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3a > Neurology (Z=>F) > Flashcards

Neurology (Z=>F) Flashcards

1
Q

Describe myelin in terms of resistance and capacitance

A
  • Increase resistance
  • Decrease capacitance (ability to store charge)
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2
Q

Is myelin found in cells of CNS or PNS?

A

both!

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3
Q

What is myelin sheath made out of ?

A

made of lipid-rich substance (mainly lipoprotein)

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4
Q

What is Multiple sclerosis (MS)?

A

Chronic and progressive condition causing demyelination and axonal loss of neurones of the CNS

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5
Q

Does MS affect CNS or PNS?

A

Just CNS. PNS not affected.

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6
Q

MS Epi?

A
  • Young adults (20 - 40)
  • more common in women
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7
Q

MS pathophysiology/aetiology?

A

Autoimmune process
- Inflammation around myelin and infiltration of immune cells => damage to myelin => affect electrical conduction along the nerve

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8
Q

How to patients often present to health services with MS?

A

present with an “attack” (e.g. episode of optic neuritis) and MRI would likely show other lions of demyelination throughout CNS

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9
Q

How does early on MS compare to later on?

A

Early disease: demyelination may occur => symptoms resolve
Later: remyelination is incomplete => symptoms gradually become worse

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10
Q

What are those buzzwords to describe MS diagnosis? what does it mean?

A

Lesions disseminated in time and space
- lesions change location over time => different nerves are affected => symptoms change over time

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11
Q

MS RF? (5)

A
  • FHx
  • EBV
  • Living further away from the equator
  • Smoking
  • Obesity
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12
Q

Signs and symptoms of MS. onset? duration?

A
  • Usually progress over >24 hrs
  • Symptoms usually last days- weeks
    (then improve)
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13
Q

What is optic neuritis ?

A

(most common MS presentation)
demyelination of optic nerve => unilateral reduced vision developing over hours-days

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14
Q

Optic neuritis symptoms (4)

A
  • Pain on eye movement
  • Vision loss
  • Central scotoma
  • Impaired colour vision

(unilateral)

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15
Q

Name some MS symptoms

A

Can affect anywhere!
- Central: fatigue, cognitive impairment, depression
- Visual: nystagmus, optic neuritis
- Speech: dysarthria
- Throat: dysphagia
- MSK: weakness, spasms, ataxia
- Sensation: pain, numbness, tingling
- Bowel: incontinence, diarrhoea, constipation
- Urinary: incontinence, frequency, retention

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16
Q

What is the first episode of demyelination + neuro signs + symptoms called? why this not MS?

A

Clinically isolated syndrome
- Cannot be diagnosed as MS with just 1 episode

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17
Q

Describe relapsing remitting MS disease course. How is it subdivided?

A

(most common)
- episodes of disease followed by recovery
- active/not active
- worsening/ not worsening

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18
Q

what does active or no active MS mean?

A

Active: symptoms developing or new lesions appearing on MRI

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19
Q

What does worsening or not worsening MS mean?

A

Worsening: overall worsening of disability over time

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20
Q

What is secondary progressive MS?

A

initially relapsing-remitting but now progressive worsening of symptoms with incomplete remissions

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21
Q

What is primary progressive MS?

A

worsening of disease + neurological symptoms without initial relapses + remissions

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22
Q

How do you get MS diagnosis? what criteria?

A
  • Based on clinical picture
  • McDonald criteria
  • Investigations can help
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23
Q

What would MRI and LP find in MS?

A

MRI: demyelinating lesions
LP: oligoclonal bands in CSF

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24
Q

MS management - 3 general bands and what do they mean?

A
  • Disease modification: disease modifying drugs => induce long term remission
  • Treating relapses: Steroids (prednisolone)
  • Symptomatic treatment: exercise, Neuropathic pain, depression, incontinence, spasticity
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25
Q

What is a stroke?

A

Acute onset of neurological symptoms of presumed vascular origin

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26
Q

What causes an ischaemic stroke? + 4 examples

A

ischaemic + infarction: caused by disruption to blood supply (thrombus, stenosis, shock (reduced BP), vasculitis)

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27
Q

What causes haemorrhage stroke?

A

haemorrhage stroke: caused by vascular rupture => intraparanchymal/SAH/…

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28
Q

What is a TIA?

A

transient ischaemic attack
- Transient neurological dysfunction secondary to ischaemia without infarction

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29
Q

Describe presentation of a stroke (5)

A
  • Asymmetrical
  • Sudden weakness of limbs
  • Sudden weakness of facial muscles
  • Sudden onset dysphasia
  • Sudden onset visual or sensory loss
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30
Q

Stroke RF (8)

A
  • CVD (angina, MI, PVD)
  • Prev stroke/TIA
  • AF
  • Hypertension
  • DM
  • Smoking
  • Vasculitis
  • Haemophilia
  • COCP
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31
Q

What screening tool is used for stroke? what does it stand for?

A

FAST
- Face
- Arms
- Speech
- Time (act fast and dial 999)

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32
Q

What risk score is associated with stroke? tell more - what is it actually used for? what does it stand for?

A

ABCD2 score: Risk of stoke in next 24 hours
- Age (>60)
- BP (>140/90)
- Clinical features
- Duration
- Diabetes

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33
Q

Patient presents with visual defects and perception disorders - what blood vessel effected?

A

Posterior Cerebral artery

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34
Q

Patient presents with sudden onset aphasia. what has likely caused this? be specific

A

ischaemic stroke
left (or dominant) brain hemisphere - Middle cerebral artery

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35
Q

patient presents with weakness and sensory loss of the left sided upper limb. what is this? what affected?

A

stroke
right ACA/MCA

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36
Q

Describe the management of stroke. starting from patient admitted to A&E?

A
  • Admit patient + exclude hypoglycaemia (blood glucose)
  • Immediate head CT
  • Aspirin 300mg stat (if CT head excludes primary intracerebral haemorrhage). continue aspirin for 2 weeks
  • Thrombolysis (alteplase)
  • Consider surgical intervention - thrombectomy
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37
Q

Management of TIA

A
  • Start aspirin 300mg daily
  • ABCD2 score to determine wither seen in 24 hrs or next 7 days
  • secondary prevention for CVD (atorvastatin)
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38
Q

ongoing management of stroke?

A
  • secondary prevention: clopidogrel (75mg once daily), atorvastatin (80mg), carotid stenting (if carotid US shows stenosis)
  • Treat modifiable RF (smoking, hypertension, DM)
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39
Q

layers of the meninges (out => in)

A

Dura => arachnoid => pia

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40
Q

What is GCS? min score? categories?

A

Glasgow Coma Scale
- min score 3/15
- Universal tool to assess consciousness: based on eyes, verbal + motor response

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41
Q

What is subdural haemorrhage usually caused by?

A

rupture of bridging veins (between dura + arachnoid mater)

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42
Q

How would subdural haemorrhage look on CT?

A
  • Cresent/banana
  • Not limited by cranial sutures
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43
Q

Epidemiology for subdural haemorrhage? Why?

A

elderly + alcoholics
- bridging veins become weaker and more atrophic

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44
Q

How does extradural haemorrhage look on CT?

A
  • Biconvex/lemon on CT
  • Limited by cranial sutures
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45
Q

describe SAH? usually caused by what?

A

bleeding into subarachnoid space (where CSF is)
- usually caused by ruptured cerebral aneurysm

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46
Q

SAH presentation

A

sudden onset occipital headache (thunderclap) often during strenuous activity (lifting weights, having sex)

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47
Q

SAH RF?

A
  • Hypertension, aneurysm, cocaine use, smoking, excessive alcohol
  • Cocaine + sickle cell anaemia
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48
Q

SAH investigations and what would they show?

A

CT: bright white bleed
LP: CSF will show raised Red cell count and xanthechromia (yellow colour due to bilirubin)
Angiography (CT or MRI): once SA is confirmed to locate the bleed

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49
Q

SAH management? (4)

A
  • Intubation and ventilation
  • Surgical intervention, repair vessel to preven re-bleeding
  • Nimidipine (CCB) to prevent vasospasm
  • LP or shunt insertion to preven hyrdocephalus
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50
Q

What is motor neurone disease?

A

Umbrella term that covers variety of specific diagnosis
- progressive + ultimately fatal condition where motor neurones stop working

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51
Q

Describe sensory symtoms in MND

A

none! no impact on sensory neurones so patient will experience no sensory symptoms

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52
Q

MND pathophysiology

A

progressive degeneration of U + LMN (sensory neurones spared)
- aetiology not fully understood

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53
Q

MND presentation? patient speak ?

A
  • Weakness of muscles throughout body affecting limbs, face, trunk, speech
  • patient speak: clumsiness, dropping things, tripping over, slurred speech
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54
Q

signs of LMN disease? (4)

A
  • muscle wasting
  • decreased tone
  • fasciculations
  • decreased reflexes
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55
Q

Signs of UMN disease? (3)

A
  • increased tone/spasticity
  • risk (increased) reflexes
  • upping plantar reflex
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56
Q

how is MND diagnosis made?

A

clinical presentation + exclude other conditions

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57
Q

MND management?

A

No way to halt or reverse progression of disease
- Riluzole can slow the progression of disease
- Symptomatic + supportive management

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58
Q

In general, for neuro syndromes, do signs or symptoms appear first? Which 2 exceptions are there to this rule?

A

Symptoms appear before signs except for…
- Myelopathy
- Peripheral neuropathy

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59
Q

What is a secondary brain problem?

A

Where the pathological process disrupting brain function is outside the brain

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60
Q

How many vital signs are there? what are they?

A

1) Pulse
2) BP
3) Temp
4) Respiratory rate
5) Oxygen saturation

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61
Q

Explain what usually causes a fixed and dilated pupil? go into detail

A

compression of the parasympathetic fibres on the outside of the third nerve (as it passes over the apex of the patriots part of the temporal bone (McDonalds burger nerve))
- Due to life-threatening brain swelling process

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62
Q

What are the 3 sections to the Glasgow Coma Scale? how many points to each one?

A
  • Best motor response (6)
  • Best verbal response (5)
  • Best eye opening response (4)
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63
Q

What do you have to do before performing a lumbar puncture?

A

ensure prior appropriate cranial imaging (CT head)

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64
Q

What do you have to do before scanning (radiology) a patient?

A

Make sure the patient is stable
- Airway secure, vital signs are normal (resuscitation is complete and respiratory support is appropriate)

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65
Q

How many cranial fossa are there

A

3
- anterior, middle and posterior

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66
Q

What separates the anterior and middle cranial fossae?

A

lesser win of sphenoid

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67
Q

What separates the middle and posterior cranial fossae? Name in important structure that runs over this

A
  • petrous part of temporal bone and foramen magnum
  • CNIII runs over apex of petrous temporal bone => prone to getting squished (McDonalds burger)
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68
Q

Which demential is associated with features of Parkinsonism

A

Demential with Lewy bodies

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69
Q

What is the first line option for most forms of epilepsy? except for which type of seizure?
Name an important SE

A

Sodium valproate
- First line option for most forms of epilepsy (except focal seizures)
- SE: teratogenic !

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70
Q

What medication is first line for focal seizures ? name a SE

A

Carbamazepine
- SE: agranulocytosis

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71
Q

What is status epileptics?

A
  • seizures lasting more than 5 minutes
  • or more than 3 seizures in one hour
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72
Q

Management of status epileptics in the hospital? think it through

A

ABCDE approach
- Secure the airway
- Give high-cons oxygen
- Assess cardiac and respiratory function
- Check blood glucose levels
- Gain IV access (insert a cannula)
- IV lorazepam (repeated 10 mins if seizure continues)
- IV phenobarbital if seizure persist

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73
Q

What causes neuropathic pain (pathophysiology) ?

A

Cuased by abnormal functioning of the sensory nerves => delivering abnormal and painful signals to the brain

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74
Q

What is Parkinsons disease? caused by?

A

Progressive reduction of dopamine in the basal ganglia => movement disorders

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75
Q

Parkinsons disease triad of symptoms?

A
  • Resting tremor
  • Cogwheel rigidity
  • Bradykinesia
    (classically asymmetrical)
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76
Q

Describe (vague) distribution of symptoms in PD:symmetrical or assymtetrical ?

A
  • Asymmetrical (one side is affected worse than the other)
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77
Q

What is the role of basal ganglia? explain how this links to PD?

A
  • Basal ganglia responsible for habitual movements (walking, looking around, controlling voluntary movements)
  • Substantia nigra produces neurotransmitter called dopamine
  • PD: gradual + progressive fall I production of dopamine form substantia nigra
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78
Q

Describe the tremor in PD: frequency? symmetry? effect of alcohol?

A

Pill rolling tremor (4-6 Hz (per second))
- asymmetrical
- No change with alcohol

79
Q

What would cause a PD tremor to improve? to get worse?

A
  • More pronounced when rising, worse if patients is distracted (asked to do task with other hand)
  • Improves with voluntary movement
80
Q

Describe the tremor in benign essential tremor: frequency? Symmetry? effect of alcohol?

A
  • Fine tremor:5-8 Hz (faster than PD)
  • Symmetrical
  • Improves with alcohol
81
Q

What would cause a benign essential tremor to improve? worsen?

A
  • Improves with rest, and alcohol, goes away when asleep
  • Worsens with intentional movement, tired/stress/caffeine
82
Q

Describe cogwheel rigidity? associated with what condition?

A

Associated with parkinsons disease
- Rigidity is resistance to passive movement of a joint
- You would feel the tension in the joint and movement in small increments (like little jerks)

83
Q

What is bradykinsia? how would it present?

A

Small + slower movements
- Smaller handwriting (micrographia), shuffling gait, difficulty initiating movement, difficulty turning around, reduced facial movements

84
Q

Other than the main triad, name other symptoms of parkinsons disease

A
  • Depressions
  • Insomnia
  • amnesia (inability to smell)
  • Postural instability
  • Memory/cognitive problems
85
Q

How is a diagnosis of PD made?

A

Clinical diagnosis based on symptoms and examination

86
Q

What 2 drugs are the main management for PD? How do they work?

A
  • Levadopa (Synthetic dopamin to boost dopamine levels)
    PLUS
  • carbidopa (peripheral decarboxylase inhibitor: stops levodopa being broken down before gets to brain)
87
Q

SE of PD drug treatment ? which drug ?

A

(levodopa SE)
excessive motor activity: dystonia, chorea, athetosis

88
Q

What is a benign essential tremor?

A

Common condition associated with older age: fine tremor affecting voluntary muscles

89
Q

Differential for a tremor (6)

A
  • Parkinsonism
  • MS
  • Huntingtons chorea
  • Hyperthyroidism
  • Fever
  • Medications (antipsychotics)
90
Q

features of a benign essential tremor?

A
  • Fien tremor
  • Symmetircal
  • More prominent on voluntary movement
  • Worse when tired/stressed/caffeine
  • Improves with alcohol
  • nascent during sleep
91
Q

Management of being essential tremor?

A

no definitive treatment
(lifestyle, caffeine, sleep, stress)

92
Q

What are brain tumours ?

A

they are abnormal growths in the brain (benign or malignant)

93
Q

How might brain tumours present ? kinda categories of presentation

A
  • Asymptomattic
  • Rocal neurological symptoms
  • Sign + symptoms of raised ICP
94
Q

What is an ocular sing of raised ICP? explain what causes this ?

A

papilloedema (swelling of the optic risk) on fundoscopy
- Due to pressure behind optic nerve

95
Q

what surrounds the optic nerve ?

A

the meninges

96
Q

Causes of raised ICP? (4)

A
  • brain tumour
  • IC haemorrhage
  • Idiopathic intracranial hypertension
  • Abscesses of infection
97
Q

Riased ICP presentation ?

A
  • headache
  • other features: change in mental state, confused/drowsy, visual field defects, seizures
98
Q

describe the headache associated with raised ICP? when worse ? (5)

A
  • constant
  • Worse at night (nocturnal)
  • Worse in morning
  • When when coughing/straining/leaning forward
  • Vomiting
99
Q

What types of brain tumour are there? (4)

A
  • Secondary metastases
  • Glioma (most common primary)
  • meningioma
  • pituitary tumours
100
Q

what are the most common secondary brain metastasis ? (4)

A
  • Lung
  • Breast
  • Renal cell carcinoma
  • Melanoma
101
Q

what are gliomas ? name some ? which is the most common type ?

A

tumours of the glial cells
(most common)
- astroglioma
- oligodendroglioma
- ependymoma
(least common)

102
Q

What hormone effects can a pituitary tumour have? name the hormone and the condition associated (4)

A
  • Acromegaly (high GH)
  • Hyperprolactinaemia (high prolactin)
  • Cushing’s disease (high ACTH)
  • Thyrotoxicosis (high TSH)
103
Q

treatment of pituitary tumours ?

A

trans-sphenoidal surgery

104
Q

Management of brain tumours overall ?

A

depends on type _ grade
- Palliative, chemo, radiotherapy, surgery

105
Q

What is a facial nerve palsy ?

A

Isolate dysfunction of the facial nerve (CN VII)

106
Q

facial nerve palsy presentation ?

A

usually present with unilateral facial weakness

107
Q

What is facial nerve function ? (all of them)

A
  • Motor: muscles of expression, stapedius (inner ear)
  • Sensory: Tast (anterior 2/3 of tongue)
  • Parasympathetic: supply submandibular + sublingual salivary glands + lacrimal gland
108
Q

Why do you need to differentiate between upper and lower motor neurone lesion (facial nerve)? what would general management for each be ?

A
  • UMN: refer urgently with suspected stroke
  • LMN: manage in community
109
Q

Describe the facial movements in an UMN lesion ?

A

forehead will be spare + patient can move forehead as forehead is controlled by UMN from BOTH sides

110
Q

Describe the facial movements in a LMN lesion ?

A

forehead no spared => patients cannot move forehead on affected side

111
Q

What type of motor neurone involved in a bells palsy ?

A

LMN

112
Q

what is bells palsy ?

A

idiopathic, unilateral LMN facial nerve palsy

113
Q

what is recovery from bells palsy like ?

A

most patients revere in several weeks to a yr (may still have some residual weakness)

114
Q

bells plays management ?

A
  • <72 hrs: prednisolone (50mg for 10 days)
  • lubricating eye drops for eye on affected side
115
Q

What is Ramsay-hunt syndrome ? associated with what ?

A

VZV causing unilateral LMN facial nerve palsy

116
Q

person present with painful + tender vesicular rash in the ear canal and a facial nerve palsy. What is this ?

A

Ramsay-Hunt syndrome
(VZV shingles of the face - facial nerve)

117
Q

Ramsay hunt syndrome treatment

A

prednisolone + aciclovir

118
Q

What is neuropathic pain ?

A

caused by abnormal functioning of the sensory nerves delivering abnormal + painful signals to the brain

119
Q

name some conditions that could cause neuropathic pain ?

A
  • Post-herpetic neuralgia from shingles
  • MS
  • Diabetic neuralgia
  • Trigeminal neuralgia
120
Q

Describe the pain/sensation in neuropathic pain ?

A
  • burning, tingles, pins+needles, electric shocks
121
Q

Management of neuropathic pain ? exception ?

A

usually amytripyline
- Carbamazepine is recommend for trigeminal neuralgia

122
Q

name the primary headaches ?

A
  • tension
  • Migraine
  • Cluster
123
Q

differential diagnosis for a headache (12)

A
  • Primary (tension, migraine, cluster)
  • sinusitis
  • GCA
  • Glucoma
  • ICH
  • SAH
  • Hormonal headache
  • Drug indiced
  • Trigeminal neuralgia
  • raised ICP
  • Brain tumours
  • Encephalitis/meningitis
124
Q

(headache red flag)
Hx of headache +
- fever, photophobia or neck stiffness ? (2)

A

meningitis or encephalitis

125
Q

(headache red flag)
Hx of headache +
- New neurological symptoms ? (3)

A
  • haemorrhage
  • Malignancy
  • Stroke
126
Q

(headache red flag)
Hx of headache +
- dizziness (1)

A

stroke

127
Q

(headache red flag)
Hx of headache +
- visual disturbance ? (2)

A
  • Temporal arteriis
  • Glaucoma
128
Q

(headache red flag)
Hx of headache +
- sudden onset occipital headache ? (1)

A

SAH

129
Q

(headache red flag)
Hx of headache +
- Worse on coughing or straining ? (1)

A

raised intracranial pressure

130
Q

(headache red flag)
Hx of headache +
- Postural, worse on staining, lying or bending over ? (1)

A

raised intracranial pressure

131
Q

(head ache red flag)
Hx of headache +
- vomiting (2)

A
  • raised ICP
  • Carbon monoxide poisoning
132
Q

(headache red flag)
Hx of headache +
- history of trauma

A

intracranial haemorhage

133
Q

(headache red flag)
Hx of headache +
- Pregnancy

A

pre-eclampsia

134
Q

in a patient presenting with a headache, what does fundoscopy look for and what would this indicate ?

A
  • looks for papilloedma
  • indicate raised ICP due to being tumour, benign intracranli hypertension, intracranial bleed)
135
Q

Tension headache, describe the:
site, character, severity, associated symptoms, timing ?

A
  • Site: bilateral, bandlike accrsos forehead
  • Character: pressing, tightening
  • Severity: mild or moderate, not disabling
  • Associated symptoms: stress, depression, dehydrated, no N&V, no photophobia
  • Timing: 30 min - 7 days
136
Q

What is a secondary headache ?

A

similar to tension bt with a clear cause
- Underlying medical condition

137
Q

what is sinisutus ?

A

headache associated with inflammation in ethmoidal/maxillary/frontal/sphenoidal sinuses
- tender over the affected areas

138
Q

What in an analgesic headache ? which drug associated with

A

caused by long term analgesic use (codeine, tramadol)

139
Q

Analgesic headache Management ?

A

analgesia withdrawal

140
Q

what is hormonal headache ? what hormone ?

A

related to (low) oestrogen => generic non-specific tension like headache

141
Q

whe likely to get hormonal headache ?

A

lower oestrogen
- 2/3 days beofre period
- around menopause
- start of pregnancyhor

142
Q

hormonal headache mangment ?

A

COCP can improve symptoms

143
Q

what is trigeminal neuralgia ? associated with what ? what type of pain is it ?

A

unilateral (90%) intense facial pain lasting second - hrs
- electricity-like shooting pain
- associated with MS
- neuropathic pain

144
Q

name the trigeminal branches ?

A
  • V1: opthalmic
  • V2: maxillary
  • V3: mandibular
145
Q

trigeminal neuralgia treatment ?

A

carbamazepine
(different to most other neuropathic pain which is treated with amitriptyline)

146
Q

What is a migraine ?

A

complex neuro condition that causes headache (no pathophysiology found)

147
Q

what are the 4 types of migraine ?

A
  • Migraines without aura
  • Migraines with aura
  • Silent migraine (aura, no headache)
  • Hemiplegic migraine
148
Q

Migraine: describe the site? character? severity? associated features? timing?

A
  • Site: unilateral (often bilateral)
  • Character (Pulsating/throbbing)
  • Severity: Moderate or severe, disabling (interferes with ability to perform)
  • Associated features: Nausea, vomiting, photophobia, photophobia
  • Timing: attacks last hours to days (4-72hrs)
149
Q

What is a migraine with aura ? describe

A

aura: visual changes associated with migraine
- Sparks in vision, blurring, lines, loss of visual fields

150
Q

what is a hemiplegic migraine? symptoms? what is it similar to ?

A

typical migraine symptoms + hemiplegia, ataxia, changes in consciousness
- Can mimic a stroke so need to exclude this

151
Q

what is hemiplegia ?

A

unilateral weakness of the limbs

152
Q

Migraine triggers ? (6)

A
  • stress
  • bright lights
  • strong smells
  • Certain foods (cheese, chocolate)
  • Dehydration
  • Menstruation
153
Q

What are the 5 stages of migraine ? duration of each stage ?

A
  • Prodromal (<3 days)
  • Aura (<60 min)
  • Headache (4-72 hrs)
  • Resolution
  • Prostdromal
154
Q

Acute management of a migraine ?

A
  • Acute: paracetamol/NSAIDs, triptans (50mg sumatriptan as soon as headache starts)
155
Q

Long-term management of migraine ?

A

Prophylaxis: propanolol (first line I think), amitriptyline

156
Q

What is Huntington’s chorea ? what inheritance ?

A

it is an autosomal dominated genetic condition that causes progressive deterioration in the nervous system

157
Q

when do symptoms start in Huntington’s chorea ?

A

usually asymptomatic until symptoms begin around 30-50

158
Q

what type of genetic mutation is huntingtons chorea ? why is this relevant ? what 2 things does this cause ?

A

trnucleotide repeat disorder => anticipation => earlier age onset + increased severity of disease

159
Q

huntingtons chorea presentation - what comes first ? followed by what ?

A

progressive worsening of symptoms
- starts with cognitive/psychiatric/mood problems
- followed by movement disorders

160
Q

describe the movement disorders associated with huntingtons disease ? (4)

A
  • Chorea (involuntary abnormal movements)
  • Eye movement disorders
  • speech difficulties (dysarthria)
  • swallowing difficulties (dysphagia)
161
Q

how is huntingtons disease diagnosed ?

A

genetic testing + pre/post test counselling

162
Q

what is the manamgnet of huntingtons chorea ?

A

now ay to stop or slow progression
- SLT: for speech + swallowing
- genetic counselling
- advance directives
- End of life management
- Medical

163
Q

what medications could be used to suppress the disordered movements associated with huntingtons disease ? (2) what type of drug

A
  • antipsychotics (olanzipine)
  • benzodiazepines (diazepam)
164
Q

what is the prognosis of HD ? let expectancy

A

life expectancy is 15-20 yrs after onset of symptoms

165
Q

what is often the cause of death in huntingtons disease ? (2)

A
  • Respiratory disease (pneumonia)
  • suicide
166
Q

cluster headache: describe the site? character? severity? associated features? and timing?

A

Site: unilateral
Character: excruciating, stabbing
Severity: very severe
Associated features: red+swollen eye, pupil constriction, lid drooping, lacrimation
Timing: attacks last 15 min - 3hr

167
Q

why are cluster headaches called cluster headaches ?

A

come in clusters of attacks + then disappear for a while

168
Q

Treatment of cluster headaches: acute (2) and long term (2) ?

A
  • Acute: triptans (sumatriptan), high flow 100% oxygen
  • prophylaxis: verapamil, prednisolone (short term to break up cluster of attacks)
169
Q

what is typical person to present with cluster headache ?

A

30-50 years old male smoker

170
Q

What is myasthenia gravis ? What makes it better/worse ?

A

autoimmune condition causing muscle weakness that gets progressively worse with activity and improves with rest

171
Q

with what other condition does myasthenia gravis have a strong link with

A

thyromas (tumours of thymus gland)

172
Q

myasthenia gravis pathophysioloy ?

A

acytlcholin receptor antibodies (autoantibodies) produce by immune system bind to post-synaptic NMJ receptors => block receptors => prevent EACh from being able to trigger muscle contraction => less effective stimulation of muscle with increased activity

173
Q

myasthenia gravis presentation ? variation throughout the day ? which muscles most affected ?

A

vary form to mild to life threatening, weakness gets worse with use and improves with rest, worst at end of day
- Mostly affects proximal muscles of head + neck
- diplopia, ptosis, difficulty swallowing, fatigue chewing, slurred speech

174
Q

what could you do to spot myasthenia gravis symptoms on examination ?

A

reptile exercises to induce fatigue (repetitive blinking)

175
Q

myasthenia gravis diagnosis ? (2)

A
  • test for relevant antibodies: ACh receptor antibodies
  • single fibre electromyography
176
Q

myasthenia gravis treatment ? (3) how does each work ?

A
  • Reversible acetylcholinesterase inhimitors (increase amount of ACh in NMJ)
  • Immunosuppression (suppress Ab production)
  • Thyrectomy
177
Q

complication of myasthenia gravis ? often triggered by what ? and management ?

A

myasthenia crisis
- Life threatening acute worsening of symptoms (often triggered by RTI) => resp failure
- May require intubation + ventilation, IVIg

178
Q

What is Guillain barre syndrome ? affects CNS or PNS ?

A

It is an acute paralytic polyneuropathy affecting the PNS

179
Q

what is Guillain barre syndrome usually caused by ? examples (3)

A

usually triggered by infection
- campylobacter jejuni
- Cytometaloverus
- EBV

180
Q

Guillain barre syndrome pathophysiology ? what is the fancy term for this process

A

molecular mimicry
- B cells make antibodies agains antigens on pathogen => these also happen to match proteins on myelin sheath or nerve axon => nerve damage (neuropathy)

181
Q

Guillain barre syndrome presentation ?

A

symmetrical ascending weakness
- Reduced reflexes (as it is a peripheral neuropathy)
- Peripheral loss of sensation of neuropathic pain

182
Q

Guillain barre syndrome diagnosis?

A

clinical (supported by Brighton criteria
- could do nerve conduction studies of LPw

183
Q

hat would be seen on LP in Guillain barre syndrome

A

high protein with normal cell count + glucose

184
Q

Guillain barre syndrome management ? (3)

A
  • IVIg
  • Supportive care
  • VTE prophylaxis (dlateparin)
185
Q

Charcot-marie tooth presentation ? (4)

A
  • peripheral neuorpathy
  • high foot acrches
  • reduced tendon reglexes
  • Inverted champagne bottle legs
186
Q

charcot-marie tooth inheritance pattern ?

A

autosomal dominant

187
Q

causes of peripheral neuropathy ?

A

ABCDE
- Alochol
- B12 deficiency
- Charcot-marie tooth
- Diabetes
- Every vasculitis

188
Q

what is neurofibromatosis ?

A

genetic condition causing neuromas (benign nerve tumours)
- benign but can still cause neurological + structural problems

189
Q

what is the more common type of neurofibromatosis ? what inheritance type is this ?

A

type 1 - autosomal dominant

190
Q

neurofibromatosis diagnosis

A

clinical
- CRABBING criteria (2/7 required)

191
Q

neurofibromatosis management ?

A

no treament
- treat complicaitons

192
Q

neurofibromatosis complications ?

A
  • migraines
  • epilepsy
  • renal artery stenosis (=> hypertension)
193
Q

patient presents with bilateral acoustic neuromas ? what disease does this indicate ?

A

neurofibromatosis type 2
(hearing loss, tints, vertigo)

3a (43 decks)

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