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3a Neurology > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the common causes of a migraine?

A 
C- chocolate and certain foods
H - hormones e.g. menstrual cycle
O- oral contraceptive pill
C- caffeine
O- obesity
L- lie ins - too much or too little sleep
A- alcohol
T- trauma, head injury
E- exercise
S - stress
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2
Q

What are common triggers for a migraine?

A 
too little/ too much sleep
stress
hormonal e.g. menstrual migraine, menopause
eating e.g. skipping meals
minor head injuries
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3
Q

How long does a migraine commonly last?

A

4 hours - 72 hours

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4
Q

What is the diagnostic criteria of a migraine?

A 
AT LEAST 2 OF:
unilateral pain
throbbing/ pulsating pain
moderate-severe intensity
motion sensitivity

AT LEAST 1 OF:
nausea/ vomiting
photophobia/ photophobia
normal examination

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5
Q

What is a migraine with an aura?

A

aura precedes the migraine, with symptoms changing as wave of spreading neuronal depression moves across cortex and focal neurological deficit

e.g. visual aura (loss of vision, shimmering, zig zag lines), motor aura (pins and needles, dysarthria, ataxia, hemiparesis), somatosensory

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6
Q

How are acute attacks of migraines managed?

A
  1. simple analgesics e.g. NSAIDs, paracetamol
  2. triptans + paracetamol e.g. sumatriptan
  3. avoid trigger
  4. anti emetics (even if not feeling nausea) e.g. prochloroperazine, metachlorpramide
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7
Q

How can migraines be managed long term if they are frequent and affecting quality of life?

A
  1. beta blockers e.g. propanolol

2. anti convulsants e.g. topiramate

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8
Q

Which group of people tend to get cluster headaches?

A

high alcohol intake
smoking
men 20-40 y/o

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9
Q

If a patient presents with a unilateral headache around one eye that has become watery/ bloodshot and has been several months without a headache, what is the most likely diagnosis?

A

cluster headache

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10
Q

What is the typical pattern of frequency of a cluster headache?

A

once/ twice daily headaches for 4-12 weeks and then non headaches for several months

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11
Q

What symptoms other than unilateral headache around one eye is associated with cluster headaches?

A 
rhinorrhoea
vomiting
Horners syndrome
agitation, pacing around
congestion of sinuses

eye symptoms: watery, blood shot, lid oedema, lacrimation

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12
Q

What is the acute management of a cluster headache?

A

subcut sumatriptan + high flow oxygen (12-15L per min via non breathe mask for 15 mins)

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13
Q

What are the risk factors for getting tension headaches?

A 
stress
noise
concentration/ visual effort
fumes/ smells
depression
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14
Q

If a patient presents with a bilateral headache that lasts for hours-days and is dull/diffuse and non pulsatile, what is your diagnosis and what other symptoms would you ask about?

A

TENSION HEADACHE

chronic
tight banding pain
scalp tenderness
pressure behind eyes
worse at the end of the day
spreads to neck
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15
Q

How are tension headaches managed?

A

avoid causative factors
analgesics e.g. paracetamol, NSAIDs, aspirin (avoid opioids)
supportive care e.g. massage, ice packs
preventative measures - acupuncture, low dose amitriptyline

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16
Q

What is temporal arteritis?

A

CHRONIC VASCULITIS OF LARGE/ MEDIUM VESSELS: granulomatous inflammation affecting the branches of external carotid artery, including the superficial temporal artery

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17
Q

What are the main clinical features of temporal arteritis?

A
  1. unilateral headache/ pain over non pulsatile temporal arteries, thickened skin
  2. visual loss - amaurosis fugax
  3. jaw claudication
  4. scalp tenderness e.g. brushing hair causes pain

+ fever, fatigue, weight loss, polymyalgia rheumatic

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18
Q

How is temporal arteritis diagnosed?

A
  1. raised ESR

2. temporal artery biopsy - granulomatous inflammation, skip lesions

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19
Q

How is temporal arteritis managed?

A

high dose corticosteroids 60mg e.g. prednisolone + urgent referral to ophthalmology (if eye symptoms)

(give gastric and bone protection e.g. PPI, bisphosphonates)

steroids gradually reduced over time

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20
Q

How is Huntingtons disease inherited?

A

autosomal dominant disorder

complete penetrance - all gene carriers have the disease

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21
Q

What is the underlying pathology of Huntingtons disease?

A

expanded trinucleatide repeat (CAG= huntingtin gene) on chromosome 4
each generation, the repeat increases in length causing a younger age of onset and worse phenotype

causes a loss of GABA and cholinergic neurones in the striatum of the basal ganglia

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22
Q

How does Huntingtons disease first present “prodrome”?

A

personality change and lack of coordination

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23
Q

What are the main symptoms of Huntingtons disease?

A

presents usually > 35 y/o

personality/behavioural change = irritable, depression, antisocial

chorea (jerky involuntary movements) = affects face/trunk/limbs, dystonia, grimacing, gait problems

dementia - late

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24
Q

How is Huntington’s disease diagnosed?

A

genetic testing - CAG repeats

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25
Q

How is Huntington’s managed?

A

no treatment prevents progression or cures

  1. dopamine blocking drugs e.g. tetrabenazine for chorea
  2. MDT approach - counsel family, SALT, physiotherapists, OT, palliative care
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26
Q

List the MDT members that are involved in managing a patient with Huntington’s disease

A 
speech and language therapists 
physiotherapists
dieticians
occupational therapists 
psychologists
palliative care team
counsellors for family
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27
Q

List the causes of parkinsonian symptoms

A

Lewy body dementia
side effects of drugs e.g anti-psychotics, metaclopramide
vascular disease
tumour in basal ganglia
parkinsons plus syndrome e.g. young onset Huntingtons, spinal cerebellar ataxia, progressive supra-nuclear palsy, normal pressure hydrocephalus

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28
Q

What is the pathology behind parkinsons disease?

A

degeneration of dopaminergic neurones in the substantial nigra
lewy bodies found in brain stem which contain alpha synuclein and ubiquitin

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29
Q

What are the cardinal features of parkinsons disease?

A

T- tremor
R- rigidity
A- akinesia/ bradykinesia
P - postural instability

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30
Q

List the clinical symptoms and signs of parkinsons disease

A

TREMOR - unilateral, pill rolling, resting
RIGIDITY - cogwheel, increased muscle tone
BRADYKINESIA- slow to initiate movements
SPEECH- slow, monotone, quiet, slurred
GAIT- reduced arm swing, shuffling, apraxic, slow to initiate movement
PSYCHIATRIC- depression, dementia, psychosis
REM SLEEP DISTURBANCE
AUTONOMIC SYMPTOMS- urinary frequency, constipated, drooling, postural hypotension, falls are late sign

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31
Q

How is parkinsons disease diagnosed?

A

clinical examination

dopamine transporter imaging - use radioactive labelled ligand binding to assess extent of nigrastriatal loss

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32
Q

How is Parkinson’s managed with medication?

A

1st line if have motor symptoms = levodopa e.g. L-dopa + decarboxylase inhibitor (carbidopa)

1st line if no motor symptoms= dopamine agonist e.g. ropinirole, bromocriptine or MAO-I e.g. seligilene

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33
Q

How does levodopa work?

A

levodopa crossed the blood brain barrier and enters nigrostriatal neurones and converted to dopamine

combined with decarboxylase inhibitor to reduce peripheral adverse effects and prolong half life

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34
Q

What are the side effects of levodopa?

A

chorea, dyskinesia, reduced efficacy over time, dry mouth, palpiatations, postural hypotension

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35
Q

Name some examples of dopamine agonists and what are their possible side effects?

A

e.g. ropinirole, pramipipexone, bromocriptine, cabergoline

psychosis, compulsive/addictive behaviour, gambling, risky behaviour, postural hypotension, excessive day time sleeping

if Ergot derived, then at risk of cardiac, pulmonary and retroperitoneal fibrosis

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36
Q

Describe an astrocytoma?

A

type of glioma
most common primary brain tumour
arise from astrocytes

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37
Q

Describe glioblastoma multiforme and what is the prognosis with this tumour?

A

highly malignant
no cell differentiation
life expectancy is <1 year

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38
Q

Describe an ependyoma?

A

derived from ependymal cells and chord plexus

better survival rate than other gliomas

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39
Q

List the different types of intracranial tumours

A
  1. gliomas
  2. meningiomas
  3. primary central nervous system lymphoma
  4. neurofibromas and schwannomas
  5. haemangioblastomas
  6. metastasis
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40
Q

Describe meningiomas

A

mostly benign tumours
arise from arachnoid membrane and granulations
compress adjacent brain structures

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41
Q

Who are primary central nervous system lymphomas most common in?

A

males
>60 y/o
immunocompromised patients

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42
Q

What are the most common types of pituitary tumours?

A

prolactinomas
growth hormone secreting adenomas
ACTH secreting adenomas

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43
Q

Which tumour might you suspect if a patient presents with visual symptoms e.g. bitemporal hemianopia

A

pituitary tumour - they comprises on the chiasma to cause visual symptoms

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44
Q

Describe haemangioblastomas

A

derived from blood vessels
occur in cerebellar parenchyma or spinal cord
associated with von hippie lindau disease, tumours in retina

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45
Q

Describe the classic triad of symptoms of raised intracranial pressure

A
  1. headache
    worse on waking, coughing, bending forward, wake up at night
  2. vomiting
  3. papilloedema
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46
Q

What is a colloid cyst?

A

cyst in 3rd ventricle that obstructs CSF flow out of the ventricle -> increases ICP -> rapidly fatal in hours

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47
Q

If a patient presents with a headache worse on bending forwards, what tumour might you suspect?

A

colloid cyst

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48
Q

Describe “cushings triad” of signs of raised intracranial pressure

A
  1. irregular respiratory rate
  2. bradycardia
  3. hypertension
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49
Q

What symptoms does herniation cause?

A

impaired consciousness
respiratory depression
bradycardia
death

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50
Q

Define coning

A

compression of medulla by herniation of the cerebellar tonsils through the foramen magnum

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51
Q

Describe “false localising signs” and why are these important?

A

important as indicate increase in brain pressure with brain shift and urgent surgery is required

6th nerve palsy
3rd nerve palsy
hemiparesis on same side as tumour

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52
Q

How do intracranial tumours present?

A
  1. effects of raised intracranial pressure
    = classic triad (headache, papilloedema, vomiting), herniation, false localising signs
  2. focal neurological signs
    = caused by direct effects of tumour and effects depend on site of tumour
  3. diffuse cereal symptoms
    e. g. seizures, cognitive symptoms
  4. tiredness
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53
Q

What are the risk factors for developing MS?

A

first degree relatives
viral infections can precipitate e.g. EBV, HHV
low levels of vitamin D and lack of sunlight - living further away from equator
women
smoking

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54
Q

Describe the pathology behind MS

A
  1. autoimmune T cell mediated demyelination of oligodendrocytes (white matter)
  2. gliosis (scarring)
  3. axonal loss
  4. conduction loss and progressive disability
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55
Q

What are the core symptoms of MS?

A

VISUAL- optic neuritis (painful eye on movement, reduce visual acuity over days, difficulty distinguishing colour, worse on heat exposure, eye pain at rest )

SENSORY - numbness, tingling, Lhermittes sign (electrical impulse down back when bend head), Uhtoffs phenomenon (symptoms worse in hot bath)

MOTOR - spastic weakness, tremor, ataxia, clumsy

OTHER SYMPTOMS - urinary incontience, neuropathic pain, fatigue, depression, sexual dysfunction

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56
Q

What are the later signs of MS?

A 
spastic tetra paresis
nystagmus 
urinary incontinence
pseudo bulbar palsy 
cognitive impairment
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57
Q

What are the 4 different clinical patterns of MS presentation?

A
  1. relapsing remitting (80%)
  2. primary progressive (10-20%)
  3. secondary progressive
  4. progressive relapsing
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58
Q

Describe the relapsing remitting MS presentation?

A

most common type
symptoms occur in attacks with a characteristic time course
unpredictable onset of attacks over days, recovery over weeks
steady increase in disability

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59
Q

Describe primary progressive MS presentation

A

gradually worsening disability without relapses or remission
usually presents later
10-20% of cases

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60
Q

Describe secondary progressive MS presentation

A

gradually worsening disability progressing over years

75% of relapsing remitting evolve to this after 30 years of onset

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61
Q

Describe progressive relapsing MS clinical pattern

A

steady decline since onset with super imposed attacks

<10%

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62
Q

How is MS diagnosed?

A

MRI - multiple lesions/ plaques across brain

CSF lumbar puncture- oligoclonal IgG bands

evoked potential testing

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63
Q

What is clinically isolated syndrome?

A

an example of one of the MS disease courses
it is the 1st episode of neurological symptoms lasting for 24 hours
in 70% of patients, they have lesions across brain in MRI and can develop MS

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64
Q

How are acute relapses of MS managed?

A

short course of steroids
IV methylprednisiolone 0.5g/day for 5 days

steroids can only be used twice a year

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65
Q

Which drugs are indicated for reducing relapse of relapsing remitting MS?

A

disease modifying drugs - beta interferon or glatiramer acetate

reduce relapse by 1/3 and reduce development of new MRI lesions
SE: flu like symptoms

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66
Q

Which drugs are used to treat more aggressive forms of MS?

A

MONOCLONAL ANTIBODIES e.g. alemtuzumab, natalizumab

prevents relapses and reduces disability
used in very agressive disease or when disease modifying drugs not working

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67
Q

What are the adverse side effects of monoclonal antibodies treating MS?

A

progressive multifocal leukoencephalopathy **
fatigue
autoimmune disorders
cardiotoxicity

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68
Q

Other than medical treatment, how should MS patients be managed?

A

MDT approach - physiotherapy, occupational therapy, psychological therapy , reviewed annually by specialist

Spasticity treated with baclofen
urinary incontinence treated with anti-muscarinics or botulinum toxin injection
fatigue treated with amantadine

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69
Q

Define Guillain Barre syndrome

A

acute inflammatory (immune mediated) demyelinating polyradiculopathy

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70
Q

How is GBS caused?

A

several weeks after an infection, for example:
food poisoning e.g. campylobacter jejuni **
HIV
vaccination
respiratory infection

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71
Q

How does GBS present?

A

distal paraesthesia** that ascends up lower limbs and body over days-weeks
symmetrical proximal weakness**
tingling, numbness
asymmetrical facial weakness
autonomic dysfunction - urinary retention, diarrhoea

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72
Q

What is a major concern with GBS?

A

if have cranial nerve involvement, at risk of intercostal muscle and diaphragmatic weakness -> RESPIRATORY FAILURE

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73
Q

What is Miller Fishers syndrome?

A

variant of GBS

symptoms include: ophthalmoplegia, ataxia, areflexia, descending paralysis ***

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74
Q

How is GBS diagnosed?

A

clinical history and examination

nerve conduction studies - slow

lumber puncture - CSF protein raised, normal cell count, mild lymphocytosis

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75
Q

How is GBS managed?

A

EMERGENCY!
IV immunoglobulin for 5 days
plasma exchange

+ continuous heart monitoring, regular vital capacity, refer to ITU for ventilation

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76
Q

What is meningitis?

A

inflammation and infection of the meninges

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77
Q

What are the main bacterial infectious causes of meningitis?

A

neisseria meningitidis
streptococcus pneumoniae
listeria monocytogenes

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78
Q

What are the main viral infectious causes of meningitis?

A

enteroviruses e.g. coxsackie*
mumps
herpes simplex

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79
Q

what is the difference between bacterial and viral meningitis?

A

bacterial meningitis is lethal and sudden onset -> need urgent treatment!

viral meningitis is self limiting lasting 4-10 days

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80
Q

What is the classic meningitic syndrome triad?

A
  1. headache
  2. neck stiffness
  3. fever
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81
Q

How does meningitis present?

A 
headache
neck stiffness
fever + rigors
intense malaise and muscle aches
photophobia
vomiting
kernigs sign - pain and resistance on knee extension
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82
Q

What are the later signs of meningitis?

A

seizures
decreased consciousness
signs of septicaemic shock
petechial rash - non blanching

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83
Q

What are the signs of meningococcal meningitis?

A

petechial rash ** - non blanching
fever
headache
neck stiffness

EMERGENCY!!!

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84
Q

How is meningitis diagnosed?

A

blood cultures and septic screen

lumbar puncture

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85
Q

If a mass lesion is suspected, why can’t you perform a lumbar puncture?

A

at risk of coning of the cerebellar tonsils
high ICP = no lumbar puncture

do a CT scan first to exclude

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86
Q

What would you expect to see in both a viral and bacterial meningitis CSF sample?

A

VIRAL
+ lymphocytes, 10-2000 white cell count, colourless, normal glucose and protein

BACTERIAL
+++ polymorphs/neutrophils, 1000-5000 white cell count, turbid colour, low glucose, raised protein, +ve gram statin

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87
Q

How is meningococcal meningitis treated?

A

slow IV benzylpenicillin - given ASAP + notify public health

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88
Q

How is unknown meningitis treated?

A

IV cefotaxime = broad spectrum

+ ciprofloxacin to close contacts

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89
Q

Define encephalitis

A

inflammation of the brain parenchyma caused by a viral infection

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90
Q

Which viruses are likely to cause encephalitis?

A 
herpes simplex
enterovirus 
adenovirus
HIV
mumps and measles
rabies
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91
Q

How does encephalitis commonly present?

A
  1. personality and behavioural change
  2. progressive reduced level of consciousness
  3. seizures
  4. fever
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92
Q

How is encephalitis investigated?

A
  1. MRI - inflammation, cerebral oedema and swelling
  2. EEG - periodic sharp and slow wave complexes
  3. CSF - viral detection, elevated lymphocytes and protein, reduced glucose
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93
Q

How is encephalitis managed?

A

IV acyclovir - EMERGENCY - for 14-21 days

early treatment reduces mortality

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94
Q

How is trigeminal neuralgia caused primarily and secondarily?

A

trigeminal neuralgia is caused by compression of the trigeminal nerve root by blood vessels e.g. superior cerebellar (primary)

secondary (15%) causes: aneurysms of intracranial vessels, tumour, MS, trauma, meningeal inflammation (should do MRI and referral to neuro if suspect)

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95
Q

How does trigeminal neuralgia present?

A

FACIAL PAIN WITH NO OTHER SYMPTOMS
unilateral, sudden, short stabbing, intense, affects mandibular and maxillary divisions of trigeminal nerve, precipitated by light touch, 10/10 pain, can occur up to 100x/day

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96
Q

How is trigeminal neuralgia treated medically?

A

carbamazepine - 200mg TDS

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97
Q

What is an extradural haemorrhage?

A

blood collects between the dura mater and bone of skull

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98
Q

How is an extradural haemorrhage usually caused?

A

there is a traumatic tear in the middle meningeal artery, usually caused by a fracture to the temporal and parietal skull

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99
Q

How does an extradural haemorrhage commonly present?

A

patient has had head injury with few hours of a lucid period

after the lucid period, patient develops focal signs, deteriorating consciousness, confusion, vomiting, severe headache

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100
Q

How is an extradural haemorrhage diagnosed?

A

CT HEAD - biconvex/lens shaped haematoma

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101
Q

how is an extradural haemorrhage treated?

A

urger referral to neurosurgeons for clot evacuation

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102
Q

What is a subdural haemorrhage?

A

accumulation of blood in the subdural space (between dura mater and arachnoid mater) following rupture of the cortical vein

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103
Q

How does a subdural haemorrhage commonly occur?

A

caused by trauma to the head in a patient with a shrunken brain e.g. alcoholics, elderly

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104
Q

What is the common history of a patient with a subdural haemorrhage?

A
  1. INJURY - minor
  2. LATENT INTERVAL - days-months
  3. SYMPTOMS START - fluctuating, drowsiness, headache, confusion, personality change, focal deficits
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105
Q

What is the classic sign of a subdural haemorrhage on the CT?

A

crescent/ sickle shape

midline shift

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106
Q

How is a subdural haemorrhage managed?

A

refer to neurosurgeons

irrigation/ evacuation via burr hole to relieve high ICP

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107
Q

What are the likely causes of a subarachnoid haemorrhage?

A
  1. TRAUMA - most common
  2. SPONTANEOUS
    saccular berry aneurysms in circle of willis (80%) - associated with Polycystic kidney disease, Ehlers danlos
    arteriovenous malformation (15%)
    Other rarer causes (<5%) - acute bacterial meningitis, tumours, coarction of the aorta
108
Q

What are the risk factors for a subarachnoid haemorrhage?

A

family history
smoking
hypertension
polycystic kidney disease

109
Q

How does a subarachnoid haemorrhage commonly present?

A

sudden severe thunderclap headache - often occipital, warning sentinel headache previous
transient loss of consciousness/ seizure
nausea and vomiting after headache
meningism symptoms: neck stiffness, papilloedema, neck stiffness

110
Q

What is a sentinel headache?

A

a generalised headache in the weeks before a subarachnoid haemorrhage due to a small leak before rupture of berry aneurysm

111
Q

What are the complications of a subarachnoid haemorrhage?

A 
rebreeding (>10%)
cerebral ischaemia
hydrocephalus 
hyponatraemia 
seizure
coma
112
Q

How is a subarachnoid haemorrhage diagnosed?

A

CT HEAD - star shaped lesion

LUMBAR PUNCTURE - 12 hours after onset of symptoms, if CT -ve but high suspicion,
CSF= xanthochromic (yellow) due to bilirubin breakdown of haemoglobin (do not do if high ICP)

113
Q

How is a subarachnoid haemorrhage managed?

A

EMERGENCY
refer to neurosurgeons
surgery = endovascular coiling within 24 hrs, whilst waiting bed rest, monitoring of BP, no exertion
medical= nimodipine for 3 weeks to control hypertension

114
Q

What are the two types of common presentation of myasthenia gravis?

A 
young women (20-35 y/o) -> acute, severely fluctuating 
older men (60-75 y/o) -> oculobulbar presentation
115
Q

What is the pathology behind myasthenia gravis?

A

autoimmune disorder where antibodies are directed against postsynaptic acetylcholine receptor at neuromuscular junctions -> decreased neurotransmission -> weakness and fatiguability

116
Q

What are the main symptoms of myasthenia gravis?

A

muscle fatiguability and fluctuating weakness :

  1. extraocular muscles - diplopia
  2. proximal muscle weakness
  3. dysphagia
  4. ptosis
117
Q

When is weakness worse in myasthenia gravis?

A 
exercise
end of day
infection
change of climate
emotion
drugs e.g. opiates, tetracycline, beta blockers
pregnancy
118
Q

What are the commonly affected muscles in myasthenia gravis and what are their presentations?

A

OCULAR **
cognans lid twitch, ptosis, diplopia

BULBAR**
dysphagia, dysphonia

PROXIMAL LIMB*
fatigue on repeated movements

RESPIRATORY MUSCLES
shortness of breath

NECK WEAKNESS
difficulty lifting head up

CRANIAL MUSCLE WEAKNESS
weak face and jaw, dysarthria

119
Q

How is myasthenia gravis diagnosed?

A
  1. TENSILON TEST**
    IV bolus of edrophonium (anti cholinesterase) and will improve fatiguability within seconds for 2-3 mins
  2. serum acetylcholine receptor antibody (85% of patients) or MUSK antibodies (50% of patients)
  3. thymus imaging - hyper plasmic thymus as a cause
120
Q

How is myasthenia graves managed long term?

A

oral acetylcholinesterase inhibitor e.g. PYRIDOSTIGMINE

- prevents destruction of acetylcholine in the synaptic space so more ACh for transmission

121
Q

What are the side effects of pyridostigmine?

A

increased salivation
sweats
lacrimation
cholinergic crisis - severe weakness, colic, diarrhoea

122
Q

How are myasthenic crises managed?

A
  1. plasmapheresis

2. IV immunoglobulin

123
Q

What is hydrocephalus?

A

excessive volume of CSF within the ventricular system of the brain and is caused by an imbalance between CSF production and absorption

124
Q

How does hydrocephalus present?

A

present with symptoms due to raised intracranial pressure including…

headache
nausea and vomiting
papilloedma
coma - severe

125
Q

how is hydrocephalus classified?

A
  1. OBSTRUCTIVE HYDROCEPHALUS = non communicating
    due to a structural pathology blocking the flow of CSF, dilatation of ventricular system is superior to site of obstruction
  2. NON OBSTRUCTIVE HYDROCEPHALUS= communicating
    due to imbalance of CSF production absorption
126
Q

What are the causes of obstructive hydrocephalus?

A

tumours
acute haemorrhage
developmental abnormalities e.g. aqueduct stenosis

127
Q

What are the causes of non-obstructive hydrocephalus?

A

increased production of CSF caused by choroid plexus tumour

failure of reabsorption e.g. meningitis, post haemorrhagic

128
Q

how is hydrocephalus diagnosed?

A
  1. lumbar puncture

2. CT head

129
Q

What is normal pressure hydrocephalus?

A

ventricular dilatation in the absence of raised CSF pressure on lumbar puncture

130
Q

What is the classic triad of features of normal pressure hydrocephalus?

A
  1. urinary incontinence
  2. dementia - reversible cause of dementia in elderly!
  3. gait abnormality
131
Q

How is normal pressure hydrocephalus diagnosed?

A

lumbar puncture - CSF pressure normal

Neuroimaging (MRI/CT) - hydrocephalus with an enlarged 4th ventricle

132
Q

How is normal pressure hydrocephalus managed?

A

Medical - carbonic anhydrase inhibitors e.g. acetazolamide

Surgical - ventriculoperitoneal shunting

133
Q

What are the most common sites for an atheromatous plaque?

A

origin of internal carotid artery
within carotid syphon
origin of vertebral arteries

134
Q

What areas of the brain does the middle cerebral artery supply?

A

largest branch of the internal carotid artery and supplies largest area of cerebral cortex:

  1. motor cortex
  2. sensory cortex
  3. wernickes area (comprehension of speech)
  4. Brocas area (expression of speech)
135
Q

Which areas of the brain does the posterior cerebral artery supply?

A 
terminal branches of basilar artery which supply...
medial inferior temporal lobes
occipital lobe
visual cortex
midbrain
thalamus
136
Q

Which structure is involved if a patient has locked in syndrome?

A

bilateral infarction in ventral pons

137
Q

If a patient presents with ataxia, dysarthria and hiccoughs, which area is affected in their brain?

A

cerebellum

138
Q

When is thrombolysis contraindicated for ischaemic strokes?

A 
major infarct 
recent surgery 
birth 
severe liver disease
INR >1.7 
on anticoagulants
139
Q

What is an epileptic seizure?

A

sudden synchronous discharge of cerebral neurones causing symptoms or signs that are apparent either to patient or witness

140
Q

What is epilepsy?

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain causing seizures

141
Q

What are the possible causes of seizures?

A 
genetic 
epilepsy 
hippocampal sclerosis * 
trauma e.g. depressed skull fracture, intracranial haemorrhage
surgery 
brain tumours 
vascular disorders
neurodegenerative disorders 
alcohol and drugs 
inflammatory conditions e.g. encephalitis, cerebral abscesses, chronic meningitis
142
Q

What is the difference between partial and generalised seizures?

A

partial/ focal seizures = caused by electrical discharge restricted to a limited part of the cortex of one cerebral hemisphere

Generalised seizures= simultaneous involvement of both hemispheres

143
Q

What are the types of partial seizures?

A

simple partial
complex partial
partial seizures with secondary generalisation

144
Q

What are the types of generalised seizures?

A

total absence (petit mal)
tonic clonic (grand mal)
myoclonic
atonic

145
Q

Describe a simple partial seizure

A

conscious
isolated limb jerking on one side
Todd paralysis can follow (local temporary paralysis of limbs)

146
Q

Describe a complex partial seizures

A

loss of consciousness and awareness for 1-2 mins
preceding aura
speech arrest, lip smacking, dystonic limb posturing
post ictal confusion

147
Q

Describe a partial seizure with secondary generalisation

A

spread of electrical activity to both sides of the brain

remember initial part of seizure before losing consciousness

148
Q

Describe total absence seizures

A

begin in childhood
loss of awareness
vacant expression for <10s before return to normal like nothing happened

149
Q

Describe tonic clonic seizures and its stages

A

Prodrome: no warning or aura

Tonic clonic phase: stiffening (tonic) followed by synchronous jerking of limbs (clonic) + tongue biting, eyes open, incontinence

Post ictal phase: period of placid unresponsiveness, confusion, drowsiness, headache

150
Q

Describe myoclonic seizures

A

sudden limb/trunk/face jerking
only clonic symptoms
eye rolling

151
Q

Describe atonic seizures

A

sudden collapse with loss of muscle tone

loss of consciousness

152
Q

How is epilepsy diagnosed?

A

Clinically based * - history of seizure, eye witness, triggers

EEG - categorise seizures and understand cause

153
Q

What is status epilepticus?

A

continuous seizures for >30 mins or 2 or more seizures without recovery of consciousness between them
mortality of 10-15%

154
Q

How is status epilepticus managed?

A
  1. lorazepam IV 4mg bolus
  2. oxygen
  3. monitor BP
  4. ECG
  5. bloods
155
Q

How is a prolonged seizure (>5 mins) managed or repeated seizures?

A

emergency!
rectal diazepam or buccal midazolam
monitor airway

156
Q

What is 1st line treatment for generalised seizures?

A

sodium valproate

increases GABA concentration and inhibits Na+ channel and inhibits glutamate decarboxylase at synapse

157
Q

What is 2nd line treatment for generalised seizures?

A

lamotrigine
carbamazepine
(choose these if women at childbearing age/ pregnant as sodium valproate is tetragenic)

158
Q

What is 1st line treatment for focal partial seizures?

A

carbamazepine

= inhibits sodium channels so decrease number of action potentials

159
Q

What are the possible causes of syncope?

A 
hypoglycaemia
vertigo
migraine
pseudo-seizure
TIA
panic attacks
postural hypotension
cardiac causes
160
Q

How does syncope present?

A

prodrome = brief, dizziness, light headed, sweating, nausea

blackout = lie still but can twitch, pale, incontinence?

recovery= quick, general fatigue

161
Q

List the types of syncope

A

cardiac syncope e.g. arrhythmias, heart attack
micturition syncope
neurogenic= inappropriate activation fo cardio inhibitory and vasodepressor reflex leading to hypotension
cough syncope
orthostatic = autonomic failure
carotid sinus syncope
convulsive syncope

162
Q

What are the causes of carpal tunnel syndrome?

A 
"MEDIAN TRAPS"
M- myxoedema 
E- enforced flexion
D- diabetic neuropathy
I- idiopathic
A- acromegaly
N- Neoplasm
T- thyroid (hypo)
R- rheumatoid arthritis
A- amyloidosis
P- pregnancy
S- sarcoidosis
163
Q

What are the muscles that the median nerve controls?

A 
muscles of precision grip "LOAF"
L- lumbricals
O- opponens pollicis
A- abductor pollicis brevis
F- flexor pollicis brevis
164
Q

Which nerves roots are the median nerve supplied by?

A

C6
C7
C8
T1

165
Q

How does carpal tunnel present?

A

tingling, pain and numbness in hand - wakes patient from sleep or in the morning, relieved by shaking of arm/hand

weakness of thenar muscles esp abductor pollicis brevis

sensory loss affects palm and maternal 3 1/2 digits

166
Q

Which 2 tests are used to diagnose carpal tunnel syndrome?

A

Tinels sign- tapping on carpal tunnel reproduces tingling and pain

Phalanx test - forced wrist flexion causes similar sensory symptoms

167
Q

How is carpal tunnel managed?

A

splint: worn at night , avoid repetitive strain at work
carpal tunnel steroid injection
surgical decompression

168
Q

What causes ulnar nerve compression?

A

fracture of the ulna **

prolonged/ recurrent pressure at ulnar e.f. screwdrivers, crutches, cycle handlebars

169
Q

How does ulnar nerve compression present?

A

tingling or numbness in the little finger/ ring finger/ ulnar side of hand distal to wrist
sensory loss
wasting of hypothenar muscles
“ulnar claw hand”

170
Q

Which muscles does the ulnar nerve supply?

A

adductor pollicis
abductor digiti minimi
interossi

171
Q

Which muscles/ areas does the radial nerve supply?

A 
triceps
brachioradialis 
supinator 
wrist and finger extensors
long thumb abductor
172
Q

How does a radial nerve compression present?

A

wrist drop
weakness of finger extension
sensation loss in anatomical snuff box

173
Q

Which nerve roots is the common peroneal nerve supplied by?

A

L4, L5, S1, S2 nerve roots

174
Q

How does compression of the common peroneal nerve present?

A

foot drop
weakness of eversion and dorsiflexion
sensory loss on the anterolateral border of shin and dorsum of foot

175
Q

How can spinal cord compression be caused?

A

trauma
degenerative disease e.g. spinal canal stenosis, spondolysis
spinal cord temps
infective lesions e.g. epidural abscess, HIV, tuberculoma
epidural haemorrhage

176
Q

How can spinal cord compression present depending on site of lesion?

A

lesions above C5 = legs and arms UMN
lesions C5- T1 = involves arms (LMN and UMN signs) and legs (UMN signs)
lesions below T1 = do not involve arms

pain
limb weakness
sensory loss below lesion
sphincter disturbance - bladder hesitancy, frequency, painless retention, constipation
spastic paraparesis
177
Q

Which diagnostic test is most appropriate if suspect spinal cord compression

A

MRI

178
Q

What is caudal equina?

A

compression of caudal equina

179
Q

What are the causes of cauda equina?

A 
disc herniation*
metastasis *
spinal infection or inflammation 
lumbar spondylosis 
lumbrosacral nerve lesions
180
Q

How does caudal equina present?

A

sudden onset and quick progression
lower back pain and radicular pain down legs
loss of sphincter tone - post void incontinence, urinary retention, constipation
saddle anaesthesia
LMN signs in lower limbs

181
Q

How is caudal equina diagnosed?

A

MRI

182
Q

How is caudal equina managed?

A

SURGICAL EMERGENCY

surgical decompression

183
Q

What are the causes of peripheral neuropathy?

A

“DAVID”

DIABETIC NEUROPATHY
“walking on cotton wool/ cobblestones”
use monofilament to assess sensation
loss of deep tendon reflexes, muscle weakness, neuropathic ulcer, callus

ALCOHOL NEUROPATHY
EMG, nerve conduction studies, LFT

VITAMIN B12 DEFICIENCY
transient, decreased vibratory and joint position sense + other signs e.g. lemon tinge, splenomegaly, pallor

INFECTIVE / INHERITED
Gullain barre syndrome: symmetrical proximal weakness and distal ascending paraesthesia
Charcot Marie tooth: glove and stocking distribution, “champagne bottle” legs

DRUGS
isoniazid, amiodarone, nitrofurantoin, metronidazole

184
Q

what is motor neurone disease?

A

progressive degeneration of motor neurones in the motor cortex and in the anterior horns of the spinal cord

185
Q

What are the 4 different presentations of motor neurone disease and do they have LMN/UMN signs?

A

amyotrophic lateral sclerosis * - UMN + LMN
progressive muscular atrophy - LMN
progressive bulbar and pseudo bulbar palsy - UMN + LMN
primary lateral sclerosis - UMN

186
Q

What is the pathology behind ALS?

A

damage to the lateral corticospinal tracts

loss of motor neurones in the motor cortex and anterior horn of cord

187
Q

How does ALS present?

A

UMN and LMN signs: progresses from one limb to another, asymmetrical
50% have cognitive impairment
10% develop fronto temporal dementia

188
Q

What is the pathology behind progressive muscular atrophy and what are the signs?

A

anterior horn cell lesion so only LMN affected
asymmetrical in small muscles of hands and feet
hands have atrophy, weakness and cramps

189
Q

What is the pathology behind progressive bulbar palsy and its prognosis?

A

degeneration of motor neurones in cranial nerves IX-XII

worse prognosis due to increased risk of aspiration

190
Q

How does bulbar palsy present?

A 
prominent fasciculations in tongue and wasting - weak tongue 
weak palate 
dysphagia 
nasal regurgitation and nasal voice
dysarthria / slurred speech 
disturbed emotional state
191
Q

How does pseudo-bulbar palsy present?

A

UMN bilaterally
spastic dysarthria
dysphagia
emotional lability

192
Q

How does primary lateral sclerosis present and what is its prognosis?

A

slower progression and better prognosis

onset in legs and progresses to arms and bulbar muscles
respiratory muscles involved
spastic tetra paresis
sensory symptoms

193
Q

What upper motor neurone signs are seen in MND?

A 
spastic paralysis 
brisk reflexes 
clonus 
extensor plantar response = babinski 
no wasting or fasciculations
194
Q

What lower motor neurone signs are seen in MND?

A 
flaccid paralysis 
muscle wasting
fasciculations 
reduced or absent reflexes 
plantar responses flexor or absent 
no clonus
195
Q

How is MND diagnosed?

A

electromyography - presence of denervation in muscles supplied by more than one spinal region
nerve conduction studies
MRI - to exclude skull base lesions

196
Q

How is MND managed medically?

A

Riluzole = glutamate receptor antagonist
increases survival by 2-3 months but no effect on disability
check liver enzymes regularly

197
Q

How are MND symptoms and signs managed? (conservative treatment)

A 
speech therapy and communication aids 
alter food consistency for safe swallowing 
baclofen for spasticity 
physiotherapy, walking aids
non invasive respiratory support
palliative care
198
Q

What is the diagnostic criteria for neurofibromatosis (NF1)?

A 
2 out of 7 criteria:
>6 cafe au last spots
axillary or inguinal freckles
>2 neurofibromas
optic nerve glioma
>2 iris haematomas
sphenoid dysplasia
1st degree relative
199
Q

What are the features of neurofibromatosis NF2?

A

bilateral acoustic neuromas
multiple intracranial schwannomas
fewer cafe au last spots

200
Q

How does cerebellar syndrome present?

A 
"DANISH"
D- dysdiadochokinesia 
A- ataxia
N- nystagmus
I- intention tremor
S- slurred speech
H- hypotonia
201
Q

What are the signs and symptom of progressive supra nuclear palsy?

A 
impairment of vertical gaze
parkinsonism
falls
slurred speech
POOR RESPONSE TO L-DOPA
202
Q

What are the signs and symptoms of multi system atrophy?

A 
poor response to l-dopa
parkinsonism
impotence
urinary retention
younger onset
203
Q

Describe the 2 pyramidal motor tracts and their function

A
  1. lateral corticospinal
  2. anterior corticospinal

controls voluntary control of musculature

204
Q

Describe the 4 extrapyramidal motor tracts and their functions

A

extrapyramidal = involuntary and autonomic control of musculature

  1. rubrospinal - fine control of hand
  2. reticulospinal - enhance and inhibit voluntary movements
  3. olivospinal - vision
  4. vestibulospinal - balance and posture
205
Q

What are the sensory ascending spinal tracts

A
  1. DORSAL COLUMN MEDICAL LEMNISCUS =fine touch, vibration and proprioception
    (cuneate fasciculus, gracile fasciculus)
  2. SPINOCEREBELLAR TRACTS = proprioception from lower limbs to ipsilateral cerebellum
  3. ANTEROLATERAL SYSTEM
    lateral spinothalamic = pain and temp
    anterior spinothalamic = crude touch and pressure
206
Q

What are the differentials for a painful red eye?

A
  1. optic neuritis
  2. conjunctivitis
  3. glaucoma
207
Q

What are the symptoms of optic neuritis?

A 
worse over 1 week
unilateral visual loss 
blurred and cloudy vision
pain on eye movement
poor discrimination of colours 
exacerbated by heat or exercise
208
Q

How is visual acuity assessed?

A

cover one eye with palm and test each eye using Snellen chart
test distant, near and colour vision

209
Q

What are the differentials for decreased visual acuity?

A

CONDITIONS AFFECTING THE EYE ITSELF - glaucoma, macular degeneration, cataracts, diabetic retinopathy

CONDITIONS AFFECTING OPTIC NERVE/ TRACT - trauma, tumour, infarction

210
Q

How are visual fields assessed?

A

patient sat in front of you, they cover one eye with palm and you close eye on same side
then bring in pin from periphery and test the 4 quadrants of visual fields and ask when they can see it

211
Q

What are the differentials for visual field loss?

A
  1. mononuclear field loss = retinal damage, ipsilateral optic nerve lesion
  2. bitemporal hemianopia = optic chiasma compression = pituitary tumour
  3. L/R homonymous hemianopia = contralateral optic tract lesion e.g. tumour, haemorrhage
212
Q

How are reflexes assessed in eyes?

A
  1. accommodation reflex - focus on distant object and move finger close to face and pupils constrict
  2. direct and consensual papillary reflex - shine light in each pupil and observe for pupil constriction
  3. swinging light reflex
213
Q

What are the differentials for loss of red reflexes in eyes?

A

retinal blastoma
cataracts
corneal scarring

214
Q

What are the signs of a CN3 (oculomotor) lesion?

A

“down and out” eye
ptosis
dilated fixed pupil

215
Q

what are the signs of a CN4 (trochlear) lesion?

A

defective downward glaze = vertical diplopia

216
Q

What are the signs of a CN6 (abducens) lesion?

A

defective abduction = horizontal diplopia

217
Q

What does a complete optic nerve lesion caused?

A

blindness in that eye

218
Q

List possible transient causes of unilateral visual loss

A 
central retinal vein occlusion
thromboembolism
uveitis 
amaurosis fugax - stroke, temporal arteritis 
migraine prodrome
219
Q

List possible persistent causes of unilateral visual loss

A 
trauma
glaucoma 
optic neuritis - MS
tumour 
retinal detachment
220
Q

List possible causes of bilateral visual loss

A

diabetic maculopathy

papilloedema

221
Q

What are the possible causes of optic neuritis?

A

= inflammation and damage to myelin of optic nerve

MS
infections e.g. lyme disease, measles, mumps, meningitis
sarcoidosis
B12 deficiency 
drugs - quinine
neuromyelitis optica
222
Q

How is optic neuritis managed?

A

methylprednisolone IV

immunoglobulin IV

223
Q

How are EEGs useful in investigating recurrent blackouts?

A

performed within 24-48 hours of first seizure and can help determine a diagnosis of epilepsy and seizure type

224
Q

What are they types of EEGs available?

A

sleep deprived
prolonged EEG
video telemetry
interictal EEF

225
Q

What are the primary prevention measures for a stroke?

A

Risk assessment tools - Q risk, CHADS2VASC

Lifestyle modifications - dietary advice, weight loss, physical activity, decrease alcohol, smoking cessation

226
Q

What are the secondary prevention measures for a stroke?

A

regular review and treatment of vascular disease risk factors
aspiring
statin
anti hypertensive medication

227
Q

What is the difference between CT and MRI for a patient with a stroke?

A

CT * - more commonly available and can easily differentiate between ischaemic and haemorrhage stroke

MRI - considered if clinical signs localise to posterior fossa or small as this might not be picked up on CT

228
Q

Who is involved in the rehabilitation of stroke patients?

A 
consultant physicians
nurses
physiotherapists
occupational therapists
SALT
psychologists 
social workers
229
Q

What are the side effects of triptans?

A 
warm sensation
tingling 
tightness
flushing
heaviness in face/ limbs/ chest

(contraindicated in ischaemic heart disease)

230
Q

how are cluster headaches managed long term?

A

verapamil

avoid analgesics as don’t work e.g. paracetamol, NSAIDs, oral triptans, opioids

231
Q

What are the possible complication of giant cell arteritis that is largely prevented by administering corticosteroids?

A 
permanent visual loss 
large artery complications e.g. aortic aneurysm, aortic dissection
depression
deafness
CVD 
peripheral neuropathy
232
Q

What are the red flags for Parkinsonism plus syndromes?

A

early falls
unresponsive to L-dopa
symmetrical

233
Q

What are the features of progressive supra nuclear palsy?

A 
Parkinsonism
impairment of vertical gaze
pseudo bulbar palsy 
dementia
falls
234
Q

What are the features of multi system atrophy?

A 
parkinsonism
urinary retention
impotence
ataxia
postural hypotension
cerebellar signs
235
Q

How is horners syndrome caused?

A

1st order: MS *, trauma, spinal cord tumours
2nd order: apical lung tumour, lymphadenopathy, neuroblastoma
3rd order: cluster headache, herpes zoster infection, temporal arteritis

236
Q

What are the features of horners syndrome?

A

compression of the faces sympathetic nerve supply

  1. ptosis - drooping of eyelid
  2. anhidrosis - loss of sweating
  3. miosis - pupil constriction

+/- enopthalmos (sunken eye)

237
Q

What are the features of Bells palsy?

A

LMN unilateral facial nerve plasy
sudden onset
post auricular pain, altered taste, dry eyes

238
Q

How is bells palsy managed?

A
  1. prednisolone for 10 days

2. eye care: eye drops, artificial tears

239
Q

Define TIA

A

transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischameia, without acute infarction

240
Q

How is a TIA caused?

A

atherothromboembolism
cardio embolism e.g. post MI, AF, valve disease
hyperviscocity e.g. polycythaemia, sickle cell anaemia

241
Q

What are the clinical features of TIA?

A 
sudden onset where symptoms improve within 24 hours
numbness
weakness
slurred speech
visual disturbance
242
Q

which features are seen in a TIA in the anterior circulation?

A

dysphagia
contralateral hemiparesis
contralateral homonymous visual field loss
amaurosis fugax

243
Q

which features are seen in a TIA in the posterior circulation?

A 
dysphagia 
diplopia
vertigo
dysarthria
ataxia
LOC
244
Q

Which risk stratifying score if used after TIA to assess the risk of stroke?

A 
ABCD2
Age >50 y/o
Blood pressure >140/90 mmHg
Clinical features e.g. unilateral weakness, speech difficulties
Diabetes
Duration of symptoms >60 mins
245
Q

How do you interrupt ABCD2 scores?

A 
>4 = assessment by specialist within 24 hours
>6 = strong risk of stroke
246
Q

If see a person who has had a TIA, how should they be managed?

A
  1. aspirin 300mg immediately
  2. if suspected tIA in last 7 days, urgent specialist referral within 24 hours
  3. do not drive for 1 month
247
Q

How should person who has had a TIA be managed long term?

A
  1. clopidogrel 1st line
  2. carotid endarterectomy if carotid stenosis >70% (often regional anaesthetic so can see if pt experience neurological symptoms during surgery)
248
Q

Define stroke

A

clinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance which lasts more than 24 hours or leads to death

249
Q

What are the 2 types of stroke?

A
  1. ischaemic stroke **

2. hemorrhagic stroke

250
Q

How are ischaemic strokes caused?

A

= neurological dysfunction due to ischaemia and death of brain, spinal cord or retinal tissue following vascular occlusion or stenosis

  1. thrombosis due to atherosclerosis
  2. embolus due to fatty material from an atherosclerotic plaque/clot
251
Q

List the possible risk factors for an ischaemic stroke?

A 
hypertension **
smoking **
alcohol misuse/ drug misuse 
hyperlipidaemia
elderly
diabetes mellitus 
physical inactivity
infective endocarditis 
valvulvar disease
sickle cell disease
anti phospholipid syndrome
CKD
obstructive sleep apnoea
252
Q

How are haemorrhage strokes caused?

A

= neurological dysfunction caused by a local collection of blood from rupture of a blood vessel either:

  1. within the brain = intracerebral
  2. subarachnoid haemorrhage
253
Q

list the risk factors for a haemorrhage stroke?

A

age
hypertension
anti coagulants
arteriovenous malformation

254
Q

List the general features of a stroke

A 
motor weakness
speech problems 
swallowing difficulties
visual field defects
balance problems
255
Q

list the features of a cerebral hemisphere infarct?

A

contralateral hemiplegia: flaccid -> paralysis
contralateral sensory loss
contralateral homonymous hemianopia
dysphagia

256
Q

List the features of posterior cerebral artery occlusion?

A

dysphagia
diplopia
dysarthria

257
Q

List the features of brainstem infarct

A

quadriplegia
lock in syndrome
horners syndrome
nystagmus

258
Q

List the features of a haemorrhage stroke?

A

decrease LOC
vomiting
headache
seizures

259
Q

what are the possible early complications of a stroke?

A

cerebral oedema
haemorrhage transformation to ischaemic stroke
seizures
venous thromboembolism
cardiac complications e.g. MI, AF
infection risk e.g. aspiration pneumonia, UTI, cellulitis from pressure sore

260
Q

List the possible late complications of stroke?

A
  1. mobility problems- hemiparesis/ hemiplegia, ataxia, falls, spasticity
  2. communication problems - dysphasia, dysarthria
  3. fatigue - disturbed sleep
  4. pain - neuropathic or MSK
  5. continence issues
  6. depression, anxiety
  7. swallowing difficulties - poor nutrition, poor oral hygiene, dysphagia
  8. cognitive - dyspraxia, impairment of attention and spatial awareness
261
Q

which system is used to classify strokes?

A

Oxford stroke classification “Bamford”
should assess:
1. unilateral hemiparesis +/- hemisensory loss
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

262
Q

What is the FAST test?

A

Face Arm Speech Test - used for rapid assessment of someone if suspect having a stroke

263
Q

what should first be done when someone presents with a stroke?

A

CT scan - differentiate between haemorrhage or ischaemic stroke

264
Q

If an ischaemic stroke and no contraindications, how are they managed?

A

IV recombinant tissue plasminogen activator e.g. alteplase given within 4.5 hours

265
Q

List the secondary prevention lifestyle advice given to stroke patients?

A
  1. encourage physical activity
  2. smoking cessation
  3. diet optimisation
  4. alcohol consumption under limits <1 units/week
  5. control diabetes
  6. arrange pre winter influenza vaccinations
  7. treat heart failure
266
Q

How are stroke patients managed with medical management?

A
  1. anti platelet therapy with clopidogrel 75mg daily + aspirin for first 3 months (+ warfarin if AF)
  2. statin e.g. atorvastatin 20-80mg daily
  3. anti hypertensives and aim for systolic <130mmHg
267
Q

what are the risks of a carotid endarterectomy?

A 
stroke risk
MI
death
wound haematoma 
at risk of damaging: hypoglossal nerve, vagus nerve

3a Neurology (2 decks)

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