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Haroon Phase 2A > Neurology > Flashcards

Neurology Flashcards

1
Q

Where is Broca’s area? What is its function?

A
  • Left frontal lobe, Brodmann‘s area 44 and 45 - Language production
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2
Q

Where is Wernicke’s area? What is its function?

A
  • Left (usually) temporal lobe, Brodmann’s area 22- Perception of language
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3
Q

What are the layers of brain covering?

A

Skin - Bone - Dura mater - Arachnoid mater - (Subarachnoid space) - Pia mater

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4
Q

Lateral corticospinal tract

A

Supplies limbs - Fine motor movement - Decussates at medulla

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5
Q

Ventral corticospinal tracts

A

Supplies trunk (proximal muscles) - Decussates at level of effector muscle - Also motor movement

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6
Q

Corticobulbar tract

A

Head and neck via cranial nerves

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7
Q

What structures are in the cavernous sinus?

A

(OTOMCAT) - Oculomotor nerve - Trochlear nerve - Ophthalmic division of trigeminal nerve - Maxillary division of trigeminal nerve - Carotid artery - Abducens nerve

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8
Q

DCML tract

A
  • Ascending (sensory) - Dorsal root -> medulla, then decussates - Fine touch, vibration and proprioception
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9
Q

Spinothalamic tract

A
  • Ascending (sensory) - Decussates at spine 1-2 levels above dorsal entry - Pain, temperature, crude touch - Anterior - trunk - Posterior - limbs
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10
Q

Brown sequard syndrome

A
  • Ipsilateral DCML loss - decussate at medulla - Ipsilateral corticospinal loss - decussate at medulla - Contralateral spinothalamic loss - decussate at spinal cord (1-2 levels above)
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11
Q

Blood supply to the pituitary gland

A

Anterior - Superior hypophyseal artery - Posterior - Inferior hypophyseal artery The hypothalamophyseal portal system is a branch of The internal carotid artery

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12
Q

Drug for bacterial meningitis in hospital

A
  • Ceftriaxone (3rd gen cephalosporin) - Cefuroxime if prgenant or under 3 months old - Amoxicillin if listeria suspected - Steroids simultaneously (dexamethasone) within 12 hrs
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13
Q

Pathophysiology of Wernicke’s encephalopathy

A

Combined B1 deficiency (caused by alcohol) and alcohol withdrawal symptoms

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14
Q

Complication on Wernicke’s encephalopathy

A

Wernicke Korsakoff syndrome: - Confabulation memory loss - make up stories to fill gaps in memory - Ataxia - Nystagmus

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15
Q

Treatment for Wernicke’s encephalopathy

A
  • Parenteral (IV) pabrinex for 5 days acutely - Oral thiamine prophylactically
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16
Q

Cause of transient ischaemic attack and ischaemic stroke

A

Carotid thrombo-emboli - Thrombosis - Emboli, eg: from atrial fibrillation

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17
Q

Risk factors of stroke

A

Hypertension - Atrial fibrillation - Ventricular septal defect - Smoking - T2DM - Obesity/hypercholestrolemia - Cannabis and cocaine

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18
Q

Where do transient ischaemic attacks happen?

A

90% - internal carotid artery (anterior circulation) 10% - vertebral artery (posterior circulation)

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19
Q

Symptoms of ACA stroke

A

Contralateral hemiparesis and sensory loss - Lower limbs > upper limbs

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20
Q

Symptoms of MCA stroke

A

Contralateral hemiparesis and sensory loss with upper limbs > Lower limbs - Homonymous hemianopia - Aphasia affecting dominant hemisphere - Hemineglect syndrome affecting non-dominant hemisphere

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21
Q

Symptoms of PCA stroke

A

Contralateral Homonymous hemianopia with macular sparing - Visual agnosia

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22
Q

Symptoms of vertebral artery strokes

A
  • Cerebellar syndrome; DANISH with the Romberg test (sensory + motorataxia) - Brainstem infarct - CN lesions 3-12
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23
Q

Amaurosis fugax in transient ischaemic attack

A
  • Decreased blood flow to retina through opthalmic, retinal, ciliary artery - Bad sign; often signals stroke is impending
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24
Q

How to differentiate between stroke and transient ischaemic attack (“mini stroke”)

A
  • Stroke: symptoms last 24+ hours, infarct - TIA: symptoms resolve within 5-15 mins usually, always <24 hours, no infarct
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25
Q

Treatment of transient ischaemic attack

A
  • Acutely = aspirin 300mg Prophylaxis long term - Lifestyle changes - Clopidogrel 75mg - Atorvastatin 20-80mg
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26
Q

What percentage of strokes are ischaemic vs haemorrhagic?

A

Ischaemic - 85% Haemorrhagic - 15%

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27
Q

What are the symptoms of stroke generally called?

A

Focal neurology

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28
Q

Types of stroke

A
  • Transient ischaemic attack (“mini stroke”) - Ischaemic stroke - Haemorrhagic stroke
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29
Q

Aetiology of haemorrhagic stroke

A

Ruptured blood vessel - Trauma, Hypertension - Berry aneurysm rupture - Can be haematomas

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30
Q

If a patient is on anticoagulants, what type of stroke would you suspect?

A

Haemorrhagic until proven otherwise

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31
Q

Symptoms of haemorrhagic stroke

A

High ICP - always contraindicated in lumbar puncture - Therefore midline shift, risk of tentorial haemorrhage/coning

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32
Q

What’s a lacunar stroke?

A

Very common type of ischaemic Stroke - Occurs in lenticulostriate arteries (supply deep brain structures) - Ischaemia to basal ganglia, internal capsule, thalamus, pons

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33
Q

Diagnosis of ischaemic and haemorrhagic stroke

A

non-contrast CT head (identifies haemorrhagic Stroke) - Gold standard: MRI brin with diffusion weightted imaging - carotid Doppler ultrasound - LFTs, FBC and HbA1c to rule out differential diagnoses - ECG

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34
Q

Pronator drift

A

Specific sign in strokes - Ask patient to lift arms to ceiling - Pronators take over, arm on affected side will pronate

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35
Q

Treatment of ischaemic stroke

A

If patient presents within 4.5 hours: Alteplase IV (thrombolytic) Prophylaxis: Aspirin 300mg for 2 weeks, lifelong clopidogrel 75mg, atorvastatin, ramipril NICE recommend carotid intervention within 1 week if internal carotid thrombus

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36
Q

Treatment for haemorrhagic stroke

A

Neurosurgery referral - IV mannitol for High ICP - Atorvastatin, ramipril

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37
Q

Pathophysiology of subarachnoid haemorrhage

A

Berry aneurysm coin rupture - Or Trauma - Most common at Anterior communicating/ACA junction

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38
Q

Risk factors for subarachnoid haemorrhage

A

Connective tissue disorders - Hypertension - PKD - Trauma - Inreasing age + family history

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39
Q

Presentation of subarachnoid haemorrhage

A

Occipital thunderclap headache - Meningism - Kernig and Brudzinski signs - Low GCS - Nerve palsies (CN3 fixed dilated pupil,#REF! non Specific sign of increased ICP)

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40
Q

What are the Kernig and Brudzinski signs?

A
  • Kernig - can’t extend leg when knee is flexed - Brudzinski - when neck is elevated, knees unintentionally flex
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41
Q

What may preceed a thunderclap headache?

A

Sentinel headache - Preceds berry aneurysm rupture for weeks - In around 50% cases - Throbbing occipital pain

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42
Q

Glasgow coma scale (GCS)

A
  • Out of 15 - Eyes (4), verbal (5), motor (6) 15: Normal 8: Comatose 3: Unresponsive
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43
Q

Differential diagnoses of subarachnoid haemorrhage

A

Meningitis (signs of infection, no thunderclap headache) - Migraine (no thunderclap headache Or Meningism)

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44
Q

Diagnosis of subarachnoid haemorrhage

A

CT head, star shape

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45
Q

What would you do if CT for subarachnoid haemorrhage is positive?

A

CT angiogram to see the extent of the rupture

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46
Q

What would you do if CT for subarachnoid haemorrhage is negative?

A
  • Lumbar puncture - Wait around 12 hours (as that’s when results are most sensitive) - Will see xanthochromia - yellowish CSF due to RBC haemolysis
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47
Q

Treatment of subarachnoid haemorrhage

A

First line: Neurosurgery + endovascular coiling - Also give nimodipine (CCB, decreases vasospasm and blood pressure)

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48
Q

Pathophysiology of subdural haemorrhage

A

rupture of bridging vein due to shearing - Deceleration injuries and in abused children (shaken baby syndrome)

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49
Q

Risk factors of subdural haemorrhage

A

Trauma - Child abuse - Low pressure bleeding - Gradual rise in ICP - Cortical atrophy (eg: dementia)

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50
Q

Presentation of subdural haemorrhage

A
  • Gradual onset with latent period (bleeding is small, accumulation + autolysis of blood) - Signs of high ICP - Fluctuating GCS - Focal neurology later (CN3 palsy)
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51
Q

Signs of high ICP

A

Cushing triad: bradycardia, High pulse pressure, irregular breathing - Papillodema - Reduced GCS

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52
Q

Complications of subdural haemorrhage

A

Brainstem herniation - Respiratory arrest

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53
Q

Diagnosis of subdural haemorrhage

A

Non-contrast CT head -> banana/cresent shaped haematoma, not confined to suture lines, midline shift

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54
Q

How to deduce nature of subdural haemorrhage from NCCT

A

If acute = hyperdense (bright) - If subacute = isodense - If chronic = hypodense (darker than brain)

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55
Q

Treatment of subdural haemorrhage

A

Burr hole + craniotomy - IV mannitol to decrease ICP - Address cause If Child abuse suspected

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56
Q

Pathophysiology of extradural haemorrhage

A

Trauma to middle meningeal artery due to damage to lateral pterygoid Bone - Can feel Fine for hours to weeks until rapid deterioration - cause old blood clots become haemolysed, taking up water, increases volume in skull and increases ICP as a result

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57
Q

Risk factors of extradural haemorrhage

A

Head trauma - Typically young adults 20-30 (as the dura adheres more firmly the more you age)

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58
Q

Presentation of extradural haemorrhage

A

High ICP signs - May have extensive traumatic injuries

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59
Q

Complication of extradural haemorrhage

A

Death from respiratory arrest - Tonsillar herniation and coning of brain = compressed respiration centres - Due to untreated high ICP

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60
Q

Diagnosis of extradural haemorrhage

A

Non-contrast CT head -> lens shaped hyperdense bleed, confined to suture lines, midline shift due to brain compression

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61
Q

Treatment of extradural haemorrhage

A

Urgent surgery - IV mannitol to reduce ICP

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62
Q

Symptoms of Wernicke’s encephalopathy

A

Classic triad: - Ataxia - Confusion - Opthalmoplegia

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63
Q

Diagnosis of Wernicke’s encephalopathy

A

Clinically recognised + supported with macrocytic anaemia and deranged LFTs

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64
Q

Pathophysiology of Duchenne muscular dystrophy

A

X linked recessive mutated dystrophin gene - Affects boys exclusively - muscle replaced with adipose

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65
Q

Symptoms of Duchenne muscular dystrophy

A
  • Gower’s sign - Difficulty getting up from lying down - Skeletal deformities (scoliosis, hyperlordosis)
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66
Q

Diagnosis of Duchenne muscular dystrophy

A

Prenatal tests - DNA genetic tests

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67
Q

Treatment of Duchenne muscular dystrophy

A

Supportive - Corticosteroids (eg: prednisone) delay progress of muscle weakening

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68
Q

Pathophysiology of Charcot-Marie-Tooth syndrome

A
  • Inherited sensory and motor PNS polyneuropathy - Autosomal dominant mutation on chromosome 17 - PUP22 gene - Childhood - adulthood onset
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69
Q

Symptoms of Charcot-Marie-Tooth syndrome

A

Foot drop - Stork legs (v thin calves) - Hammer toes (always curled) - Pes planus (flat feet) Or Pes cavus (arched feet) - Reduced deep tendon reflex

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70
Q

Diagnosis of Charcot-Marie-Tooth syndrome

A

Nerve conduction study - Nerve biopsy - genetic testing

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71
Q

Treatment of Charcot-Marie-Tooth syndrome

A

Supportive - Orthotics - Physio

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72
Q

What is tetanus caused by?

A
  • Clostridium tetani (gram +ve bacillus) - Inoculation by stepping in dirty soil
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73
Q

Pathophysiology of tetanus

A

Tetanospasmin toxin produced - Retrograde travels up axons - Causes involuntary muscle spasms

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74
Q

Treatment of tetanus

A

VACCINE …if a patient has a wound that is susceptible to tetanus and has not been adequately vaccinated, boosters may need to be given

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75
Q

What is varicella zoster virus?

A
  • 90% under 16s have this as chicken pox - Reactivation -> shingles
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76
Q

Pathophysiology of shingles

A

Peripheral nerves attacked via dorsal root (sensory)

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77
Q

Symptoms of herpes zoster

A

Painful rash confined to a dermatome

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78
Q

Treatment of herpes zoster

A

Oral acliclovir (antiviral)

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79
Q

Pathophysiology of Creutzeldt-Jakob disease

A

Idiopathic misfolded proteins deposited in cerebrum and especially cerebellum - Severe Cerebellar dysfunction

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80
Q

Treatment of Creudzfeldt-Jakob disease

A

Rare. no treatment - Rapidly progressive and always fatal. Death usually within one year of onset of illness

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81
Q

Diagnosis of Creutzfeldt-Jakob syndrome

A

Brain biopsy or autopsy

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82
Q

Primary headaches

A

Migraines - Cluster - Tension - Drug overdose - Trigeminal neuralgia

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83
Q

Secondary headaches

A

Due to underlying condition: - GCA - Infection - SAH - Trauma - Cerebrovadcular diseae - Eye, ear, sinus pathology

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84
Q

What are migraines?

A

Episodes of recurrent throbbing headache, sometimes with aura beforehand - Often with change in vision - Most common cause of recurrent headache - May be associated with nausea and vomiting

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85
Q

Who do migraines affect?

A

Most common in women under 40 - often during PMS

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86
Q

Triggers of migraines 🍫

A

Chocolate Hangovers Orgasms Cheese Oral contraceptives Lie ins Alcohol Tumult (noise) Exercise

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87
Q

Women with oral contraceptive pill with migraines

A

STOP, offer alternatives because it can: - Be a trigger - Increase stroke risk - Decrease triptan efficacy

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88
Q

Stages of migraine

A

Prodrome (days before) - Mood change Aura (part of attack, minutes before headache) - Visual phenomena; zig zag lines Throbbing headache lasting 4-72 hours

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89
Q

Clinical diagnosis of migraines

A

2 ≤ of: - Unilateral pain - Throbbing - Motion sickness - Mod-severely intense AND 1 ≤ of: - Nausea and vomiting - Photophobia/phonophobia with normal neuro exam

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90
Q

Treatment of migraines

A

Acute: - Oral triptan (sumatriptan) - or aspirin 900mg Prophylaxis: - Propanolol (topirimate if asthmatic) - Or TCA - Avoid triggers - Consider antiemetics - eg: metoclopramide for n+v - Don’t use opiates - Risk of dependence or worsening nausea

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91
Q

What are cluster headaches

A
  • Unilateral periorbital pain with autonomic features - 15-180 minutes - Most disabling primary headache - Many headaches clustered in small amounts of time
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92
Q

Risk factors for cluster headaches

A

Male - Smoking - Genetics (Autosomal dominant link)

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93
Q

Symptoms of cluster headaches

A

Crescendo Unilateral periorbital excruciating pain, May affect temples too - autonomic features and face flushing

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94
Q

Autonomic features as symptoms

A

Conjunctival injection and lacrimation (watery bloodshot eye) - Ptosis (droopy eyelid) - Miosis (constriction of Unilateral pupil) - Rhinorrhoea

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95
Q

Diagnosis of cluster headaches

A
  • Clinically - 5 ≤ similar attacks confirms
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96
Q

Treatment of cluster headaches

A

Acute: Triptans (sumatriptan) Prophylaxis: Verapamil (CCB), TCA second line

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97
Q

What is a tension headache?

A

Bilateral generalised headache, radiates to neck - Most common primary headache - Triggered by STRESS

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98
Q

Symptoms of tension headaches

A

Tight rubber band feeling around hear - pain Also felt in trapezius - Mild-moderate severity - no motion sickness, photophobia Or aura

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99
Q

Diagnosis of tension headaches

A

Clinically from history

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100
Q

Treatment of tension headaches

A

Simple analgesia - aspirin Or paracetamol - Avoid opiates due to dependence

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101
Q

What is trigeminal neuralgia?

A
  • Unilateral pain in 1 ≤ trigeminal branches - No pain between attacks
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102
Q

Risk factors for trigeminal neuralgia

A
  • MS (20x more likely!!!) - Increasing age (50-60) - Female
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103
Q

Triggers for trigeminal neuralgia

A

Eating - Shaving - Talking - Brushing teeth - Putting on makeup - Wind on face

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104
Q

Symptoms of trigeminal neuralgia

A
  • Electrical shock pain - Seconds - 2 minutes - In V1/2/3
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105
Q

Diagnosis of trigeminal neuralgia

A

Clinical, 3 ≤ attacks with symptoms

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106
Q

Treatment of trigeminal neuralgia

A

Carbamazepine (anticonvulsant) Surgery last line - Percutaneous procedures - Sterotactic radiosurgery - Microvascular decompression

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107
Q

Causes of seizures

A

Vascular Infecion Trauma Autoimmune, eg: SLE Metabolic eg: hypocalcaemia Idiopathic -> epilepsy Neoplasms Dementia and Drugs (cocaine) Eclampsia and everything else

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108
Q

Pathophysiology of seizures

A

Balance between GABA and glutamate shifts to glutamate - More excitatory - increased GABA inhibition and glutamate stimulation

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109
Q

Risk factors of epilepsy

A
  • Familial inherited - Dementia (10x more likely)
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110
Q

What is epilepsy?

A
  • Idiopathic cause of seizures - 2 ≤ episodes more than 24hr apart
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111
Q

Unique features of epileptic seizures

A

Eyes open - Synchronous movements - Can occur in sleep

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112
Q

Stages of epileptic seizures

A

Prodrome - Mood change, days before Aura - Minutes before - Deja vi + automatisms (lip smacking, rapid blinking) - Not always present, mostly seen in temporal lobe epilepsy Ictal event - seizure Post ictal period

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113
Q

Features of post ictal period

A
  • Headache - Confusion + low GCS - Todd’s paralysis - temporary paralysis and muscle weakness if motor cortex affected - Dysphasia - Amnesia - Sore tongue
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114
Q

What are generalised seizures?

A

Bilateral - always loss of consciousness - Two types: tonic clonic and absence

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115
Q

Tonic clonic generalised seizures (grand mal)

A
  • No aura - Tonic phase -> rigidity, fall to floor - Clonic phase -> jerking of limbs - Upgazing open eyes, incontinence, tongue bitten
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116
Q

What parts of the brain are affected in generalised seizures

A

All cortex + deep brain - Bilaterally affected

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117
Q

Absence generalised seizures (petit mal)

A
  • Childhood - Moments of staring blankly into space (seconds-minutes) then carrying on where they left off - 3Hz spike on EEG
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118
Q

Tonic vs myoclonic vs atonic generalised seizures

A

tonic - just rigid - Myoclonic - just jerking limbs - Atonic - sudden floppy limbs + muscles

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119
Q

What are focal seizures?

A

features confined to a region, eg: temporal - May progress to secondary generalised

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120
Q

Simple focal seizures

A

no loss of consciousness - patient awake and aware - just uncontrollable muscle jerking - no basal ganglia + thalamus involvement

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121
Q

Complex focal seizures

A

loss of consciousness - patient unaware - Post ictal period positive - basal ganglia and thalamus involved

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122
Q

Symptoms of temporal focal seizures

A

aura - Dysphasia - Post ictal period

123
Q

Symptoms of frontal focal seizures

A
  • Jacksonian march (abnormal movement or sensation limited to one part of the body) - Todd’s palsy (temporary paralysis follows seizures)
124
Q

Symptoms of parietal focal seizures

A

Parasthesia

125
Q

Symptoms of occipital focal seizures

A

Change in vision

126
Q

Diagnosis of epilepsy

A
  • CT head + MRI (examine hippocampus, check bleeds, tumours) - EEG - 3 Hz wave in absence - Bloods - rule out metabolic cause/infection
127
Q

Treatment for epilepsy

A
  • Sodium valproate to all - Except females of childbearing age (15-45) as it’s teratogenic - give Lamotrigine instead
128
Q

Complication of epilepsy

A

Status epilepticus - neuro emergency - Seizures without a break back to back OR - Seizures lasting over 5 minutes (long time)

129
Q

Treatment for status epilepticus

A

Benzodiazepines - Lorazepam 4mg IV - Again if it doesn’t work, then phenytoin

130
Q

Risk factors for Parkinson’s disease

A

family history - Males - Increasing age - Smoking seems to be protective?

131
Q

Pathophysiology of parkinson’s disease

A

loss of dopaminergic neurones from substantia nigra pars compacta - Therefore harder to initiate movement

132
Q

Normal physiology for initiation of movement

A

Nigrostriatal pathway signals striatum to stop firing to substantia nigra pars compacta - Stops movement inhibition

133
Q

Cardinal symptoms of Parkinson’s disease

A

Bradykinesia - Resting tremor - Rigidity - Postural instability

134
Q

Diagnosis of Parkinson’s disease

A
  • Clinical - Bradykinesia and 1 ≤ other cardinal symptoms
135
Q

Pharmacological treatment of Parkinson’s disease

A
  • DA agonists (first line in younger patients)- Levodopa + dopa decarboxylase inhibitor (co-beneldopa or co-careldopa) - MOA-B inhibitor can also be used
136
Q

Issues with Levodopa

A
  • Initially works very well but soon body becomes resistant to it so effects wear off - So don’t give it too early (v.mild symptoms)
137
Q

Differential diagnosis of Parkinson’s disease

A

Lewy body dementia - Parkinson symptoms then dementia = Parkinson dementia - Parkinson symptoms after dementia = Lewy body dementia w/ parkinsonism

138
Q

Pathophysiology of Alzheimer’s disease

A

Beta amyloid plaques are a breakdown product of amyloid precursor protein - Beta amyloid plaques + tau neurofibrillary tangles in cerebral cortex - increased Cortical scarring + brain atrophy, Decreased Ach neurotransmitter

139
Q

Risk factors for Alzheimer’s disease

A

Down’s syndrome (inevitable; APP gene mutation) - ApoE4 allele in familial Alzheimer’s, late onset (1/4 cases)

140
Q

Symptoms of Alzheimer’s disease

A
  • Agnosia - don’t recognise things - Apraxia - can’t do basic motor skills - Aphasia - can’t talk as well as normal
141
Q

Alzheimers vs vascular dementia

A

Alzheimer’s - steady decline Vascular - stepwise decline

142
Q

Aetiology of vascular dementia

A

Cerebrovascular damage, eg: stroke, TIA

143
Q

Symptoms of vascular dementia

A

UMN signs - General decrease in cognition

144
Q

Pathophysiology of lewy body demenia

A

Lewy bodies (synuclein + ubiquitin aggregates) accumulate in cortex

145
Q

Symptoms of lewy body dementia

A

Cognitive decline - Parkinsonism

146
Q

Risk factors for frontotemporal dementia

A
  • Family history; autosomal dominant change in tau protein (chromosome 17) - Family history of MND (TDP-43)
147
Q

Symptoms of frontotemporal dementia

A

Shows frontotemporal atrophy: - Speech and language mostly = temporal moreso affected - Thinking + memory affected = frontal moreso

148
Q

Pathophysiology of frontotemporal dementia

A

Proteins clump in frontal and temporal lobe

149
Q

Risk factors for Lewy body dementia

A
  • Age - Parkinson’s - REM sleep behaviour disorder
150
Q

Incidence of each type of dementia

A
  • Alzheimer’s - 60% - Vascular - 20% - Lewy body - 10% - Frontotemporal - 5%
151
Q

Diagnosis of dementia

A

Mini mental state exam (/30) >25 = normal 18-25 = impaired <17 = severely impaired Brain MRI shows cortical atrophy

152
Q

Conservative treatment for dementia

A

Conservative; social stimulation, exercise

153
Q

Treatment for vascular dementia

A

Antihypertensives eg: ramipril

154
Q

Treatment of Alzheimer’s

A

Achase-1 (donepezil/rivastigmin)

155
Q

Pathophysiology of Huntington’s disease

A
  • Autosomal dominant with full penetrance (all genotypes with express phenotypes) - Lack of GABA and excessive nigrostriatal pathway - CAG appears on chromosome 4, affecting HTT gene
156
Q

Trinucleotide expansion repeats in Huntington’s

A

< 35 = no Huntington’s 35-55 = Huntington’s 60+ = severe Huntington’s The more trinucleotide repears, the earlier and more severely symptoms present; anticipation

157
Q

Symptoms of Huntington’s

A

Chorea (excessive limb jerking) - dementia - Psychiatric issues - Depression

158
Q

Diagnosis of Huntington’s disease

A
  • Clinical - Family history of earlier + more severe Huntington’s - Genetic test if necessary
159
Q

Treatment of Huntington’s

A

extensive counselling - DA antagonist for Chorea + tetrabenazine

160
Q

What is Guillain-Barre syndrome?

A
  • Post infection (gastroenteritis/URTI) result in demyelenating response vs PNS myelating oligodendrocytes - Equivalent of MS in the PNS
161
Q

Risk factors for Guillain-Barre syndrome

A

Males 15-30, 50-70

162
Q

Prognosis of Guillain-Barre syndrome

A

85% recovery

163
Q

Aetiology of Guillain-Barre syndrome

A
  • C.Jejuni (mc) - Viruses; CMV, EBV, HZV
164
Q

Pathophysiology of Guillain-Barre syndrome

A

Molecular mimickry - Organism antigens very similar to those on Schwann cells - Results in antibody production vs Schwann cells -> Demyelination and acute polyneuropathy

165
Q

Symptoms of Guillain-Barre syndrome

A

Post infection presentation of: - Ascending symmetrical muscle weakness (+paralysis) - Loss of deep tendon reflexes - Autonomic involvement in about 50% - Resp failure in 35% -> so always monitor breathing

166
Q

Diagnosis of Guillain-Barre syndrome

A
  • Nerve condution studies (low conduction/block) - Lumbar puncture at L3/4 -> raised protein + normal WCC ( = inflammation, no infection)
167
Q

Treatment for Guillain-Barre syndrome

A
  • IV Ig for 5 days + plasma exchange - Allergic reaction in IgA deficient patients (CI) - If FVC <0.8, consider intubation + ITU
168
Q

What is myasthenia gravis?

A
  • Type 2 hypersensitivity - Autoimmune response vs nmj post synaptic receptors - Nicotinic Ach-R and MUSK
169
Q

Myasthenia gravis in females vs males

A

Females - 40 year olds - Related to autoimmune disease Males - 60 years old - Related to thymoma (thymus tumours)

170
Q

Pathophysiology of myasthenia gravis when anti Ach-R

A
  • 85% - Bind to post synaptic receptor + inhibit, competitively - More binding with exertion -> worse symptoms later on - Activate complement causing nmj destruction
171
Q

Pathophysiology of myasthenia gravis when anti MUSK

A
  • 15% - MUSK helps synthesis Ach-R - Therefore, decreased Ach-R expression on post synaptic membrane
172
Q

Symptoms of myasthenia gravis

A
  • Muscle weakness - Weak eye muscles - diplopia and ptosis - Jaw fatiguability - Speech fatiguability - Swallowing difficulty (bulbar weakness) - Myasthenic snarl - fig. 1 fig.1
173
Q

Nature of muscle pain in myasthenia gravis

A

Worse later on and with exertion - Starts at head+neck and goes to Lower body - Better with rest

174
Q

Differential diagnosis of myasthenia gravis

A

Lambert eaton syndrome - Autoimmunity vs presynaptic Ca2+ channels - Symptoms improve with exertion - Associated with SCLC (not thymoma) - Symptoms start at extremities then move to head + neck - Treated with steroids (prednisolone) and immunosuppression (IVIg)

175
Q

Diagnosis of myasthenia gravis

A
  • Serology -> Anti Ach-R and Anti MUSK high - Tensilon/edrotropium test (increased muscle posert when edrotropium given) - CT thymus - Bedside: icepack test and upward gaze fatiguability
176
Q

Treatment of myasthenia gravis

A
  • First line: Achase inhibitors; neostigmine/pyridostigmine - Second line: Immunosuppression (steroids)
177
Q

Complication of myasthenia gravis

A

Myasthenic crisis - Acute symptoms worsening with severe respiratory weakness - Treated with plasma exchange and IVIg - + BiPAP for resp failure

178
Q

Where do CN3-12 originate?

A

Brainstem - Therefore caused by Brainstem pathology eg: Trauma, MS, tumours

179
Q

What does a CN 3+4+6 lesion cause?

A

Non-functioning eye

180
Q

CN3 lesion

A

Ptosis (eyelid drooping) - Down and out eye - fixed dilated pupil due to EW nuclei dysfunction

181
Q

CN4 lesion

A

diplopia looking Down - RARE: always due to Trauma

182
Q

CN6 lesion

A

Adducted eye, sign of increased intracranial pressure

183
Q

CN5 lesion

A

Jaw deviates towards affected side - loss of corneal reflex - Trigeminal neuralgia

184
Q

CN7 lesion

A
  • Facial drop with no forehead sparing - Bell’s palsy, parotid inflammation
185
Q

CN8 lesion

A
  • Hearing loss - Loss of balance - Skull change (eg: Paget’s), compression, middle ear disease
186
Q

CN9+10 lesion

A
  • Impaired gag reflex (+ swallowing, resp, vocal issues) - Jugular foramen lesion
187
Q

CN11 lesion

A

Can’t shrug shoulders or turn head vs resistance

188
Q

CN12 lesion

A

Tongue deviation towards side of lesion

189
Q

How do spinal cord lesion signs present?

A

Ipsilateral sensory signs - Contralateral motor signs

190
Q

Spinal cord reflexes

A

L3/4 = knee jerk - L5 = big toe jerk - S1 = ankle jerk

191
Q

Types of paralysis

A

Hemiplegia = one side of the body, brain lesion Paraplegia = both legs, cord lesion

192
Q

Compression of what parts of which vertebrae causes myelopathy?

A

C1 -> L1/2 (the spinal cord)

193
Q

Compression of what parts of which vertebrae causes cauda equina syndrome?

A

L3 -> conus medullaris and cauda equina

194
Q

Causes of myelopathy

A
  • Verterbral body neoplasms, mc: mets from lung, breast, RCC, melanoma - Spinal pathology (eg: disc prolapse/herniation)
195
Q

Symptoms of myelopathy

A
  • Progressive leg weakness with UMN signs - Sensory loss below lesion (as ascending roots send info up) - Sphincter involvement uncommon (late = v bad sign)
196
Q

Diagnosis of myelopathy

A

MRI cord ASAP (risk of permanent damage If not ASAP) - CxR If malignancy suspected

197
Q

Treatment of myelopathy

A

Neurosurgery (laminectomy, microdiscectomy)

198
Q

Cause of cauda equina syndrome

A

Occurs in 2% lumber herniation (L4/5 or L5/S1)

199
Q

Symptoms of cauda equina syndrome

A

leg weakness with LMN signs - Saddle anaethesia (perianal numbness) - Bladder/bowel dysfunction + Sphincter involvement common

200
Q

Diagnosis of cauda equina syndrome

A

MRI cord (diagnostic) - testing Nerve roots/reflexes

201
Q

Treatment of cauda equina syndrome

A

ASAP neurosurgery (eg: microdiscectomy, spinal fixation)

202
Q

Mechanisms of peripheral neuropathy

A
  • Demyelination - Axonal damage - Nerve compression - Vasa nervorum infarction - Wallerian degeneration (nerve cut; distally dies)
203
Q

What are vasa nervorum?

A

Small arteries that provide blood supply to peripheral nerves

204
Q

Aetiology of peripheral neuropathy

A

Demyelination (mc Guillain Barre,#REF! def) - T2DM - surgery - pathology, eg: infection, endocrine, rheumatoid arthritis

205
Q

Types of peripheral neuropathy

A

Mononeuropathy - single Nerve - Mononeuritis multiplex - several individual nerves - polyneuropathy - diffuse, Often symmetrical pathology

206
Q

Causes of mononeuritis multiplex

A

Wegeners AIDS/amyloidosis Rheumatoid arthritis DMT2 Sarcoidosis Polyarteritis nodosa Leprosy Carcinomas

207
Q

Pathophysiology of carpal tunnel syndrome

A

pressure on median Nerve, passing through carpal tunnel - Nerve roots #REF! - T1

208
Q

Risk factors of carpal tunnel syndrome

A

F > M - Hypothyroidism - Acromegaly - Pregnancy - rheumatoid arthritis - Obesity

209
Q

Symptoms of carpal tunnel syndrome

A

Gradual onset - Weakness of grip + aching hand/forearm - Parasthesia of the hand - Wasting thenar eminence

210
Q

Nature of carpal tunnel syndrome pain

A

Bad at night - Relieved by hanging hand over bed - WAKE and SHAKE

211
Q

Diagnosis of carpal tunnel syndrome

A

Phalen’s test - Flex hands at wrist for 1 minute - Parasthesia + pain = +ve Tinel test - Tapping wrist causes tingling Electromyography diagnostic if above tests uncertain

212
Q

Treatment of carpal tunnel syndrome

A

Wrist splint at night + steroid injection (Acutely v painful) - last resort = surgical decompression

213
Q

Wrist drop

A

Radial Nerve palsy - roots C5 - T1 - Mostly innervates extensor arm muscles

214
Q

Claw hand

A
  • Ulnar nerve palsy - Nerve roots C8 + T1 - 4th and 5th fingers claw up
215
Q

Foot drop

A

common peroneal Nerve palsy - Nerve roots L4 - S2 - Smaller of Two terminal branchers of sciatic Nerve, other one being The tibial Nerve

216
Q

Trendelenburg sign

A

Superior gluteal Nerve palsy - Nerve roots S4 - L1

217
Q

Aetiology of sciatica

A

L5/S1 lesion due to: - Spinal: IV disc herniation/prolapse - Non spinal: Piriformis syndrome, tumours, pregnancy

218
Q

Symptoms of sciatica

A
  • Pain from buttock down lateral leg -> pinky toe - Weak plantarflexion + absent ankle jerk
219
Q

Diagnosis of sciatica

A
  • Exam - can’t do straight leg raise test without pain - MRI cord to confirm
220
Q

Treatment of sciatica

A

analgesia + Physio - Neurosurgery

221
Q

Distribution of polyneuropathy

A
  • “Glove + stocking” distribution - Mostly peripheries affected
222
Q

Types of polyneuropathy

A

Mostly motor = Guillain Barre syndrome - Mostly sensory = Diabetic neuropathy

223
Q

Other causes of polyneuropathy

A

Vasculitis - malignancy -#REF! deficiency - rheumatoid arthritis

224
Q

Diagnosis of polyneuroathy

A

Find an underlying cause through bloods, serology, ESR/CRP

225
Q

Treatment for polyneuropathy

A

Analgesia + treat underlying cause (eg: TCA)

226
Q

Pathophysiology of multiple sclerosis

A
  • Type 4 sensitivity vs myelin basic protein of oligodendrocytes - Leading to demyelination of CNS neurons
227
Q

Risk factors of multiple sclerosis

A

females - 20-40 - Autoimmune disease - family history - EBV

228
Q

What is primary progressive remiting multiple sclerosis?

A

Gradual deterioration without recovery

229
Q

Types of multiple sclerosis

A

Relapsing remiting - common in early stages, often becoming progressive Primary progressive - from disease onset Secondary progressive - following a period of relapsing/remitting disease (75% evolve to this)

230
Q

Symptoms of multiple sclerosis

A
  • Parasthesia - Blurred vision - Uthoff’s phenomenon - symptoms exacerbated by heat 🚿
231
Q

Signs of multiple sclerosis

A

Optic neuritis - Internuclear opthalmoplegia - brain signs - sensory signs - UMN signs (not LMN) - Lhermitte phenomenon - Charcot neurological triad

232
Q

What is optic neuritis?

A
  • First presenting symptom of multiple sclerosis - Inflamed optic nerve - Can’t see red properly - Usually unilateral
233
Q

What is internuclear opthalmoplegia?

A

lateral gaze Impaired - Damaged medial longitudinal fasciculus

234
Q

What is the lhermitte phenomenon?

A

Electric shock sensation with neck flexion

235
Q

Charcot neurological triad

A

Dysarthria - staccato Speech - Nystagmus - repetitive involuntary eye movement - Intention tremor

236
Q

Diagnosis of multiple sclerosis

A

Mcdonald criteria - 2 ≤ attacks disseminated in time and space (separate events and different parts of the CNS affected) Also: - MRI brain and cord is diagnostic - CSF from lumbar puncture (oligoclonal IgG bands) - Evoked potentials - delayed reactions to stimuli

237
Q

What does an MRI brain and cord show for multiple sclerosis

A

Dissemination in space and time - Space - Where is white demyelination? - Time - give gadolinium contrast to show how long these have been there for

238
Q

Treatment of multiple sclerosis

A
  • Acutely (in episodes) - IV Methylprednisolone - Prophylaxis - beta inteferon (DMARD; biologic)
239
Q

Where does UMN lesion come from?

A

Precentral gyrus - to Anterior spinal cord

240
Q

UMN lesions signs

A

Everything UP - Hypertonia; rigidity + spasticity (rigid w movement) - Hyperreflexia - No fasciculation - Babinski positive - Arms: power of flexors > extensors - Legs: power of flexors < extensors

241
Q

LMN lesion signs

A

Everything DOWN: - Hypotonia (flaccid) + muscle wasting - Hyporeflexia - Fasciculations - Babinski negative - Generall low power

242
Q

Where does an LMN lesion come from

A

Antispinal cord - to The muscles innervated

243
Q

Presentation of MND

A
  • Mixed UMN + LMN signs - No eye, sensory, cerebellar or Parkinson’s signs
244
Q

Decussation of UMN

A

Decussation - lateral, 90% fibres No decussation - anterior, 10% fibres

245
Q

Risk factors for MND

A
  • Male - Family history (SOD-1 mutation) - Increasing age
246
Q

What is amyotrophic lateral sclerosis (ALS) ?

A
  • Most common classification of MND - Can progress to bulbar palsy - May see “split hand sign” - disproportionately high wasting of thenar muscles compared to hypothenars
247
Q

Types of ALS

A

progressive muscular atrophy - LMN only - primary lateral sclerosis - UMN only

248
Q

What is progressive bulbar palsy?

A
  • CN 9-12 affected - Worst progrnosis, high chance of respiratory failure
249
Q

Diagnosis of MND

A

Mainly Clinical - Electromyography shows fibrillation potentials - due to denervation of muscles with LMN dysfunction

250
Q

Treatment of MND

A

MDT management - Riluzole (antiglutaminergic) - Supportive - Physio and breathing support If necessary

251
Q

Complications of MND

A

resp failure - Aspiration pneumonia - Swallowing failure

252
Q

Types of primary brain tumour

A
  • Glioma, mc type: astrocytoma (90%) (2nd mc paediatric cancer after ALL) - Oligidodendrocytoma - Meningioma + Schwannoma
253
Q

Secondary brain tumours

A

Much More common, mets form NSCLC (mc) + SCLCBreastMelanomaRenal cell (RCC) Gastric cancerTesticularColorectal

254
Q

Treatment of secondary brain tumours

A
  • Often metastasised = grade 3/4 (severe) - Chemo, palliative care
255
Q

WHO grading for astrocytomas

A

1-4 1 = benign 4 = globlastoma (v bad prognosis, death within 1 year)

256
Q

Symptoms of primary brain tumours

A

High ICP signs including headaches - Focal neurology - Epileptic seizures - Lethargy and weight loss

257
Q

Diagnosis of primary brain tumours

A

MRI head to locate tumour - Then biopsy to determine grade - no lumbar puncture because High ICP of undetermined cause = massive CI

258
Q

Treatment of primary brain tumours

A

craniotomy - + chemo before/during/after surgery - Steroids (eg: dexamethasone) May help

259
Q

What is meningitis?

A

infection of The meninges of The brain - Notifiable to Public Health England

260
Q

Causes of meningitis

A
  • Viral (mc, less severe) -> enteroviruses (eg: coxsackie) and HSV-2, VZV - Bacterial (lc, very severe) -> mainly s.pneumoniae + n.meningitidis
261
Q

Risk factors for meningitis

A

Extremes of age - Immunocompromised - Crowded environments - non-vaccinated

262
Q

Bacterial causes of meningitis in neonates (0-3 months)

A

Group B alpha haem strep (s.agalactiae) - Listeria - E.coli

263
Q

Bacterial causes of meningitis in infants (3 months - 6 years)

A

S.pneumoniae - N.meningitidis

264
Q

Bacterial causes of meningitis in non-neonates

A

S.pneumoniae - N.meningitidis

265
Q

Bacterial causes of meningitis in the elderly (60+ years)

A

S.pneumoniae - N.meningitidis - Listeria

266
Q

Meningitis caused by n.meningitidis

A
  • Gram negative diplococcus - Vaccines available; men B + C, MenACWY - Non blanching purpuric rash (meningococcal septicemia -> DIC -> v easy bleeds)
267
Q

Meningitis caused by s.pneumoniae

A
  • Gram positive diplococcus in chains - PCV vaccine - 25% mortality
268
Q

Meningitis caused by Group B strep

A
  • Gram positive coccus in chains - Most common cause of neonatal meningitis - Because it colonises maternal vagina !!!
269
Q

Meningitis caused by listeria monocytogenes

A

gram positive bacillus - Affects Extremes of age and maternal (pregnant ladies) - Found in cheese 🪤

270
Q

Presentation of meningitis

A
  • Meningism - headache, neck stiffness, photophobia, fever - Kernig - can’t extend knee without pain when hip is flexed - Brudzinski - when neck is flexed, knees and hips automatically flex - Pyrexia
271
Q

Diagnosis of meningitis

A
  • Lumbar puncture + CSF analysis (contraindicated in high ICP due to tentorial herniation/coning risk) - Sample taken from L3/4 and analysed
272
Q

CSF sample in meningitis caused by bacteria

A
  • High opening pressure - Cloudy yellow - Neutrophilia - High protein (>1g/L) - Low glucose (<50% serum levels)
273
Q

CSF sample in meningitis caused by virus

A
  • Normal opening pressure - Clear, normal appearance - Lymphocytosis - Normal/high proteins (<1g/L) - Glucose >60% serum level
274
Q

CSF sample in meningitis caused by fungus/TB

A

Same as bacteria but also fibrinous and high lymphocytes instead of neutrophils

275
Q

Treatment for viral meningitis

A

Nothing If enteroviruses - Aciclovir If HSV Or VZV

276
Q

Contact tracing for meningitis

A
  • Antibiotic prophylaxis for contacts with 7+ days prolonged contact preceding symptoms (eg: cohabitation) - One off dose of ciprofloxacin
277
Q

What is meningococcal disease?

A

Any illness caused by bacteria called Neisseria meningitidis (n.meningitidis)

278
Q

Complications of meningitis

A

DIC (meningococcal septicaemia) - Waterhouse friedrichsen syndrome (adrenal insufficiency caused by intraadrenal haemorrhage as a result of meningococcal DIC)

279
Q

What is encephalitis?

A

Viral infection of brain parenchyma

280
Q

Aetiology of encephalitis

A
  • 95% of cases: HSV-1 - Others: CMV, EBV, HIV, toxoplasmosis (close contact with cats; parasitic infection)
281
Q

Risk factors of encephalitis

A

Immunocompromised - Extremes of age

282
Q

Symptoms of encephalitis

A
  • Fever - Headache - Encephalopathy - Focal neurology (temporal lobe mc affected - eg: aphasia)
283
Q

Encephalitis that presents with meningism symptoms

A

Meningo-encephalitis (2-in-1 offer🛍)

284
Q

Diagnosis of encephalitis

A
  • CSF may show veraemia (viruses in blood, high lymphocytes, consider PCR) - MRI head = unilateral usually temporal encephalitis - Also non-specific EEG firing of 2Hz periodically
285
Q

Treatment for encephalitis

A

Aciclovir (works well against HSV)

286
Q

img

A
  1. Caudate nucleus 2. Putamen 3. Globus pallidus 4. Subthalamic nucleus 5. Substantia nigra
287
Q

Visual pathway

A

img

288
Q

CN3 - Oculomotor

A
  • Motor to MR, SR, IO, LPS - Carries parasympathetic fibres into the orbit -> constrict the pupil
289
Q

Pupillary light reflex

A

Afferent limb (input) = CN2 Efferent limb (output) = Parasympathetic fibres in CN3 To test: Shine light into one eye Ipsilateral pupil constricts = direct response Contralateral pupil constricts = consensual response

290
Q

What is acoustic neuroma?

A

Also called vestibular schwannoma - Peogressive Unilateral Hearing loss and dizziness

291
Q

Pathophysiology of intracerebral haemorrhage

A

Spontaneous due to aneurysm Or vessel rupture - small perforating vessels prone to rupture, especially If hypertensive

292
Q

Diagnosis of intracerebral haemorrhage

A

acute (fresh) bleed is hyperdense on CT - blood seen in The substance of The brain - Mass effect seen If large (eg: midline shift)

293
Q

What does the brainstem include

A

Midbrain - pons - medulla oblongata Contains Ascending and descending tracts

294
Q

Function of the cerebellum

A

Balance, posture and motor coordination - Operates subconciously

295
Q

Differential diagnosis of stroke

A

Epileptic seizure - space occupying lesion - infection - Metabolic problems: thyroid, diabetes - MS - Functional neurological disorder - Migraine

296
Q

Aetiology of brain tumours

A
  • Majority no cause found - Ionising radiation (radiotherapy) - 5% family history - associated genetic syndromes eg, neurofibromatosis, Von Hippel-Lindau disease, tuberose sclerosis - Immunosuppression (CNS lymphoma)
297
Q

Symptoms of vertebrobasilar artery stroke

A

Cerebellar signs - Reduced consciousness - Quadriplegia Or hemiplegia

298
Q

Weber’s syndrome

A

Midbrain infarct - branches of PCA - Oculomotor palsy - Contralateral hemiplegia

299
Q

What to investigate for if a young person presents with stroke

A

Aortic dissection

300
Q

Non-movement related symptoms of Parkinson’s disease

A

Autonomic problems - Constipation - Increased urinary frequency (but incontinence not typical) - Anosmia seen early (loss of sense of smell) Depression and anxiety Dementia

301
Q

Parkinsonian tremors vs essential tremors

A

Parkinsons: unilateral resting/pill rolling tremor that usually affects limbs (can become bilateral) Essential tremor: bilateral symmetrical active tremor that worsens with movement

302
Q

Gait patterns in Parkinson’s

A

Reduced armswing - Shuffling gait - Festination - Stooped posture

303
Q

Treatment for wrist drop and claw hand

A

Splint + simple analgaesia

Haroon Phase 2A (14 decks)

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