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Neuro Flashcards

1
Q

What is Myasthenia Gravis?

A

AI neuromuscular disease of nicotonic AChR resulting in impaired NMJ transmission

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2
Q

In order state the muscle groups that are affected in MG

A 
Extra-ocular
Bulbar
Face
Neck
Limb 
Trunk
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3
Q

Give 3 symptoms of Myasthenia gravis

A

Diplopia, blurred vision, difficulty swallowing/chewing, difficulty climbing stairs

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4
Q

Give 3 signs of Myasthenia gravis

A

Ptosis
Myasthenic snarl
Dysphonia (voice fades)

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5
Q

What antibodies are present in 90% of PTs with MG?

If -ve for these ABs, what other antibodies can you look for?

A

Anti- AChR- Antibodies

MUSK Antibodies

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6
Q

What other investigation could you perform for MG? What would you see?

A

Electromyography

Decreased muscle response to repeated stimuli

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7
Q

What is the characteristic pattern of muscle weakness in MG patients?

A

Increasing muscle fatigue throughout day, improves with rest. PT struggles with repetitive movements.

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8
Q

What class of drugs is used for symptomatic control of myasthenia gravis? Give an example

A

Anti-cholinesterase e.g. Pyridostigmine

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9
Q

What is a myasthenic crisis?

A

Acute, life-threatening exacerbation of myasthenic symptoms + weakness of respiratory muscles that leads to respiratory failure.

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10
Q

What is the treatment for myasthenic crisis?

A

Intubation + mechanical ventilation
Plasmaphoresis to remove anti-AChR ABs if bulbar symps
IVIg

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11
Q

What is Lambert-Eaton Myasthenic Syndrome?

A

AI condition whereby pre-synaptic VG Ca2+ channels are attacked, resulting in disruption of synaptic transmission

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12
Q

LEMS is often paraneoplastic to what type of cancer?

A

Small cell lung cancer

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13
Q

Give 3 clinical features of Lambert-Eaton Myasthenic Syndrome

A

Proximal weakness- improves with exercise
Hyporreflexia
Autonomic symptoms: dry mouth, constipation + impotence

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14
Q

What antibody would be detected in a LEMS PT?

A

Anti- VGCC ABs (75/95% PTs)

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15
Q

What other investigation might you want to do in PT with LEMS symptoms?

A

CXR/CT- weakness symptoms may precede associated lung cancer

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16
Q

What treatment is often combined with anti-cholinesterase’s for myasthenia gravis?

A

Immunosuppression e.g. Oral Prednisolone

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17
Q

Give 3 differences between MG +LEMS

A

MG: increasing muscle weakness with activity, starts with weakness of extraocular, no autonomic symps, normal reflexes, post-synaptic AChR ABs
LAMS: decreasing muscle weakness with activity, starts with weakness of lower limbs, autonomic symps (constipation, dry mouth, impotence), hyporeflexia, pre-synaptic VGCC ABs

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18
Q

What is a migraine?

A

Recurrent, throbbing, pulsatile headache often preceded by an aura, N&V + visual changes

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19
Q

Name some triggers for migraine

A 
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptive
Lie-ins
Alcohol
Travel
Exercise
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20
Q

State the clinical features of a migraine

A 
Unilateral
Throbbing + pulsatile
Can be preceded by an aura
4-72hrs
Moderate-severe pain
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21
Q

A PT presents with a headache. You suspect it is a migraine. What are the differential diagnoses?

A

Tension headache: often bilateral + band like
Cluster headache: autonomic symptoms
Meningitis: fever, neck stiffness, photophonia
SAH: sudden onset “thunderclap”
TIA: max deficit presents immediately

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22
Q

What is an aura? What type of headache are they common in?

A

Transient, focal, neurological symptoms that usually precede headache e.g. visual (scotoma, zig-zags), paresthesia. MIGRAINES (25% have aura)

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23
Q

How is migraine diagnosed? What other investigations might you consider if suspect something more sinister?

A

Clinical diagnosis

CT head [SAH]

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24
Q

Give a possible reason why an episodic headache may become a chronic daily headache

A

Medication overuse headache (Paracetamol + opiates, triptans)

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25
Q

A PT develops a medication overuse headache, what do you do?

A

STOP ANALGESIA. Consider prevention when off other drugs.

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26
Q

What is a primary headache?

A

Primary headaches are headaches which are not associated with another underlying condition

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27
Q

What is a secondary headache?

A

Secondary headaches are headaches which occur as a result of underlying local or systemic pathology such as intracerebral haemorrhage, malignancy or infection.

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28
Q

What is diagnostic criteria for PT with migraine without aura?

A

5 attacks lasting 4-72hrs with:

  1. 1 or more: N&V, photophobia, phonophobia
  2. 2 or more: unilateral, pulsating/throbbing, mod-severe pain impairs routine activity
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29
Q

What is the diagnostic criteria for PT with migraine with aura?

A

2 attacks with:

  1. Reversible aura symp (visual, paresthesia/numbness, speech, motor weakness)
  2. 3 or more: unilateral aura, aura lasting 5-60mins, + aura symp, 1 aura symp over at least 5 mins, aura followed within 60mins of headache
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30
Q

What is the recommended treatment for mild-mod migraines?

A

NSAIDs e.g. Ibuprofen +/- anti-emetic

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31
Q

What group of drugs should be given to PT with severe migraine? Give an example

A

Triptan’s e.g. Sumatriptan

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32
Q

What is 1st line prophylaxis for migraine?

A

Beta-blockers e.g. propanolol

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33
Q

Give 3 classes of drug used in prophylaxis of migraine

A

Beta-blocker- Propanolol
TCA: Amitriptyline
Anti-convulsant: Topiramate (CI in pregnancy)

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34
Q

What is the most common type of primary headache? Describe it

A

Tension headache: bilateral and band-like headache with feeling of pressure or tightening

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35
Q

Name 3 triggers of tension headaches

A

Stress, anxiety/depression, sleep deprivation, noise/fumes, overexertion, conflict, clenched jaw

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36
Q

Give 3 differences between tension headache and migraine

A

TH: bilateral, band-like non-pulsatile, N&V/aura/photophobia, not aggravated by routine activity
Migraine: unilateral, pulsatile/throbbing, no aura/ N&V, aggravated by routine activity

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37
Q

What is the diagnostic criteria for a tension headache?

A

Clinical diagnosis

  1. Lasts 30mins-7days
  2. 2 or more bilateral, band-like tightening, mild-moderate, not exacerbated by routine activity
  3. Both of following- no N&V, no more than one of photo/phonophobia
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38
Q

A PT with a history of tension headaches requires some lifestyle advice to help. What would you tell them?

A

Good sleep hygiene
Stress relief
Exercise
Treat depression

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39
Q

What treatment would you advice for episodic tension headaches?

A

NSAIDs/aspirin/paracetamol

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40
Q

What treatment would you advice for chronic tension headaches?

A

TCA- Amitriptyline

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41
Q

What is a cluster headache?

A

Recurrent 15mins-3hr attacks of agonising, strictly unilateral headaches in peri-orbital/forehead regions
Primary headache

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42
Q

Give 3 clinical features of cluster headaches

A

Excruciating pain around eye, unilateral, abrupt onset, short recurring attacks in clusters (4-12wk episodes), PT restless

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43
Q

What autonomic signs may indicate a PT has cluster headaches? Where will these autonomic features present?

A

Lacrimation/bloodshot eye, Miosis +/- ptosis, rhinorrhoea

Autonomic signs will present on ipsilateral side of headache

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44
Q

What demographic of population are most likely to have cluster headaches?

A

20-40yo males

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45
Q

What treatment would you use in acute cluster headache?

A

100% FiO2 Oxygen therapy

Triptan e.g. Sumatriptan

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46
Q

What treatment would you use in prophylaxis for cluster headache?

A

Ca2+ channel blocker e.g. Verapamil
Corticosteroid e.g. Prednisolone
Avoid triggers e.g. alcohol

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47
Q

What is encephalitis?

A

Inflammation of brain parenchyma often as result of infection (HSV)

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48
Q

What is most common cause of encephalitis?

A

Herpes Simplex Virus

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49
Q

What demographic tend to develop encephalitis?

A

Younger (<20) + older (>50)

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50
Q

Give some features of an infectious prodrome that encephalitis PTs may present with?

A 
Fever/Pyrexia
Headache
N&amp;V
Lymphadenopathy
Rash
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51
Q

Give 3 symptoms of encephalitis

A

Fever
Headache
Photophobia
Confusion

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52
Q

Give 3 signs of encephalitis

A

ODD/ENCEPHALOPATHIC BEHAVIOUR
Focal neurological deficits (aphasia/ataxia)
Seizures
Decreased consciousness

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53
Q

Encephalitis may resemble meningitis, what factors are more likely to indicate encephalitis

A

Altered mental state, focal neurological deficits, seizures

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54
Q

Why might you want to take bloods in PT with encephalitis?

A

Blood cultures, viral PCR, Toxoplasma IgM titre, malaria film

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55
Q

What might a contrast CT scan show in PT with encephalitis?

A

Focal bilateral temporal lobe involvement (HSV encephalitis)

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56
Q

What is gold-standard diagnosis for encephalitis?

A

LP + viral PCR on CSF

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57
Q

What is 1st-line treatment for Herpes Simplex Encephalopathy? What are guidelines for treatment?

A

Aciclovir

Start within 30mins of PT arriving, HSE progresses quickly. Start before definitive diagnosis

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58
Q

What is risk with aciclovir?

A

Nephrotoxicity- taper dose and hydrate PT!

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59
Q

What is a cerebral abscess?

A

Focal, suppurative (pus-filled) lesion in brain

Rare but life-threatening

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60
Q

What are causes of cerebral abscess?

A
  1. Direct spread from sinus/ear/dental infections
  2. Skull fracture + subsequent inoculation
  3. Haematogenous spread from infective loci (e.g. endocarditis)
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61
Q

What is clinical presentation of PT with cerebral abscess?

A

Fever, headache, focal neurological deficit, N&V, drowsiness/confusion, papilloedema, seizures

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62
Q

Give 3 symptoms of PT with cerebral abscess

A

Fever, headache, N&V, seizure, drowsiness, confusion, focal neuro symps

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63
Q

Give 3 signs of PT with cerebral abscess

A

Pyrexia, seizure, papilloedema, decreased mental state, raised BP/ bradycardia, focal neuro signs

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64
Q

Give 3 DD’s for brain abscess

A

Encephalitis, meningitis, brain tumour/space-occupying lesion

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65
Q

State two results you would see in lab tests from cerebral abscess PTs

A

Raised CRP/ESR/WCC [Leukocytosis]

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66
Q

What investigation may you avoid in PT with cerebral abscess + why?

A

Lumbar puncture, tentorial herniation risk if raised ICP

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67
Q

What is investigation of choice for cerebral abscess?

A

CT head [+ contrast]: shows ring enhancement + radiolucent [black] space-occupying lesion

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68
Q

A PT CT shows a cerebral abscess. What is the treatment for this?

A
  1. Burr-hole + surgical drainage of abscess
  2. Take biopsy and send pus for culture
  3. Prolonged ABX
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69
Q

What empirical ABX should be given to PT with suspected cerebral abscess?

A
  1. 3rd generation cephalosporin (Ceftriaxone)
  2. Metronidazole
  3. +/- Vancomycin [if staph]
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70
Q

What is the difference between meningitis and encephalitis?

A

E: inflammation of brain parenchyma
M: inflammation of meninges

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71
Q

State 3 common causative organisms of bacterial meningitis in neonates

A

Listeria monocytogenes
E.coli
Group B Haemolytic strep (Strep agalactiae)
Strep pneumoniae

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72
Q

State 2 common causative organisms of bacterial meningitis in infants

A

Neisseria meningitidis
Strep. pneumoniae
Haemophilus influenza

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73
Q

State 2 common causative organisms of bacterial meningitis in adults

A

Neisseria meningitidis

Strep pneumoniae

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74
Q

State 2 common causative organisms of bacterial meningitis in the elderly

A

Neisseria meningitidis
Strep pneumoniae
Listeria monocytogenes

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75
Q

Give 3 risk factors for meningitis

A

Young age, elderly, intra-thecal injection, immunocompromised, crowding, bacterial endocarditis

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76
Q

What would indicate meningococcal septicaemia?

A

Appearance of non-blanching purpuric rash

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77
Q

What is meningococcal septicaemia?

A

Dissemination of bacteria into blood stream (sepsis) + presenting as purpuric rash

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78
Q

How is bacterial meningitis spread?

A

Close contact via droplets or secretions from respiratory tract

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79
Q

How does pneumococcal disease usually enter body?

A

Colonises nasopharyngeal mucosa (spread via droplets/direct contact)

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80
Q

What can be said about neonates clinical presentation of meningitis? State some symps/signs of neonatal meningitis

A

NON-SPECIFIC (without classic triad)
Lethargy, high-pitched crying, hypo/hyperthermia, hypotonia, poor appetite, irritability, abnormal breathing, bulging fontanelle

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81
Q

What is classic triad of symptoms for meningitis?

A

Fever
Headache
Neck stiffness

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82
Q

State 3 non-specific symptoms of meningitis

A

Fever, headache, N&V, lethargy, irritability, muscle/joint pain, loss of appetite, leg pains

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83
Q

Give 3 signs of meningitis

A

+ve Kernig’s sign, +ve Brudzinski’s sign, seizures/focal neuro deficits, change in skin colour, shock (decreased BP + increased CRT), cold hands/feet

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84
Q

A PT presents with suspected meningitis, what is the first investigation you do?

A

BLOOD CULTURES- 1st thing in suspected meningitis

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85
Q

In a meningitic PT with no signs of septicaemia/shock/raised ICP, how should you acutely manage them?

A
  1. Blood cultures first
  2. Lumbar Puncture
  3. Empirical ABs
    LP delayed–> Give ABs
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86
Q

What empirical AB should you give to a PT with suspected meningitis in a primary care setting?

A

Benzopenicillin

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87
Q

What empirical AB should you give to a PT with suspected meningitis in a hospital setting?

A

IV Cefotaxime (+/- Amoxicillin- elderly/immunocompromised)

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88
Q

Why do you give IV Dexamethasone to meningitis PT?

A

Reduce neurological complications (hearing loss, motor or cognitive deficit)

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89
Q

What prophylactic AB should you give to contacts of meningitis PTs?

A

Ciprofloxacin stat

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90
Q

What is shingles?

A

Dermatological rash with painful blistering caused by reactivation of varicella zoster virus

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91
Q

Give an overview of the pathophysiology of shingles

A
  • Initial VZV in childhood
  • Virus lies dormant in DRG
  • VZV reactivated in immunocompromised
  • Virus replicates and travels through affected peripheral sensory nerve in dermatomal distribution
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92
Q

Where does VZV commonly reactivate in shingles?

A

Thoracic nerves + ophthalmic division of trigeminal nerve

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93
Q

What is the most common complication of herpes zoster infection?

A

Post-herpatic neuralgia (pain after 90 days of rash onset)

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94
Q

How can symptoms present in immunocompromised people?

A

Widespread across multiple dermatomes

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95
Q

What is the main prodromal symptom in a shingles PT? Give some other prodromal symptoms

A

PAIN
Headache
Fever/fatigue

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96
Q

Describe the rash seen in shingles PTs

A

Dermatomal distribution, does not cross midline, painful/itchy/tingly

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97
Q

Describe the course of the rash in herpes zoster

A
  1. Erythematous maculopapular rash
  2. Vesicular rash
  3. Crusting + involution
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98
Q

What is Herpes Zoster Ophthalmicus?

A

Reactivation of VZV in ophthalmic division of trigeminal nerve

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99
Q

What are the risks of HZ ophthalmicus?

A

Corneal ulceration, optic neuritis, glaucoma, BLINDING

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100
Q

What is Herpes Zoster oticus?

A

Reactivation of VZV in facial and vestibulocochlear nerves (Ramsey Hunt Syndrome)

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101
Q

What are risks of HZ oticus?

A

7th nerve: facial paralysis

8th nerve: hearing loss/vertigo

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102
Q

What is Hutchinson’s sign? What is significance of this sign?

A

Involvement of nasociliary nerve (HZOpth)–> Zoster lesion at tip of nose.

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103
Q

Why might Hutchinson’s sign be significant in herpes zoster ophthamicus?

A

Prognostic factor for eye inflammation/permanent corneal denervation

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104
Q

When might you want to admit shingles PT?

A

Immunocompromised adult/child [systemic/widespread rash]
Serious complications [meningitis, encephalitis]
HZ Ophthalmicus (eye symps)

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105
Q

What is 1st line treatment for shingles?

A

Aciclovir- give IV if PT immunocompromised

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106
Q

What is guillain-barre syndrome?

A

Acute inflammatory and demyelinating condition of PNS, characterised by ascending and symmetrical muscle weakness

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107
Q

Who tends to develop GBS?

A

PTs with URT/GI infection 1-4wks previous

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108
Q

State some pathogens associated with GBS

A

Campylobacter jejuni, Cytomegalovirus, EBV, Mycoplasma pneumoniae

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109
Q

What is pathophysiology of GBS?

A

Cross-reactive auto-antibodies attack host’s own axonal antigens–> demyelination–> Decreased peripheral nerve conduction

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110
Q

What is main clinical presentation of GBS?

A

Symmetrical ascending muscle weakness

111
Q

Which muscles are most affected by GBS?

A

Proximal muscles- trunk, respiratory + cranial nerves (esp VII)

112
Q

Give some other clinical features of GBS

A

Back/limb pain

Tingling/numbness in extremities

113
Q

Give 3 signs that a PT with GBS may present with

A

Dec. sweating, Inc. pulse, BP changes (autonomic)
Facial nerve palsy
Hyporreflexia

114
Q

What investigations would be used to diagnose GBS? What would you see?

A

Nerve conduction studies (decreased conduction)
Lumbar puncture (raised protein, normal cell count/glucose)
Serological (bloods): detect causative pathogen

115
Q

Why might you do lung function tests in GBS?

A

To determine respiratory muscle involvement [potential fatal].

116
Q

When might you consider mechanically ventilating a GBS PT?

A

FVC < 1.5L
PaO2< 10kPa
PaCO2>6kPa

117
Q

What are the treatment options for GBS?

A

V- Ventilation (if sig. respiratory involvement)
I- Immunoglobulins
P- Plasmapheresis

118
Q

What is Wernicke’s Encephalopathy?

A

Acute, reversible condition caused by severe thiamine (vitamin B1) deficiency

119
Q

What is Korsakoff’s syndrome?

A

Chronic, irreversible condition caused by thiamine deficiency

120
Q

What is the main cause of Wernicke Korsakoff Syndrome? Give two other causes

A

CHRONIC ALCOHOLISM
Eating disorders
Prolonged vomiting (chemotherapy)

121
Q

What is Wernicke-Korsakoff’s syndrome?

A

Spectrum of disorders:

  1. Wernicke’s Encephalopathy [frequently progresses into…]
  2. Korsakoff’s syndrome
122
Q

What is classic triad of symptoms for Wernicke’s Encephalopathy?

A
  1. Confusion
  2. Ataxia/Gait ataxia
  3. Ophthalmoplegia
123
Q

What are the clinical features of a PT with Korsakoff’s syndrome?

A
  1. Severe memory impairment (anterograde/retrograde)
  2. Confabulation
  3. Lack of insight/apathy (personality changes if frontal lobe)
124
Q

Give 3 differential diagnoses of Wernicke-Korsakoff’s syndrome

A

Hepatic encephalopathy, drug use, dementia, cerebrovascular disease, post-ictal state

125
Q

What is main way to diagnose Wernicke- Korsakoff’s syndrome?

A

Clinical diagnosis

126
Q

What other investigations might you do to diagnose Wernicke- Korsakoff’s syndrome?

A

MRI brain: peri-ventricular haemorrhages/atrophy to mammillary bodies
Lab: low serum thiamine, dysfunctional LFTs, decreased red cell transkeletase

127
Q

When do you treat Wernicke’s encephalopathy?

A

Medical emergency- immediately! Stop progression Korsakoff’s syndrome

128
Q

How do you treat Wernicke’s encephalopathy?

A
  1. Immediate IV Thiamine/Vitamin B1
  2. Add glucose if PT hypoglycaemic (thiamine first)
  3. Give vitamin B1/6/12 + folic acid replacement
  4. Stop drinking
129
Q

How do you treat Korsakoff’s syndrome?

A

Irreversible condition, thiamine supplementation, stop drinking and psychiatric/psychological therapy

130
Q

What is cerebral palsy?

A

Group of disorders affecting movement + posture (motor disorder).

131
Q

What causes cerebral palsy?

A

Damage to developing brain during in utero, neonatal or early infant stages

132
Q

What are different types of cerebral palsy?

A
  1. Spastic [75%]: spastic paresis (inability of voluntary movement + spasticity)
  2. Ataxic: intention tremor, loss of balance/coordination
  3. Dyskinetic: abnormal involuntary movements
    PTs may have mixed type
133
Q

How are the different types of cerebral palsy classified?

A

Dependant on part of brain affected + resultant motor dysfunction

134
Q

State some antenatal RFs for cerebral palsy

A

Preterm birth, congenital malformations, intrauterine infections (HIV, toxoplasmosis), toxic/teratogenic agents, maternal GU/RESP infections

135
Q

State some perinatal RFs for cerebral palsy

A

Neonatal sepsis, low birth weight, maternal GU/RESP infections

136
Q

State some postnatal RFs for cerebral palsy

A

Head trauma, hypoxia, intracranial haemorrhage, meningitis

137
Q

Is cerebral palsy a progressive disease?

A

BRAIN DAMAGE NOT PROGRESSIVE

Clinical features may change as brain matures

138
Q

Give some early signs that may indicate a PT has cerebral palsy

A 
Fidgety/abnormal movements
Hand preference before 1yo (suggests weakness on other side)
Problems feeding
Abnormal tone
Failure to meet motor milestones
139
Q

What clinical features can affect all types of cerebral palsy sufferers?

A 
Delay reaching motor milestones
Intellectual disability
Pain
Seizures
Dysphagia/Dysarthria
140
Q

Give some features of spastic cerebral palsy

A 
Increased muscle tone (1 or more limbs)
Scissor gait
Toe walking
Muscle weakness/atrophy
MSK problems (scoliosis, hip dislocation)
141
Q

Give some features of ataxic cerebral palsy

A

Abnormal coordination/balance
Poor precise movements
Intention tremor

142
Q

Give some features of dyskinetic cerebral palsy

A

Abnormal involuntary movements
Dystonic: random, slow uncontrolled movements in limbs/trunk
Chorea: random, dance-like movements

143
Q

How is cerebral palsy diagnosed?

A

Clinical diagnosis + parental observation

144
Q

What other investigations may help to diagnose cerebral palsy?

A

Cranial ultrasound (neonates)
MRI (older infants)
To detect causative lesion

145
Q

What is aim of treating cerebral palsy?

What is essential in treating cerebral palsy?

A

Improve function + quality of life, non-curable. MDT ESSENTIAL

146
Q

What members of MDT might be important in treating cerebral palsy PT?

A

Neurologist, speech therapist, physiotherapist, OT’s, orthapaedic surgeon

147
Q

What medical treatment might be useful for cerebral palsy PT + why?

A

BOTOX: reduce hypertonia (reducing associated pain + improving motor func)
DIAZEPAM: pain crisis, rapid effect
BACLOFEN: relieve spasticity, discomfort + improve motor function

148
Q

Why might surgery be useful in cerebral palsy PTs?

A 
Loosen muscles (hypertonia)
Relieve joint contractures
Aim: to improve function
149
Q

What is Huntington’s disease?

A

Neurodegenerative movement disorder characterised by involuntary and irregular movements

150
Q

How is huntington’s inherited? What is chance offspring will inherit?

A

Autosomal dominant- 50%

151
Q

What triplet of bases is repeated in HD PTs? What AA does this encode?

A

CAG (36 or more times)

Glutamine

152
Q

What clinical features would you expect to see in prodromal phase?

A

Irritability
Lack of coordination (clumsiness)
Personality changes
Depression

153
Q

What classic movements are seen in Huntington’s PTs?

A

Chorea: involuntary, irregular movements of limbs, head and face, “dance-like”

154
Q

Give some clinical features of huntington’s disease?

A

Chorea–> Hypokinetic motor symptoms (dystonia)
Oculomotor disorders: hypometric saccades
Personality changes
Depression/psychosis
Motor impersistence: inability to sustain simple acts

155
Q

What are the clinical features of advanced Huntington’s?

A

Immobility, dementia, mutism

156
Q

How do you diagnose huntington’s?

A

Clinical- PT history/examination
Genetic testing
CT/MRI: striatal atrophy + neuronal loss in cortex, not useful in early disease

157
Q

What is the meaning of anticipation (genetic)?

A

Increased severity and/or earlier manifestation of disease in next generation [seen in HD- more CAG repeats]

158
Q

What is average age of onset for HD?

159
Q

What general management options may be used in HD?

A

MDT: neurologists, speech therapists, physiotherapists
Genetic counselling (genetic testing may reveal offspring likely to have disease–> Depression)
Psychotherapy

160
Q

What might you give to PT with depression caused by HD?

A

SSRIs e.g. Citalopram

161
Q

What might you give to PT with psychosis caused by HD?

A

Atypical anti-psychotics e.g. Clozapine

162
Q

A PT with HD presents with chorea, what medication options are there?

A

Dopamine-depleting agents- Tetrabenazine

Neuroleptics- Clozapine

163
Q

What is Bell’s palsy?

A

Acute, unilateral facial nerve weakness or paralysis of rapid onset (<72hrs) and unknown cause

164
Q

Name some other causes of VII nerve palsy

A

Infection: TB, meningitis, Lyme disease, HIV, Herpes Zoster
Brainstem lesion: stroke, tumour, MS
Systemic disease: DM, GBS, sarcoidosis
Local disease: Parotid tumour, orofacial granulomatosis, skull trauma

165
Q

What is the motor function of facial nerve?

A

Muscles of facial expression, digastric and stylohyoid muscles

166
Q

What is the sensory function of the facial nerve?

A

Anterior 2/3 of tongue

167
Q

What is parasympathetic function of facial nerve?

A

Supply submandibular and sublingual glands–> Produce saliva (via chorda tympani). Lacrimal glands

168
Q

If the facial nerve is dysfunctional, what is the general result?

A

Weakness/paralysis of facial muscles

169
Q

If there is a central upper motor neuron lesion, what impact would this have on the facial muscles?

A

Resembles stroke paralysis

Drooping of lower face + lid, FOREHEAD SPARED

170
Q

If there is a peripheral lower motor neuron lesion, what impact would this have on the facial muscles?

A

Resembles Bell’s palsy

Drooping of lower face, lid and forehead. NO FOREHEAD SPARING

171
Q

What are the risk factors for Bell’s palsy?

A

Pregnancy
Diabetes mellitus
Obesity
Hypertension

172
Q

What is the most common clinical presentation of Bell’s palsy?

A

Rapid onset, facial muscle weakness in upper and lower face. Decreased ipsilateral movement, drooping of eyelid and corner of mouth, absence of nasolabial fold. Primarily unilateral

173
Q

State some other symptoms of Bell’s palsy

A

Ear/post-auricular pain
Difficulty chewing, changes in taste + dry mouth
Incomplete eye closure, watery or dry eye
Speech problems/drooling

174
Q

How would you diagnose Bell’s palsy?

A

Clinical examination- history + examination
CNVII: frown, whistle, inflate cheeks, show teeth, close eyes tightly. Observe asymmetries
Rule out other causes

175
Q

How might you rule out other causes of CNVII palsy?

A

Bloods: VSV ABs, Borrelia ABs, ESR

CT/MRI: space-occupying lesions, stroke, MS

176
Q

What treatment may speed up recovery time in Bell’s Palsy PTs if given within 72hrs?

A

Corticosteroids e.g. Prednisolone

177
Q

What organ must you consider in management of Bell’s Palsy? How?

A

EYE

  • Artificial tears for lubrication
  • Sunglasses to protect eye
  • Tape eye during sleep
178
Q

What is a bulbar palsy?

A

LMN palsy that affects nuclei of cranial nerves IX, X, XI, XII.

179
Q

What is a pseudobulbar palsy?

A

UMN palsy that affects the corticobulbar tracts of V, VII, IX, X, XI, XII

180
Q

Give 2 causes of a bulbar palsy

A

Brainstem stroke/tumours
Neurodegenerative disorders: MND, MS, syringobulbia
AI neuropathies: MG, GBS
Infectious neuropathies

181
Q

Give 2 causes of a pseudobulbar palsy

A

Tumours/injury higher up on brain stem [than nuclei]
Stroke
Neurodegenerative disorders: MND, MS

182
Q

State 3 clinical features of a bulbar palsy

A

Tongue: flaccid, fasciculating, wasting
Speech: quiet, hoarse or nasal
Dysphagia/drooling
Palatal movement absent

183
Q

State 3 clinical features of a pseudobulbar palsy

A 
Tongue: spastic, difficulty with protrusion, no wasting/fasciculations
Speech: dysarthria
Dysphagia/drooling
Palatal movement absent
Expressionless face
Emotional incontinence
184
Q

State some supportive treatments that may be useful in PTs with bulbar or pseudobulbar palsy

A 
Baclofen (spasticity in PBP)
Speech + language theraoy
PEG: dysphagia or recurrent aspiration pneumonia
Anti-cholinergics: drooling
SSRIs: pseudobulbar affect
185
Q

Name a common complication of bulbar + pseudobulbar palsies

A

Recurrent aspiration pneumonia

186
Q

What is narcolepsy?

A

Neurological condition of sleep/wake cycle characterised by irresistible attacks of inappropriate sleep

187
Q

What are the classic tetrad of symptoms for narcolepsy?

A

Excessive daytime sleepiness
Cataplexy
Sleep paralysis
Hypogognic hallucinations

188
Q

What is a typical PT for narcolepsy?

A 
Adolescent male (approx. 15yo)
Second peak at 35yo
189
Q

What is cataplexy?

A

Bilateral loss of tone in anti-gravity muscles
Provoked by emotions such as anger/excitement
Highly specific for narcolepsy

190
Q

Give some clinical features of cataplexy

A 
Falls
Dysarthria
Mutism
Phasic muscle jerking around mouth 
No loss of awareness
191
Q

What is sleep paralysis?

A

State whereby PT aware but unable to move, open eyes or speak
Can occur when PT falling asleep/awakening

192
Q

What is difference between hypopompic and hypogognic hallucinations? Which is more common in narcolepsy?

A

Hypopompic: as PT waking up
Hypogognic: as PT going to sleep [more common]

193
Q

How is narcolepsy diagnosed?

A

Primarily clinical- history + analysis of sleep patterns
Sleep studies
Measure CSF orexin levels

194
Q

What is diagnostic criteria for narcolepsy without cataplexy?

A

Excessive daytime sleepiness most days ≥ 3 months
Must have confirmation by sleep studies (nocturnal polysomnography then MSLT)
Hypersomnia not better explained by another condition

195
Q

What is diagnostic criteria for narcolepsy with cataplexy?

A

Excessive daytime sleepiness most days ≥ 3 months
Cataplexy
If possible… sleep studies
Hypersomnia not better explained by another condition

196
Q

Give for differential diagnoses for excessive daytime sleepiness

A

Drug/toxins, obstructive sleep apnoea, sleep deprivation

197
Q

Give differential diagnoses for cataplexy

A

Drop attack, syncope, seizures/epilepsy, TIA

198
Q

What is normal sleep like in a PT with narcolepsy?

A

PTs usually have normal sleep + feel rested

199
Q

What is first line treatment for narcolepsy?

A

Modafinil (CNS stimulant, non amphetamine)

200
Q

What treatment can be used for narcolepsy?

A

Modafinil

Methylphenidate (amphetamine)

201
Q

What medication is most effective for cataplexy? What other group of drugs can be used?

A

Sodium oxybate

SSRIs (Citalopram)/TCAs

202
Q

What are risks with giving an amphetamine like Methylphenidate for narcolepsy?

A

Dependence

Psychosis

203
Q

What non-pharmacological advice might you give to a PT with narcolepsy?

A

Good sleep hygiene
Strategic daytime naps
Exercise (increase energy)
Education of family/friends

204
Q

What is neurofibromatosis?

A

Genetic disorders causing lesions to nervous system, and in some cases the skeleton + skin

205
Q

What are the two types of neurofibromatosis?

A

Neurofibromatosis type 1Neurofibromatosis type 2

206
Q

How is neurofibromatosis inherited?

A 
Autosomal dominant (50%)
De novo- new mutation (50%)
207
Q

State two skin changes that may indicate type 1 neurofibromatosis

A

Freckling e.g. axillae/groin)

Cafe au lait

208
Q

How might the eye be affected by type 1 neurofibromatosis?

A 
Lisch nodules 
Optic glioma (tumour of optic nerve)
209
Q

State some of skeletal complications in type 1 neurofibromatosis

A

Scoliosis

Bone fractures/ cortical thinning/ pseudoarthosis

210
Q

State the different types of neurofibroma

A

Cutaneous neurofibromas
Spinal neurofibromas
Plexiform neurofibromas-

211
Q

Give some other clinical features that may be a sign of type 1 neurofibromatosis

A 
Macrocephaly
Hypertension
Short stature
GI bleeds/obstruction
Mild learning disability
212
Q

What investigations may support diagnosis of neurofibromatosis?

A 
History + dermatological examination
MRI: neurofibromas + meningiomas
Genetic testing
Slit lamp 
X-ray
213
Q

Who is important in treatment of neurofibromatosis?

A

MDT involvement- surgeons, neurologists, geneticist

214
Q

What is the treatment option for a neurofibroma? When is this most likely to be done?

A

Surgical removal when pressing on vital structures

215
Q

What type of neurofibromatosis does not tend to involve skin lesion? What does it tend to present with?

A

NF2 = no skin lesions

CNS tumours common

216
Q

What is a neurofibroma?

A

Benign peripheral nerve sheath tumours

217
Q

What clinical features would indicate type 2 neurofibromatosis?

A

Hearing loss/tinnitus, vertigo- Bilateral vestibular schwannoma
Meningiomas

218
Q

What diagnostic tests might you use if neurofibromatosis type 2 is suspected?

A

Hearing tests

MRI

219
Q

What management is there for PTs with vestibular schwannomas? What are the risks?

A

Surgical removal

Risk of hearing loss/facial palsy

220
Q

What is hydrocephalus?

A

Abnormal enlargement of cerebral ventricles as a result of excess CSF

221
Q

What are the two classifications of hydrocephalus?

A
  1. Obstructive/Non-communicating

2. Communicating

222
Q

What age groups tend to suffer from hydrocephalus?

A
  1. Congenital form: birth

2. Acquired form: all ages

223
Q

Give 3 risk factors for congenital hydrocephalus?

A
  1. Pre-eclampsia
  2. Absence of ante-natal care
  3. Maternal hypertension (pregnancy)
  4. Alcohol use (pregnancy)
224
Q

Give an overview of what happens in obstructive/non-communicating hydrocephalus

A

Flow of CSF OBSTRUCTED within ventricles or between ventricles and subarachnoid space

225
Q

Give an overview of what happens in communicating hydrocephalus

A
  • Communicating of CSF within ventricles intact
  • Reduced absorption of CSF
  • Increased production of CSF
226
Q

Give 3 potential causes of congenital non-communicating hydrocephalus

A
  1. Arnold-Chiari malformation
  2. Dandy-Walker malformation
  3. Intra-uterine infections
227
Q

Give 3 potential causes of communicating hydrocephalus associated with an increase in CSF production

A
  1. Choroid plexus papilloma
  2. Choroid plexus carcinoma
  3. Inflammation
228
Q

Give 3 potential causes of communicating hydrocephalus associated with a decrease in CSF absorption

A
  1. Arachnoid villi inflammation
  2. Congenital absence of arachnoid villi
  3. Subarachnoid/IV haemorrhage–> Inflammation–> Fibrosis–> Loss of villi
229
Q

Give 3 potential causes of acquired non-communicating hydrocephalus

A
  1. Aqueduct stenosis
  2. Brain tumours: ventricular or posterior fossa e.g. Ependymoma
  3. Inflammation
230
Q

What proportion of hydrocephalus cases in adults are idiopathic?

231
Q

Give some clinical features of an infant with hydrocephalus

A

Macrocephaly
Setting sun sign
Tense fontanelle/dysjunction of sutures/ dilated scalp veins
Increased limb tone

232
Q

In what condition would you see the setting sun sign? Describe the sign

A

Downward deviation of ocular globes
Upper lids retracted
White sclera visible above eye

233
Q

Give some acute clinical features you would expect to see in older children and adults with hydrocephalus

A

Vomiting
Headache
Papilledema

234
Q

Give some gradual clinical features you would expect to see in older children and adults with hydrocephalus

A 
Unsteady gait (spasticity in legs)
Large head (later presentation in adults)
6th nerve palsy
235
Q

Give some adult specific features you may observe in a hydrocephalus PT

A

Cognitive impairment
Neck pain
blurred vision
Incontinence

236
Q

What is primary investigation used to diagnose hydrocephalus in the antenatal or early infant (<6months) period?

A

Ultrasound

Shows enlarged lateral ventricles

237
Q

What is primary investigation used to diagnose hydrocephalus in infants (>6months) and adult period?

238
Q

What type of hydrocephalus would show generalised dilatation of ventricles on a CT scan?

A

Communicating hydrocephalus

239
Q

If a PT has non-communicating hydrocephalus, what would you see in a CT scan?

A

Ventricles upstream of obstruction are dilated

240
Q

What is the definitive treatment for hydrocephalus

A

Neurosurgery: CEREBRAL SHUNT to drain excess CSF

241
Q

Name some interim medications that could be used to delay neurosurgery for hydrocephalus

A

Furosemide/acetazolamide: decreased CSF secretion

Isosorbide: increases CSF absorption

242
Q

State some interim therapies for hydrocephalus to delay neurosurgery

A

Medication

Lumbar puncture

243
Q

What is normal pressure hydrocephalus?

A

Ventricular dilatation in absence of raised CSF pressure

244
Q

Why is diagnosis of normal pressure hydrocephalus important?

A

NPH is a reversible cause of dementia

245
Q

Who tends to suffer from normal pressure hydrocephalus?

A

Elderly PTs (>60yo)

246
Q

What is classic triad for normal pressure hydrocephalus?

A 
Urinary incontinence (WET)
Dementia (WACKY)
Apraxic gait (WOBBLY)
247
Q

Are signs of raised ICP observed in normal pressure hydrocephalus PTs?

248
Q

What other condition may be confused with normal pressure hydrocephalus and why?

A

Parkinson’s disease

NPH PTs present with slow, broad-based + shuffling movements.

249
Q

How do you differentiate between Parkinson’s disease and normal pressure hydrocephalus?

A

NPH: less marked rigidity + tremor

Give Levodopa therapy + observe reaction

250
Q

What investigations are used to diagnose normal pressure hydrocephalus?

A

CT/MRI: showing ventricular enlargement

LP/CSF tap: normal/mildly elevated CSF pressure, CSF removal should improve symps

251
Q

What is diagnosis of normal pressure hydrocephalus based upon?

A

Triad (wet, wacky, wobbly)
Neuroimaging
Absence of ICP signs
Symp improvement on LP

252
Q

What is primary treatment for normal pressure hydrocephalus?

A

Cerebral shunt (VP then VA)

253
Q

What treatment is only advised for PTs who cannot be operated on?

A

Serial LPs

Acetazolamide

254
Q

What is Horner’s syndrome?

A

Neurological disorder characterised by a triad of

  1. Partial ptosis
  2. Miosis
  3. Anhidrosis
255
Q

Give a brief overview of the pathophysiology of Horner’s syndrome

A

Interruption of face’s sympathetic supply
Can occur on 1st order neurons (brainstem, SC), 2nd order neurons (thoracic outlet, superior cervical ganglion) or 3rd order neurons (ICA)

256
Q

Give 3 causes of horner’s syndrome in first order neurons

A
  1. Brainstem stroke/haemorrhage
  2. Demyelinating disease (MS)
  3. Brain tumours (pituitary/skull base)
  4. Neck trauma- cervical vertebrae dislocation
  5. Syringomyelia
  6. Meningitis
257
Q

Give 3 causes of horner’s syndrome in second order neurons

A
  1. Apical lung tumour (pancoast tumour)
  2. Lymphadenopathy (TB, leukaemia, lymphoma)
  3. Trauma/surgery to head/neck
258
Q

Give 3 causes of horner’s syndrome in third order neurons

A
  1. Cluster headache
  2. Herpes zoster infection
  3. ICA dissection
259
Q

What investigations might reveal the underlying pathology behind Horner’s syndrome?

A
  1. CXR: apical lung cancer
  2. CT/MRI: Cerebrovascular event
  3. CT angiography: carotid artery dissection
260
Q

How do you manage Horner’s syndrome?

A

Diagnose + treatment of underlying condition

261
Q

What may be used to help confirm diagnosis of Horner’s syndrome?

A

Cocaine drops: dilatation of normal eye, no dilatation in Horner’s
Apraclonidine drops: no effect on normal pupil, dilatation of pupil in Horner’s

262
Q

What is a myelopathy?

A

Disease or disorder of the spinal cord

263
Q

Spinal cord compression is an example of what type of syndrome?

A

Myelopathy

264
Q

What is the most common cause of a myelopathy?

A

Osteophyte- disc compression

265
Q

Give 3 causes of spinal cord compression

A
  1. Tumours
  2. Trauma
  3. Infection
  4. Haematoma
  5. Prolapsed IV disc
  6. Cervical spondylosis
266
Q

What symptoms may a PT with spinal cord compression present with?

A

Motor weakness, sensory changes (numbness/paresthesia), sphincter disturbances, back/neck pain, erectile problems

267
Q

What motor dysfunction would a cervical lesion present with?

A

Quadriplegia (paralysis of 4 limbs and trunk)

If above C3,4,5–> Paralysis of diaphragm

268
Q

What motor dysfunction would a thoracic lesion present with?

A

Paraplegia (paralysis of legs)

269
Q

Give 4 red flags for sinister causes of back pain

A 
Sphincter disturbance
Neurological deficit
Worse when supine/at night
Age: <20yo, >55yo
Fever, night sweats, weight loss
History of malignancy
270
Q

In a myelopathy, which appears first, symptoms or signs? Give some examples

A

Signs

Long tract/ upper motor signs: spastic gait, hypertonia, hyperreflexia, +ve Babinski, loss of fine finger movements

271
Q

How serious is an acute spinal cord compression? Why?

A

MEDICAL EMERGENCY- swift diagnosis to prevent irreversible spinal cord injury + long term disability

272
Q

What investigations may be useful in diagnosis of spinal cord compression?

A

MRI of full spine
X-ray of spine
Other investigations will depend on underlying cause

273
Q

What medication should be given to a PT with spinal cord compression whilst they await definitive treatment?

A

Dexamethasone (corticosteroid)

Analgesia

274
Q

What is definitive treatment for spinal cord compression?

A

Surgery e.g. Laminectomy, posterior decompression

Start before neurological deterioration (ideally 24hrs)

Phase 3A (3 decks)

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