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My Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Name 3 acute causes of headaches

A

VICIOUS

  1. Vascular –> haemorrhage, infarction, venous thrombosis
  2. Infection –> meningitis, encephalitis, abscesses
  3. Compression –> obstructive hydrocephalus, pituitary enlargement
  4. ICP –> intracranial HTN
  5. Ophthalmic –> acute glaucoma
  6. Unknown –> situational, cough, exertion
  7. Systemic –> HTN, phaeochromocytoma, infections, toxins (CO)
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2
Q

Name 3 chronic causes of headaches

A
  1. Migraine
  2. Cluster headaches
  3. Tension headaches
  4. Trigeminal neuralgia
  5. Medication overuse headaches
  6. GCA
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3
Q

Give 2 primary causes of headaches

A
  1. Migraine
  2. Tension
  3. Cluster
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4
Q

Give 2 secondary causes of headaches

A
  1. Meningitis
  2. Subarachnoid haemorrhage
  3. GCA
  4. Medication overuse headache
  5. Idiopathic intracranial HTN
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5
Q

Give 3 red flags for secondary headache

A
  1. HIV or immunosuppressed
  2. Fever
  3. Thunderclap
  4. Seizure and new headache
  5. Suspected meningitis or encephalitis
  6. Acute glaucoma
  7. Headache and focal neurology
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6
Q

Give 3 red flags of a suspected brain tumour

A
  1. New onset headache and history of cancer
  2. Cluster headache
  3. Seizure
  4. Significantly altered consciousness, memory, confusion, coordination
  5. Papilloedema
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7
Q

Define migraine

A

Recurrent headaches for 4-72 hours with to without aura or GI disturbance
- Episodic cerebral oedema and dilation of the cerebral vessels

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8
Q

Give 3 triggers of migraines

A
  1. Chocolate
  2. Cheese
  3. OCP
  4. Alcohol
  5. Caffeine
  6. Anxiety
  7. Travel
  8. Sleep
  9. Exercise
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9
Q

What are the features of a migraine?

A
  • Unilateral
  • Pulsating
  • Aggravated by routine physical activity
  • MOderate/severe pain
  • Nausea
  • Photophobia or phonophobia
  • 4 to 72 hours
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10
Q

What are the features of aura?

A
  • Precedes migraine by 15-30 minutes
  • Zigzag lines or scotoma
  • Hemianopia
  • Paraesthesia
  • Dysphagia
  • Ataxia
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11
Q

Describe the clinical presentation fo prodrome

A

Precedes migraine by hours and days

  • Yawning
  • Food Cravings
  • Changes in sleep, appetite and mood
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12
Q

Describe the diagnosis criteria of migraine

A 
>5 attacks lasting 4-72 hours with N+v or photophobia/phonophbia 
AND 2 of 
- Unilateral pain 
- Throbbing pain 
- Pain aggravated by physical activity 
- Moderate/severe pain
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13
Q

What is the acute treatment for migraines?

A
  • NSAIDS
  • Triptans (5HT agonist) = sumatriptan
    +/- anti-emetics
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14
Q

What are the prophylactic treatments for migraines?

A
  • BB = propranolol
  • Topiramate (teratogenic)
  • Amitriptyline
  • Acupuncture
  • Valproate, pizotifen, gabapentin
    If aura is present, can’t use OCP
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15
Q

What are the features of cluster headaches

A
  • Rapid onset
  • Severe unilateral orbital pain - 15-180 minutes
  • Autonomic symptoms =lid swelling, lacrimination, facial flushing, rhinorrhoea, mitosis, ptosis
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16
Q

Describe the classification of the cluster headaches

A

Episodic = >2 cluster periods lasting 7 days to a year separated by pain free periods lasting >1 month

Chronic = attacks occurs for more than 1 year without remission or with remission lasting <1 month

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17
Q

What is the management for an acute cluster headache?

A
  1. minutes 100% O2 and triptan (sumatriptan)
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18
Q

What is the preventative management for cluster headaches?

A
  • Avoid triggers
  • Short term corticosteroids
  • Verapamil (CCB)
  • Lithium
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19
Q

What are the features of a tension headache?

A
  • Lasts 30 mins - 7 days
  • Bilateral
  • Pressing/tight band
  • Mild/moderate pain
  • Not aggravated by exercise
  • Photophobia OR phonophobia
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20
Q

Describe the classification of tension headaches

A 
Episodic = <15 days/month 
Chronic = >15 days/month for at least 3 months
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21
Q

Give 3 causes of tension headaches

A
  1. Stress
  2. Depression
  3. Alcohol
  4. Skipping meals
  5. Dehydration
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22
Q

Describe the management of tension headaches

A
  • Exercise, stress relief

- Symptomatic = aspirin, paracetamol, NSAIDS, NO opioids

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23
Q

Define medication overuse headache

A

Chronic headaches resulting from the overuse of medication –> opioids, mixed analgesia, ergotamine, triptans

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24
Q

What is the diagnostic criteria for a medication overuse headache?

A
  1. Headaches present for >15 days/month
  2. Regular overuse for >3 months of >1 symptomatic treatment drugs
  3. Headache has developed or markedly worsened during drug use
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25
Q

What is the management of a medication overuse headache?

A
  • Remove analgesia

- Aspirin/naproxen

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26
Q

Define trigeminal neuralgia

A

Paroxysms of unilateral intense stabbing pain the trigeminal distribution precipitated by innocuous stimuli

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27
Q

Name 2 triggers for trigeminal neuralgia

A
  1. Washing
  2. Shaving
  3. Eating
  4. Talking
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28
Q

Give 2 secondary causes of the trigmeinal neuralgia

A
  1. Compression CN
  2. MS
  3. Zoster
  4. Chiara malformation
  5. Meningeal inflammation
  6. Tumour
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29
Q

What is the clinical features of trigeminal neuralgia?

A
  • No radiation outside of the trigeminal distribution
  • Reoccurring paroxysmal attacks from a fraction of a second to 2 minutes
  • Severe intensity
  • Electric shock like, shutting, stabbing, sharp
  • Precipitated by innocuous stimuli to the affected side of the face
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30
Q

What is the management for trigeminal neuralgia?

A
  • Anticonvulsant –> carbamazepine, lamotrigine, phenytoin, gabapentin
  • Microvascular decompression
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31
Q

What is Giant Cell Arteritis (GCA)?

A

Systemic immune medicated chronic vasculitis affecting medium to large size arteries

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32
Q

What condition is GCA associated with?

A

Polymyalgia rheumatica (PMR)

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33
Q

What is the epidemiology of GCA?

A

Primarily over 50s

Female > Males

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34
Q

What are the symptoms of the headache in GCA?

A
  • New onset unilateral temple/scalp pain and tenderness/headache
  • Thickened pulseless, nodular or tender temporal artery
  • Jaw claudication
  • Amaurosis fugax, diplopia
  • Systemic features = fever, fatigue, anorexia, weight loss, depression
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35
Q

What investigative results would indicate GCA?

A

Increased ESR

Abnormal Temporal artery biopsy

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36
Q

What is the treatment for GCA?

A

High dose prednisolone (40-60mg oral OD)

- For 2 years

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37
Q

Give 2 potential complications of GCA

A
  1. Vision loss
  2. Large artery complications –> aortic aneurysm, aortic dissection, large artery stenosis
  3. CVD
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38
Q

Define subarachnoid haemorrhage

A

Spontaneous arterial bleeding into the subarachnoid space (between arachnoid and pia)

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39
Q

Give 2 causes of a SAH

A
  1. Berry aneurysm rupture (80%)
  2. Arteriovenous malformation (10%)
  3. Trauma –> contusion, skull base fracture, cerebral artery rupture/dissection
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40
Q

Give 4 risk factors for subarachnoid haemorrhages

A
  1. Previous berry aneurysms
  2. Smoking
  3. HTN
  4. Alcohol
  5. Family history
  6. Disease that predisposes aneurysms –> PCKD, Ehlers dances, coarctation
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41
Q

Where are Berry aneurysms most likely to form?

A
  • Junction between posterior communication artery and internal carotid (30%)
  • Junction between anterior communicating artery and anterior cerebral (35%)
  • Bifurcation of the Middle cerebral artery (22%)
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42
Q

Give 3 symptoms of a SAH

A
  1. Sudden onset severe occipital headache (thunderclap)
  2. Vomiting
  3. Meningism –> neck stiffness, N+V, photophobia
  4. Seizures
  5. Decreased consciousness –> coma
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43
Q

Give 2 signs of a SAH

A
  1. Kernig’s sign = can’t straighten leg past 135 degrees
  2. Brudzinski’s sign = neck flexed, hip and knee flex
  3. Papilloedema
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44
Q

What investigations might you carry out in someone with a suspected SAH?

A

CT = star pattern (blood in sulci)

LP (after 12 hours) = bloody then xanthochromic (bilirubin)

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45
Q

How do you manage someone with a SAH?

A
  • Nimodipine (CCB) –> reduce vasospasm
  • Endovascular surgery –> CT angiography and coiling/cliping
  • Bed rest, hydration, BP control
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46
Q

Give 2 possible complications of a SAH

A
  1. Rebleeding
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
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47
Q

Define and describe the pathophysiology of a subdural haemorrhage

A

Bleeding of bridging veins between the cortex and sagittal sinus –> accumulating haematoma –> raised ICP –> tentorial herniation/coning

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48
Q

What is the most common cause of a subdural haemorrhage?

A

Minor head injury –> especially deceleration injuries

- May have happened 8-10 weeks previously

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49
Q

Name 3 at risk groups of a subdural haemorrhage

A
  1. Alcoholics
  2. Epileptics
  3. Elderly –> falls
  4. People of anticoagulants
  5. Shaken babies
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50
Q

What are the symptoms of a subdural haemorrhage?

A
  1. Headache
  2. Fluctuating consciousness level
  3. Confusion and personality change
  4. Sleepiness/drowsiness
  5. Unsteadiness
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51
Q

What is a sign of a subdural haemorrhage?

A

Raised ICP –> seizures, papilloedema

Tentorial herniations and coning

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52
Q

What would you see on a CT for someone with a subdural haematoma?

A

Unilateral crescent shaped blood collection
Midline shift
Clots goes from white to grey over time

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53
Q

What is the management for someone with a subdural haematoma?

A
  • Mannitol –> decrease ICP

- Surgical evacuation of the clot –> burr holes, craniotomy

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54
Q

Define an extradural haemorrhage

A

Often due to a fractured temporal or parietal bone –> laceration of middle meningeal artery/vein –> bleed between bone and dura

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55
Q

When should you suspect an extradural haemorrhage?

A

Head injury –> LOC –> lucid interval –> worsening of symptoms

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56
Q

How does an extradural haemorrhage present?

A
  1. Lucid interval (hours/days)
  2. Reduced GCS
  3. Increased ICP
    - Headache
    - N+V
    - Confusion
    - Seizures
    - Ipsilateral blown pupil (3nd nerve plasy)
  4. Brainstem compression –> deep irregular breathing –> death
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57
Q

What investigations would you do on someone with a suspected extradural haemorrhage?

A
  • CT = lens shaped (biconvex) haematoma and possible skull fracture
  • LP is CONTRAINDICATED
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58
Q

What is the management of a extradural haematoma?

A
  • Neuroprotective ventilation
  • Mannitol = decrease ICP
  • Craniotomy for clot evacuation
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59
Q

Give 3 differences in the presentation of a patient with a subdural haemorrhage compared to someone with an extradural haemorrhage

A
  1. Time Frame = extradural symptoms are more acute
  2. GCS = subdural GCS will fluctuate, extradural GCS will drop suddenly
  3. CT = extradural ill have a rounder more contained appearance
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60
Q

Define Stroke

A

Rapid onset of focal neurological deficit which is the result of a vascular lesion and is associated with infarction of central nervous tissue lasting >24 hours or leading to death with no apparent cause other than vascular origin

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61
Q

What are the 2 main types of stroke?

A
  1. Ischaemic (80%)

2. Haemorrhagic (15-20%)

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62
Q

Give 2 possible causes of an ischaemic stroke

A
  1. Atheroma –> MCA, small vessel, carotid (atherothromboembolism)
  2. Embolism –> cardiac from AF, endocarditis, MI
  3. Systemic hypo perfusion
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63
Q

Give 2 possible causes of an haemorrhagic stroke

A
  1. HTN
  2. Trauma
  3. Aneurysm rupture
  4. Carotid artery dissection
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64
Q

Give 4 risk factors for a stroke

A
  1. HTN
  2. Smoking
  3. DM
  4. Heart disease –> valvular, ischaemic, AF
  5. Peripheral vascular disease
  6. FHx or previous TIA history
  7. COCP
  8. Ethnicity (increased in blacks and asians)
  9. Clotting abnormalities
  10. Alcohol use
  11. Hyperlipidaemia
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65
Q

What investigations would you do to determine whether someone has had a haemorrhagic or an ischaemic stroke?

A

CT scan

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66
Q

What investigations might you do for a suspected stroke?

A
  • CT head (excludes haemorrhage)
  • MRI –> identify ischaemic stroke
  • Carotid doppler –> carotid stenosis
  • ECG –> MI, AF
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67
Q

What is the criteria of a Total Anterior Circulation Stroke (TACS)?

A

= Large infarct of MCA, ACA or carotid
ALL 3 of:
1. Contralateral hemiparesis and sensory deficit (>2 of face, arm, leg)
2. Homonymous hemianopia (contralateral)
3. Higher cerebral dysfunction –> dysphagia/dysarthria (dominant), visuospatial

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68
Q

What is the criteria of a Partial Anterior Circulation Stroke (PACS)?

A

2/3 of:

  1. Contralateral hemiparesis and sensory deficit (>2 of face, arm, leg)
  2. Homonymous hemianopia (contralateral)
  3. Higher cerebral dysfunction –> dysphagia/dysarthria (dominant), visuospatial
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69
Q

What is the criteria of a Posterior Circulation Stroke/Syndrome (POCS)?

A

1 of:

  1. Cranial nerve palsy and a contralateral motor/senosry deficit
  2. Bilateral motor/senosry deficit
  3. Conjugate eye movement disorder (e.g. gaze palsy)
  4. Cerebellar dysfunction –> ataxia, nystagmus, vertigo
  5. Isolated homonymous hemianopia or cortical blindness
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70
Q

What is the criteria of a Lacunar Infarct?

A 
= Perforating arteries supplugng internal capsule and basal ganglia 
1 of:
- Pure sensory stroke 
- Pure motor store 
- Sensori-motor stroke 
- Ataxic hemiparesis
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71
Q

Give 3 signs of a ACA stroke

A
  1. Lower limb weakness and loss of sensation
  2. Gait apraxia (unable to initiate walking)
  3. Incontinence
  4. Drowsiness
  5. Akinetic mutism = decrease in spontaneous speech
  6. FACE is SPARED
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72
Q

Give 3 signs of a MCA stroke

A
  1. Contralateral arm and leg weakness and contralateral sensory loss
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial droop
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73
Q

Give 3 signs of a PCA stroke

A
  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agnosia = inability to recognise or interpret visual information
  4. Prosopagnosia = inability to recognise a familiar face
  5. Dyslexia, anomic aphasia
  6. Unilateral headache
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74
Q

What are the symptoms of a lacunar stroke?

A

Absence of:

  • Higher cortical dysfunction
  • Homonymous hemianopia
  • Drowsiness
  • Brainstem signs
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75
Q

Give 3 signs of a brainstem stroke

A
  1. Hemi/quadra-peresis
  2. Conjugate gaze palsy
  3. Horner’s syndrome
  4. Facial weakness
  5. Nystagmus, vertigo
  6. Dysphagia, dysarthria
  7. Decreased GCS
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76
Q

What is the treatment for an ischaemic stroke?

A
  • Aspirin 300mg PO (once haemorrhagic stroke excluded)
  • Thrombolysis <4.5 hours after symptom onset (alteplase)
  • Decompressive hemicraniotomy for some MCAs
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77
Q

What non pharmacological treatments are there for people after a stroke?

A
  1. Specialised stroke units = rehab
  2. SALT help
  3. Physiotherapy
  4. Home modifications
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78
Q

What are the primary preventative measures for stroke prevention?

A

= Before stroke occurs

  • Control ris factors –> HTN, lipids, DM, smoking, cardiac disease
  • Lifelong anticoagulation in AF (CHADVASC)
  • Exercise
  • Carotid endocardectomy is symptomatic 70% stenosis
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79
Q

What are the secondary preventative measures for stroke prevention?

A

= preventing another stroke occurring

  • Statin
  • Aspirin and clopidogrel for 2 weeks then just 75mg clopidogrel OR 75mg aspirin OD + 200mg dipyridamole (warfarin is cardioembolic stroke)
  • Antihypertensives
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80
Q

Define ITA

A

Sudden onset focal neurology lasting <24 hours due to temporary occlusion of part of the cerebral circulation without evidence of an acute infarct

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81
Q

Give 2 possible causes of a TIA

A
  1. Atherthromboembolism of carotid
  2. Cardioembolism –> post MI, AF, valve disease
  3. Hyperviscosity –> polycythaemia, SCD
  4. Vasculitis
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82
Q

Give 2 signs of a carotid (90%) TIA

A
  1. Amaurosis fugax = retinal artery occlusion, descending curtain of vision loss
  2. Aphasia
  3. Hemiparesis
  4. Hemisensory loss
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83
Q

Give 2 signs of a vertebrobasilar (10%) TIA

A
  1. Diplopia
  2. Vomiting
  3. Choking
  4. Ataxia
  5. Hemisenosry loss
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84
Q

What is essential to do in someone who has had a TIA?

A

ABCD2 score = risk of stroke in the next 7 days

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85
Q

What is the ABCD2 score?

A

Assesses his of a stroke in next 7 days

  • Age >60
  • BP >140/90
  • Clinical features
    a) Unilateral weakness (2 points)
    b) Speech disturbance without weakness (1 point)
  • Duration
    a) 10-59 minutes (1 point)
    b) >1 hour (2 points)
  • Diabetes

High risk stroke patients = ABCD2 score >4, AF, >1 TIA in a week

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86
Q

What do the scores from an ABCD2 mean?

A 
>6 = high risk stroke
>4 = assess within 24 hours
<4 = assess within 1 week
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87
Q

What is the management of someone with a TIA

A
  1. Control risk factors –> statin, antihypertensives, DM control, diet and exercise
  2. Antiplatelet therapy = 2 weeks aspirin and clopidogrel then longterm clopidogrel
  3. Specialist referral to TIA clinic and ABCD2 score
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88
Q

Give 4 causes of transient loss of consciousness

A
  1. Epileptic seizures
  2. Non-epileptic seizures
  3. Syncope
  4. Intoxication
  5. Hypoglycaemia
  6. Acute hydrocephalus
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89
Q

Define Seizure

A

A convulsion caused by paroxysmal discharge of cerebral neurones
Abnormal and excessive excitability of neurones

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90
Q

Give 3 causes of seizures

A
  1. Epilepsy
  2. Febrile convulsions
  3. Alcohol withdrawal
  4. Psychogenic non epileptic seizures
  5. Brain injury or tumour
  6. Infection
  7. Trauma
  8. Metabolic imbalances
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91
Q

Define epilepsy

A

Recurrent, spontaneous, intermittent, abnormal electrical activity in part of the brain manifesting seizures
- At least 2 or more unprovoked seizures occurring >24 hours apart

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92
Q

What 2 categories can epileptic seizure be broadly divided into?

A
  1. Focal epilepsy = only 1 hemisphere of the brain is involved, often structural cause
  2. Generalised = widespread seizure activity in both hemispheres
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93
Q

Give 3 examples of focal seizures

A
  1. Simple partial seizures
  2. Complex partial seizures
  3. Secondary generalised seizures
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94
Q

What are simple partial seizures?

A

Aura = epigastric rising, deja vu, smells, lights, sounds

  • Awareness unimpaired
  • Non memory, autonomic or psychic symptoms
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95
Q

What are the features of a complex partial seizure?

A

Disturbance of consciousness or awareness, 5As

  • Aura
  • Autonomic –> change in sin colour, temp, palpitations
  • Awareness los –> motor arrest, motionless stare
  • Automatism –> lip smacking, fumbling, chewing, swallowing
  • Amnesia
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96
Q

What is a secondary generalised seizure?

A

Focal seizure = generalise

Aura –> tonic clonic

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97
Q

Give 4 types of generalised epilepsy

A
  1. Absence
  2. Tonic-clonic
  3. Myoclonic
  4. Atonic
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98
Q

Describer the features of a absence seizure

A

Often seen in childhood

  • Ceases activity and states
  • Abrupt onset and offset
  • <10 seconds
  • Eye = blank stare and glazed
  • 3Hz spike and wave on EEG
  • Stimulated by hyperventilation and photics
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99
Q

Describe the features of a tonic-clonic seizure

A
  • Rigid phase (tonic) –> rhythmic jerking (clonic)
  • LOC
  • Tongue bring, incontinence, drowsiness
  • POst ictal confusion
  • Lasts 1-2 minutes
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100
Q

Describe the features of a myoclonic seizure

A
  • Sudden isolated jerk of limb, face or trunk and stiffening
  • Movement cessation/falling
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101
Q

Describe the features of a atonic seizure

A
  • Sudden loss of muscle tone –> fall forwards
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102
Q

What features localise a seizure to the temporal lobe?

A
  1. Automatisms = lip smacking, chewing, fumbling
  2. Deja vu
  3. Delusional behaviours
  4. Emotional disturbance = terror, panic, anger
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103
Q

What features localise a seizure to the frontal lobe?

A

Motor features –> arrest, Jacksonism march, Todds plays (post ictal temporary weakness)

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104
Q

What features localise a seizure to the parietal lobe?

A

Sensory disturbance –> tingling, numbness

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105
Q

What features localise a seizure to the occipital lobe?

A

Visual phenomenon –> spots, lines, flashes

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106
Q

What are the treatments for generalised seizures (excluding absence)?

A

Sodium valproate –> lamotrigine –> carbamazepine

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107
Q

What are the treatments for absence seizures?

A

Sodium valproate –> ethosuximide –> lamotrigine

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108
Q

What are the treatments for focal seizures?

A

Carbamazepine –> lamotrigine –> Keppra (levetiracetam)

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109
Q

What are the treatments for acute seizures?

A

Diazepam and lorazepam

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110
Q

Give 2 side effects of sodium Valporate

A
  1. Teratogenic (neural tube defects) –> not given to women of child bearing age
  2. Increased appetite
  3. Liver failure
  4. Pancreatitis
  5. Hair loss
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111
Q

Give 2 side effects of Lamotrigine

A
  1. Skin rash
  2. Diplopia and blurred vision
  3. Vomiting
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112
Q

Give 2 side effects of Carbamazepine

A
  1. Agranulocytosis
  2. Skin rashes
  3. Decreased effectiveness of OCP
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113
Q

Give 2 side effects of Phenytoin

A
  1. Teratogenic (cleft palate)
  2. tremor
  3. Cerebellar syndrome
  4. Diplopia
  5. Decreased effectiveness of OCP
114
Q

Which anti epileptics should pregnant women take?

A

Lamotrigine

  • Avoid valporate
  • CBA and PHE reduce effectiveness of OCP (enzyme inducers)
115
Q

What is status epilepticus?

A

Seizure lasting >5 minutes or recurrent seizures without recovery

116
Q

What is the management of status epilepticus?

A
  • Benzodiazepine (lorazepam 0.1mg/kg, diazepam), buccal midazolam if no IV
  • Further dose after 10 minutes (if not settled)
  • Non response –> phenytoin
  • Intubation and GA
117
Q

Define syncope

A

Transient global cerebral hypoperfusion = insufficiency blood or O2 supply to the brain causes paroxysmal changes in behaviours, sensation and cognitive processes

118
Q

Give 3 signs that a transient loss of consciousness is due to syncope

A
  1. Situational
  2. 5-30 seconds
  3. Sweating
  4. Nausea
  5. Pallor
  6. Dehydration
  7. Rapid recovery
119
Q

Give 3 causes of Syncope

A
  1. Reflex = associated with a sudden decreased in BP and HR in response to a trigger
  2. Orthostatic = associated with a sudden drop in BP after standing up
  3. Cardiogenic = until ruled out, DO ECG
120
Q

Give 3 possible causes of reflex syncope

A
  1. Vasovagal = triggered by posture, provoking factors (pain, anxiety, medical, stress, heat), prodromal symptoms
  2. Situational = triggered by cough, defecation, sense, post micturition, post exercise
  3. Carotid sinus hypersensitivity = triggered by sudden head turning, tight collar, shaving
121
Q

What is the criteria for orthostatic syncope?

A
  • Fall in BP of 20mmHg or a fall in diastolic BP of at least 10mmHg within 3 minutes of standing

Due to drugs (antihypertensives, antidepressants), autonomic failure (PD), DM, hypovolvaemia

122
Q

Define psychogenic non epileptic seizures (pseudo seizures)

A

Mental processes associated with psychological distress cause paroxysmal changes in behaviour, sensation and cognitive processes

123
Q

Give 3 signs of a pseudo seizure

A
  1. Situational
  2. 1-20 minutes
  3. Eyes closed
  4. Emotional = crying, speaking
  5. Pelvic thrusting
  6. History of psychiatric illness
124
Q

Define Huntington’s disease

A

Neurodegenerative disorder characterised by the lack of inhibitory neurotransmitter GABA

125
Q

What is the inheritance pattern seen in Huntington’s disease?

A

Autosomal dominant = 50% chance of inheritance

126
Q

What is the pathophysiology behind Huntington’s disease?

A

Degeneration of cholinergic and GABA neurones in the striatum (caudate nucleus and putamen) of the basal ganglia –> decreased inhibition o f dopamine –> excessive thalamic stimulation

127
Q

What triplet code is repeated in Huntington’s disease?

A

CAG in the HTT gene on chromosome 4
>35 = possible HD
>39 = adult onset
>60 = early onset

128
Q

Give 3 features of Huntington’s disease

A
  1. Chorea
  2. Psychiatric problems = personality change, depression, psychosis
  3. Dementia
  4. Saccidic eye movement
  5. Lack of coordination, ataxia
  6. Seizures
129
Q

What is the management of Huntington’s disease?

A

Incurable, symptomatic control

  • Chorea = sulpiride (neuroleptic, decreases nerve function), tetrabenazine (dopamine depleting)
  • Depression = SSRI
  • Psychosis = haloperidol
  • Aggression = risperidone
130
Q

Give 3 causes of Parkinsonism?

A
  1. Parkinson’s disease
  2. Parkinson Plus Syndromes
  3. Infection –> syphilis, HIV, CJD
  4. Vascular –> multiple infarcts
  5. Drugs
  6. Genetic –> Wilsons
131
Q

Name 3 drugs known to induce parkinsonism

A
  1. Antipsychotics (aripiprazole)
  2. Anti-emetics (metoclopramide)
  3. SSRIs
  4. CCBs
  5. Lithium
  6. Valporate
  7. Cholinesterase inhibitors
132
Q

What are the cardinal signs of Parkinsonism?

A
  1. Asymmetric tremor = worse at rest, exacerbated by distraction, 4-6Hz, pin rolling
  2. Rigidity = lead pipe (increased tone in all muscle groups) or cog wheel (rigidity and tremor)
  3. Bradykinesia = slow initiation of movements, reduced amplitude and speed on repetition, expressionless face, monotonous voice, microgrpahia

Also festinating gait = short shuffling steps, stooped, decreased arm swing

133
Q

What is Parkinson’s disease?

A

Degenerative movement disorder caused by a reduction in dopamine in the substantial nigra (pars compact) of the basal ganglia

134
Q

Briefly describe the pathophysiology of PD

A

Loss of dopamine –> thalamus inhibited –> decreased in movement + symptoms present

B amyloid plaques, neurofibrillary tangles and hyperphosphorylated tau

135
Q

Give 5 features of PD

A
  1. Asymmetric tremor
  2. Cog wheel rigidity
  3. Bradykinesia
  4. Postural instability
  5. Hyposmia
  6. Excessive salvia production
  7. Dementia
  8. Sleep disorders = insomnia, EDS
  9. Depression
  10. Autonomic dysfunction = postural hypotension, urinary symptoms, ED, constipation
136
Q

What investigations might you do in someone you suspect to have PD?

A
  • Response to L-Dopa
  • DaTSCAN
  • MRI and PET scans
137
Q

What is the management of PD?

A
  • Levodopa = dopamine precursor (tyrosine –> L-dopa –> dopamine)
  • Dopamine Recepto agonist = bromocriptine, ropinirole, cabergoline –> 1st line in <60y/o
  • MAO-B inhibitors = rasagiline, selegiline (inhibits dopamine breakdown)
  • COMT inhibitors = entacapone, tolcapone (inhibits dopamine breakdown)
  • Anticholinergics (reduce tremor), SSRI (depression)
  • Surgical = deep brain stimulation
138
Q

Give 2 possible side effects of L-dopa

A
  1. Dyskinesia –> dystonia, chorea, athetosis
  2. On-off phenomena = motor fluctuations
  3. Psychosis
  4. Insomnia
  5. Mouth dryness
  6. N+V
  7. Excessive daytime sleepiness
139
Q

Give 2 possible side effects of dopamine receptor agonists

A
  1. Tiredness
  2. Gambling
  3. Hypersexuality
  4. Dystonia
140
Q

What are the 4 Parkinson Plus Syndromes?

A
  1. Multiple systems atrophy
  2. Progressive supranuclear palsy
  3. Corticobasiliar degeneration
  4. Lewy body Dementia
141
Q

What are the signs of Multiple systems atrophy?

A
  • Symmetrical onset
  • Falls at presentation
  • Parkinsonism with autonomic, corticospinal and cerebellar dysfunction
  • Autonomic = postural hypotension, impotence, incontinence, increased sweat
  • Hot cross bun sing on MRI
142
Q

What are the signs of progressive supra nuclear palsy?

A
  • Postural instability leading to falls
  • Speech disturbance
  • Vertical gaze plazy
  • Hummingbird sing on MRI
143
Q

What are the signs of corticobasiliar degeneration?

A
  • Aphasia, dysarthria, apraxia
  • Akinetic rigidity I 1 limb
  • Alien limb phenomenon = patient perceives that 1 of their limbs doesn’t belong to them
144
Q

What are the signs of lewy body dementia?

A
  • Fluctuating cognition
  • Visual hallucinations and delusions
  • REM sleep disorders
145
Q

Define dementia

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving, attention or language
There is a progressive decline in cognitive function with no impairment of consciousness but interferes with ADLs

146
Q

What are the 4 main types of dementia?

A
  1. Alzheimers (65%)
  2. Vascular (20%)
  3. Lewy body (10%)
  4. Fronto-temporal (5%)
147
Q

Give 3 differentials of dementia

A
  1. Old Age
  2. Depression
  3. Delirium
  4. Vitamin, thiamine, B12 or folate deficiency
  5. Hypothyroidism
  6. Infection –> HIV, HSV
  7. Normal Pressure hydrocephalus
148
Q

Give 3 risk factors for dementia

A
  1. FHx
  2. Age
  3. Downs Syndrome m
  4. Alcohol use
  5. Obesity, HTN, hypercholesterolaemia, DM
  6. Atherosclerosis
  7. Depression
149
Q

Give 3 cognitive impairment symptoms of dementia

A
  1. Memory loss
  2. Problems with reasoning and communication
  3. Difficulty making decision
  4. Dysphagia
  5. Difficulty carrying out coordinated movements
  6. Disorientation and unawareness of time and place
  7. Impairment of executive function
150
Q

Give 3 behavioural and psychological symptoms of dementia (BPSD)

A
  1. Psychosis
  2. Agitation and emotional lability
  3. Depression and anxiety
  4. Withdrawal and apathy
  5. Disinhibition
  6. Sleep cycle disturbance
151
Q

What investigations might you do for someone with suspected dementia?

A
  1. Good history and examination
  2. 6CIT
  3. Blood test –> FBC, LFTs, thyroid, B12, folate
  4. MMSE
  5. ACE 3
  6. Psychometric testing
  7. MRI
  8. PET and SPECT
152
Q

Give 3 ways in which dementia can be prevented

A
  1. Stop smoking
  2. Healthy diet
  3. Regular exercise
  4. Healthy weight
  5. Low alcohol intake
  6. Education decreased the risk
  7. BP control
153
Q

What medication might you give someone with dementia?

A
  • Acetylcholineesterase inhibitors –> donepezil, rivastigmine
  • Anti-glutamate –> memantine
  • BP control –> reduce vascular damage
154
Q

What is pseudo dementia?

A

Cognitive impairment secondary to mental illness –> depression, anxiety

155
Q

Describe the pathophysiology of Alzheimers disease

A

Degeneration of posterior cerebral cortex and medial temporal lobe

Accumulation of Beta amyloid peptide –> progressive neuronal damage, neurofibrillary tangles (accumulation of Tau protein), cortical atrophy

156
Q

Give 3 clinical features of Alzheimers disease

A
  1. Global memory/cognitive decline
  2. Episodic memory loss, short term memory first
  3. Visuospatial problems
  4. 4As = aphasia, anomia, acalculia, ADL decline
  5. Later = Psychosis, delusions, hallucinations, motor signs
157
Q

What would you see on functional imaging of someone with Alzheimers?

A
  • Reduced blood flow and reduced glucose metabolism in the tempo parietal regions
  • Cortical atrophy
  • Enlarged ventricles
158
Q

What is the treatment for Alzheimers?

A
  • Acetylcholinesterase inhibitors –> donepezil, rivastigmine
  • Antidepressants/psychotics
  • Emotional and social stimulation
159
Q

25% of all patients with AD will develop what?

A

Parkinsonism

160
Q

What is the pathophysiology of vascular dementia?

A

Brain damage due to cerebrovascular disease –> multiple infarcts or major stroke s

161
Q

Give 3 risk factors of vascular dementia

A
  1. History of stroke or TIA
  2. AF
  3. Smoking
  4. HTN
  5. DM
  6. Hyperlipidaemia
  7. Coronary artery disease
  8. Obesity
162
Q

Give 3 symptoms of vascular dementia

A
  1. Stepwise deterioration with patchy deficits –> mental and physical decline
  2. Sundowning
  3. Shuffling gait
  4. Attention problems
  5. Focal neurological abnormalities –> visual disturbance, sensory or motor symptoms
  6. Vascular risk factors
163
Q

What is the management for vascular dementia?

A
  • Manage predisposing factors –> especially BP
164
Q

What is the pathophysiology of Lewy body dementia?

A

Deposition of Lewy bodies (alpha synuclein) in the brainstem and neocortex

165
Q

Give 3 features of Lewy body dementia

A
  1. Fluctuating cognitive impairments
  2. Visual hallucinations
  3. Parkinsonism = bradykinesia, tremor, rigidity
  4. Sleep disorders
  5. Psychosis
166
Q

What would you see on psychometric testing in someone with Lewy body dementia?

A
  1. Deficits in attention
  2. Executive function decline
  3. Fluctuation fo cognitive performance
  4. Preservation of episodic memory loss
167
Q

What is the treatment for Lewy body dementia?

A
  • Cholinesterase inhibitors –> donepezil and rivstigmaine

- Memantine (antiglutamate)

168
Q

What is the pathology of frontotemporal dementia?

A
  • Selective degeneration of frontal and temporal lobes
  • Pick bodies (spherical aggregations of tau protein)
  • Neurofibrillary tangles
  • Senile plaques
169
Q

Which disease is front-temporal dementia associated with?

A

MND

170
Q

Give 3 clinical features of front-temporal dementia

A
  1. Onset <65 years old
  2. Insidious onset
  3. Personality change
  4. Emotional unconcern
  5. Disinhibition
  6. Aphasia
171
Q

What would be seen on an MRI of someone with Pick’s disease?

A

Atrophy of fronto-temporal dementia

172
Q

Define MND

A

Cluster of major degenerative diseases characterised by selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells

173
Q

What are the causes of MND?

A

Unknown
10% = familial (SOD1 mutation)
90% = sporadic

174
Q

What is the classification of MND?

A
  1. Amyotrophic lateral sclerosis (ALS)
  2. Progressice bulbar plasy
  3. Progressive muscular atrophy
  4. Primary lateral sclerosis
175
Q

What is affected in ALS?

A

Loss in motor cortex and anterior horn –> UMN and LMN signs
- Asymmetrical proximal muscle weakness

176
Q

What is affected in progressive bulbar palsy?

A

CN 9-12 affected = LMN signs only

- Dysarthria, dysphagia, wasting and fasciculations of tongue

177
Q

What is affected in progressive muscular atrophy?

A

Anterior horn lesion –> LMN signs only

- Distal to proximal

178
Q

What is affected in Primary lateral sclerosis?

A

Loss of Betz cells in motor cortex leading –> UMN signs

- Marked spastic leg weakness, pseudo bulbar plays (spastic slow tongue movements, brisk jaw jerk)

179
Q

Do you get sensory loss and sphincter disturbance in MND?

A

NO

180
Q

Are eye movements affected in MND?

A

NO

181
Q

What are the features of MND?

A

Mixed UMN and LMN signs

  • UMN = hypertonia (spasticity), hyperreflexia, +ve babinski, muscle weakness (pyramidal pattern, upper limb flexors > extensors, Lower limb extensors > flexors)
  • LMN = hypotonia, muscle wasting, fasciculations, hyporeflexia
182
Q

Give 2 possible bulbar signs of MND

A
  1. Dysarthria
  2. Dysphagia
  3. Brisk jaw jerk
  4. Wasting and fasciculations of the tongue
183
Q

Give 2 possible respiratory signs of MND

A
  1. Dyspnoea
  2. Orthopnoea
  3. Poor sleep
184
Q

Give 2 possible Limb onset signs of MND

A
  1. Weakness
  2. Clumsiness
  3. Wasting muscles
  4. Foot drop
185
Q

What investigations would you do on someone with suspected MND?

A
  • Head and spinal MRI
  • Blood tests = muscle enzymes, autoantibodiea
  • LP = oligoclonal IgG bands
  • NCS and EMG = denervation
186
Q

What is the medical management of MND?

A

Disease modifying drugs = Riluzole (anti-glutamatergic)

- Prolongs life by 3 months

187
Q

What is the supportive treatment for MND?

A 
Dribbling = propantheline or amitriptyline
Dysphagia = NG tube or PEG
Respiratory failure = NIV 
Pain = analgesic ladder 
Spasticity = baclofen, botox 
Counselling
188
Q

Define multiple sclerosis

A

A chronic inflammatory autoimmune T cell mediated condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space

189
Q

Describe the epidemiology of MS

A
  • Presents between 20-40 y/o
  • Females >Males
  • More popular in temperate climates = low vitamin D
190
Q

Describe the aetiology of MS

A
  • Environmental –> EBV
  • Genetic = HLA-DRB1
  • Unknown
  • Vit D deficiency, smoking, obesity
191
Q

Where would MS plaques be seen histologically?

A
  • Optic nerves
  • Spinal cord
  • Cerebral hemispheres
  • Medulla
  • Pons
192
Q

Describe the classifications of MS

A
  1. Relapsing remitting (85%) = defined relapses with no progression between attacks
  2. Secondary progressive = initially relapsing remitting followed by progression with or without occasional relapse, minor remission or plateaus
  3. Primary progressive = disease progression from onset
193
Q

Define relapse and pseudo relapse in MS

A

Relapse = experienced by patient but may be confirmable by examination which last >48 hours

Pseudo-relapse = Infection causes relapse symptoms

194
Q

Name 4 clinical features of MS

A

DEMYELINATION

  1. Diplopia
  2. Eye movement painful = optic neuritis (unilateral eye pain on movement and loss of central vision)
  3. Motor weakness = progressive spastic weakness
  4. nYstagmus
  5. Elevated temperature worsens = Uthoff’s phenomenon
  6. Lhermitte’s sign = flexion os neck causes shock down spine
  7. Intention tremor
  8. Neuropathic pain –> e.g. trigeminal neuralgia
  9. Ataxia
  10. talking slurred
  11. Impotence
  12. Overactive bladder/incontinence
  13. Numbness/tingling
    - Also can present as transverse myelitis = focal inflammation fo spinal cord –> paraesthesia, weakness, lhermittes, urinary Sx
195
Q

What investigations might you do for someone with suspected MS?

A
  • MRI brain and spinal cord
  • LP –> oligoclonal bands
  • NCS and EMG = delayed suggests demyelination
  • Visual provoked potential = prolonged reaction
  • Antibodies = anti-MBP, NMO-IgG
196
Q

What is the diagnostic criteria for MS?

A

McDonald criteria

  • An inflammatory demyelinating disease of the CNS, >2 lesions
    - Dissemination in space
    - Dissemination in time
    - No alternative neurological disease which may explain the signs and symptoms
  • Need at least 1 episode of typical relapse
197
Q

What are the lifestyle management options for MS?

A
  • Regular exercise
  • Reduce stress
  • Smoking/alcohol cessation
198
Q

What is the drug management of someone having an acute MS attack?

A

Methylprednisolone

199
Q

Describe the drug management to prevent an MS relapse

A

DMARDS

  • Beta interferon
  • Naralizumab
  • Dimethyl fumarate
  • Alemtuzumab
200
Q

What symptomatic treatment is there for MS patients?

A

Spasticity = baclofen, botox
Tremor = botox , gabapentin, BB, clonazepam
Thalamic surgery = stereotactic thalamotomy, thalamic electrostimulation
Physio, OT, psychology service, speech therapy

201
Q

What is Myasthenia Gravis?

A

Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction
- Mediated by antibodies (anti-AchR Abs) against nicotinic Act receptors which interferes with neuromuscular transmission via depletion of working post synaptic receptor sites

202
Q

What is myasthenia graves associated with in <50 year olds?

A

More common in women

Associated with other AI disease –> pernicious anaemia, SLE, RA, thymic hyperplasia

203
Q

What is myasthenia graves associated with in >50 year olds?

A

More common in men

Associated with thymic atrophy or thymic tumour

204
Q

What is the presentation of myasthenia gravis?

A
  • Fatiguable weakness
  • Extraocular = ptosis, diplopia
  • Bulbar = voice deteriorates on counting to 50
  • Face = myasthenia snarl
  • Neck = head droop
  • Limbs = asymmetric, proximal weakness
  • Normal tendon reflexes but may be fatiguable
  • Weakness worsened by pregnancy, hypokalaemia, infection, emotion, exercise, drugs (opiates, BB, gent)
205
Q

What investigations would you carry out in someone with suspected myasthenia gravis?

A

Antibodies –> Anti-AchR, anti-MuSK
CT thorax –> thymus
EMG
Ice test = ice applied to affected lip and ptosis improves
Tension test (edrophonium test = short acting acetylcholinesterase causes improvement in muscular strength

206
Q

What is the treatment for myasthenia gravis?

A
  • Acetylcholinesterase inhibitors –> pyridostigmine or neostigmine (slow reuptake of Ach)
  • Immunosuppression –> prednisolone, azathioprine, methotrexate
  • Thymectomy
207
Q

Give 2 possible side effects of anti cholinesterase inhibitors?

A

Increased

  • Salivation
  • Lacrimation
  • Sweating
  • Vomiting
  • Diarrhoea
  • Miosis
208
Q

What are the potential complications fo myasthenia gravis?

A

Myasthenic Crisis
- Weakness of respiratory muscles during relapse
- Monitor FVC
Treat with plasmapheresis or IVIg

209
Q

What is Lambert Eaton Syndrome?

A

Antibodies to VGCC which decreases the influx of Ca2+ during presynaptic excitation leading to decreased presynaptic Ach vesicle fusion

210
Q

What are the 2 main causes of Lambert Eaton Syndrome?

A
  1. AI

2. Paraneoplastic from small cell lung carcinoma

211
Q

How does Lambert Eaton Syndrome present?

A 
- Same as myasthenia gravis = diplopia, ptosis, slurred speech, dysphagia 
AND LEMS 
- Leg weakness early 
- Extra m= autonomic and areflexia 
- Movement improves symptoms 
- Small response to edrophonium
212
Q

Describe the management of Lambert Eaton Syndrome

A

IVIg

213
Q

Define Guillain Barre Syndrome

A

Acute inflammatory demyelinating ascending polyneuropathy affects PNS Schwann cells following URTI or GI infection

214
Q

What are the causes of GBS?

A

Post infection
Bacterial = Campylobacter, mycoplasma
VIral = CMV, EBV, HIV

215
Q

Give 3 clinical features of GBS

A
  1. Symmetrical ascending flaccid weakness/paralysis
  2. LMN signs = areflexia, fasciculations
  3. Back pain
  4. Little sensory disturbance
  5. Autonomic = sweating, tachycardia, BP changes, arrhythmias
216
Q

What investigations might you do on someone with suspected GBS?

A
  • NCS = slow conduction
  • LP –> raised protein, normal WCC
  • Anti GM1 antibodies (25% of patients)
  • Spirometry –> for resp involvement (ITU if decreased)
217
Q

What is the management of GBS?

A
  • IVIg

- Plasma exchange

218
Q

What is Miller Fisher Syndrome?

A

Variant of Guillain Barre

  • Ophthalmoplegia, ataxia, areflexia (eyes affected first)
  • Descending paralysis
219
Q

What is Charcot Marie Tooth Disease?

A

A group of inherited motor and sensory neuropathies that cause dysfunction in the myelin or the axons
- Genetic tests for PMP22 gene mutation

220
Q

Give 3 causes of Charcot Marie Tooth Disease

A

ABCDE

  1. Alcohol
  2. B12 deficiency
  3. Cancer and CKD
  4. DM
  5. Every vasculitis
221
Q

Give 3 clinical features of Charcot Marie Tooth Disease

A
  1. High foot arches (per cavus)
  2. Distal muscle wasting (inverted Champagne bottle legs)
  3. Weakness in lower legs (loss of ankle dorsiflexion)
  4. Symmetrical muscle atrophy –> claw hand
  5. Foot drop with high stoppage gait
  6. Peripheral sensory loss –> stocking distribution
222
Q

What is the management of Charcot Marie Tooth Disease?

A

Supportive with physio, podiatry and orthoses

223
Q

What is meningitis?

A

Inflammation of the meninges of the brain and spinal cord

224
Q

What are the causes of meningitis in

a) Neonates
b) Children
c) Adults
d) Viral

A

a) Strep agalactiae, E.coli, strep pneumoniae, listeria monocytogenes
b) N. meningitides (g-ve diplocci), strep pneumoniae, HiB
c) Strep pneumoniae (g+ve cocci chain)
d) Enteroviruses (coxsackie), HSV2, CMV, VZV

225
Q

Give 3 risk factors for meningitis

A
  1. Intrathecal drug administration
  2. Immunocompromised
  3. Incomplete immunisation
  4. Elderly and pregnant
  5. Crowding
  6. Endocarditis
  7. DM
  8. IVDU
226
Q

Give 5 signs of meningitis

A
  1. Headache
  2. Fever
  3. Neck stiffness
  4. Photophobia
  5. Kernigs sign = unable to straighten leg greater than 135 without pain
  6. Brudzinskis sign = hip and knees flex when neck is flexed
  7. Increased ICP –> papillodema, decreased GCS, focal seizures
227
Q

Give 3 signs of meningococcal sepsis

A
  1. Petechial non blanching rash
  2. Fever
  3. Decreased BP
  4. Increased HR
  5. DIC
228
Q

What investigations might you do for someone with suspected meningitis?

A
  1. Blood cultures
  2. Throat swabs
  3. Bloods –> FBC, U&Es, CRP, serum glucose, lactate
  4. LP
  5. CT head
229
Q

What does an LP show with a bacterial infection?

A
  • Turbid
  • High opening pressure
  • High protein
  • Low glucose
  • Neutrophils
230
Q

What does an LP show with a viral meningitis infection?

A
  • Clear
  • Normal opening pressure
  • Normal protein
  • Normal glucose
  • Lymphocytes
231
Q

What does an LP show with a TB meningitis infection?

A
  • Fibrin web
  • Massive increase in protein
  • Lymphocytic/mononuclear
232
Q

Give 2 contraindications of an LP

A
  1. Thrombocytopenia
  2. Increases ICP
  3. Unstable –> cardio or resp
  4. Coagulation disorder
  5. Infection at LP site
233
Q

What is the treatment for bacterial meningitis?

A

Ceftriaxone/Cefotaxime IV

+ amoxicillin is >60 or immunocompromised

234
Q

What is the treatment given to someone seen in primary care with suspected meningitis?

A

Benzylpenicillin

235
Q

What is the treatment for viral meningitis?

A

Watch and wait

Acyclovir if severe

236
Q

What is encephalitis?

A

Inflammation of brain parenchyma

237
Q

Give 2 viral and non-viral causes of encephalitis

A

Viral

  1. HSV1/2
  2. CMV
  3. EBV
  4. VZV
  5. HIV

Non viral

  1. Bacterial meningitis
  2. TB
  3. Malaria
  4. Listeria
  5. Lyme disease
238
Q

What investigations would you do with carry out in someone with suspected encephalitis?

A
  • Bloods –> cultures, viral PCR, malaria film
  • LP –> increased protein, normal glucose, lymphocytes, PCR
  • Contract CT –> SOL
  • EEG
239
Q

What is the management of encephalitis?

A

Acyclovir

240
Q

Give 3 possible causes of spinal cord compression

A
  1. Vertebral tumour (mets = lung, breast, kidney, prostate, myeloma)
  2. Disc herniation = centre of disc moved out through annulus
  3. Disc prolapse = nucleus pulposus moves and presses against annulus
  4. Trauma
  5. Infection
241
Q

Give 3 signs of a spinal cord compression

A
  1. Back pain
  2. Progressive spastic leg weakness
  3. UMN signs below level = hypertonia, hyperreflexia
  4. Sensory loss below lesion
  5. LAte = bladder/sphincter problems
242
Q

What is the management of a spinal cord compression?

A

Dexamethasone
Radiotherapy (if malignancy)
Decompressive surgery

243
Q

What is cauda equina?

A

Compression of spinal cord at cauda equina level = L1 or below
= Surgical emergency

244
Q

Give 2 possible causes of cauda equina

A
  1. Lumbar disc herniation –> L4/5, L5/S1
  2. Tumour
  3. Trauma
  4. Infection
245
Q

Give 3 signs of cauda equina

A
  1. Flaccid and areflexic leg weakness
  2. Bilateral sciatica
  3. Saddle paraesthesia
  4. Loss of sphincter tone –> bladder and bowel dysfunction
  5. Erectile dysfunction
246
Q

What investigations might you do for someone with suspected cauda equina?

A
  • MRI/CT back and legs
  • DRE = reduced anal tone
  • Reflex tests
247
Q

What is the management of someone with cauda equina?

A
  • Immediate surgical decompression

- Treat cause

248
Q

What is spondylysis and give 2 causes?

A

Degenerative disc disease

  1. Degernation due to trauma/ageing
  2. IV dic collapse
  3. Osteophytes
249
Q

How does spondylysis present?

A
  • Asymptomatic
  • Neck stiffness and crepitus
  • Stabbing/dull ache in arm
  • Upper limb motor and sensory disturbance according to level of compression
250
Q

What are the 2 specific signs of cervical spondylysis?

A
  1. Lhermitte’s = neck flexion causes tingling down the spine
  2. Hoffman’s = flick middle finger pulp and causes a brief pincer flexion of thumb and index finger
251
Q

What is myelopathy?

A

Spinal cord disease = UMN problems

252
Q

What is radiculopathy?

A

Spinal nerve root disease = LMN problem

253
Q

What nerve root compression causes sciatica?

A

L4-S3 compression

254
Q

What is a mononeuroapthy?

A

Lesions of individual peripheral or cranial nerves

255
Q

What is Carpal Tunnel Syndrome?

A

Medical nerve neuropathy = C6-T1

256
Q

Give 2 risk factors for Carpal Tunnel Syndrome

A
  1. Pregnancy
  2. Obesity
  3. RA
  4. Hypothyroidism
  5. Acromegaly
257
Q

What are the motor and sensory symptoms of carpal tunnel syndrome?

A 
Motor = LLOAF muscle dysfunction and thenar wasting 
Sensory = radial 3 and a half fingers, decreased 2 point discrimination
258
Q

What nerve neuropathy causes a +ve Fromet’s sign?

A

Ulnar nerve neuropathy = C7-T1

259
Q

What are the features of a common perineal neuropathy?

A

= L4-S1
Motor = foot drop, weak ankle dorsiflexion and eversion
Sensory = loss of sensation below the knee laterally

260
Q

What is mononeuritis multiplex?

A

When 2 or more peripheral nerves are affected

261
Q

Give 3 causes of mononeuritis multiplex

A

WAARDS PLC

  1. Wegner’s
  2. AIDS
  3. Amyloid
  4. RA
  5. DM
  6. Sarcoidosis
  7. PAN
  8. Leprosy
  9. Carcinomatosis
262
Q

Give 2 sensory causes of polyneuropathy

A
  1. Alcohol
  2. B12
  3. DM m
  4. Vasculitis
263
Q

Give 2 motor causes of polyneuropathy

A
  1. GBS
  2. Lead poisoning
  3. CMT
  4. Paraneoplastic
264
Q

What does an UMN facial nerve palsy indicate?

A

A stroke

- Forehead SPARING due to dual innervation

265
Q

What does a LMN facial nerve palsy indicate?

A

Bells Palsy

- Acute unilateral facial nerve weakness or paralysis of rapid onset (<72 hours)

266
Q

What is the treatment for Bells Palsy?

A

Prednisolone within 72 Horus
Valavivlovir if zoster suspected
Protect the eye –> dark glasses, artificial tear, tape closed at night

267
Q

Outline the Glasgow Coma Scale

A

Eyes

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

Verbal

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

Motor Response

  • Obeys commands = 6
  • Localises pain = 5
  • Normal flexion = 4
  • Abnormal flexion = 3
  • Extends = 2
  • None = 1
268
Q

Give 3 possible causes of a coma

A
  1. Drugs and toxins –> opiates, alcohol
  2. Anoxia –> post arrest
  3. Toxins –> CO
  4. Mass lesions –> bleeds, head injuries
  5. Infections –> bacterial meningitis
  6. Infarcts –> brainstem
  7. Metabolic –> hypoglycaemia, DKA, herpatic encephalopathy, uraemia, Wernicke’s
  8. SAH
  9. Epilepsy
  10. Tumours
269
Q

What spinal cord tracts carry sensory fibres?

A

Ascending

  1. Dorsal column medical lemniscal pathway (DCML)
  2. Anterolateral system (spinothalamic)
  3. Spinocerebellar tracts

= 3rd order neurones

270
Q

What information is carried by the DCML pathway?

A

Fine touch, vibration and proprioception

  • Upper limbs (T6 and aboce) = Tavel in fasciculus cuneatus (lateral)
  • Lower limbs (below T6) = Tavel in fasciculus gracilis (medial)

Decussate in medulla

271
Q

What information is carried by the lateral spinothalamic tract?

A

Pain and temperature

272
Q

What information is carried by the anterior spinothalamic tract?

A

Crude touch and pressure

273
Q

What information is carried by the spinocerebellar pathway?

A

Unconscious sensation from muscles to the cerebellum

274
Q

What information is carried by the posterior and anterior spinocerebellar tract?

A

Proprioceptive information from lower limbs to ipsilateral cerebellum

  • Anterior = decussate twice end ipsilateral
275
Q

What information is carried by the cuneocerebellar and rostral tracts?

A

Proprioceptive information from the upper limbs to the ipsilateral cerebellum

276
Q

What spinal cord tracts carry motor fibres?

A

Descending

  1. Pyramidal = corticopsinal, corticobulbar
  2. Extrapyramidal = rubrospinal, tectospinal and vestibulospinal
277
Q

What information do the pyramidal descending tracts carry?

A

Voluntary control of musculature of body and face, originate in cerebral cortex

278
Q

Describe the corticospinal tracts

A

Musculature of body

  1. Lateral = motor cortex –> decussate in medullar –> limb muscles
  2. Medial = motor cortex –> ipsilateral –> axial muscles (head and trunk)
279
Q

What information do the extrapyramidal descending tracts carry?

A

Involuntary autonomic control of all musculature in the body = muscle tone, balance, posture, locomotion
- Originate in brainstem

280
Q

What is Brown Sequard Syndrome?

A

Hemisection fo the spinal cord

  • Damage to the RIGHT corticopsinal tract at L1 = ipsilateral UMN sings in right leg
  • Damage to RIGHT dorsal columns at L1 = ipsilateral loss of fine touch, propriocpetion and vibration in right leg
  • Damage to lateral spinothalamic tracts = contralateral absence of pain and temperature sensation in left leg

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