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Phase 2A revision > NEURO > Flashcards

NEURO Flashcards

1
Q

Name 3 types of primary headache

A

No underlying cause

  1. Migraine
  2. Tension headache
  3. Cluster headache
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2
Q

Name 2 types of secondary headache

A

Underlying cause

  1. Meningitis
  2. Subarachnoid haemorrhage
  3. Giant cell arteritis
  4. Idiopathic intracranial hypertension
  5. Medication overuse headache
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3
Q

Give an example of a tertiary headache

A

Trigeminal neuralgia

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4
Q

Give 6 questions that are important to ask when taking a history of headache

A
  1. Time = onset, duration, frequency, pattern
  2. Pain = severity, quality, site, spread
  3. Associated symptoms - n/v, photophobia, phonophobia
  4. Triggers/aggravating/relieving factors
  5. Response to attack = is medication useful?
  6. What are the symptoms like between attacks?
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5
Q

Give 5 red flags for suspected brain tumour in a patient presenting with a headache

A
  1. New onset headache and history of cancer
  2. Cluster headache
  3. Seizure
  4. Significantly altered consciousness, memory, confusion
  5. Papilloedema
  6. Other abnormal neurological exam
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6
Q

How long do migraine attacks tend to last for?

A

Between 4-72 hours

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7
Q

Briefly describe the pathophysiology of migraines

A
  1. Cerebrovascular constriction –> aura, dilation –> headache
  2. Spreading of cortical depression
  3. Activation of CN V nerve terminals in meninges and cerebral vessels
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8
Q

what are the main triggers of migraines?

A

CHOCOLATE

C - chocolate
H - hangovers
O - oral contraceptives
C - cheese
O - orgasms
L - lie-ins
A - alcohol
T - tumult i.e. loud noises
E - exercises
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9
Q

Describe the pain of a migraine

A

A symptoms:

  1. Unilateral
  2. Throbbing
  3. Moderate/severe pain
  4. Aggravated by physical activity
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10
Q

What other symptoms may a patient with a migraine experience other than pain?

A

B symptoms:

  1. Nausea
  2. Photophobia
  3. Phonophobia
  4. Aura
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11
Q

What is a prodrome for migraines?

A

Precedes migraine by hours-days

  • yawning
  • food cravings
  • changes in sleep, appetite or mood
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12
Q

what is a migraine aura?

A

Precedes migraine attacks and can be a variety of symptoms
- Visual = lines, dots, zig-zags
- somatosensory = paraesthesia, pins and needles
Dysphagia
Ataxia

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13
Q

what are the differential diagnoses for a migraine?

A
  1. Other headache type
  2. Hypertension
  3. TIA
  4. Meningitis
  5. Subarachnoid haemorrhage
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14
Q

What is the diagnostic criteria for a migraine?

A
  • classified as with or without aura
  • at least 2 of:
    • unilateral pain (usually 4-72hrs)
    • throbbing-type pain
    • moderate > severe intensity
    • motion sensitivity

plus at least 1 of:

 - nausea/vomiting
 - photophobia/phonophobia

there must also be a normal examination and no attributable cause

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15
Q

How can migraines be subdivided?

A
  1. Episodic with (20%)/without (80%) aura

2. Chronic migraine

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16
Q

what is the treatment for migraines

A
  • triptans e.g. sumatriptan
  • NSAIDs e.g. naproxen
  • anti-emetic e.g. prochlorperazine
  • AVOID opioids and ergotamine
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17
Q

How does triptan work?

A

Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain

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18
Q

How long do tension headaches usually last for?

A

From 30 minutes to 7 days

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19
Q

what are tension headaches?

A

most common chronic daily and recurrent headache

Can be episodic <15 days/month or chronic >15 days/month (for at least 3 months)

There is no known organic cause, however a number of triggers exist

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20
Q

Would a patient with a tension headache experience any other symptoms other than pain?

A

NO

Nausea, photophobia and photophobia would NOT be associated

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21
Q

How do you treat a tension headache?

A

avoidance of triggers and stress relief

symptomatic relief:

  • aspirin
  • paracetamol
  • ibuprofen / diclofenac
  • AVOID OPIOIDS

limit analgesics to no more than 6 days per month to reduce risk of medication-overuse headaches

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22
Q

what is the clinical presentation of a cluster headache?

A
  • rapid onset excruciating pain, classically around the eye (or temples/forehead)
  • pain is unilateral and localised.
  • pain rises to crescendo over a few minutes and lasts for 15-160 minutes, once or twice daily (usually around the same time)
  • ipsilateral autonomic features:
    • watery/bloodshot eye
    • facial flushing
    • rhinorrhoea (blocked nose)
    • miosis (pupillary constriction) +/- ptosis
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23
Q

How can cluster headaches be subdivided?

A 
Episodic = >2 cluster periods lasting 7 days - 1 year separated by pain free periods lasting >1 month 
Chronic = attack occur for >1 year without remission or remission lasting <1 month
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24
Q

How long do cluster headaches tend to last?

A

Between 15 minutes and 3 hours

Mostly nocturnal

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25
Q

what is the treatment for cluster headaches?

A

FOR ACUTE ATTACKS:
- analgesics are unhelpful

  • 15L 100% O2 for 15mins via non-rebreather mask
  • triptans e.g. sumatriptan
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26
Q

What is the most common type of secondary headache?

A

Medication overuse headache - episodic headache becomes daily chronic headache

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27
Q

Describe the pain of trigeminal neuralgia

A
  1. Unilateral face pain
  2. Severe intensity
  3. Electric shock like, shooting, stabbing or sharp
  4. No radiation beyond the trigeminal distribution
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28
Q

Describe the epidemiology of trigeminal neuralgia

A

Peak age = 50-60 years

Women > men

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29
Q

Give 3 causes of trigeminal neuralgia

A
  1. Compression of trigeminal nerve by a loop of vein or artery
  2. Aneurysms
  3. Meningeal inflammation
  4. Tumours
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30
Q

How long does the pain associated with trigeminal neuralgia usually last for?

A

A few seconds

Maximum 2 minutes

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31
Q

What is the treatment for trigeminal neuralgia?

A

Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery

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32
Q

What features might be present in the history of a headache that make you suspect meningitis?

A
  1. Pyrexia
  2. Photophobia
  3. Neck stiffness
  4. Non-blanching purpura rash
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33
Q

At what level is a lumbar puncture done and why is an LP done?

A

L3/4 or L4/5

To obtain a CSF sample

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34
Q

What does a small response on an nerve conduction study suggest?

A

There is axon loss

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35
Q

What does a slow response on an nerve conduction study suggest?

A

There is myelin loss

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36
Q

Define encephalopathy

A

Reduced level of consciousness/diffuse disease of brain substance

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37
Q

Define neuropathy

A

Damage to one or more peripheral nerve, usually causing weakness and/or numbness

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38
Q

Define myelitis

A

Inflammation of the spinal cord

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39
Q

Define meningitis

A

Infection and inflammation of the meninges of the brain

it is a notifiable disease

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40
Q

Name 3 bacterial organisms that cause meningitis in adults

A
  1. N. meningitidis
  2. S. pneumoniae
  3. H. influenzae
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41
Q

Name 2 bacterial organisms that cause meningitis in neonates

A
  1. E.coli

2. Group B strep - strep agalactiae

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42
Q

Name 3 viruses that can cause meningitis

A
  1. Enterovirus (most common viral)
  2. HSV
  3. CMV
  4. Varicella zoster virus
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43
Q

Name 2 organisms that can cause meningitis in immunocompromised patients

A
  1. CMV
  2. Cryptococcus
  3. TB
  4. HIV
  5. herpes simplex
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44
Q

Give the main triad of symptoms of meningitis

A

Headache + neck stiffness + fever

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45
Q

what are the symptoms of meningitis

A
  1. Neck stiffness
  2. Photophobia
  3. Papilloedema (due to increased ICP)
  4. Petechial non-blanching rash
  5. Headache
  6. Fever
  7. Decreased GCS
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46
Q

what are the signs of meningitis

A

Kernig’s sign = unable to straighten leg more than 135 degrees without pain when hip is flexed to 90 degrees

Brudzinski’s sign = severe neck stiffness cause hip and knees to flex when neck is flexed

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47
Q

How would you describe the rash associated with meningococcal sepsis?

A

Petechial non-blanching rash

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48
Q

What investigations might you do in someone you suspect has meningitis?

A
  1. Blood cultures (pre LP)
  2. Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate
  3. Lumbar puncture (contraindicated with raised ICP)
  4. CT head - exclude lesions
  5. Throat swabs - bacterial and viral
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49
Q

What is the treatment of bacterial meningitis?

A
  • ABCDE + support
  • Empirical therapy = IV Benzylpenicillin
    Assess GCS
  • First line = Ceftriaxone / Cefotaxime
  • Add IV Benzylpenicillin for rash
  • Penicillin allergy = Chloramphenicol
  • Immunocompromised ( Risk of Listeria) = Amoxicillin / Ampicillin

oral dexamethasone to reduce cerebral oedema

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50
Q

What is the treatment of viral meningitis?

A

Watch and wait

acyclovir

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51
Q

What is the treatment for meningococcal septicaemia?

A

IV BENZYLPENICILLIN (in community)

IV CEFOTAXIME (in hospital)

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52
Q

What can be given as prophylaxis against meningitis?

A

IV CIPROFLOXACIN (all ages and pregnancy) and IV RIFAMPICIN (all ages but NOT pregnancy)

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53
Q

For which bacteria is meningitis prophylaxis effective against?

A

N. meningitidis

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54
Q

Give 4 potential adverse effect of a lumbar puncture

A
  1. Headache
  2. Paraesthesia
  3. CSF leak
  4. Damage to spinal cord
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55
Q

What investigations would you do on a CSF sample?

A

Protein and glucose levels
MCS
Bacterial and viral PCR

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56
Q

When would you do a CT before an LP?

A 
>60
Immunocompromised
History of CNS disease
New onset/recent seizures
Decreased GCS
Focal neurological signs 
Papilloedema
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57
Q

What is the colour of the CSF in someone with a bacterial infection?

A

Cloudy (normally it is clear)

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58
Q

Give 4 reasons why a lumbar puncture might be contraindicated

A
  1. Thrombocytopenia
  2. Delay in Abx admin
  3. Signs of raised ICP
  4. Unstable cardio or resp systems
  5. Coagulation disorder
  6. Infections at LP site
  7. Focal neurological signs
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59
Q

Define encephalitis

A

Infection and inflammation of the brain parenchyma

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60
Q

In what group of people is encephalitis common?

A

Immunocompromised

the infections are most frequent in children and elderly

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61
Q

What area of the brain does encephalitis mainly affect?

A

Frontal and temporal lobes

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62
Q

what are the viral causes of encephalitis

A
  1. Herpes simplex (most common)
  2. CMV
  3. Epstein Barr
  4. varicella zoster
  5. HIV
  6. measles
  7. mumps
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63
Q

what are the non-viral causes of encephalitis

A
  1. Bacterial meningitis
  2. TB
  3. Malaria
  4. Lyme’s disease
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64
Q

Name the main triad of symptoms of encephalitis

A

Fever + headache + altered mental state

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65
Q

what is the clinical presentation of encephalitis?

A

begins with features of viral infection:
- fever, headaches, myalgia, fatigue, nausea

progresses to:

  • personality & behavioural changes
  • decreased consciousness, confusion, drowsiness
  • focal neurological deficit - hemiparesis, dysphagia
  • seizures
  • raised ICP and midline shift
  • coma
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66
Q

What would the LP show from someone with encephalitis?

A
  • CSF shows elevated lymphocyte count

- viral detection by CSF PCR

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67
Q

What investigations might you do on someone with encephalitis?

A
  • MRI - shows areas of inflammation, may be midline shifting
  • EEG - periodic sharp and slow wave complexes
  • lumbar puncture
  • blood and CSF serology
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68
Q

What is the treatment for encephalitis?

A
  • IV Acyclovir immediately - even before investigation results
  • Primidone = anti-seizure medication if needed
  • IV benzylpenicillin if meningitis is suspected
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69
Q

How does herpes zoster occur?

A

Reactivation of varicella zoster virus, usually within the dorsal root ganglia

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70
Q

where does herpes zoster commonly occur?

A
  • thoracic nerves
  • ophthalmic division of trigeminal nerve
  • cervical, lumbar and sacral nerve roots
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71
Q

what is the clinical presentation of herpes zoster?

A
  • Pain and paraesthesia in dermatomal distribution priced rash for days
  • Malaise, myalgia, headache and fever can be present
  • Can be over a week before eruption appears
  • Rash - consists of papules and vesicles
    RESTRICTED to SAME DERMATOME:
    • Neuritic pain
    • Crust formation and drying occurs over the next week with resolution in 2-3 weeks
    • Patients are infectious until lesions are dried
    • RASH DOES NOT EXTEND OUTSIDE DERMATOME
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72
Q

Describe the treatment for herpes zoster

A

Antiviral therapy within 72 hours of rash onset - ACYCLOVIR or VALICICLOVIR or FAMCICLOVIR

Analgesia - IBUPROFEN

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73
Q

Briefly describe the pathophysiology of herpes zoster

A

Latent virus is reactivated in dorsal root ganglia –> travels down affected nerve via sensory root in dermatomal distribution –> perineural and intramural inflammation

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74
Q

What dermatome is herpes zoster most likely to affect?

A

Thoracic nerves

Then ophthalmic division of trigeminal

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75
Q

Give 2 complications of herpes zoster

A
  1. Ophthalmic branch of trigmeinal = damages sight

2. Post herpetic neuralgia - pain lasts >4 months after

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76
Q

What is MS?

A

A chronic autoimmune, T-cell mediated inflammatory condition of the CNS characterised by multiple plaques of demyelination within the brain and spinal cord, occurring sporadically over years

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77
Q

Briefly describe the pathophysiology of MS

A
  • Autoimmune inflammation causes CD4 mediated destruction of oligodendrocytes
  • This causes demyelination of CNS neurones. The myelin sheath regenerates but is less efficient
  • Repeated demyelination leads to axonal loss and incomplete recovery between attacks
  • Poor demyelination healing results in relapsing and remitting symptoms
  • Multiple areas of sclerosis (scar tissue) form along neurones which slow/block conduction of signals thus impairing movement and/or sensation
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78
Q

What is MS characterised by?

A

Disseminated in space and time
Hypercellular plaque formation
BBB disruption

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79
Q

what are the different types of MS?

A
  1. Relapsing remitting (80%)
  2. secondary progressive MS
  3. primary progressive MS
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80
Q

what are the causes/risk factors of MS?

A 
Unknown
Environment and genetic components
- exposure to EBV in childhood
- low levels of sunlight and vitamin D
- female
- white
- living far from equator
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81
Q

Describe the epidemiology of MS

A

Presenting between 20-40 y/o
Females > Males
More common in white populations

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82
Q

what are the symptoms of MS?

A

TEAM

  • Tingling
  • Eye = optic neuritis
  • Ataxia
  • Motor - spastic paraparesis, pyramidal weakness (UL = extensors, LL = flexors)
  • swallowing disorders
  • bladder incontinence
  • dizziness, falls
  • constipation
  • fatigue
  • cognitive impairment, depression
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83
Q

what are the signs of MS?

A
  • Lhermitte sign - electric jolt felt down the spine when flexing neck
  • Uhthoff phenomenon - symptoms worse with heat, e.g. hot bath/exercise
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84
Q

What can exacerbate the symptoms of MS?

A

Heat (e.g. a warm shower)

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85
Q

Name 3 differential diagnosis’s of MS

A
  1. SLE
  2. Sjogren’s
  3. AIDS
  4. Syphilis
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86
Q

What investigations might you do in someone to see if they have MS?

A

● Symptoms must be disseminated in time and space

MRI = gold standard
- GD-enhancing plaques

● Lumbar puncture = oligoclonal IgG bands

● Bloods = rule out other causes

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87
Q

What is the diagnostic criteria for MS?

A

> 2 CNS lesions disseminated in time and space (>2 attack affected different parts of the CNS)

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88
Q

Describe the non-pharmacological treatment for MS

A

must notify DVLA

Regular exercise, smoking and alcohol cessation, low stress lifestyle
Psychological therapies
Speech therapists
Physio and OR

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89
Q

Describe the pharmacological treatment for MS

A

acute relapse
- steroids = IV METHYLPREDNISOLONE

chronic/frequent relapse

  • biological - SC BETA INTERFERON (contraindicated in pregnancy)
  • DMARDs - IV alentuzumab, IV natalizumab
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90
Q

What symptomatic treatments can you give to those with MS?

A

Spasticity

  • BACLOFEN (GABA analogue, reduces Ca2+ influx)
  • TIZANIDINE (alpha-2 agonist)
  • BOTOX INJECTION (reduces ACh in neuromuscular junction)

urinary incontinence = catheterisation

incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs

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91
Q

What medication might you give to someone to reduce the relapse severity of MS?

A

Short course steroids - methylprednisolone

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92
Q

Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

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93
Q

Define epileptic seizure

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excess, hypersynchronous neuronal discharge in the brain

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94
Q

Give 5 causes of epilepsy

A
  1. Idiopathic (2/3)
  2. cortical scarring
  3. tumour
  4. stroke
  5. alzheimers dementia
  6. alcohol withdrawal
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95
Q

What 2 categories can epileptic seizures be broadly divided into?

A
  1. Focal epilepsy - only one portion of the brain is involved
  2. Generalised epilepsy - whole brain is affected
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96
Q

Give 2 examples of focal epileptic seizures

A
  1. Simple partial seizures

2. Complex partial seizures

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97
Q

Give 3 examples of generalised epileptic seizures

A
  1. Absence seizures
  2. Tonic-clonic seizure (grand mal)
  3. Myoclonic seizure (isolated jerking)
  4. Atonic seizure (floppy)
  5. tonic seizure (high tone)
  6. clonic seizure (jerking)
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98
Q

what are the different components of an epileptic seizure?

A
  • prodrome
  • aura
  • post-ictal
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99
Q

What is aura?

A
  • Part of the seizure where the patient is aware & often precedes other manifestations
  • Eg. strange feelings in gut, déjà vu, strange smells, flashing lights
  • Often implies a partial seizure
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100
Q

If a patient experienced epilepsy with aura, what other symptoms would they get?

A

Strange feeling in gut
Deja vu
Strange smells
Flashing lights

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101
Q

Name 3 post-ictal symptoms

A
  1. Headache
  2. Confusion
  3. Myalgia
  4. Temporary weakness (focal seizure)
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102
Q

What is the diagnostic criteria for epilepsy?

A

At least 2 or more unprovoked seizures occurring >24 hours apart

One unprovoked seizure + probability of future seizures

Epileptic syndrome diagnosis

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103
Q

What is the treatment for focal epileptic seizures?

A 
Lamotrigine = 1st line
Carbamazepine = 2nd line
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104
Q

How do lamotrigine and Carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

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105
Q

What is the treatment for generalised epileptic seizures?

A

Sodium valproate = 1st line

Lamotrigine = 2nd line

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106
Q

How does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

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107
Q

What medication can control seizures?

A

Diazepam or lorazepam

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108
Q

What possible surgery could you do to treat epilepsy?

A

Vagal nerve stimulation

Resection of affected area

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109
Q

Give 4 potential side effects of anti-epileptic drugs (AED’s)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
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110
Q

Give 4 differential diagnosis’s of epilepsy

A
  1. Syncope
  2. Non-epileptic seizure
  3. Migraine
  4. Hyperventilation
  5. TIA
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111
Q

Define syncope

A

Insufficient blood or oxygen supply to the brains causes paroxysmal changes in behaviour, sensation and cognitive processes
Caused by sitting/standing
5-30 seconds duration

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112
Q

Define non-epileptic seizure

A

Mental processes associated with psychological distress causes paroxysmal changes in behaviour, sensation and cognitive processes
1-20 minute duration
Closed eyes and mouth

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113
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient had their eyes closed, was speaking and there was waxing/waning/pelvic thrusting. They say the seizure lasted for about 5 minutes. Is this likely to be an epileptic or a non-epileptic seizure?

A

A non-epileptic seizure

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114
Q

A patient complains of having a seizure. An eye-witness account tells you that the patient was moving their head and biting their tongue. They say the seizure lasted for just under a minute. Is this likely to be an epileptic or a non-epileptic seizure?

A

An epileptic seizure

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115
Q

A patient complains of having a ‘black out’. They tell you that before the ‘black out’ they felt nauseous and were sweating. They tell you that their friends all said they looked very pale. Is this likely to be due to a problem with blood circulation or a disturbance of brain function?

A

This is likely to be due to a blood circulation problem e.g. syncope

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116
Q

Name 3 intra-cranial haemorrhages

A
  1. Sub-arachnoid haemorrhage
  2. Sub-dural haemorrhage
  3. Extra-dural haemorrhage
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117
Q

What can cause a subarachnoid haemorrhage?

A
  • Traumatic injury
  • Berry aneurysm rupture
    (70-80%) - at common points round Circle of Willis
  • Arteriovenous malformations (15%) - abnormal tangle of blood vessels connecting arteries and veins
  • Idiopathic (15-20%)
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118
Q

Give 3 risk factors for a subarachnoid haemorrhage

A

Hypertension
Known aneurysm
Previous aneurysmal SAH

Smoking
Alcohol
Family history
Bleeding disorders

  • associated with berry aneurysms:
    • Polycystic Kidney Disease
    • Coarctation of aorta
    • Ehlers-Danlos syndrome & Marfan syndrome
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119
Q

Briefly describe the pathophysiology of a subarachnoid haemorrhage

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
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120
Q

what are the symptoms of a subarachnoid haemorrhage?

A
  1. sudden onset excruciating headache - thunderclap, worst headache, typically occipital
  2. sentinel headache - before main rupture, sign of warning leak
  3. nausea
  4. vomiting
  5. collapse
  6. loss of/depressed consciousness
  7. seizures
  8. vision changes
  9. coma - can last for days
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121
Q

what are the signs of a subarachnoid haemorrhage?

A

signs of meningeal irritation

  1. Kernig’s sign (can’t straighten leg past 135 degrees)
  2. neck stiffness
  3. Brudzinski’s sign (Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed)
  • retinal, subhyaloid and vitreous bleeds
    • worse prognosis
    • with/without papilloedema
  • neurological signs - e.g. 3rd nerve palsy
  • increased BP
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122
Q

What investigations might you do to see if someone has a subarachnoid haemorrhage?

A
  1. urgent Head CT = star pattern (diagnostic)
  2. Lumbar Puncture = xanthochromia -> RBC breakdown (only if normal ICP and after 12 hrs)
  3. MR/CT angiography - to establish source of bleeding
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123
Q

Describe the treatment for a subarachnoid haemorrhage

A
  • NIMOPIDINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
  • surgery = endovascular coiling
  • IV fluids - maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
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124
Q

Give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
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125
Q

What can cause a subdural haematoma?

A

Head injury –> vein rupture

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126
Q

Describe the pathophysiology of a subdural haematoma

A
  1. bleeding from bridging veins into the subdural space forms a haematoma
  2. then bleeding stops
  3. weeks/months later the haematoma starts to autolyse - massive increase in oncotic and osmotic pressure. Water is sucked in and haematoma enlarges
  4. gradual rise in ICP over weeks
  5. midline structures shift away from side of clot - causes tentorial herniation and coning
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127
Q

What causes water to be sucked up into a subdural haematoma 8-10 weeks after a head injury?

A

Clot starts to break down and there is massive increase in oncotic pressure –> water is sucked up by osmosis into the haematoma

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128
Q

Give 3 risk factors of a subdural haematoma?

A
  1. Elderly - brain atrophy, dementia
  2. Frequent falls - epileptics, alcoholics
  3. Anticoagulants
  4. babies - traumatic injury (“shaking baby syndrome”)
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129
Q

what are the signs and symptoms of a subdural haematoma?

A

SYMPTOMS:

  1. Fluctuating GCS
  2. Headache
  3. Confusion - may fluctuate
  4. Drowsiness
  5. physical and intellectual slowing
  6. personality change
  7. unsteadiness

SIGNS

  1. raised ICP - seizures
  2. localising neurological signs (unequal pupils, hemiparesis)
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130
Q

Name 3 differential diagnosis’s of a subdural haematoma

A
  1. Stroke
  2. Dementia
  3. CNS masses (tumour vs abscess)
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131
Q

What are the investigations for a subdural haematoma?

A
  • CT SCAN:
    • crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time)
      • unilateral
      • shows midline shift
  • MRI SCAN
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132
Q

What is the treatment for a subdural haematoma?

A

SURGERY

  • 1* = irrigation via burr-hole craniostomy
  • 2* = craniotomy

IV MANNITOL - to reduce ICP

address cause of trauma

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133
Q

What can cause an extradural haematoma?

A

Traumatic head injury resulting in a skull fracture (often temporal bone) –> middle meningeal artery rupture –> bleed

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134
Q

what is the pathophysiology of extradural haematoma?

A

Blood accumulates rapidly in the space between the dura and the skull (over minutes to hours)

After a lucid interval there is:

  • rapid rise in ICP
  • pressure on the brain
  • midline shift
  • tentorial herniation
  • coning
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135
Q

what is the clinical presentation of an extradural haematoma?

A
  • initial injury followed by lucid period
  • period of rapid deterioration
  • rapid decline in GCS
  • increasing severe headache
  • vomiting
  • seizures
  • hemiparesis
  • coma
  • UMN signs
  • ipsilateral pupil dilation
  • bilateral limb weakness
  • deep and irregular breathing - due to coning
  • late signs = bradycardia and raised BP
  • death from respiratory arrest
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136
Q

What investigations might you do to see if someone has an extradural haematoma? What are the results

A

CT SCAN

  • lens shaped haematoma = LEMON SHAPE
    • doesn’t cross suture lines
    • shows midline shift

SKULL X-RAY
- fracture lines may be seen

LP is CONTRAINDICATED

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137
Q

What do the ventricles do to prolong survival in someone with an extradural haematoma?

A

Get rid of CSF to prevent rise in ICP

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138
Q

What is the treatment for an extradural haematoma?

A

STABILISE PATIENT

URGENT SURGERY

  • clot evacuation
  • ligation of bleeding vessel

IV MANNITOL
- to reduce ICP

airway care
- intubation and ventilation

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139
Q

Give 3 differences in the presentation of a patient with a subdural haematoma in comparison to an extradural haematoma

A
  1. Time frame: extra-dural symptoms are more acute
  2. GCS: sub-dural GCS will fluctuate whereas GCS will drop suddenly in someone with an extra-dural haematoma
  3. CT: extra-dural haematoma will have a lens appearance whereas subdural will have a crescent shaped haematoma
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140
Q

Define weakness

A

Impaired ability to move a body part in response to will

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141
Q

Define paralysis

A

Ability to move a body part in response to will is completely lost

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142
Q

Define ataxia

A

Willed movements are clumsy, ill-direction or uncontrolled

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143
Q

Define involuntary movements

A

Spontaneous movement independent of will

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144
Q

Define apraxia

A

Disorder of conscious organised pattern of movement or impaired ability to recall acquired motor skills

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145
Q

Give 3 things that modulate LMN action potential transmission to effectors

A
  1. Cerebellum
  2. Basal ganglia
  3. Sensory feedback
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146
Q

Give 3 disease that are associated with motor neurone damage

A
  1. Motor neurone disease
  2. Spinal atrophy
  3. Poliomyelitis
  4. Spinal cord compression
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147
Q

Give 3 pathologies that are associated with ventral spinal root damage

A
  1. Prolapsed intervertebral disc
  2. Tumours
  3. Cervical or lumbar spondylosis
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148
Q

Name a disease associated with NMJ damage

A

Myasthenia Gravis

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149
Q

Describe the pyramidal pattern of weakness in the upper limbs

A

Flexors are stronger than extensors

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150
Q

Describe the pyramidal pattern of weakness in the lower limbs

A

Extensors are stronger than flexors

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151
Q

What is a UMN?

A

A neurone that is located entirely in the CNS

Its cell body is located in the primary motor cortex

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152
Q

Give 3 causes of UMN weakness

A
  1. MS
  2. Brain tumour
  3. Stroke
  4. MND
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153
Q

Give 4 sites of UMN damage

A
  1. Motor cortex lesions
  2. Internal capsule
  3. Brainstem
  4. Spinal cord
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154
Q

Give 4 signs of UMN weakness

A
  1. Spasticity
  2. Increased muscle tone (hypertonia)
  3. Hyper-reflexia
  4. Positive babinski’s reflex
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155
Q

Give 4 signs of LMN weakness

A
  1. Flaccid
  2. Hypotonia
  3. Hypo-reflexia
  4. Muscle atrophy
  5. Fasciculation’s
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156
Q

Define motor neurone disease (MND)

A

A group of neuro degenerative disorders that selectively affect the motor neurons

Most in the anterior horn, cells of the spinal cord and the motor cranial nuclei

There are no sensory problems

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157
Q

Does MND affect UMN or LMN?

A

Both UMN and LMN can be affected

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158
Q

Does MND affect eye movements?

A

Never affects eye movements (clinical feature of myasthenia gravis)

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159
Q

Does MND cause sensory loss or sphincter disturbance?

A

No (clinical feature of MS)

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160
Q

What is the epidemiology of MND?

A
  • relatively uncommon
  • males > females (3:2)
  • often fatal in 2-4 years
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161
Q

What is the clinical presentation of MND?

A
  • results in mixed UMN and LMN presentation (LMN symptoms predominate)
  • wrist drop/foot drop
  • change in appearance of hands - wasting
  • gait disorders/tendencies to trip
  • excessive fatigue
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162
Q

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

A 
Head/spine MRI
Blood tests = muscle enzymes, autoantibodies 
Nerve conduction studies 
EMG
Lumbar Puncture
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163
Q

What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

  1. Presences of LMN and UMN degeneration and progressive history
  2. Absence of other disease processes
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164
Q

What is the treatment for MND?

A
  • MDT care
  • anti-glutaminergic drugs - ORAL RILUZOLE - Na+ channel blocker, inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
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165
Q

Give 3 limb onset symptoms of MND

A
  1. Weakness
  2. Clumsiness
  3. Wasting of muscles
  4. Foot drop
  5. Tripping
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166
Q

Give 3 respiratory onset symptoms of MND

A
  1. Dyspnoea
  2. Orthopnoea
  3. Poor sleep
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167
Q

Would you do a LP in a patient that has a raised ICP?

A

NO

LP is contraindicated if they have a raised ICP due to the risk of coning

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168
Q

Give 4 signs of raised ICP

A
  1. Papilloedema
  2. Focal neurological signs
  3. Loss of consciousness
  4. New onset seizures
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169
Q

What is the treatment for raised ICP?

A

Osmotic diuresis with mannitol

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170
Q

Explain the ICP/volume curve

A

Volume increase –> ICP plateau (compensate) –> rapid ICP increase

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171
Q

What are the 4 cardinal presenting symptoms of brain tumours?

A
  1. Raised ICP –> headache, decrease GCS, n+v, papilloedema
  2. Progressive neurological deficit –> deficit of all major functions (motor, sensory, auditory, visual) + personality change
  3. Epilepsy
  4. lethargy/tiredness - caused by pressure on brainstem
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172
Q

You ask a patient with a brain tumour about any facts that aggravate their headache, what might they say?

A
  1. Worse first thing in the morning

2. Worse when coughing, straining or bending forward

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173
Q

Name 2 differential diagnosis’s for a brain tumour

A
  1. Aneurysm
  2. Abscess
  3. Cyst
  4. Haemorrhage
  5. Idiopathic intracranial hypertension
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174
Q

What investigations might you do in someone you suspect to have a brain tumour?

A

CT/MRI head and neck
Biopsy - via burr hole
blood tests - FBC, U&E, LFTs, B12
LP = CONTRAINDICATED (high ICP)

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175
Q

Where might secondary brain tumours arise from?

A
  1. non-small cell lung cancer
  2. small cell lung cancer
  3. breast
  4. melanoma
  5. renal cell carcinoma
  6. GI
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176
Q

Describe the treatment for secondary brain tumours

A
  1. surgery - if age <75yrs
  2. radiotherapy
  3. chemotherapy
  4. palliative therapy
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177
Q

From what cells to primary brain tumours originate?

A

Glial cells (gliomas)
- Astrocytoma (85-90%)
- Oligodendroglioma
Other primary = meningioma, schwannoma, medulloblastoma

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178
Q

Describe the WHO glioma grading

A

Grade 1 = benign paediatric tumour
Grade 2 = Pre-malignant tumour (benign)
Grade 3 = ‘Anaplastic astrocytoma’ (cancer)
Grade 4 = Glioblastoma multiforme (GBM) - malignant

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179
Q

Describe the epidemiology of grade 2 gliomas

A

Disease of young adults

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180
Q

Give 3 causes of grade 2 glioma deterioration

A
  1. Tumour transformation to a malignant phenotype
  2. Progressive mass effect due to slow tumour growth
  3. Progressive neurological deficit form functional brain destruction by tumour
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181
Q

Describe the common pathway to a GBM (grade 4 brain tumour)

A

Initial genetic error of glucose glycolysis –> Isocitrate Dehydrogenase 1 mutation –> excessive build up of 2-hydroxyglutarate –> genetic instability of glial cells –> grade II-IV glioma transform into glioblastoma

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182
Q

Give 5 good prognostic factors for GBM

A
  1. <45 y/o
  2. Aggressive surgical therapy
  3. Good performance post-surgery
  4. Tumour that has transformed from previous lower grade tumour
  5. MGMT mutant - will respond will to chemo
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183
Q

Describe the treatment for GBM

A
  1. Resective surgery
  2. Adjuvant chemotherapy with Temozolomide
  3. Dexamethasone - reduces tumour inflammation/oedema
  4. anticonvulsants - oral carbimazepine
  5. palliative care
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184
Q

How does Temozolomide work in treatment for GBM?

A

Methylates guanine in DNA making replication impossible

MGMT gene reverses it = tumour resistance

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185
Q

Define dementia

A

A set of symptoms that may include memory loss and difficulties with thinking, problem solving or language
There is a progressive decline in cognitive function

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186
Q

Describe the epidemiology of dementia

A

Rare <55
10% of people >65
20% of people >80

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187
Q

Give 3 causes of dementia

A
  1. Alzheimer’s disease (50%)
  2. Vascular dementia (25%)
  3. Lewy body dementia (15%)
  4. Fronto-temporal (Pick’s)
  5. Huntington’s
  6. Liver failure
  7. Vitamin deficiency - B12 or folate
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188
Q

Give 3 risk factors of dementia

A
  1. Family history
  2. Age
  3. Down’s syndrome
  4. Alcohol use, obesity, HTN, hyperlipidaemia, DM
  5. Depression
  6. ? Head injury
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189
Q

Describe the pathophysiology of Alzheimer’s disease

A

Degeneration of temporal lobe and cerebral cortex, with cortical atrophy

Accumulation of beta-amyloid peptide –> progressive neuronal damage, neurofibrillary tangles, increase in number of amyloid places and loss of ACh

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190
Q

what is the clinical presentation of Alzheimer’s Disease

A 
● Memory - episodic and semantic
● Language - difficulty understanding or
finding words
● Attention and concentration issues
● Psychiatric changes, e.g. withdrawal,
delusions
● Disorientation, e.g. time and surroundings
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191
Q

Give 2 histological signs of Alzheimer’s dementia

A
  1. Plagues of amyloid

2. Neurofibrillary tangles

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192
Q

25% of all patients with Alzheimer’s Disease will develop what?

A

Parkinsons

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193
Q

What does vascular dementia often present with?

A

● Characterised by stepwise progression - Periods of stable symptoms, followed by a sudden increase in severity
● Presentation varies massively but can include:
- Visual disturbances,
- UMN signs (e.g. muscle weakness, overactive reflexes, clonus),
- attention deficit,
- depression,
- incontinence,
- emotional disturbances
○ If infarct was subcortical, then expect to see dysarthria and parkinsonisms

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194
Q

Describe the pathophysiology of Lewy body dementia

A

● Characterised by eosinophilic intracytoplasmic neuronal inclusion bodies (Lewy bodies) in the brainstem and neocortex
● Also see substantia nigra depigmentation and amyloid deposits

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195
Q

what are the clinical features of Lewy body dementia

A

● Dementia is often presented initially
○ Memory loss, spatial awareness difficulties,
loss of cognitive function
● Parkinsonisms, e.g. tremor, rigidity, change in gait
● Visual hallucinations
● Sleep disorders, restless leg syndrome

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196
Q

Frontal lobe atrophy is seen on an MRI, what kind of dementia is this patient likely to have?

A

Fronto-temporal

= frontal and temporal lobe atrophy

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197
Q

Give 3 symptoms of Fronto-temporal dementia

A

● Onset tends to be insidious and progressive
● Present with 3 main symptoms:
○ Behavioural issues, e.g. loss of inhibition/empathy, compulsive behaviours, difficulty planning
○ Progressive aphasia, e.g. slow, difficult speech, grammatical errors
○ Semantic dementia, e.g. loss of vocabulary, problems understanding

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198
Q

What is functional memory dysfunction?

A

Acquired dysfunction of memory that significantly affects a person’s professional/private life in absence of an organic cause

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199
Q

How could you determine whether someone has functional memory dysfunction or a degenerative disease?

A

When asked the question ‘when was the last time your memory let you down?’, someone with functional memory dysfunction would give a good detailed answer whereas someone with degenerative disease would struggle to answer

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200
Q

What investigations can you do in primary care to determine whether someone might have dementia?

A
  1. Good history of symptoms
  2. 6 item cognitive impairment test (6CIT)
  3. Blood tests - FBC, liver biochemistry, TFTs, vitamin B12 and folate
  4. Mini mental state examination = screening
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201
Q

What questions are asked in 6CIT?

A
  1. What year is it?
  2. What month is it?
  3. Give an address with 5 parts
  4. Count backwards from 20
  5. Say the months of the year in reverse
  6. Repeat the address
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202
Q

What secondary care investigation can you do to investigate a dementia diagnosis?

A

Brain MRI - where and extent of atrophy
Brain function tests = PET, SPECT and functional MRI
Brain CT
Myeloid and tau histopathology

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203
Q

Name the staging system that classifies the degree of pathology in AD

A

Braak staging
Stage 5/6 = high likelihood of AD
Stage 3/4 = intermediate likelihood
Stage 1/2 = low likelihood

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204
Q

Give 3 ways in which dementia can be prevented

A
  1. Smoking cessation
  2. Healthy diet
  3. Regular exercise
  4. Low alcohol
  5. Engaging in leisure activités
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205
Q

What support should be offered to patients with dementia?

A

Social suport
Cognitive support
Specialist memory service

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206
Q

What medications might you use in someone with dementia?

A 
Acetylcholinesterase inhibitors - increase ACh = donepezil, rivastigmine
Control BP (ACEi) to reduce further vascular damage
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207
Q

What is myasthenia gravis?

A

Autoimmune disease against nicotinic acetylcholine receptors in the neuromuscular junction

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208
Q

what is the pathophysiology behind myasthenia gravis?

A

Autoantibodies (IgG) attach to ACh receptor and destroy them –> fewer action potentials fire –> muscle weakness and fatigue

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209
Q

what are the causes/risk factors for myasthenia gravis?

A

If <50 = associated with other AI conditions (pernicious anaemia, SLE, RA) and more common in women
If >50 = associated with thymic atrophy, thymic tumour, SLE and RA and more common in men

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210
Q

what are the clinical features of myasthenia gravis?

A
  1. Muscle weakness
  2. Increasing muscular fatigue
  3. Ptosis
  4. Diplopia
  5. Myasthenic snarl
  6. Tendon reflexes normal but fatigable
● Weakness is more marked in proximal muscles
● Weakness might be seen in:
    ○ Small muscle of the hands
    ○ Deltoid and triceps muscles
    ○ Bulbar muscles
    ○ Muscles involved in chewing
● No muscle wasting, sensation is unimpaired
● Seizures can occur
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211
Q

What muscle groups are affected in myasthenia gravis?

A

muscle groups affected in order:

  • extra-ocular
  • bulbar - chewing and swallowing
  • face
  • neck
  • trunk
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212
Q

What can weakness due to myasthenia gravis be worsened by?

A 
Pregnancy
Hypokalaemia
Infection 
Emotion
Exercise 
Drugs (opiates, BB, gentamicin, tetracycline)
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213
Q

What investigations might you do to see if someone has myasthenia gravis?

A
  • mostly clinical examination
  • positive tensilon test
  • anti-AChR antibodies
  • TFTs
  • EMG
  • CT of thymus
  • crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis
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214
Q

Give 3 possible differential diagnosis’s for myasthenia gravis

A
  1. MS
  2. Hyperthyroidism
  3. Acute Guillain-Barre syndrome
  4. Lamert-Eaton myasthenia syndrome
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215
Q

What is treatment for myasthenia gravis?

A

Anti-cholinesterase = pyridostigmine
Immunosuppression = prednisolone (with alendronate - bisphosphonate)
Steroids can be combined with azathioprine or methotrexate
Thymectomy

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216
Q

When is a thymectomy considered as a treatment for myasthenia gravis?

A

Onset <50 y/o and it is poorly controlled

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217
Q

Give a complication of myasthenia gravis

A

Myasthenic crisis
Weakness of respiratory muscle during relapse
Treatment = plasmapheresis and IV immunoglobulin

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218
Q

Define Parkinson’s disease

A

Degenerative movement disorder caused by a reduction in dopamine in the pars compacta of the substantia nigra

219
Q

what is the pathway of dopamine production?

A

Tyrosine –> L-dopa –> Dopamine

220
Q

Describe the pathophysiology of Parkinson’s disease

A

destruction of dopaminergic neurones (in substantia nigra) –> reduced dopamine supply –> thalamus inhibits –> decrease in movement + symptoms
Lewy body formation in basal ganglia

221
Q

What is the 3 cardinal symptoms for Parkinsonism?

A

resting tremor
rigidity
bradykinesia
postural instability

222
Q

what are the clinical features of Parkinson’s disease

A

● Often an insidious onset

  • impaired dexterity,
  • fixed facial expressions,
  • foot drag

● Common associated symptoms:

  • dementia,
  • depression,
  • urinary frequency,
  • constipation,
  • sleep disturbances
223
Q

Would you describe the symptoms of Parkinson’s disease as symmetrical or asymmetrical?

A

Asymmetrical = One side is always worse than the other

224
Q

You ask a patient who you suspect to have Parkinson’s disease to walk up and down the corridor to assess their gait, what features would be suggestive of PD?

A

Stooped posture
Asymmetrical arm swing
Small steps
Shuffling

225
Q

Give 2 histopathological signs of Parkinson’s disease

A
  1. Loss of dopaminergic neurones in the substantia nigra

2. Lewy bodies

226
Q

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

A

DaTscan

Functional neuroimaging - PET

Can confirm by reaction to levodopa

227
Q

Describe the pharmacological treatment for Parkinson’s disease

A

young onset + fit

  • Dopamine agonist (ropinirole)
  • MAO-B inhibitor (rasagiline)
  • L-DOPA (co-careldopa)

frail + co-morbidities

  • L-DOPA (co-careldopa)
  • MAO-B inhibitor (rasagiline)
228
Q

How does L-dopa work in the treatment of PD?

A

Precursor to dopamine and can cross the BBB (unlike dopamine)
- once in the brain it can be converted to dopamine

229
Q

How do dopamine agonists work in the treatment of PD and give an example of one?

A

Reduced risk of dyskinesia
First line in patient <60
Ropinirole, pramipexole

230
Q

How do MAO-B inhibitors work in the treatment of PD and give an example of one?

A

Inhibit MAO-B enzymes which breakdown dopamine -> increases amount of dopamine available
Rasagiline, selegiline

231
Q

How do COMT inhibitors work in the treatment of PD and give an example of one?

A

Inhibit COMT enzymes which breakdown dopamine

Entacapone, tolcapone

232
Q

What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

233
Q

Define Huntington’s disease

A

Neurodegenerative disorder characterised by the lack of inhibitory neurotransmitter GABA - too much dopamine
autosomal dominant - 100% penetrance

234
Q

Define chorea

A

Continuous flow of jerky, semi-purposeful movements, flitting from one part of the body to another

235
Q

Describe the inheritance pattern seen in Huntington’s disease

A

Autosomal dominant inheritance

100% penetrance

236
Q

What triplet code is repeated in Huntington’s disease?

A

CAG triplet repeat on chromosome 4

>35 CAG = huntingtons

237
Q

Briefly describe the pathophysiology of Huntington’s disease

A

Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)

238
Q

Name the cardinal features of Huntington’s disease

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety

239
Q

Name 3 signs of Huntington’s disease

A
  1. Abnormal eye movements
  2. Dysarthria
  3. Dysphagia
  4. Rigidity
  5. Ataxia
240
Q

What investigations might you do in someone you suspect to have Huntington’s disease?

A

● MRI/CT - loss of striatal volume

● Genetic testing

241
Q

Describe the treatment of Huntington’s disease

A

poor prognosis - no treatment
● Benzodiazepines/valproic acid - chorea
● SSRIs = depression
● Haloperidol = psychosis

242
Q

What nerve is affected in carpal tunnel syndrome?

A

The median nerve (C6-T1)

243
Q

what are the causes/risk factors of carpal tunnel syndrome

A
  1. Pregnancy
  2. Obesity
  3. RA
  4. DM
  5. Hypothyroidism
  6. Acromegaly
244
Q

Describe the symptoms of carpal tunnel syndrome

A
  • Intermittent and gradual onset
  • Pins and needles, index and middle fingers
    tend to be affected first
  • Pain in thumb, index, middle and 1/2 ring fingers and palm, can reach
    to the shoulder
  • Numbness in same areas
  • Weakness of same fingers, and loss of grip
  • Worse at night, relieved by shaking
245
Q

What investigations might you do in someone who you suspect to have carpal tunnel syndrome?

A

clinical diagnoses based on symptom presentation

EMG = slowing conduction velocity in median sensory nerves
Phalen’s test = 1 min maximal wrist flexion –> symptoms
Tinel’s test = tapping over nerve at wrist –> tingling

USS or MRI if other damage is suspected

246
Q

What is the treatment for carpal tunnel syndrome?

A
  • 1 in 4 cases will be self-limiting (usually 1 year)
  • Pregnancy cases will resolve postpartum
  • Rest the wrist, and try to avoid gripping/squeezing actions
  • Splinting at night
  • Local steroid injection
  • Decompression surgery
247
Q

What is autoimmune Guillain-Barre syndrome?

A

Acute inflammatory demyelinated ascending polyneuropathy affecting the PNS following an upper respiratory tract infection or GI infection

248
Q

What can cause Guillain-Barre syndrome?

A

Bacteria

  • Camplylobacter jejuni
  • Mycoplasma

Viruses

  • CMV
  • EBV
  • HIV
  • Herpes zoster
249
Q

Describe the pathophysiology of Guillain-Barre syndrome

A

Same antigens on infectious organisms as Schwann cells (PNS) –> autoantibody mediated nerve cell damage -> via molecular mimicry
Schwann cell damage consists of demyelination, which results in a reduction in peripheral nerve conduction –> causes acute polyneuropathy

spreads from proximal to distal

250
Q

what are the clinical features of Guillain-Barre syndrome

A 
Breathing problems
Back pain 
Sensory disturbance
Sweating
Urinary retention
  1. Ascending symmetrical muscle weakness 1-3 weeks post-infection (proximal muscles most affected - trunk, respiratory, CN) TOES TO NOSE WEAKNESS
  2. Pain in legs, back is rare
  3. sensory loss in lower extremities
  4. Reflexes lost early on (LMN sign)
  5. Autonomic features =
    • reduced sweating
    • reduced heat tolerance
    • paralytic ileus - intestinal obstruction w/o blockage
    • urinary hesitancy
251
Q

What investigations might you do in someone you suspect has Guillain-Barre syndrome?

A
  • Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
  • Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
  • bloods - FBC, U&E, LFT, TFT
  • Spirometry = respiratory involvement
  • ECG
252
Q

Describe the treatment for Guillain-Barre syndrome

A
  • If FVC <1.5L/80% = ventilate and ITU monitoring
  • IV immunoglobulin (IvIg) for 5 days = decrease duration and severity of paralysis
  • Plasma exchange
  • Low molecular weight heparin (LMWH) - SC ENOXAPARIN
  • Analgesia
253
Q

When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?

A

If a patient has IgA deficiency - can cause severe allergic reaction

254
Q

Define stroke

A

Rapid onset of neurological deficit due to a vascular lesion lasting >24 hours and associated with infarction of central nervous tissue

poor blood flow to the brain causes cell death

255
Q

How can strokes be classified?

A
  1. Ischaemic (85%) - blood clot in the blood vessel to the brain
  2. Haemorrhagic (15%) - bleed in small blood vessel in/around brain
256
Q

What are the causes of an ischaemic stroke?

A
  • small vessel occlusion by thrombus
  • atherothromboembolism (e.g. from carotid artery)
  • cardioembolism (post MI, valve disease, IE)
  • hyper viscosity
  • hypoperfusion
  • vasculitis
  • fat emboli from a long bone fracture
  • venous sinus thrombosis
257
Q

What are the causes of an haemorrhagic stroke

A

Bleeding from the brain vasculature

  1. Hypertension - stiff and brittle vessels, prone to rupture
  2. Secondary to ischaemic stroke - bleeding after reperfusion
  3. Head trauma
  4. Arteriovenous malformations
  5. Vasculitis
  6. Vascular tumours
  7. Carotid artery dissection
258
Q

what are the risk factors for ischaemic stroke?

A
  1. Age
  2. Male
  3. Hypertension
  4. Smoking
  5. Diabetes
  6. Recent/past TIA
  7. Heart disease - IHD, AF, valve disease
  8. Combined oral contraceptive
259
Q

Give 3 signs of an ACA stroke

A
  1. Leg weakness - contralateral
  2. Sensory disturbance in legs
  3. Gait apraxia
  4. Incontinence
  5. Drowsiness
  6. Akinetic mutism - decrease in spontaneous speech (in a stupor)
  7. truncal ataxia - can’t sit or stand unsupported
260
Q

Give 3 signs of a MCA stroke

A
  1. Contralateral arm and leg weakness and sensory loss
  2. Hemianopia
  3. Aphasia
  4. Dysphasia
  5. Facial droop
261
Q

Give 3 signs of a PCA stroke

A

visual issues

  1. Contralateral homonymous hemianopia
  2. Cortical blindness
  3. Visual agonisa
  4. Prosopagnoisa
  5. Dyslexia
  6. Unilateral headache
262
Q

What is visual agnosia?

A

An inability to recognise or interpret visual information

263
Q

What is prosopagnosia?

A

Inability to recognise a familiar face

264
Q

A patient presents with upper limb weakness and loss of sensory sensation to the upper limb. They also have aphasia and facial drop. Which artery is likely to have been occluded?

A

Middle cerebral artery

265
Q

A patient presents with lower limb weakness and loss of sensory sensation to the lower limb. They also have incontinence, drowsiness and gait apraxia. Which artery is likely to have been occluded?

A

Anterior cerebral artery

266
Q

A patient presents with a contralateral homonymous hemianopia. They are also unable to recognise familiar faces and complain of a headache on one side of their head. Which artery is likely to have been occluded?

A

Posterior cerebral artery

267
Q

Give 3 differential diagnosis’s for a stroke

A
  1. Hypoglycaemia
  2. Intracranial tumour
  3. Head injury +/- haemorrhage
268
Q

What investigation could you do to determine whether someone has had a haemorrhagic or ischaemic stroke?

A

Head CT scan (before treatment)

269
Q

What is the treatment for an ischaemic stroke?

A

Immediate management:

  • CT/MRI to exclude haemorrhagic stroke
  • aspirin 300mg

Antiplatelet therapy

  • aspirin 300mg for 2 weeks
  • clopidogrel daily long term

Anticoagulation (e.g. warfarin) for AF

thrombolysis

  • within 4.5 hrs of onset
  • IV alteplase
  • lots of contraindications (can cause massive bleeds)

mechanical thromboectomy
- endovascular removal of thrombus

270
Q

How does alteplase work?

A

Converts plasminogen –> plasmin

So promotes breakdown of fibrin clot

271
Q

When can you do thrombolysis in someone with an ischaemic stroke?

A

Up to 4.5. hours post onset of symptoms

272
Q

What is primary prevention of strokes?

A

Risk factor modifcaiton

  • Antihypertensives for HTN
  • Statins for hyperlipiaemia
  • Smoking cessation
  • Control DM
  • AF treatment = warfarin/NOAC’s
273
Q

What is secondary prevention of strokes?

A

2 weeks of aspirin –> long term clopidogrel

274
Q

What non-pharmacological treatment options are there for people after a stroke?

A
  1. Specialised stroke units
  2. Swallowing and feeding help
  3. Phsyio and OT
  4. Neurorehab - physio + speech therapy
275
Q

What is a TIA?

A

sudden onset, brief episode of neurological deficit due to temporary, focal cerebral ischaemia
symptoms are maximal at onset and lasts 5-15 mins (<24hrs)

276
Q

Give 3 causes of a TIA

A
  1. Artherothromboembolism of the carotid - main cause (can hear carotid bruit)
  2. Cardioembolism - in AF, after MI, valve disease/prosthetic valve
  3. Hyperviscosity - polycythaemia, sickle cell, high WBCC
  4. hypoperfusion - postural hypotension, decreased flow
277
Q

Describe the pathophysiology of a TIA

A

Cerebral ischaemia due to lack of O2 and nutrients –> cerebral dysfunction without infarction (no irreversible cell death)

symptoms are maximal at onset -> usually last 5-15 mine (<24hrs)

278
Q

what are the signs of a carotid TIA?

A
  1. Amaurosis fugax = retinal artery occlusion –> vision loss
  2. Aphasia
  3. Hemiparesis
  4. Hemisensory loss
  5. hemianopia
279
Q

what are the signs of a vertebrobasilar TIA?

A
  1. Diplopia, vertigo, vomiting
  2. Choking and dysarthria
  3. Ataxia
  4. Hemisensory loss
  5. Hemianopic/bilateral visual loss
  6. tetraparesis
  7. loss of consciousness
280
Q

what are the differential diagnosis’s for a TIA

A
  1. Migraine aura
  2. Epilepsy
  3. Hypoglycaemia
  4. Hyperventilation
  5. retinal bleed
  6. syncope - due to arrhythmia
281
Q

What investigations would you do in someone who you suspect to have a TIA?

A

first line = diffusion weighted MRI or CT

second line = carotid imaging (doppler ultrasound followed by angiography if stenosis is found)

Bloods

  • FBC - look for polycythaemia
  • ESR - raised in vasculitis
  • U&Es, glucose

ECG

echocardiogram

282
Q

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

A

Assess their risk of having stroke in the next 7 days = ABCD2 score

283
Q

What is the ABCD2 score?

A

Assesses risk of stoke in the next 7 days for those who have had a TIA

  • age
  • BP
  • clinical features - unilateral weakness, speech disturbance
  • duration of TIA
  • presence of diabetes mellitus
284
Q

What classifies as a high risk stroke patient?

A
  • have ABCD2 score >4
  • have AF
  • > 1 TIA in a week
285
Q

Within how long should someone with a suspected TIA been seen by a specialist?

A

Within 7 days

286
Q

What is the treatment for a TIA?

A

immediate treatment = aspirin 300mg and refer to specialist within 24hrs

control CV risk factors

  • BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN)
  • smoking cessation
  • statin - SIMVASTATIN
  • no driving for 1 month

antiplatelet therapy
- ASPIRIN 75mg daily (With Dipyridamole)
or
- CLOPIDOGREL daily

anticoagulation (e.g. WARFARIN) for patients with AF

carotid endarterectomy

  • if >70% carotid stenosis
  • reduces stroke/TIA risk by 75%
287
Q

Give 3 causes of spinal cord compression

A
  • trauma,
  • tumours - most common spinal metastases are
    breast, prostate and lung cancer
  • central disc protrusion,
  • prolapsed disc (L4-5 and L5-S1 most common),
  • epidural haematoma,
  • infection,
  • cervical spondylitic myelopathy
288
Q

Give 3 signs and symptoms of spinal cord compression

A 
Red flag signs:
- Loss of bladder or bowel function, 
- UMN signs in the lower limbs (e.g. clonus, hyperreflexia), 
- LMN signs in the upper
limbs (e.g. atrophy)

● Symptoms depend on the injury type and site

  • Can include paraplegia,
  • pain,
  • paraesthesia,
  • changes to tendon reflexes
289
Q

What investigations might you do in someone with suspected spinal cord compression?

A

Urgent MRI/CT scan

● X-ray whole spine
● MRI if indicated
● Renal function
● Haemoglobin - monitor blood loss

290
Q

What is the treatment for spinal cord compression?

A

● Acute spinal cord compression is a neurosurgical emergency
● Dexamethasone until treatment plan confirmed
● Catheterisation
● Analgesia
● Surgical decompression if indicated
● Chemotherapy if indicated

291
Q

Briefly describe the pathophysiology of cauda equina syndrome

A

Spinal compression at or caudal to L1 –> disrupts sensation and movement - flaccid and areflexic weakness

292
Q

Give 3 causes of cauda equina syndrome

A
  1. Lumbar disc herniation at L4/5 or L5/S1
  2. Tumour
  3. Trauma
  4. Infection
  5. late-stage ankylosing spondylitis
  6. post-operative haematoma
  7. sarcoidosis
293
Q

what are the clinical features of cauda equina syndrome

A 
● Sudden onset - hours
● Saddle paraesthesia
● bilateral sciatica
● Bladder/bowel dysfunction
● erectile dysfunction
● Motor problems
● Lower back pain
● Bilateral LMN weakness, absent ankle reflex (flaccid and areflexic)
294
Q

What investigations might you do to see if someone has cauda equina syndrome?

A

● Medical emergency
- immediate referral
● Rectal exam - loss of anal tone/sensation
● MRI spine
● knee flexion (L5-S1) and ankle plantar flexion (S1-S2)

295
Q

How do you treat cauda equina syndrome?

A 
● Surgical decompression is essential
● Immobilise spine
● Anti-inflammatory agents
● Antibiotics if infection present
● Chemotherapy if indicated
  • Microdiscectomy - removal of part of the disc - may tear dura!
  • Epidural steroid injection - more effective for leg pain
  • Surgical spine fixation - if vertebra slipped
  • Spinal fusion - reduces pain from motion and nerve root inflammation
296
Q

What is treatment for sciatica without neurological signs?

A

Conservative management - physio and NSAIDs

297
Q

Define spondyloisthesis

A

Slippage of vertebra over the one below

298
Q

Define spondylosis

A

Degenerative disc disease

299
Q

What are the 4 stages of a seizure?

A
  1. Prodromal - often emotional signs
  2. Aura
  3. Ictal
  4. Post-ictal - often drowsy and confused
300
Q

Give 3 activities that can trigger trigeminal neuralgia

A
  1. Washing your face
  2. Eating
  3. Shaving
  4. Talking
301
Q

How long do you wait for before doing a lumbar puncture in someone with a suspected subarachnoid haemorrhage?

A

At least 12 hours
You need to wait or the Hb to break down and then CSF will become yellow - sign that there is a bleeding in subarachnoid space (xanthochromia)

302
Q

what are the investigations for alzheimer’s disease?

A

● MMSE
● Bloods - TFTs, B12 (check for other causes)
● Memory clinic assessment
● MRI

303
Q

what is the treatment for alzheimer’s disease?

A

No cure
● Supportive therapy, e.g. carers, changes to the home, help with daily activities
● Medication to manage symptoms
○ Acetylcholinesterase (AChE) inhibitors, e.g. rivastigmine, galantamine, memantine

304
Q

what is the epidemiology of Alzheimer’s disease?

A

Most common type of dementia

● Mainly affects those over 65

305
Q

what are the risk factors for Alzheimer’s disease?

A
  • Down’s syndrome,
  • ApoE E4 allele homozygosity,
  • reduced cognitive activity,
  • depression/loneliness
306
Q

what is the epidemiology of frontotemporal dementia?

A

● Progressive dementia

● More common dementia in those under 65, but still only 5% of dementias

307
Q

what is the pathophysiology of frontotemporal dementia?

A

● Atrophy of the frontal and temporal lobes
● Loss of neurons, but no plaque formation
● Tau +ve or TDP-43 +ve inclusions

308
Q

what are the risk factors for frontotemporal dementia?

A

50% dominant inheritance

309
Q

what are the investigations for frontotemporal dementia?

A

Bloods - B12, TFTs, U&Es (?other causes)
● FBC and LFTs for suspected encephalopathy
● MMSE
● MRI - frontal/temporal atrophy

310
Q

what is the treatment for frontotemporal dementia?

A

● No cure
● Supportive therapy, e.g. carers, help setting up a stable routine, home changes for motor difficulties, speech and language therapy
● SSRIs - help with behaviour symptoms
● Levodopa/carbidopa if Parkinson’s symptoms present
● Stopping exacerbating drugs

311
Q

what is the epidemiology of vascular dementia?

A

● Second most common dementia, globally
○ 17% of dementia in the UK
● Result of multiple, small infarcts

312
Q

what are the risk factors for vascular dementia?

A 
smoking, 
history of TIAs, 
AF,
hypertension, 
DMT1, 
hyperlipidaemia, 
obesity,
coronary heart disease
313
Q

what is the pathophysiology of vascular dementia?

A

is based on the location and size of the original infarct, and number and location of consequent infarcts
● A single stroke double the risk of developing vascular dementia

314
Q

what are the investigations for vascular dementia?

A

● Full history important - previous stroke/TIA?
● Cognitive impairment screen
○ Orientation, attention, language function,
visuospatial functions, motor control
● Medication review - ?other cause
● MRI - looking for previous infarcts

315
Q

what is the treatment for vascular dementia?

A

● Supportive therapy, e.g. carers, home changes,
routine help, cognitive simulation programmes
● No pharmacological treatment for the dementia
itself
● SSRIs or anti-psychotics to control symptoms,
e.g. lorazepam
● Prognosis is 3-5 years from diagnosis

316
Q

what are the investigations for Lewy Body dementia?

A

● MMSE or 6-item cognitive impairment test (6-CIT)
● Bloods - B12, TFTs, U&E, MRI (?other cause)
● MSU to check for urine infection

317
Q

what is the diagnostic criteria for Lewy Body dementia?

A

○ Presence of dementia with 2 of:

- fluctuating attention and concentration, 
- recurrent well-formed visual hallucinations, 
- spontaneous Parkinsonism

○ If there is only 1 of the 3 core features, diagnosis can also be made with a SPECT or PET scan showing low dopamine transporter uptake in basal ganglia

318
Q

what is the treatment for Lewy Body dementia?

A

● Refer to a specialist
● Supportive therapy - cognitive stimulation, exercise programmes, at-home care
● Cholinesterase inhibitors, e.g. rivastigmine suggested to treat cognitive decline
● Avoid use of neuroleptic drugs, e.g. haloperidol, as they can produce severe
sensitivity reactions

319
Q

what is the epidemiology of Parkinson’s disease?

A

Second most common neurodegenerative disorder (after Alzheimer’s)

Typically develops between 55-65 years of age

320
Q

what are the other causes of Parkinson’s disease?

A
  • Drug induced Parkinsonism - caused by dopamine
    antagonists, e.g. clozepine
  • encephalitis
  • exposure to certain toxins, e.g. manganese dust
321
Q

what is the 3 step diagnostic pathway for diagnosing Parkinson’s disease?

A

1) Diagnosis of Parkinsonian syndrome
○ Bradykinesia (required) plus one of rigidity, resting tremor, or postural instability

2) Exclusion criteria (none to be met)
○ History of stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, babinski’s sign, early severe dementia, negative response to large L-dopa dose

3) Supportive criteria (3 or more required)
○ Unilateral onset, rest tremor present, progressive, excellent response to L-dope (70-100%), visual hallucinations

322
Q

what is foot drop?

A

Difficulty in lifting the front part of the foot,
resulting in dragging of the toes
● Can be permanent or temporary

323
Q

Damage to which nerve causes foot drop?

A

Caused by damage to the common peroneal nerve - L4-S1 (also called common fibular
nerve)

324
Q

what are the causes of foot drop?

A 
injury, 
lower back damage,
tumour, 
hip replacement, 
cauda equina syndrome, 
multiple sclerosis
325
Q

what are the clinical features of foot drop?

A 
● Unilateral symptoms
● Complaint of one foot dragging across the
floor when walking
● Tripping
● Numbness in the same side
● Weakness in the same side
326
Q

what are the investigations for foot drop?

A

● Foot drop itself can be a clinical diagnosis
● Need to find the underlying cause:
○ X-ray, USS, CT, MRI
○ Nerve conduction study

327
Q

what is the treatment for foot drop?

A 
● Brace or splint
● Physiotherapy
● Specialised shoes - prevent foot drop when walking
● Nerve stimulation
● Surgery if indicated
328
Q

what is the epidemiology of TIA?

A
  • 15% of strokes are preceded by TIA
  • can foreshadow MI
  • male > female
  • more common in black people (predisposition to hypertension and atherosclerosis)
329
Q

what are the risk factors for TIA?

A
  • age
  • hypertension
  • smoking
  • diabetes
  • heart disease - AF
  • combined oral contraceptive pill
  • hyperlipidaemia
  • peripheral artery disease
  • clotting disorder
  • vasculitis
330
Q

what are the differential diagnoses for TIA?

A 
Hypoglycaemia
Migraine aura
Focal epilepsy
Vasculitis
Syncope - E.g. due to an arrythmia
Retinal bleed
331
Q

what percentage of TIAs are found in the carotid territory?

A 
90% = carotid territory
10% = vertebrobasilar territory
332
Q

what is the pathophysiology of an ischaemic stroke?

A
  • arterial disease and atherosclerosis is the main pathological process
  • thrombosis occurs at the site of atheromatous plaque in carotid/vertebral/cerebral arteries
  • Emboli arise from atheromatous plaques in the carotid/vertebrobasilar arteries or from the left atrium in atrial fibrillation
  • Cardiac artery stenosis, hypoperfusion
333
Q

what is the pathophysiology of haemorrhagic stroke?

A

bleeds caused by trauma, aneurysm rupture, thrombolysis, carotid artery dissection

334
Q

what are lacunar infarcts (ischaemic stroke)?

A
  • Small infarcts
  • From occlusion of a single small perforating artery supplying a subcortical area
  • Can happen in:
    • Internal capsule
    • Basal ganglia
    • Thalamus
    • Pons
335
Q

what is the clinical presentation of lacunar infarcts (ischaemic stroke)?

A

Depends on the area affected

One of:

  • Sensory loss
  • Weakness (unilateral)
  • Ataxic hemiparesis
  • Dysarthria
  • Motor speech problems
336
Q

which areas of the brain can be affected by lacunar infarcts (ischaemic stroke)?

A

Internal capsule
Basal ganglia
Thalamus
Pons

337
Q

what is the clinical presentation of brainstem infarcts (ischaemic stroke)?

A
  • Quadriplegia
  • Facial numbness & paralysis
  • Gaze & vision disturbances
  • Dysarthria & speech impairment
  • Vertigo, nausea, vomiting
  • Cerebellar signs
  • Palatal paralysis & diminished gag reflex
  • Altered consciousness
  • Locked-in syndrome
  • Coma
338
Q

what are the investigations for ischaemic stroke?

A
  • urgent head CT before treatment
    - shows site
  • pulse, BP and ECG
    • look for AF and MI
  • bloods
    • FBC - look for polycythaemia
    • glucose - rule out hypoglycaemia
    • ESR - raised in vasculitis
    • cholesterol
    • INR - if on warfarin
    • U&Es
  • MRI
    • more sensitive but may be negative in first few hours after infarct
    • indicated if diagnosis is uncertain
339
Q

what are the different types of haemorrhagic stroke?

A
  • intracerebral haemorrhage

- subarachnoid haemorrhage

340
Q

what are the contraindications of thrombolysis (IV alteplase)?

A
  • Recent surgery last 3 months
  • Recent arterial puncture
  • History of active malignancy (highly vascular thus increased
    bleeding risk)
  • Evidence of brain aneurysm
  • Patient on anticoagulation
  • Severe liver disease (abnormal clotting)
  • Acute pancreatitis
  • Clotting disorder
341
Q

what is the treatment for haemorrhagic stroke?

A
  • frequent GCS monitoring
  • anticoagulants are contraindicated (any anticoagulants should be reversed with vitamin K)
  • control hypertension
  • decompression of raised ICP - MANNITOL
  • surgery may be required
342
Q

what is an intracerebral haemorrhage?

A
  • Sudden bleeding into brain tissue
  • Due to rupture of a blood vessel within the brain
  • Like an ischaemic stroke, this leads to infarction, due to O2 deprivation
  • Pooling blood increases intracranial pressure (ICP)
  • ~10% of strokes
  • Higher mortality: up to 50%
343
Q

what are the major risk factors for intracerebral haemorrhage?

A 
Hypertension
Age
Alcohol
Smoking
Diabetes

Anticoagulation
Thrombolysis

344
Q

what are the causes of intracerebral haemorrhages?

A
  • Hypertension
    • Stiff & brittle vessels, prone to rupture
    • Microaneurysms
  • Secondary to ischaemic stroke
    • Bleeding after reperfusion
  • Head trauma
  • Arteriovenous malformations
  • Vasculitis
  • Vascular tumours
  • Brain tumours
  • Cerebral amyloid angiopathy
  • Carotid artery dissection
345
Q

what is the pathophysiology of intracerebral haemorrhage?

A
  1. Increased ICP puts pressure on skull, brain & blood vessels - healthy tissue can die
  2. CSF obstruction - hydrocephalus
  3. Midline shift
  4. Tentorial herniation
  5. Coning - compression of
    brainstem
346
Q

what is the clinical presentation of intracerebral haemorrhage?

A

similar to ischaemic stroke

pointers to haemorrhage:

  • sudden loss of consciousness
  • severe headache
  • meningism
  • coma
347
Q

what are the investigations for intracerebral haemorrhage?

A
  • same as ischaemic stroke

- CT/MRI is essential

348
Q

what is the management for intracerebral haemorrhage?

A
  • stop anticoagulants immediately
    • effects reversed with clotting factor replacement
  • control of BP - IV drugs
  • reduce ICP
    • mechanical ventilation
    • IV mannitol
  • refer for neurosurgical intervention if:
    • hydrocephalus
    • coma
    • brainstem compression
349
Q

what are the differential diagnoses for subarachnoid haemorrhages?

A
  • headache - migraine, cluster headache
  • meningitis
  • intracerebral haemorrhage
  • cortical vein thrombosis
  • carotid/vertebral artery dissection
350
Q

what is a subarachnoid haemorrhage?

A

Spontaneous bleeding into subarachnoid space

Space between arachnoid mater & pia mater

Can be catastrophic

351
Q

what is a subdural haematoma?

A
  • Bleeding into subdural space - space between dura mater & arachnoid mater
  • Due to rupture of a bridging vein - run from cortex to venous sinuses. They are vulnerable to deceleration injury
  • Usually due to head trauma
  • Other causes include dural metastases
  • Massive latent interval – weeks to months
  • Very treatable
352
Q

what are migraines?

A

recurrent throbbing headache often preceded by an aura & associated with nausea, vomiting and visual changes

353
Q

what is the epidemiology of migraines?

A

Most common causes of episodic headache ie. Recurrent

More common in females (roughly 3x)

90% have onset before 40yrs

354
Q

what are the risks for migraines?

A
  • genetics - family history
  • female
  • age - majority of first migraines are in adolescence
355
Q

what are the investigations for migraines?

A
  • usually made with little/no investigations, however if there are red flags further investigation is required
  • always examine eyes, BP, head and neck (muscles, scalp, temporal arteries)
  • lab tests e.g. CRP, ESR
  • CT/MRI
  • LUMBAR PUNCTURE
356
Q

what are the red flag indications for CT/MRI in migraines?

A
  • worst/severe headache i.e. “thunderclap”
  • change in pattern of migraine
  • abnormal neurological exam
  • onset > 50yrs
  • epilepsy
  • posteriorly located headache
357
Q

what are the red flag indications for a lumbar puncture in migraines?

A
  • thunderclap headache

- severe, rapid onset headache / progressive headache / unresponsive headache

358
Q

when are triptans contraindicated?

A

in ischaemic heart disease, coronary spasm and uncontrolled high BP

family history of CVD, stroke, DM and high cholesterol

359
Q

what are the side effects of triptans?

A
  • arrhythmias
  • angina +/- MI
  • recurrence of migraines - higher frequency
360
Q

what preventative measures can be taken for migraines?

A
  • beta blockers e.g. propranolol
  • TCAs e.g. amitriptyline
  • anticonvulsant e.g. topiramate
  • acupuncture
361
Q

when should preventative measures be taken for migraines?

A
  • if >2 attacks per month

- require acute meds >2x per week

362
Q

what is a cluster headache?

A

Episodic headaches lasting from 7 days up to 1 year (although usually 2-3wks) with pain-free periods in between that last ~4wks

363
Q

what is the epidemiology of cluster headache?

A

Considered the most disabling of primary headaches

Much rarer than migraines, and more common in males (~4x)

Typically affects adults with onset usually 20-40yrs

364
Q

what are the risk factors of cluster headaches?

A

Smoker
Alcohol
Male
Genetics - autosomal dominant gene has a link

365
Q

what are the preventative measures for cluster headaches?

A
  • 1st line = verapamil (CCB)
  • prednisolone
  • reduce alcohol consumption and stop smoking
366
Q

what are the investigations for cluster headaches?

A
  • diagnosed by clinical examination

- at least 5 attacks fulfilling the presentation criteria

367
Q

what are the triggers for tension headaches?

A
  • stress
  • sleep deprivation
  • bad posture
  • hunger
  • eyestrain
  • anxiety
  • noise
368
Q

what is the clinical presentation of tension headache?

A

usually one of the following:

  • bilateral
  • pressing/tight and non-pulsatile (like an elastic band)
  • mild/moderate intensity
  • +/- scalp tenderness

no aura, vomiting or sensitivity to head movement

can be some pressure behind the eyes, but pain isn’t localised to be around the eye

369
Q

which medications commonly cause medication-overuse headaches?

A
  • worsens whilst on regular analgesia, especially opioids

- mixed analgesics e.g. paracetamol + codeine/opiates, ergotamine and triptans

370
Q

why are lumbar punctures contraindicated in brain tumours?

A

withdrawing CSF may provoke immediate coning

371
Q

which is more common out of primary and secondary brain tumours?

A

secondary brain tumours are 10 times more common

372
Q

what is wernicke’s encephalopathy caused by?

A

depletion of thiamine (vitamin B1)

373
Q

what is the clinical presentation of wernicke’s encephalopathy?

A
  • classic triad
    • confusion
    • ataxia
    • ophthalmoplegia
  • sign
    • asterixis (liver flap) - general sign of metabolic encephalopathy
374
Q

what diseases does wernicke’s encephalopathy occur in?

A
  • chronic alcoholism
  • severe starvation
  • prolonged vomiting
375
Q

what are the investigations for wernicke’s encephalopathy?

A
  • diagnosed via clinical examination
376
Q

what is the management for wernicke’s encephalopathy?

A
  • pabrinex - IV B-vitamins (including thiamine)
377
Q

what are the complications of wernicke’s encephalopathy?

A

if not managed appropriately

  • fatal in 20%
  • can progress to korsakoff’s syndrome
378
Q

what is korsakoff’s syndrome?

A
  • irreversible
  • long term brain damage due to vitamin B1 deficiency
  • symptoms = decreased ability to acquire new memories, retrograde amnesia, confabulation (invented memories)
379
Q

what are the causes and risk factors of MND?

A
  • usually sporadic and unknown cause

- 5-10% are familial = SOD-1 mutation

380
Q

what is the pathophysiology of MND?

A
  • degenerative condition affecting anterior horn motor neurone cells in the brain and the spinal cord
  • damage is caused by oxygen species which damage DNA,, lipids and proteins
  • causes both UMN and LMN dysfunction
  • there is no sensory loss or sphincter disturbance
  • it never affects eye movements
381
Q

what are the 4 different types of MND? do they affect LMN or UMN?

A

amyotrophic lateral sclerosis (ALS) - UMN + LMN

progressive muscular atrophy (PMA) - LMN only

progressive bulbar palsy (PBP) LMN only

primary lateral sclerosis (PLS) UMN only

382
Q

what is the epidemiology of ALS (MND)?

A
  • most common form of MND (50%)
  • some familiar inheritance - SOD1 and C90RF72 genes
  • common ages of onset 40-50 (familial) and 58-63 (sporadic)
383
Q

what is the clinical presentation of ALS?

A

● Presents with signs of degeneration of upper and
lower motor neurons
● progressive paralysis and eventual respiratory failure
● Asymmetric onset
● Babinski sign +ve
● Fasciculations of the tongue
● Any corticobulbar signs indicate a worse prognosis:
○ Brisk jaw reflex
○ Dysarthria (difficulty speaking)
○ Dysphagia (difficulty swallowing)
○ Sialorrhoea (excess salivation)

384
Q

what are the clinical features of progressive bulbar palsy (PBP) in MND?

A

CN 9-12

  • LMN in the brain stem
  • pharyngeal muscle weakness
  • progressive loss of speech (hoarse, quiet, nasal)
  • tongue atrophy (flaccid)
385
Q

what are the clinical features of primary lateral sclerosis (PLS) in MND?

A
  • UMN of the arm, legs and face
  • movements become slow
  • progressive tetraparesis
386
Q

what are the clinical features of progressive muscular atrophy (PMA) in MND?

A
  • LMNs only
  • muscle wasting
  • clumsy hand movements
  • fasciculations
  • muscle cramps
387
Q

what are the risk factors for Guillain-Barre syndrome (GBS)?

A
  • history of respiratory or GI infection 1-3 weeks prior to onset
  • vaccinations have been implicated
  • post-pregnancy
388
Q

what is the epidemiology of Guillain-Barre syndrome?

A

● Increased incidence in males

● Peak ages are 15-35, and 50-75

389
Q

what are the side effects of pyridostigmine used to treat myasthenia gravis?

A
  • increased salivation
  • lacrimation
  • sweats
  • vomiting
  • miosis (excessive pupillary constriction)
  • diarrhoea
390
Q

what is myasthenic crisis?

A

a complication of myasthenia gravis

weakness of the respiratory muscles during a relapse can be life-threatening

391
Q

what is the treatment for myasthenic crisis?

A
  • monitor FVC
  • plasmapheresis and IV immunoglobulin
  • identify and treat trigger of relapse e.g. infection, medications
392
Q

where are MS demyelination plaques commonly found?

A
  • optic nerves
  • around ventricles of the brain
  • brainstem and cerebellar connections
  • corpus callosum
  • cervical cord (corticospinal tract and dorsal columns)
393
Q

what is relapsing and remitting MS?

A
  • MOST COMMON PATTERN of MS
  • Symptoms occur in attacks (relapses) with onset over days and typically recovery, either partial or complete, over weeks
  • Periods of good health or remission are followed by sudden symptoms or relapses
  • Patients may accumulate disability over time if they do not recover fully after relapses
394
Q

what is secondary progressive MS?

A

• Follows on from relapsing & remitting MS

• Late stage of MS that consists of gradually worsening symptoms with
fewer remissions

• 75% of patients with relapsing-remitting MS will eventually evolve into a secondary progressive MS by 35yrs after onset

395
Q

what is primary progressive MS?

A

• Gradually worsening disability WITHOUT relapses or remissions

• Typically presents later and is associated with fewer inflammatory
changes on MRI

396
Q

what is the classic presentation of MS in exams?

A

○ A female 20-40 years old
○ Any 2 of the symptoms of MS
○ Optic neuritis is often shown as first symptom - disseminate in space!

397
Q

what are the investigations for herpes zoster?

A
  • clinical diagnosis

- eruption of rash is virtually diagnostic

398
Q

what are the risk factors of herpes zoster?

A
  • increasing age
  • immunocompromised
  • HIV, hodgkin’s lymphoma and bone marrow transplants
399
Q

what is the epidemiology of herpes zoster?

A
  • 90% of children have been exposed to chicken pox before 16 years
  • can affect all ages - more seen in elderly
  • incidence and severity increases with age
400
Q

what is the pathophysiology of herpes zoster?

A
  • viral infection affecting peripheral nerves
  • when latent virus is reactivated in the dorsal root ganglia it travels down the affected nerve via sensory root in dermatomal distribution over 3-4 days
  • results in perineural and intramural inflammation
401
Q

what is post-herpetic neuralgia?

A
  • pain lasting for more than 4 months after developing shingles
  • occurs in 10% of patients - often elderly
  • burning, intractable pain
  • responds poorly to analgesics
402
Q

what is the treatment for post-herpetic neuralgia?

A
  • tricyclic antidepressant - AMITRIPTYLINE
  • anti-epileptic - GABAPENTIN
  • anti-convulsant - CARBAMEZAPINE
403
Q

what is sciatica?

A
  • pain numbness and tingling sensation

- radiates from lower back and travels down one of the legs to the foot and toes

404
Q

what are the lumbar puncture results for meningitis caused by bacteria?

A
  • cells = polymorphs
  • proteins = raised
  • glucose = low
  • CSF = turbid colour
405
Q

what are the lumbar puncture results for meningitis caused by TB?

A
  • cells = lymphocytes
  • proteins = raised
  • glucose = normal/low
406
Q

what are the lumbar puncture results for meningitis caused by viruses?

A
  • cells = lymphocytes
  • proteins = normal
  • glucose = normal
407
Q

what antibiotic is used in meningitis if S. Pneumoniae is suspected?

A

vancomycin

408
Q

what antibiotic is used in meningitis if listeria is suspected?

A

ampicillin (or amoxicillin) and gentamycin

409
Q

what is the treatment for viral meningitis?

A

no specific treatment
analgesia
antipyretics
hydration

410
Q

what are the risk factors for meningitis?

A
  • immunosuppression
  • elderly
  • pregnant
  • crowding (university)
  • diabetes
  • malignancy
  • IV drug use
  • sickle cell anaemia
  • adrenal insufficiency
411
Q

what is the pathophysiology of meningitis?

A
  • Microorganisms reach the meninges from the ears,
    nasopharynx, cranial injury or congenital meningeal defect or by bloodstream spread
  • Acute bacterial meningitis:
    • Typically sudden
    • The pia-arachnoid is congested with polymorphs
    • A layer of pus forms which may organise to form adhesions causing
    cranial nerve palsies and hydrocephalus
  • Chronic infection e.g. TB:
    • Brain is covered in a viscous grey-green exudate with numerous
    meningeal tubercles
  • Viral meningitis:
    • Predominantly lymphocytic inflammatory CSF reaction WITHOUT PUS FORMATION
    • no cerebral oedema
412
Q

what is meningococcal septicaemia?

A
  • When bacteria invades into blood
  • Presence of endotoxin in bacteria leads to a inflammatory cascade
  • Petechial rash + signs of sepsis = meningococcal septicaemia
413
Q

what is the cardinal sign of meningococcal septicaemia?

A

Petechial rash + signs of sepsis = meningococcal septicaemia

414
Q

what are the risk factors for epilepsy?

A

FHx
Premature babies, especially if they are small for their gestational age
Abnormal cerebral blood vessels
Drugs eg. cocaine

415
Q

what is the prodrome element of a seizure?

A
  • Precedes the seizures, usually by hours/days

- Weird feeling eg. mood/behaviour changes

416
Q

what is the post-ictal element of a seizure?

A
  • The period after a seizures
  • Headache, confusion, myalgia, sore tongue (often bitten)
  • Temporary weakness after focal seizure in motor cortex = Post-Ictal Todd’s palsy
  • Dysphasia following temporal lobe seizure
417
Q

what are primary/generalised seizures?

A
  • Simultaneous electrical discharge throughout the whole cortex, with no features that suggest localisation to only one hemisphere/lobe
  • Bilateral and symmetrical motor manifestations
  • ALWAYS ASSOCIATED WITH LOSS OF CONSCIOUSNESS & LACK OF AWARENESS
418
Q

what are focal (partial) seizures?

A
  • Focal onset with features that can be referrable to a single lobe eg. temporal lobe
  • Often seen with underlying structural disease ie. There is an underlying cause
  • Electrical discharge is limited to one lobe, in one hemisphere
  • These may later progress to become generalized seizures
419
Q

what are tonic seizures?

A 
High tone (hence the name) = rigid, stiff limbs
Will fall to floor if standing due to stiff limbs
420
Q

what are clonic seizures?

A

Rhythmic muscle jerking (ie. Clonus, the UMN sign)

421
Q

what are tonic-clonic seizures (grand mal)?

A

As the name suggests a combination of tonic & clonic seizures
This is your stereotypical “Shaking” seizures due to the mix of on/off rigidity & muscle jerking

422
Q

what is a myotonic seizure?

A

Isolated jerking of a limb/face/trunk

“disobedient limb” or “thrown to the floor”

423
Q

what is an atonic seizure?

A

Complete opposite to tonic seizure, loss of muscle tone = floppy

424
Q

what is an absence (petit mal) seizure?

A

Common in childhood but usually goes by adulthood, however there is an increased risk of developing generalized tonic-clonic seizures as an adult

Will go pale and ”stare blankly” for a few seconds

Often suddenly stop talking mid-sentence & do not realise they have had an attack

425
Q

what are simple focal (partial) seizures?

A
  • No affect on consciousness or memory
  • Awareness unimpaired but will have focal motor, sensory, autonomic or psychic symptoms depending on the affected lobe
  • No post-ictal symptoms
426
Q

what are complex focal (partial) seizures?

A

Memory/awareness is affected before, during or immediately after the seizure

Most commonly arises from the temporal lobe > affects speech, memory & emotion

Post-ictal confusion is common if temporal lobe, whereas recovery is often swift if the frontal lobe is affected

427
Q

what are the characteristics of temporal lobe specific seizures?

A

Aura (80%); deja-vu, auditory hallucinations, funny smells, fear

  • Anxiety, out-of-body experiences
  • Automatisms eg. lip smacking
428
Q

what are the characteristics of frontal lobe specific seizures?

A

Motor features eg. posturing, peddling movements of leg

JACKSONIAN MARCH – seizures march up/down the motor homunculus

Post-Ictal Todd’s palsy

Starts distally in a limb & works its way upwards to the face

429
Q

what are the characteristics of parietal lobe specific seizures?

A

Sensory disturbances eg. tingling/numbness

430
Q

what are the characteristics of occipital lobe specific seizures?

A

Visual phenomena eg. spots, lines, flashes

431
Q

what is a partial seizure with secondary generalization?

A

2/3 patients with partial seizures will develop generalized seizures, usually generalized tonic-clonic

These start focally & spread widely throughout the cortex

432
Q

what are the characteristics of non-epileptic seizures?

A

Non-epileptic seizures are entirely situational
Eg. metabolic disturbances; low Na+, hypoxia
Can be related to syncope

Non-epileptic seizures are typically longer with closed eyes & mouth

Non-epileptic do not occur during sleep and do not involve incontinence or tongue-biting

There are pre-ictal anxiety symptoms in non-epileptic eg. they know they are about to happen

433
Q

what clinical signs indicate a diagnosis of epilepsy rather than syncope?

A 
Tongue-biting
Head turning
Muscle pain
LOC
Cyanosis
Post-ictal symptoms
434
Q

what are the investigations for epilepsy

A

Electroencephalogram (EEG) = supports diagnosis

MRI/ CT head = rule out space-occupying lesions

Bloods
FBC, Ca2+, electrolytes, U&Es, LFTs, blood glucose = rule out metabolic disturbances

Genetic testing
If suspected genetic cause -> juvenile myoclonic epilepsy

435
Q

what is the emergency treatment for epilepsy?

A
  • ABCDE
  • check glucose
  • RECTAL/IV DIAZEPAM or LORAZEPAM
  • IV PHENYTOIN loading
  • mechanical ventilation
436
Q

what is the treatment for generalised tonic-clonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

437
Q

what is the treatment for generalised tonic/atonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

438
Q

what is the treatment for generalised myoclonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Levetiracetam/Topiramate to females of childbearing potential

439
Q

what is the treatment for absence (petit mal) epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Ethosuximide to females of childbearing potential

440
Q

what are the side effects of sodium valproate?

A
  • weight gain
  • hair loss
  • liver failure
441
Q

why is sodium valproate not prescribed to women during pregnancy?

A

it is teratogenic

442
Q

what are the side effects of lamotrigine?

A

maculopapular rash
blurred vision
vomiting

443
Q

what are the side effects of carbamazepine?

A 
diplopia
rashes
leucopenia
impaired balance
drowsiness
444
Q

what are the side effects of ethosuximide?

A

rashes

night terrors

445
Q

what is status epilepticus?

A
  • medical emergency

- continuous seizures for over 5 minutes without recovery of consciousness

446
Q

what is trigeminal neuralgia?

A

described as a chronic, debilitating condition resulting in

intense and extreme episodes of pain

447
Q

what are the risk factors for trigeminal neuralgia?

A
  • Hypertension is the main risk factor
  • Triggers:
    • Washing affected area,
    shaving,
    eating,
    talking
    dental prostheses
448
Q

what is the clinical presentation of trigeminal neuralgia?

A
  • ALMOST ALWAYS UNILATERAL
  • At least 3 attacks of unilateral facial pain
  • Facial pain occurs in one or more distributions of the
    trigeminal nerve, with no radiation beyond the trigeminal
    distribution
  • Pain has at least 3 of the following:
    • Reoccurring in paroxysmal (sudden and frequent) attacks from a fraction
    of a second to 2 minutes• Severe intensity
    • Electric shock like, shooting, stabbing or knife-like
    • Precipitated by innocuous (non-harmful) stimuli by the affected side of
    the face e.g. washing or shaving area
449
Q

what are the investigations for trigeminal neuralgia?

A
  • In order to diagnose needs to be at least 3 attacks with unilateral facial pain
  • Clinical diagnosis based on criteria above and based on history
  • MRI to exclude secondary causes or other pathologies
  • Not attributed to another disorder
450
Q

what are brainstem lesions caused by?

A
  • Tumour
  • MS
  • Trauma
  • Aneurysm
  • Vertebral artery dissection resulting in infarction
  • Infection - cerebellar abscess from ear
451
Q

what are the signs of a CN3 palsy?

A
  • Ptosis - dropping eyelids
  • Fixed dilated pupil - loss of PARASYMPATHETIC outflow from EDINGER
    WESTPHAL NUCLEUS which supply pupillary sphincter and ciliary bodies -
    lens accommodation
  • Eye down and out
452
Q

what are the causes of CN3 palsy?

A
  • Raised ICP
  • Diabetes
  • Hypertension
  • Giant cell arteritis
453
Q

what are the signs of a CN4 palsy?

A

Innervate superior oblique muscle and results in a head tilt to correct the
extortion that results in diplopia on looking down e.g. walking downstairs

454
Q

what are the causes of a CN4 palsy?

A

Trauma to the orbit - rare

455
Q

what are the signs of a CN6 palsy?

A

Innervate the lateral rectus muscle thus eyes will be adducted

456
Q

what are the causes of CN6 palsy?

A
  • MS
  • Wernicke’s encephalopathy
  • Pontine stroke - presents with fixed small pupils +/- quadriparesis
457
Q

what are the signs of CN3,4,6 palsy?

A
  • Non-functioning eye
458
Q

what are the causes of CN3,4,6 palsy?

A
  • Storke
  • Tumours
  • Wernicke’s encephalopathy
459
Q

what are the signs of CN5 palsy?

A
  • Jaw deviates to side of lesion

- Loss of corneal reflex

460
Q

what are the causes of CN5 palsy?

A

trigeminal neuralgia (pain but no sensory loss),
herpes zoster,
nasopharyngeal cancer

461
Q

what are the signs of CN7 palsy?

A

Facial droop and weakness

462
Q

what are the causes of CN7 palsy?

A

• Bells palsy is the most common lesion of the facial nerve - will see
dribbling out the side of mouth
• Fractures of the petrous bones
• Middle ear infections
• Inflammation of the parotid gland - which facial nerve passes through

463
Q

what are the signs of CN8 palsy?

A
  • Hearing impairment

- Vertigo and lack of balance

464
Q

what are the causes of CN8 palsy?

A

• The vestibulocochlear nerve runs very close to the bone
• Is also very affected by surrounding tumours - if a tumour arises in the
internal acoustic meatus then this will press on the vestibulocochlear
& facial nerve
• Skull fracture
• Toxic drug effects
• Ear infections

465
Q

what are the signs of CN9,10 palsy?

A
  • Gag reflex issues
  • Swallowing issues
  • Vocal issues
466
Q

what are the causes of CN9,10 palsy?

A

jugular foramen lesion

467
Q

which conditions are associated with berry aneurysms?

A
  • Polycystic Kidney Disease
    • Coarctation of aorta
    • Ehlers-Danlos syndrome & Marfan syndrome
468
Q

give an example of an SSRI

A

citalopram
fluoxetine
sertraline

469
Q

what conditions do SSRIs treat?

A
  • first line for moderate to severe depression
  • mild depression if other treatments have failed
  • panic disorder
  • OCD
470
Q

what is the mechanism of action for SSRIs?

A

SSRIs preferentially inhibit neuronal reuptake of serotonin from the synaptic cleft -> increases availability for neurotransmission

471
Q

what are the side effects of SSRIs?

A
  • GI disturbance
  • appetite and weight disturbance
  • hypersensitivity reactions
  • hyponatraemia
  • suicidal thoughts
  • seizures
  • prolonged QT interval
472
Q

what are the contraindications of SSRIs?

A
  • contraindicated with other monamine oxidase inhibitors -> may cause serotonin syndrome
  • other drugs that cause prolonged QT interval
  • increase bleeding when used with anticoagulants
473
Q

give an example of a tricyclic antidepressant

A

amitriptyline

474
Q

what are the indications for using tricyclic antidepressants?

A

As a second line treatment for moderate to severe depression where SSRIs
are ineffective

475
Q

what is the mechanism of action for tricyclic antidepressants?

A
  • inhibits neuronal uptake of serotonin and noradrenaline from the synaptic cleft -> increase availability for neurotransmission
476
Q

why do tricyclic antidepressants have extensive side effects?

A
  • they block a wide range of receptors
477
Q

what are the side effects of tricyclic antidepressants?

A
  • dry mouth
  • constipation
  • urinary retention
  • blurred vision
  • sedation
  • hypotension
  • arrhythmias
  • QT and QRS prolongation
  • hallucinations
  • sexual dysfunction
478
Q

when are tricyclic antidepressants contraindicated?

A
  • with other monoamine oxidase inhibitors
479
Q

give an example of a benzodiazepine

A

diazepam

lorazepam

480
Q

what are the indications for using a benzodiazepine

A
  • First line treatment of seizures and status epilepticus
  • Management of alcohol withdrawal reactions
  • SHORT TERM treatment of severe anxiety or insomnia
481
Q

what is the mechanism of action for benzodiazepines?

A
  • Benzodiazepines target the GABA-a receptor, which is a chloride channel that opens in response to binding by GABA (the main INHIBITORY NEUROTRANSMITTER)
  • opening the channel allows chloride to enter making the cell more resistant to depolarisation
  • They facilitate the enhanced binding of GABA to GABA-a receptors and have a widespread depressant effect on synaptic transmission
482
Q

what are the side effects of benzodiazepines?

A

cause dose dependent drowsiness, sedation and coma

483
Q

when are benzodiazepines contraindicated?

A
  • in elderly
  • those with respiratory or hepatic impairment
  • neuromuscular disease
  • has sedative effects with alcohol, opioids and CYP450 inhibitors
484
Q

what are the side effects of carbamazepine?

A
  • GI disturbance
  • dizziness
  • ataxia
  • hypersensitivity rash
  • oedema
  • hyponatraemia
485
Q

when is carbamazepine contraindicated?

A
  • prior anti-epileptic hypersensitivity syndrome

- caution in hepatic, renal and cardiac disease

486
Q

what is the mechanism of action for gabapentin and pregabalin?

A

it is closely related to GABA

  • It binds voltage sensitive Ca2+ channels, where it prevents inflow of Ca2+ and thus inhibits neurotransmitter release
  • interfering with synaptic transmission and reducing neuronal excitability
487
Q

what are the side effects of gabapentin and pregabalin?

A
  • drowsiness
  • dizziness
  • ataxia
488
Q

what are the contraindications of gabapentin and pregabalin?

A
  • renal impairment

- other sedating drugs

489
Q

what are the side effects of levo-dopa?

A 
nausea
drowsiness
confusion
hallucinations
hypertension
490
Q

what are the contraindications for levo-dopa?

A
  • take care in elderly

- caution in CVS disease

491
Q

why is levo-dopa always given alongside a decarboxylase inhibitor (Co-Careldopa)?

A
  • reduce levo-dopa’s peripheral conversion before it is able to enter the brain
    this reduces nausea and lowers dose required
492
Q

give an example of a dopamine deleting drug

A

reserpine

493
Q

what are the indications for using a dopamine depleting drug (reserpine)?

A
  • treat dyskinesia in Huntington’s

- can be used as antipsychotic and antihypertensive drug

494
Q

what is the mechanism of action for dopamine depleting drugs (reserpine)?

A
  • irreversibly blocks vescicular monoamine transporter (VMAT)
495
Q

what are the side effects of dopamine depleting drugs (reserpine)?

A
  • nasal congestion
  • GI disturbance
  • drowsiness/dizziness
  • hypotension
  • bradycardia
496
Q

what are the contraindications for dopamine depleting drugs?

A
  • asthma

- CVS disease

497
Q

give an example of MAO inhibitor?

A

selegiline

rasagiline

498
Q

what are the contraindications of MAO inhibitors?

A
  • aged cheese and alcohol -> can cause hypertensive crisis

- antidepressants and adrenaline

499
Q

give an example of ACh inhibitor

A

rivastigmine

donepezil

500
Q

what are the indications for ACh inhibitors?

A
  • alzheimers
  • Lewy body dementia
  • parkinsons
  • myasthenia gravis
501
Q

what is the mechanism of action for ACh inhibitors

A

inhibits ACh breakdown by blocking site of acetylcholinesterase

502
Q

what are the side effects of ACh inhibitors?

A
  • bradycardia
  • hypotension
  • hypersecretion
  • bronchoconstriction
  • GI tract hyper motility
  • prolonged muscular contraction
503
Q

what are the contraindications of ACh inhibitors?

A

urinary retention

CVS disease

504
Q

which nerve root is compressed in sciatica?

A

S1

505
Q

what are the causes of primary syncope?

A

Dehydration
Missed meals
Extended standing in a warm environment, such as a school assembly
A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood

506
Q

what is bell’s palsy?

A
  • acute unilateral facial nerve palsy
507
Q

what is the cause of bell’s palsy?

A

viral infection - reactivation of herpes simplex virus 1 (HSV1)

this leads to swelling of CN VII

508
Q

what is the clinical presentation of Bell’s palsy?

A
  • unilateral LMN facial weakness
  • altered taste
  • post auricular pain - pain behind ears
509
Q

how do you tell the difference between Bell’s palsy and a stroke?

A
  • stroke = forehead still innervated - forehead sparing

- Bell’s palsy = both forehead and lower face are affected on one side

510
Q

what are the investigations for Bell’s palsy?

A
  • usually a clinical diagnosis

- can do more investigations to rule out other conditions

511
Q

what is the treatment for Bell’s palsy?

A
  • prednisolone
  • eye care
  • ?antivirals
512
Q

what visual field defect would be caused by an optic nerve lesion?

A

monocular vision loss

- loss of vision in one eye

513
Q

what visual field defect would be caused by an optic chiasm lesion?

A

bitemporal hemianopia

514
Q

what visual field defect would be caused by an optic tract lesion?

A
  • contralateral homonymous hemianopia
515
Q

what visual field defect would be caused by a lesion on one of the optic radiations?

A

homonymous quadrantanopia

516
Q

where is the primary visual centre located?

A

calcarine sulcus of occipital lobe

517
Q

what are the 2 components of an intervertebral disc?

A
  • nucleus pulposus

- annulus fibrosus

518
Q

what are the characteristics of cushing’s triad?

A
  • bradycardia
  • irregular respirations
  • widened pulse pressure
519
Q

what is cushing’s reflex?

A
  • nervous system response to increased ICP
  • as ICP increases cerebral perfusion pressure (CPP) decreases, resulting in reduced cerebral perfusion
  • sympathetic nervous system is activated which increases BP
520
Q

what are the clinical presentation of cushing’s reflex?

A
  • cushing’s triad - bradycardia, irregular respirations and widened pulse pressure
  • hypertension
  • headache
  • vomiting
  • blurred vision
521
Q

what are the investigations for cushing’s reflex?

A
  • measure ICP - lumbar puncture or continuous monitoring via catheter in ventricle of brain
  • CT/MRI
522
Q

what is the treatment for cushing’s reflex?

A
  • mannitol
  • duiretics - furosemide
  • steroids - methylprednisolone
  • sedatives - propofol
  • hyperventilation
  • elevate head to 30 degrees (reverse trendelenburg position)
  • drain CSF
  • craniotomy
523
Q

what are the complications of cushing’s reflex?

A
  • herniation -> death

- brain tissue infarction

524
Q

what is the pathophysiology of horner’s syndrome?

A

unilateral damage to the sympathetic chain

525
Q

what are the causes of 1st order horner’s syndrome?

A

stroke, tumours of hypothalamus, spinal cord lesions

526
Q

what are the causes of 2nd order horner’s syndrome?

A

tumours of upper chest cavity, trauma to the neck

527
Q

what are the causes of 3rd order horner’s syndrome?

A

lesions to carotid artery, middle ear infections, injury to base of the skull

528
Q

what are the clinical features of horner’s syndrome?

A

MAPLE

  • Miosis
  • Anhydrosis
  • Ptosis
  • Loss of ciliospinal reflex
  • Endophthalmos (sunken eyeball)
529
Q

what is the treatment for horner’s syndrome?

A

treat underlying cause

530
Q

what are the investigations for horner’s syndrome?

A

clinical examination

MRI - detect lesions

531
Q

what is brown-sequard syndrome?

A

hemisection of the spinal cord

DCML, corticospinal tract and spinothalamic tract are affected on one side

532
Q

what is the presentation of brown-sequard syndrome?

A
  • DCML = ipsilateral loss of proprioception and vibration sensation
  • spinothalamic = contralateral loss of temperature and pain sensation
  • corticospinal = ipsilateral spastic paralysis below lesion
533
Q

what are the signs of a vertebrobasilar artery infarction?

A

balance and co-ordination

534
Q

what are the signs of lateral medullary syndrome in ischaemic stroke?

A

Sudden vomiting and vertigo

Ipsilateral Horner’s syndrome = reduced sweating, facial numbness, dysarthria, limb ataxia, dysphagia

535
Q

what are the signs of a brainstem infarction?

A 
Quadriplegia 
Facial paralysis, numbness
Gaze, vision 
Coma 
Locked in syndrome 
Altered consciousness, 
Vertigo , vomiting
536
Q

what is Todd’s palsy?

A

temporary weakness after a focal seizure in the motor cortex

537
Q

what are the causes of status epilepticus?

A
  • Abruptly stopping anti epileptic treatment
  • Alcohol abuse
  • Poor compliance to therapy
538
Q

what is the prognosis for huntington’s disease?

A
  • poor prognosis
539
Q

what is the most common cause of death for huntington’s disease?

A

Most common cause of death = Pneumonia

Second most common cause = suicide

540
Q

give one differential diagnosis for huntington’s disease

A

Sydenham’s chorea (Rheumatic fever)

541
Q

what are the secondary causes of syncope?

A 
Hypoglycaemia
Dehydration
Anaemia
Infection
Anaphylaxis
Arrhythmias
Valvular heart disease
Hypertrophic obstructive cardiomyopathy
542
Q

what are the clinical features of syncope?

A 
Hot or clammy
Sweaty
Heavy
Dizzy or lightheaded
Vision going blurry or dark
Headache
543
Q

`what are the investigations for syncope?

A

Full history and examination

ECG, particularly assessing for arrhythmia and the QT interval for long QT syndrome

24 hour ECG if paroxysmal arrhythmias are suspected

Echocardiogram if structural heart disease is suspected

Bloods, including a FBC (anaemia), U&E (arrhythmias and seizures) and blood glucose (diabetes)

544
Q

what is the management for syncope?

A

avoid triggers in primary syncope.

management of underlying pathology

Phase 2A revision (38 decks)

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