria necessary for a diagnosis of MS to be made?

A

2 CNS lesions
With symptoms that last >24 hours

Disseminated in time (>1 month apart)
And space (clinically or on MRI)

MCDONALD CRITERIA

162
Q

What causes MS?

A

Unknown

Thought to have a genetic component

Thought to have a link to vitamin D status – early exposure to sunlight and vitamin D thought to be protective

163
Q

What are some risk factors for MS?

A

Female gender

Living further from the equator

164
Q

What are the 4 different subtypes of MS?

A

Relapsing remitting (most common type, gets worse with each episode)

Primary progressive

Secondary progressive

Benign (they will have relapses and remissions but the overall progress will never worsen)

165
Q

What are some typical symptoms of MS?

A

Visual loss – optic neuritis (first presentation in ~10%)
Pyramidal weakness, spastic paraparesis
Sensory disturbance – most common presentation, in association with weakness
Cerebellar symptoms (nystagmus, vertigo, tremor, ataxia, dysarthria)
Bladder involvement
Sexual dysfunction
Fatigue – MS patients complain of extreme tiredness
Cognitive impairment – quite common in MS (but generally not a presenting symptoms)

166
Q

What are the 2 named signs that people with MS experience?

A

Lhermitte’s sign – electric shock sensation down trunk and limbs when they flex their neck

Uhthoff’s phenomenon – symptoms worse in hot bath/hot environment

167
Q

What are some other signs seen in MS?

A

UMN signs – spasticity, brisk reflexes, increase in tone
Don’t usually get LMN signs
Sensory signs – i.e. loss of sensation
Cerebellar signs
Optic atrophy
RAPD
Internuclear opthalmoplegia

168
Q

What is internuclear opthalmoplegia?

A

Decreased adduction of the ipsilateral eye
Nystagmus on abduction of the contralateral eye

The lesion is in the medial longitudinal geniculus

169
Q

How is MS diagnosed?

A

Clinical diagnosis

MRI scan aids diagnosis – should show MS plaques – need >2 disseminated in time and space

LP – oligoclonal bands

170
Q

How is MS treated?

A

Methylprednisolone – steroid used to treat relapses. Shortens acute relapses but no overall effect on prognosis (high dose IV for acute relapses)

Interferons – IFN-1beta and IFN-1alpha – used to maintain remissions. Decreases the number of relapses and lesions on MRI

Monoclonal antibodies

171
Q

What are some side effects of interferons?

A

Depression

Flu symptoms

Miscarriage

172
Q

What is the definition of epilepsy?

A

A continuing tendency to have seizures

173
Q

What is the definition of a seizure?

A

A paroxysmal event in which changes of behaviour, sensation, cognition and consciousness are caused by excessive, hypersynchronous neurological discharges in the brain

174
Q

How long does a seizure normally last?

A

30-120 seconds

175
Q

What’s the difference between focal and generalised seizures?

A

Partial/focal seizures are confined to one area of the cortex with recognisable pattern, they usually have unilateral movement abnormalities meaning one hemisphere is affected
May affect one body part e.g. mouth/hand – jerking movements followed by a temporary paralysis

Generalised seizures – activity in both hemispheres, diffuse throughout the brain, bilateral movement abnormalities.

176
Q

What are 2 examples of generalised seizures?

A

Absence seizures

Tonic-clonic seizures

177
Q

What causes epilepsy?

A

Genetics/family history
Trauma, hypoxia, surgery (any brain injury)
Tumours/abscesses - SOL
Vascular/degenerative brain disorders
Encephalitis/meningitis
Alcohol/drugs
Pyrexia/photosensitvity

178
Q

How do typical absence seizures present?

A

Begins in childhood
Activity stops – patient is still/doesn’t talk
May be an eyelid twitch/few muscle jerks
Can progress to tonic clonic later in life

179
Q

How do tonic-clonic seizures present?

A

Tonic - vague warning, tonic rigidity. Patient falls and may make sound, tongue usually bitten
Clonic – convulsions, bilateral rhythmic muscle jerks
Self-limiting

Post-ictal phase 🡪 drowsy, confused, may be asleep/comatose for several hours

180
Q

How do focal seizures present (i.e. not generalised)?

A

Temporal lobe seizures – déjà vu, vertigo, hallucinations

Frontal lobe seizures – strange smells (olfactory bulbs)

Parietal lobe seizures – sensory disturbances e.g. feeling skin crawl, odd noises

181
Q

What are the symptoms of the ictal and post-ictal phases of seizures?

A

Ictal phase – early phase, causes positive symptoms such as excessive activity (jerking movements etc.)

Post-ictal phase – causes negative symptoms such as weakness, numbness, tired/drowsy

182
Q

What are some differential diagnoses for epileptic seizures?

A

Postural syncope, cardiogenic syncope
TIA
Migraine
Hypoglycaemia (treat w/glucose)
Non-epileptic attack disorder
Dystonia
Vertigo

183
Q

What investigations do you do if someone presents with seizures?

A

Clinical diagnosis of epilepsy - EEG is not completely sensitive or specific
FBC, U&E, LFT, glucose
EEG
Brain imaging - CT/MRI if focal neurological signs and concerend about SOL

184
Q

How is epilepsy treated?

A

During seizure – ensure as little harm as possible, maintain airway but don’t restrain

Anti-epileptic drugs – only give when firm clinical diagnosis
Carbamazepine, lamotrigine, valproate, ethosuccimide (absence seizures)

If AEDs fail – vagal stimulation, surgery (hemispherectomy, non-dominant lobectomy)

185
Q

What is status epilepticus?

A

Medical emergency condition where the seizure does not self-limit

Can occur for any type of seizure

186
Q

What are the specific timings to know for status epilepticus?

A

T0 = when the seizure starts

10 mins = T1 = when the seizure should stop

30 mins = T2 = when brain injury occurs

187
Q

What is the most common cause of status epilepticus in someone with known epilepsy?

A

Poor adherence to medication

Other causes:
Infections i.e. meningitis
Worsening of the primary cause of the epilepsy – i.e. if it’s caused by a brain tumour, the tumour may have grown
Alcohol

188
Q

What are the causes of status epilepticus as a first presentation of epilepsy?

A

Alcohol abuse – most common and main reason

Any acute brain problem – stroke, trauma, infections, insulin OD causing hypoglycaemia

189
Q

How does status epilepticus present?

A

Convulsions tend to occur for 2-3 mins
Followed by slow activity/rest period
Followed by more convulsions etc.
The whole process continues although individual seizures don’t

190
Q

What are some pointers that may make you think the attack is a NEA rather than status epilepticus?

A

May have lots of other unexplained medical problems/explorative operations/psych involvement in the past
They aren’t a known epileptic
In NEA, they may be able to respond to you but they will NOT be able to in SE
In NEA – they may have continuous convulsions whereas they will stop for a “break” in status
More likely to have normal vital signs in NEA than SE (SE – may be cyanosed/deranged O2 sats)
NEA will not respond to medications, staus will (NEA can be fatal if mistreated with excessive medications – respiratory depression)

191
Q

What investigations do you do in someone with suspected status epilepticus?

A

EEG
FBC, LFT U&E, glucose
If pyrexic – blood cultures – meningitis and other infections can cause status

192
Q

How do you manage NEA?

A

Correct diagnosis vital
Speak to the patient, reassure them and wait for it to pass
They do not need medication – they just need time to feel better

193
Q

How is status epilpeticus managed?

A

Benzos followed by AEDs:
2 doses of benzo e.g. 2 x lorazepam
Then IV valproate OR phenytoin OR phenobarbitol

Find and treat the underlying cause
If thought to be alcohol related – treat with THIAMINE
If the medication is NOT working and they don’t respond to any drugs 🡪 think could it be NON epileptic
Status can be stopped with anaesthesia – but this is very dangerous and has all the usual risks of anaesthesia

194
Q

What is the prognosis of status epilepticus?

A

10% mortality

Also carries long-term morbidity after the episode – particularly if hypoxic brain injury occurred during

195
Q

What are the risk factors for ischaemic stroke?

A

Biggest risk factor = HYPERTENSION
Hypercholesterolaemia
Diabetes
Smoking
Atrial fibrillation
Previous TIA
Carotid stenosis – endarterectomy within 2 weeks for symptomatic disease (stroke, TIA) and if there’s 50-90% stenosis

196
Q

How would you assess someone’s risk of a stroke if they have AF?

A

CHADSVASC

Congestive heart failure – 1
Hypertension - 1
Age > 75 – 2
Previous stroke/TIA/VTE – 2
Vascular disease – 1
Age > 65
Sex category female – 1

197
Q

How would you assess someone’s stroke risk following a TIA?

A

ABCD2

Age > 60
Blood pressure > 140/90
Clinical features – unilateral weakness 2, speech 1
Duration >1hr – 2, 0-60mins - 1
Diabetes - 1

198
Q

When should someone be seen by a specialist after a TIA?

A

Within 24 hours

199
Q

What are the risk factors for haemorrhagic strokes?

A

Hypertension – often causes bleeds in the basal ganglia
AVM
Aneurysm
If taking anticoagulants
Recreational drugs/substance abuse

200
Q

What are some common presentations of stroke?

A

Unilateral weakness – often in arms and face
Slurred speech (dysarthria)
Dysphasia (unable to understand words or communicate what they mean)
MCA stroke – leg sparing

201
Q

What are the features of a total anterior circulation infarct and which blood vessels does this involve?

A

Problem with the internal carotid artery and therefore MCA, ACA, PCA

Causes cognitive impairment, speech troubles, unilateral weakness/incoordination, unilateral numbness or loss of sensation, dysarthria, unilateral visual loss or loss in 1 visual field

202
Q

What are the features of a lacunar stroke and which vessel(s) does this involve?

A

Weakness or paralysis of the face, arm, leg, foot or toes
Sudden numbness
Difficulty walking
Difficulty speaking
Clumsiness of hand or arm
Weakness of paralysis of eye muscles

203
Q

What are the clinical features of a posterior circulation infarct and which vessels are involved?

A

Vertigo
Imbalance
Unilateral limb weakness
Slurred speech
Double vision
Headache
Nausea and vomiting
Gait ataxia, limb ataxia, nystagmus

Vessels involved – basilar or vertebral arteries

204
Q

Posterior circulation and brainstem strokes:

A

Posterior = balance problems and cranial nerve palsies

Brain stem or any ‘big stroke’ = drowsiness

205
Q

What are some differential diagnoses for strokes?

A

Migraine – hemi-paretic migraine (genetic type of migraine), but any type of migraine can cause this kind of presentation

Seizure – focal type causing Todd’s paralysis

MS

Hypoglycaemia in a diabetic patient

206
Q

What is the most important investigation to do if stroke is suspected?

A

CT SCAN

Essential to perform a CT scan before any treatment – need to determine whether it’s ischaemic or haemorrhagic

207
Q

What are some early CT signs of stroke?

A

May be none
Hyperdense MCA
Loss of grey white matter differentiation and sulcal effacement (squishing) – cortical infarction
Hypodense basal ganglia (deep vessel infarct)

208
Q

What are some primary prevention methods for stroke?

A

Smoking cessation
Control hypertension – medications and diet (reduce salt intake)
Control hypercholesterolaemia (diet and medications)
Control diabetes (diet and medications)
Encourage active lifestyle and weightloss
Reduce alcohol intake
In patients with AF – CHADSVASC to see whether they need anticoagulating, HASBLED to assess bleeding risk. Usually the stroke risk is higher so you will anti-coagulate

209
Q

What are the factors for consideration in HASBLED?

A

Hypertension
Kidney disease
Liver disease
Previous stroke
Age > 65
Previous major bleed or bleeding predisposition
Labile INR
On drugs that cause bleeding
Alcohol use

210
Q

What are some secondary prevention measures for stroke after TIA?

A

Investigations – 72 hour ECG to look for paroxysmal AF, carotid doppler to look for carotid stenosis, BP, echo (to look for patent foramen ovale or endocarditis – can throw clots), if neck pain – investigate for dissectino with CTA/MRA

Drugs – aspirin, clopi, antihypertensives, statins, dietary controla nd diabetes management

PHYSIOTHERAPY AND MDT APPROACH TO REHAB

211
Q

How is an acute ischaemic stroke managed?

A

Aspirin – 300mg for 2 weeks
Potential for thrombolysis

Seen by specialist within 24 hours

Control BP – particularly after stroke diagnosis is confirmed

Swallow assessment and supportive care
FBC, LFT, U&E

212
Q

How is an acute haemorrhagic stroke managed?

A

Control bleeding

Control blood pressure

213
Q

What is the time cut-off for thrombolysis?

A

Within 4.5 hours of the onset of symptoms

So very important to determine onset time

Ischaemic strokes only

214
Q

What medication is given for thrombolysis?

A

Alteplase

Streptokinase

215
Q

What needs to be done within 24 hours of thrombolysis therapy?

A

Second CT scan to check if they’ve had a bleed

216
Q

What are some contraindications of thrombolysis?

A

On anticoagulants (can if on warfarin and below 1.7)
Haemorrhagic stroke
> 6 hours after onset of symptoms
Recent surgery or GI bleed
If active cancer
Hypertension – cut off 185/110

217
Q

What are some benefits of thrombolysis therapy?

A

Improves chances of patients being independent on discharge
Benefits decrease with time – less brain preservation the longer you leave it to thrombolyse
No increased risk of death

218
Q

What are some risks of thrombolysis?

A

Haemorrhage – 1 in 20

Reaction to rTPA

219
Q

What are some complications of stroke?

A

Raised ICP – cerebral oedema, haemorrhage (signs = hypertension, new neurological signs, reduced GCS)
Aspiration (if the stroke affects their swallowing
Pneumonia
VTE due to immobility
Pressure sores
Depression
Cognitive impairment
Long-term disability

220
Q

What is a subarachnoid haemorrhage?

A

Spontaneous bleeding into the subarachnoid space

Bleeding from the arteries that supply the brain

221
Q

What causes SAH?

A

Rupture of berry aneurysms (80%)

AVM (15%)

No known cause in < 15%

222
Q

What are some medical conditions associated with berry aneurysms?

A

Polycystic kidneys

Coarctation of the aorta

Ehlers-Danlos syndrome (hypermobile joints and skin elasticity)

223
Q

What are some risk factors for SAH?

A

Smoking
Alcohol misuse
Hypertension
Bleeding disorders
Infected aneurysm
Family history

224
Q

What are the symptoms of SAH?

A

Sudden onset “thunderclap” headache - ”worst headache ever”, 10/10 pain – may say “i thought I’d been kicked in the head”
Vomiting
Collapse
Seizures
Coma (coma/drowsiness may last for days)
May experience a “sentinel headache” earlier on – perhaps due to a warning leak from the aneurysm

225
Q

What signs are associated with SAH?

A

Neck stiffness
Photophobia

Kernig’s sign (takes 6h to develop) – lay the patient alt on their back, bend the knee and try to fully extend it. If unable to extend due to pain = positive Kernig’s sign

Bleeds in the eyes

226
Q

What investigations should be done for suspect SAH?

A

CT head – detects >90% of SAH within 48 houts – looks like a WHITE STAR SHAPE ON CT – ventricles show up white when they should normally be black (can be hard to spot)

LP if CT –ve and no contraindications >12 hours after headache onset

CT angiogram to locate aneurysms before surgical procedure

227
Q

What would be seen on an LP for SAH?

A

Xanthochromia (yellow CSF) – confirms SAH

228
Q

How is SAH treated?

A

Immediate neurosurgery referral

Nimodipine – calcium channel blocker - for 3 weeks to reduce vasospasm and thus consequent morbidity from cerebral ischaemia

Endovascular coiling

Surgical clipping

229
Q

What are some complications of SAH?

A

Re-bleeding – commonest cause of death, occurs in 20% in the first few days after

Cerebral ischaemia – due to vasospasm, may lead to CNS defecit

Hydrocephalus

Hyponatraemia

230
Q

What is a subdural haemorrhage? Is it venous or arterial in nature?

A

Bleed in between the dura and arachoid mater

Venous bleeds – from the dural venous sinuses

Consider in all whose conscious level fluctuates

231
Q

What is the most common cause of subdural haemorrhage?

A

Trauma – often forgotten/minor trauma from up to 9 months ago

Particularly elderly people, alcoholics (shrunken brains) and shaken babies

232
Q

What are the symptoms of a subdural haemorrhage?

A

Fluctuating level of consciousness
Insidious onset of physical/intellectual slowing
Sleepiness
Headache
Personality change
Unsteadiness

233
Q

What are some signs of subdural haemorrhage?

A

Raised ICP

Seizures

Localising neurological symptoms – unequal pupils, hemiparesis

234
Q

How is a subdural haemorrhage investigated?

A

CT scan – showing conCAVE bleed (towards the skull, away from the brain)
Half moon shape/crescent shape

235
Q

What’s the difference in appearance of a CT head of a chronic vs acute subdural haemorrhage?

A

Acute – blood appears white on CT

Chronic – blood appears darker on the CT

236
Q

What are some differentials for a subdural haemorrhage?

A

Stroke

Dementia

Massess – tumours, abscess

237
Q

How is a subdural haemorrhage treated?

A

Evacuate the bleed – burr holes, craniostomy

238
Q

Where does an extra-dural haemorrhage occur and is it venous or arterial in origin?

A

Happens in the space between the dura and the skull – blood accumulates between the blood and the dura

Usually arterial – middle meningeal artery

But 25% venous – if fractures disrupt the venous sinuses

239
Q

What is a big red-flag symptom for an extra-dural haemorrhage?

A

LUCID INTERVAL after head injury before becoming drowsy

Then conscious level falls or is slow to improve

240
Q

What is often the cause of an extra dural haemorrhage?

A

Often due to a fractured temporal or parietal bone - causing laceration of the middle meningeal artery and vein

Typically after trauma to the temple/just lateral to the eye – e.g. getting punched in the face

241
Q

How do extra-dural haemorrhages present?

A

Deteriorating consciousness after a head injury that initially produced no LOC
Lucid interval – drowsy at first, fine again, then drowsy. Or fine at first and go drowsy later
May last a few hours/days before a bleed presents as decreased GCS from rising ICP
Headache, vomiting, confusion, fits, +/- hemiparesis with brisk reflexes and up-going plantars
If bleeding continues – ipsilateral pupil dilates, coma, bilateral limb weakness, breathing becomes deep and irregular due to brainstem compression
Respiratory depression can lead to death

242
Q

What are some differential diagnoses of extra-dural haemorrhage?

A

Epilepsy

Carotid dissection

Carbon monoxide poisoning

243
Q

What investigations should be done for a suspected extradural haemorrhage?

A

CT head – conVEX blood (coming away from the skull, into the brain)

X-Ray skull – may be normal or may show fracture lines crossing the course of the middle meningeal vessels

Lumbar puncture CONTRAINDICATED

244
Q

How is an extradural haemorrhage treated?

A

Stabilise – A to E assessment

Transfer to neurosurgery – clot evacuation and stabilisation of the bleeding vessel

245
Q

What is meningitis?

A

Inflammation of the meninges

Can be an infection (bacterial or viral)
Or can be aseptic (autoimmune, reactive)

246
Q

What are the common causes of meningitis?

A

Bacterial – Neisseria Meningitidis (meningococcus) or steptococcus pneumoniae (pneumococcus)

Viral – CMV, EBV, HSV

Aseptic – MS

Myoplasma TB

247
Q

What are the symptoms of meningitis?

A

Early – general unwellnes (aches, cold hands and feet, headache, abnormal skin colour)
Fever
Headache
Photophobia
Neck stiffness
Altered mental state
Later symptoms – seizures, focal CNS signs, opisthotonos, decreased conscious level/coma

248
Q

What are some signs seen in meningitis?

A

Neck stiffness
Photophobia
Positive Kernig’s sign
Positive Brudzinski sign

Non-blanching petechial rash (later sign of meningococcal septicaemia)

249
Q

What are some differential diagnoses of meningitis?

A

Malaria
Encephalitis
Septicaemia
Subarachnoid
Dengue
Tetanus

250
Q

What investigations would you do for suspect meningitis?

A

Blood cultures
Blood glucose
LP – send for MC&S, glucose, virology
Throat swab – looking for meningococcus

251
Q

What LP findings would you see in someone with a bacterial meningitis?

A

LOW glucose – compared to blood glucose

Raised polymorphs (neutrophils, eosinophils, basophils)

Raised protein

Cloudy appearance of fluid

252
Q

What LP findings would you see in viral meningitis?

A

Raised lymphocytes

Normal/slightly low glucose

Normal protein

Clear appearance

253
Q

How is meningitis treated?

A

As soon as suspected – stat dose of IM BenPen before admitting to hospital
In hospital – take cultures and treat before cultures come back with IV cefotaxime
If viral – IV acyclovir
Once cultures come back – adjust treatment according to sensitivities
Prophylaxis for all household/close contacts –rifampicin

254
Q

What is encephalitis?

A

Inflammation/infection of the brain

Cause is normally viral but often never identified

255
Q

What type of presentation should always raise suspicion of encephalitis?

A

Whenever odd behaviour, decreased consciousness, focal neurology or a seizure
Is preceded by an infectious prodrome (e.g. pyrexia, rash, lymphadenopathy, sores, conjunctivitis, meningeal signs)

256
Q

What should be considered with the same presentation minus the infectious prodrome?

A

Encephalopathy

E.g. hypoglycaemia, hepatic, DKA, drugs, hypoxic brain injury, SLE, uraemia

257
Q

What are the viral causes of encephalitis?

A

HSV
CMV
EBV
VZV
HIV
Measles
Mumps
Rabies
West Nile virus
Tick-borne encephalitis

258
Q

What are some non-viral causes of encephalitis?

A

Any bacterial meningitis
TB
Malaria
Listeria
Lyme disease
Legionella
Aspergillosis
Schistosomiasis
Typhus

259
Q

How does encephalitis present?

A

Bizarre behaviour/confusion
Decreased GCS/coma
Fever
Headache
Focal neurological signs
Seizures
History of travel or animal bite

260
Q

How is suspected encephalitis investigated?

A

Blood cultures and serology for viral PCR
CT
LP
EEG – can aid diagnosis but not assist finding the cause

261
Q

How should encephalitis be treated?

A

Start acyclovir within 30 mins of patient arriving if suspected encephalitis

Supportive therapy in HDU or ICU if needed

Symptomatic treatment – i.e. phenytoin for seizures

262
Q

What is the most common cell type seen in primary brain tumours?

A

Glial cell in origin - 90% are astrocytomas, 5% oligodendrocytoma

Oligodendrocytes = myelination of the central nervous system
(same job as schwann cells in the peripheral NS)

263
Q

Brain tumours are more commonly secondary tumours from other sites. Which types of cancer spread to the brain?

A

Lung – 40%

Breast – 15%

Melanoma – 10%

GI tract

Kidney

264
Q

What is the triad of presenting symptoms for brain tumours?

A

Symptoms of raised ICP

Loss of function/focal neurological deficit

Seizures/epilepsy

265
Q

What are the symptoms of raised ICP?

A

Headache worse in the morning
Worse when laying down/leaning forwards/coughing
Drowsiness
Confusion
Vomiting
Papilloedema 🡪 cardinal sign, seen on fundoscopy
Symptoms may not be present for a while but will then have a rapid onset
If not dealt with can lead to coma and death in short space of time

266
Q

What symptoms of loss of function/focal neurological deficit would occur due to a brain tumour?

A

Depends on location of tumour

Progressive – due to tumour growth (i.e. the symptoms will get more severe)

Possible deficits include – motor, sensory, speech, visual, deafness, memory, change in personality

267
Q

What type of seizures would be caused by a brain tumour?

A

FOCAL seizures rather than generalised

Recent new onset of seizures suggests sinister aetiology

268
Q

What is the gold standard investigation for a suspected brain tumour?

A

MRI brain

269
Q

How are brain tumours managed?

A

PALLIATIVE CARE INVOLVEMENT

Dexamethasone – high strength steroid, reduced brain inflammation and swelling

Surgery - for single mets in younger patients with controlled primary cancer (aim = improve QoL)

Radio/chemo – stereotactic radiotherapy/gamma knife

270
Q

What is an important side effect of giving dexamethasone?

A

Insomnia

So give in the mornings – do not give after lunchtime

271
Q

What is the median survival time of brain tumour?

A

12 months

272
Q

What is the pathological process behind Parkinson’s disease?

A

Loss of dopaminergic neurones from the substantia nigra of the midbrain

273
Q

What are some histopathological features you’d seen in Parkinson’s disease?

A

Lewy bodies – made up of alpha-synuclein and ubiquitin

Loss of dopaminergic neurones in the substantia nigra of the midbrain (which projects to the basal ganglia)

274
Q

What are the cardinal features of Parkinson’s disease?

A

Brady/akinesia (slowness of movement)

Resting tremor/pill rolling tremor (worse when concentrating)

Rigidity – lead pipe/cogwheel

Shuffling gait and postural instability

275
Q

What are the premotor symptoms of PD?

A

Anosmia (90%) – occurs around 7 years before the motor symptoms
Depression/anxiety – depression is also a later symptom
Sleep disorders
Constipation

276
Q

What are the motor symptoms of PD and what is the timeframe of their onset?

A

Onset – insidious
Reduced arm swing on one side
Akinesia/bradykinesia
Tremor – often worse on one side (all PD starts worse on one side)
Rigidity – posture and gait disturbances
Difficulty initiating movement
Progressive fatigue and detriment in amplitude of movements – ask the patient to tap their foot on the floor and it will start to slow

277
Q

What’s the gold standard diagnosis for PD?

A

None – it’s a clinical diagnosis

Can be differentiated from other causes of Parkinsonism using MRI or simply on clinical grounds

278
Q

What are some medications that can cause PD symptoms and how is it treated?

A

Haloperidol (dopamine blockade)

Metoclopramide/ domperidone (anti-emetic)

Managed with anticholinergics (e.g. oxybutinin)

279
Q

How is PD managed?

A

Education, exercise, physio (speech and movement)
Dopamine replacement – L-Dopa (plus carbidopa – stops levodopa breaking down into Dopamine outside the brain to reduce side effects)
Dopamine agonists – e.g. bromocriptine
MAO-B inhibitors – rasagiline, selegiline – inhibit dopamine breakdown

Deep brain stimulation

280
Q

What are some side effects of L-dopa?

A

Nausea

Dyskinesia (chorea-like movements)

Effectiveness decreases over time, even with increasing dose

281
Q

Which Parkinson’s medication is most associated with gambling addiction?

A

Dopamine agonists (cabergoline, bromocriptine)

Associated with gambling/other inhibition disorders such as sexual disinhibition

282
Q

What are some complications of PD?

A

Infections
Aspiration pneumonia
Falls
Depression

283
Q

What are the main causes of Guillian Barre syndrome?

A

Usually triggered by infection

Has been associated with campylobacter jejuni, EBV and CMV

284
Q

What is the likely pathophysiology behind the mechanism of GBS?

A

Thought that the infective organisms share molecular patterns with an antigen in the peripheral nerve tissue – leading to an auto-antibody mediated nerve cell damage

Similar pathogenesis to MS but affects PNS rather than CNS (demyelination)

285
Q

How does GBS present?

A

Progressive onset of limb weakness/paralysis and peripheral neuropathy
Starts distally and works its way up
Usually symmetrical
Reflexes lost early in illness (hyporeflexia)
Often sensory symptoms
Can involve the facial muscles 🡪 bulbar palsy
And respiratory muscles

286
Q

What is Miller-Fisher syndrome?

A

Related variant to GBS that affects the CNS and eye muscles

Characterised by ophthlamoplegia (eye muscle paralysis) and ataxia

287
Q

What are some differential diagnoses of GBS?

A

Other causes of neuromuscular paralysis can usually be excluded on clinical grounds or investigation – hypokalaemia, polymyositis, botulism, poliomyelitis

MRI spine may be needed to exclude transverse myelitis or cord compression

288
Q

What investigations need to be done for GBS?

A

It’s a clinical diagnosis so no diagnostic test

Nerve conduction studies – show slowing of motor conduction

CSF – protein elevated, normal glucose, normal cell count

MONITOR FVC SERIALLY – GBS can cause respiratory depression (do spirometry)

289
Q

How is GBS treated?

A

Watch and watch – supportive therapy – heparin to prevent thrombosis, physio to prevent contractures, NG or PEG feeding for patients with swallowing problems

IVIG – reduces duration and severity of paralysis, contraindicated in patients with IgA deficiency (causes severe allergic reactions)

IVIG, plasmapheresis, DVT prophylaxis

290
Q

What is the prognosis or GBS?

A

Recovery begins from a few days – 6 weeks from onset of symptoms

10% diet – respiratory failure, PE, infection

20% have permanent neurological damage

291
Q

What are the 2 main complications of GBS?

A

Respiratory failure

Prolonged disability

292
Q

What is motor neurone disease?

A

Relentless and unexplained destruction of upper motor neurones and anterior horn cells in the brain and spinal cord

293
Q

What causes MND?

A

Most causes are spontaneous and idiopathic with no family history

Rare familial cases – mutations in SOD-1 suggests that free radical damage responsible MN destruction

MORE COMMON IN MEN
Presents in middle age

294
Q

What are the symptoms of MND?

A

Weakness (progressive in nature)
Dysarthria
Dysphagia

NO SENSORY SYMPTOMS

295
Q

What are the signs associated with MND?

A

Fasciculations (particularly in the tongue) – LMN
UMN symptoms – hypertonia, brisk reflexes
Muscle wasting

You can get UMN signs too (especially in amyotrophic lateral sclerosis – the most common type)

296
Q

What are some differential diagnoses for MND?

A

Cervical spine lesion – may present with UMN

297
Q

What is the diagnostic tool used for MND?

A

El-Escorial diagnostic criteria

298
Q

How is MND treated?

A

No curative treatment

Supportive therapy essential – ventilation, NG feeding, antidepressants

Palliative care

299
Q

What medication can be used to help the symptoms of MND?

A

Riluzole

Not curative – aims to increase survival by 2-3 months and increase their time before needing ventilation

300
Q

What are some complications of MND?

A

UTI

Pneumonia

Constipation

Pressure sores

301
Q

What is the prognosis of MND?

A

Most patients die within 3 years from respiratory failure or pneumonia

As a result of bulbar palsy (impairment of CN 9, 10, 11, and 12)

302
Q

What type of dementia is associated with MND?

A

Frontotemporal dementia (Pick’s disease)

303
Q

What is myasthenia gravis?

A

An autoimmune condition

Antibodies form against acetylcholine receptors (anti-ACH receptor antibodies)

Associated with thymic hyperplasia in 70% (large thymus – produces immune cells)

304
Q

What are some RF for MG?

A

Female gender

Family history

Other autoimmune conditions

305
Q

How does MG present?

A

Eye drooping
Weakness and fatigueability of muscles – ocular, bulbar and proximal limb muscles
Struggle with
Hair, chairs, stairs (proximal muscle weakness)
Speech
Face and neck weakness
Mastication and swallowing
Respiratory muscles – causing breathing difficulty
Eventually muscle atrophy/wasting
Heart NOT affected but lungs are

306
Q

What are some signs of MG?

A

Ptosis

307
Q

What is the disease pattern of MG?

A

Fluctuating relapsing/remitting pattern

Dangerous features indicating advacnement of disease – respiratory impairment and dysphagia

308
Q

What investigations need to be done for MG?

A

Anti-AChR antibodies (90%)
Anti-MuSK antibodies (10%)
Mediastinal CT or MRI to look for thymoma and lung cancer (Lambert-Eaton syndrome – small cell lung cancer)
Repetitive nerve stimulation shows reduction

SERIAL MONITORING OF RESPIRATORY FUNCTION

309
Q

Which medications can worsen symptoms of MG?

A

Antibiotics
CCBs
Beta blockers
Lithium
Statins

310
Q

How do you treat myasthenia gravis?

A

Anti-cholinesterases – pyridostigmine or rivastigmine

Immune suppress – steroids, azathioprine

Thymectomy – in patients with thymoma or anti-Ach R+ve disease

Plasmapheresis - for severe relapsing cases

311
Q

What is a myaesthenic crises and what can trigger it?

A

Difficulty breathing or speaking, increased WOB with intercostal recessions, tiredness, trouble swallowing

Triggers – infection (coughs, colds), thyroid disease, monthly periods/pregnancy, trauma/surgery, change in medication etc.

Treatment – ventilation, anticholinesterases, immunosuppressives, IVIG, IV fluids, plasmapheresis

312
Q

What type of inheritance pattern is seen in Duchenne muscular dystrophy?

A

X-linked recessive

No male to male transmission

Females are carriers but not affected

313
Q

How does Duchenne’s present?

A

Proximal muscle weakness – Gower’s sign
Delayed milestones

314
Q

What’s the progression of DMD?

A

Wheelchair by 13 y/o
Cardiac involvement – 100% by 15 years
Respiratory involvement
Survival >30 years is unusual
Many muscle groups end up involved

Can get DMD associated cardiomyopathy – another phenotype with little/no skeletal muscle involvement

315
Q

How is Duchenne’s investigated?

A

Clinical examination – Gower’s test positive

Genetic testing to confirm

316
Q

How is DMD treated?

A

Supportive – physiotherapy, wheelchair
Scoliosis correction in children
Manage congestive HF and arrhythmias – beta blocker, ACEi, transplant
NIV for respiratory failure
Gene therapy

STEROIDS – best treatment, improve QoL, longer life expectancy and decreased progression of heart problems
Prednisolone – unclear why it helps so much, other immune suppressants have no benefit

317
Q

What is the “typical patient” you’d expect to see presenting with idiopathic intracranial hypertension?

A

Obese woman
Narrowed visual fields
Blurred vision +/- diplopia
6th nerve palsy
Enlarged blind spot if papilloedema present
Consciousness and cognition preserved

(Patient presents as if there were a mass, but none is found – headache, papilloedema, raised ICP symptoms)

318
Q

What causes idiopathic intracranial hypertension?

A

Unknown
Secondary to venous sinus thrombosis
Drugs – tetracycline, nitrofurantoin, vitamin A, isotretionoin (roaccutane), danazol, somatropin

319
Q

What investigations can be done for IIH?

A

CT head - shows no SOL

Lumbar puncture – increased opening pressure

320
Q

How can IIH be treated?

A

Weight loss – first line
Acetozolamide (also used for glaucoma)

Topiramate can also be used and has added benefit of weight loss
Therapeutic lumbar puncture
Surgery – optic nerve sheath decompression and fenestration to prevent optic nerve damage
Lumboperitoneal or ventriculoperitoneal shunt

321
Q

What is hydrocephalus and what are the different subtypes?

A

Hydrocephalus = abnormal build-up of CSF around the brain

Subtypes:
Congenital hydrocephalus – born with excess fluid on the brain
Acquired – develops at some point after birth due to injury or illness
Normal pressure hydrocephalus – uncommon and poorly understood, usually only develops in >60 year olds

322
Q

What is the role of the CSF?

A

Protects the brain from damage

Removes waste products from the brain

Provides the brain with nutrients to function properly

323
Q

What causes congenital hydrocephalus?

A

Spina bifida

Infection during pregnancy (mumps, rubella)

324
Q

What are the causes of acquired hydrocephalus?

A

Usually develops after illness or injury e.g. head injury or brain tumour

325
Q

What causes normal pressure hydrocephalus?

A

Can develop after head injury or stroke

Most causes unknown

The symptoms come on gradually and are similar to more common conditions such as Alzheimer’s – so can be difficult to diagnose

326
Q

What are the symptoms of normal pressure hydrocephalus?

A

Abnormal gait (ataxia?)

Urinary incontinence

Dementia

327
Q

What are the general symptoms of hydrocephalus?

A

Headache
Vomiting
Blurred vision
Difficulty walking

328
Q

How is hydrocephalus investigated?

A

CT and MRI scans used to diagnose congenital and acquired hydrocephalus

NPH – diagnostic criteria = walking, mental ability and bladder control (important to diagnose NPF correctly because unlike Alzheimer’s the symptoms can be relieved with treatment)

329
Q

How is hydrocephalus managed?

A

Vetriculo-peritoneal shunt – surgically implanted into the brain to drain away excess fluid

Endoscopic third ventriculostomy – alternative to shunt surgery – hole made in the floor of the third ventricle to allowed trapped CSF to escape to the surface where it can be re-absorbed

Complications – shunt can become blocked or infected

330
Q
A

Phase 3a (11 decks)

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