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Finals Revision > Neurology > Flashcards

Neurology Flashcards

1
Q

What is an acoustic neuroma?

A

benign tumours of the Schwann cells surrounding the auditory nerve (vestibulocochlear nerve) that innervates the inner ear.

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2
Q

Symptoms of acoustic neuroma

A 
o	Patient usually 40-60 yo
o	Vertigo (CNVIII)
o	Hearing loss – unilateral sensorineural hearing loss (CNVIII)
o	Tinnitus – unilateral (CNVIII)
o	Absent corneal reflex (CNV)
o	Facial palsy (CNVII) – if the tumour grows large enough to compress the facial nerve (NO FOREHEAD SPARING = LMN lesion)
o	Dizziness / imbalance 
o	Sense of fullness in the ear
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3
Q

Are acoustic neuromas unilateral or bilateral?

A
  • Usually, unilateral

- Bilateral vestibular schwannomas = neurofibromatosis type 2

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4
Q

What CNs are affected by acoustic neuromas?

A

cranial nerves V, VII and VIII

trigeminal, facial and vestibulocochlear

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5
Q

IX for acoustic neuroma

A
  1. Audiometry: to assess hearing loss (sensorineural pattern)
  2. Auditory brainstem reflexes: results will be abnormal
  3. Brain CT/MRI: diagnosis of tumour
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6
Q

Mx for acoustic neuroma and risks with the treatment

A
  • URGENT ENT REFERRAL
  • ENT management:
    o Conservative – monitoring if there are no symptoms
    o Surgery – to remove tumour
    o Radiotherapy – to reduce tumour growth
  • Risks with treatment:
    o Vestibulocochlear nerve injury – permanent hearing loss or dizziness
    o Facial nerve injury – facial weakness
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7
Q

Other names for acoustic neuroma

A

Vestibular schwannoma

Cerebellopontine angle tumours

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8
Q

What is Bell’s palsy?

A

an acute unilateral facial nerve weakness or paralysis of rapid onset (less than 72 hours) and unknown cause.

The history and examination otherwise are unremarkable. Deficits in all facial zones equally that fully evolve within 72 hours.

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9
Q

Cause of Bell’s palsy

A

Idiopathic

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10
Q

Symptoms of bells palsy

A
  • Single episode
  • Unilateral lower motor neurone facial nerve palsy – involves upper and lower parts of the face
    o Reduction in movement on the affected side
    o Drooping of eyebrow and corner of mouth
    o Loss of nasolabial fold
  • Rapid onset (less than 72 hours)
  • Ear and postauricular region pain
  • Difficulty chewing, dry mouth and change in taste
  • Incomplete eye closure, dry eye, eye pain or excessive tearing
  • Numbness / tingling in cheek + mouth
  • Speech articulation problems, drooling
  • Hyperacusis
  • 3-6 months later – synkinesis (abnormal & involuntary synchronous movement of a facial region with reflex or voluntary movement in another facial region)
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11
Q

Diagnosis of bells palsy

A

clinical diagnosis of exclusion

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12
Q

Mx for bells palsy

A

• If patient presents within 72 hours of symptom onset = PREDNISOLONE:
o 60mg OD for 5 days, then reduce by 10mg daily

• Eye protection
o Lubricating eye drops
o Tape eye shut at night
o Sunglasses outdoors

• Antivirals (with prednisolone) may offer small benefit, discuss with specialist

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13
Q

Complications of bells palsy

A
  1. Exposure keratopathy – eye pain, requires ophthalmology review
  2. Eye injury, corneal ulceration, vision loss
  3. Synkinesis – abnormal facial muscle contraction during voluntary movements
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14
Q

Recovery from bells palsy

A
  • Most patients fully recover over several weeks, can take 12 months to recover
  • 1/3rd are left with some residual weakness
  • Refer to a facial nerve specialist if there is no improvement after 3 weeks of treatment, there’s incomplete recovery 5 months after initial onset or there are any atypical features.
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15
Q

What is a brain abscess?

A

a suppurative collection of microbes (most often bacterial, fungal or parasitic) within a gliotic capsule occurring within the brain parenchyma. Lesions can be single or multi-focal.

It is potentially life threatening

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16
Q

Causes of brain abscesses

A
  1. Bacterial: strep pyogenes, strep milleri, staph aureus
  2. Fungal: aspergillus fumigates, candida albicans, cryptococcus neoformans
  3. Parasitic: toxoplasma gondii
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17
Q

How do brain abscesses happen?

A
  • Haematogenous spread through bloodstream

- From an infected adjacent area e.g., ears or sinuses

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18
Q

Risk factors for brain abscess

A
  • Sinusitis
  • Otitis media
  • Recent dental procedure or infection
  • Recent neurosurgery
  • Skull fracture
  • Meningitis
  • Congenital heart disease
  • Endocarditis
  • DM
  • HIV or immunocompromised
  • IVDU
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19
Q

Symptoms of brain abscess

A
  • Seizures
  • Fever
  • Localising signs
  • Signs of increased ICP
  • Signs of infection elsewhere
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20
Q

Ix for brain abscess

A
  • CT/MRI = ring enhancing lesion
  • Raised WCC
  • Raised ESR
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21
Q

Mx for brain abscess

A
  1. Neurosurgery referral
  2. Antibiotics: CEFTRIAXONE
  3. Treat raised ICP
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22
Q

Common cancers that metastasise to the brain

A

Lung
Breast
Renal cell carcinoma
Melanoma

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23
Q

Symptoms of brain mets

A 
-	Increased ICP
o	Headache worse on waking, lying down, bending forwards, coughing and straining
o	Vomiting 
o	Papilloedema 
o	Reduced GCS
-	Seizures
-	Evolving focal 
-	Subtle personality change
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24
Q

Ix for brain mets

A
  • CT/MRI brain

- Consider biopsy

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25
Q

What is cerebral palsy?

A

umbrella term referring to a non-progressive disease of the brain originating during the antenatal, neonatal or early post-natal period while brain neuronal connections are still evolving, that results in disorders of movement and posture development.

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26
Q

Prevalence of cerebral palsy

A

2 in 1000

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27
Q

Impairments seen in cerebral palsy

A
  • Disorders of movement
  • Disorders of posture
  • Learning impairment
  • Visual impairment and squint
  • Hearing loss
  • Speech and language difficulties
  • Behavioural problems
  • Epilepsy
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28
Q

Presentation of cerebral palsy

A
  • Delayed motor milestones
  • Abnormal tone in infancy
  • Persistence of primitive reflexes
  • Abnormal gait
  • Feeding difficulties
  • Other developmental delays e.g., language and social
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29
Q

What are the primitive reflexes

A 
Moro's (startle) reflex
Rooting reflex
Sucking reflex
Tonic neck reflex
Grasping reflex
Stepping reflex
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30
Q

Causes of cerebral palsy

A

• Antenatal (80%)
o Cerebral malformation
o Cerebral dysgenesis
o Congenital infection

• Intrapartum (10%)
o Hypoxic-ischaemic encephalopathy (birth asphyxia)

•	Post-natal (10%)
o	Cerebral ischaemia 
o	Intraventricular haemorrhage 
o	Head trauma
o	Hydrocephalus 
o	Non-accidental head injury 
o	Hyperbilirubinaemia (severe neonatal)
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31
Q

What are the 3 types of cerebral palsy?

A

Spastic
Ataxic hypotonic
Dyskinetic

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32
Q

Ix for cerebral palsy

A
  1. Brain imaging – USS in neonates, CT or MRI
  2. Congenital infection screen
  3. Metabolic screen
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33
Q

Mx of cerebral palsy

A

MDT

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34
Q

What is hypoxic-ischaemic encephalopathy?

A
  • Seen in neonates.
  • Ischaemic damage to the brain causes a disturbance of neurological behaviour
  • Areas most affected are the ‘watershed zones’ between the major arteries as they’re most susceptible to hypoperfusion.
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35
Q

How is hypoxic-ischaemic encephalopathy classified

A

mild (resolves over a few days)
moderate
severe (50% of mortality and 80% risk of cerebral palsy)

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36
Q

Symptoms of HIE

A

floppy after birth, seizures, irregular breathing, hypertonic

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37
Q

Ix for HIE

A 
APGAR score
fetal umbilical artery pH <7
arterial base deficit >12
MRI brain
EEG
presence of multisystemic organ failure
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38
Q

Tx of HIE

A

therapeutic hypothermia (33-35°C for 72 hrs within first 6hrs of life) and supportive measures

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39
Q

What is chronic fatigue syndrome?

A

4 months + of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain the symptoms.

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40
Q

risk factors for chronic fatigue syndrome

A

Female

Past psychiatric history

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41
Q

Symptoms of chronic fatigue syndrome

A
  • Fatigue
  • Sleep problems
  • Muscle/joint pain
  • Headaches
  • Painful lymph nodes without enlargement
  • Sore throat
  • Cognitive dysfunction
  • Physical or mental exertion makes symptoms worse
  • General malaise
  • Dizziness
  • Nausea
  • Palpitations
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42
Q

Ix for chronic fatigue syndrome

A 
•	Screening blood tests to exclude other pathology
o	FBC
o	U&E
o	LFT
o	Glucose
o	TFT
o	ESR
o	CRP
o	Calcium
o	CK
o	Ferritin 
o	Coeliac screen
o	Urinalysis
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43
Q

Mx for chronic fatigue syndrome

A
  1. CBT
  2. Graded exercise therapy
  3. Pacing
  4. Low dose amitriptyline
  5. Referral to pain management clinic
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44
Q

What is CNI, its function and foramen?

A

Olfactory
smell
Cribriform plate

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45
Q

What is CNII, its function and foramen?

A

Optic
Sight
OPtic canal

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46
Q

What is CNIII and its function

A

Oculomotor

Eye movements = superior, inferior and medial rectus & inferior oblique

Pupil constriction
Accommodation
Eyelid opening

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47
Q

What happens in CNIII palsy?

A

Palsy results in

  • Ptosis
  • Down and out eye
  • Dilated fixed pupil
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48
Q

CNIII foramen

A

Superior orbital fissure

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49
Q

Causes of CNIII palsy

A

o DM
o Vasculitis e.g., temporal arteritis, SLE
o False localising sign due to uncal herniation through tentorium if raised ICP
o Posterior communicating artery aneurysm: pupil dilated + pain
o Cavernous sinus thrombus
o Weber’s syndrome – ipsilateral third nerve palsy with contralateral hemiplegia, caused by midbrain strokes
o Amyloid
o MS

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50
Q

CNIV name, function, palsy symptoms and foramen

A

Eye movement (Superior oblique)

Palsy = defective downward gaze = vertical diplopia

Superior orbital fissure

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51
Q

What is CNV, its function and 3 foramen?

A

Trigeminal

facial sensation and mastication

V1 = superior orbital fissure
V2 = foramen rotundum
V3 = foramen ovale
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52
Q

What happens in CNV lesions?

A

Lesions =

  • Trigeminal neuralgia
  • Loss of corneal reflex (afferent)
  • Loss of facial sensation
  • Paralysis of mastication
  • Deviation of jaw to weak side
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53
Q

What is CNVI, its function, symptoms of palsy and foramen?

A

VI = abducens

Eye movement
- Lateral rectus

Palsy = defective abduction = horizontal diplopia

Superior orbital fissure

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54
Q

What is CNVII, its function, symptoms of palsy and foramen?

A

VII = facial

Facial movement
Taste anterior 2/3rds
Lacrimation
Salivation

  • Flaccid paralysis of the upper and lower face
  • Loss of corneal reflex (efferent)
  • Loss of taste
  • Hyperacusis

Internal auditory meatus

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55
Q

What is CNVIII, its function, symptoms of palsy and foramen?

A

VIII = vestibulocochlear

Hearing
Balance

Hearing loss
Vertigo
Nystagmus
Acoustic neuroma

Internal auditory meatus

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56
Q

What is CNIX, its function, symptoms of palsy and foramen?

A

IX = glossopharyngeal

Taste (posterior 1/3rd)
Salivation
Swallowing
Mediated input from carotid body & sinus

Hypersensitive carotid sinus reflex
Loss of gag reflex (afferent)

Jugular foramen

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57
Q

What is CNX, its function, symptoms of palsy and foramen?

A

X = vagus

Phonation
Swallowing
Innervates viscera

Uvula deviates away from site of lesion
Loss of gag reflex (efferent)

Jugular foramen

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58
Q

What is CNXI, its function, symptoms of palsy and foramen?

A

XI – accessory

Head and shoulder movement

Weakness turning head to contralateral side

Jugular foramen

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59
Q

What is CNXII, its function, symptoms of palsy and foramen?

A

XII – hypoglossal

Tongue movement

Tongue deviates towards side of lesion

Hypoglossal canal

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60
Q

Afferent and efferent limb of corneal reflex

A 
Ophthalmic nerve (V1)
Facial nerve
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61
Q

Afferent and efferent limb of jaw jerk

A

Mandibular nerve

Mandibular nerve

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62
Q

Afferent and efferent limb of gag reflex

A

glossopharyngeal nerve

Vagal nerve

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63
Q

Afferent and efferent limb of carotid sinus reflex

A

Glossopharyngeal nerve

Vagal nerve

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64
Q

Afferent and efferent limb of pupillary light reflex

A

Optic nerve

Oculomotor nerve

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65
Q

Afferent and efferent limb of lacrimation reflex

A 
Ophthalmic nerve (v1)
Facial nerve
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66
Q

What is dementia

A

a syndrome characterised by deterioration in cognition resulting in impairment in the activities of daily living. Cognitive decline often affects multiple domains.

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67
Q

Memory screening tools

A 
o	10 point cognitive screener 
o	6 item cognitive impairment test
o	Abbreviated mental test score
o	GP assessment of cognition 
o	Mini mental state examination (MMSE score <24 = dementia)
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68
Q

Bloods for impaired memory

A 
o	FBC
o	U&E
o	LFT
o	Calcium 
o	Glucose
o	ESR/CRP
o	TFTs
o	Vitamin B12
o	Folate
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69
Q

causes of dementia

A
  • Alzheimer’s disease
  • CVS – multi infarct dementia
  • Lewy bpdy dementia
  • Huntington’s
  • CJD
  • Pick’s disease – atrophy of frontal and temporal lobes
  • HIV
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70
Q

Symptoms of Alzheimer’s disease

A

Progressive persistent global cognitive impairment. Short term memory impairment.
Irritable, behaviour/mood change. Apathy.

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71
Q

causes of Alzheimer’s disease

A

Unknown

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72
Q

Risk factors for Alzheimer’s disease

A

amyloid precursor protein gene mutations and old age

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73
Q

Ix for Alzheimer’s disease

A

MMSE

CT head

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74
Q

Pathology of Alzheimer’s disease

A

Accumulation of B-amyloid peptide that results in progressive neuronal damage, neurofibrillary tangles, amyloid plaques and loss of ACh

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75
Q

Tx for Alzheimer’s disease

A

Acetylcholinesterase inhibitors e.g. donepezil, rivastigmine, galantamine.

NMDA antagonist = memantine

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76
Q

Symptoms of vascular dementia

A

Sudden onset and stepwise deterioration

Cognitive impairment, motor disorders and changes in behaviour.

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77
Q

Cause of vascular dementia

A

Cumulative effect of many small strokes.

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78
Q

RFs for vascular dementia

A

HTN, DM, hyperlipidaemia, old age, TIA, AF, smoking, obesity, CAD

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79
Q

Ix for vascular dementia

A

MMSE
US of carotids
Cranial MRI – infarcts and extensive white matter changes

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80
Q

Mx for vascular dementia

A

There’s damage to grey and white matter from vascular causes

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81
Q

Tx for vascular dementia

A

Treat risk factors.

Antiplatelet therapy e.g. aspirin to prevent strokes/TIA

There is often co-morbid Alzheimer’s so then give a cholinesterase inhibitor

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82
Q

What are the 3 main subtypes of vascular dementia?

A

3 main subtypes:

  • Stroke related VD
  • Subcortical VD (small vessel disease)
  • Mixed dementia – VD + alzheimer’s
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83
Q

Symptoms of frontotemporal dementia

A

Onset in middle age, before 65 yo.
Slow onset
Inappropriate social behaviour and motor deficits/akinetic Parkinsonism in later stages.
Relatively preserved memory.

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84
Q

types of frontotemporal dementia

A
  • Pick’s disease
  • Chronic progressive aphasia (CPA) – non fluent speech
  • Semantic dementia – fluent progressive aphasia
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85
Q

cause of frontotemporal dementia

A

Genetic component

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86
Q

ix for frontotemporal dementia

A

MMSE

CT/MRI

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87
Q

pathology of frontotemporal dementia

A 
Atrophy of frontal and temporal lobes.
Pick bodies (cytoplasmic inclusions of aggregated tau proteins – silver staining). Associated w Pick’s disease
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88
Q

tx for frontotemporal dementia

A

Cholinesterase inhibitors and memantine are usually not effective & can worsen symptoms.

Give SSRIs for depression
Give olanzapine for agitation, hallucinations, insomnia

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89
Q

symptoms of lewy body dementia

A

Dementia with extrapyramidal / Parkinson’s motor symptoms, visual hallucinations, falls, rapid eye movement sleep behaviour disorder

Cognition may be fluctuating – in contrast to other forms of dementia

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90
Q

ix for lewy body dementia

A

SPECT (called a DaTscan)– decreased occipital perfusion / metabolism

Clinical diagnosis

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91
Q

pathology of lewy body dementia

A

Cerebral atrophy.

Lewy bodies = alpha-synuclein-positive cytoplasmic inclusions in neurones which cause neuronal degeneration

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92
Q

mx for lewy body dementia

A

Can treat Parkinsonian symptoms with Parkinson’s drugs

Acetylcholinesterase inhibitors (donepezil) and memantine can be used

Avoid antipsychotics – can develop irreversible parkinson’s

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93
Q

important differentials for dementia that are possibly treatable

A
  • Hypothyroidism
  • Addison’s
  • B12/folate/thiamine deficiency
  • Syphilis
  • Brain tumour
  • Normal pressure hydrocephalus
  • Subdural haematoma
  • Depression
  • Chronic drug use e.g., alcohol, barbiturates
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94
Q

how do cholinesterase inhibitors work and what are they used for?

A
  • Reversible cholinesterase inhibition leads to increased Ach concentration = improves dementia symptoms
  • 1st line = Alzheimer’s dementia (mild-moderate) & vascular dementia
  • Can be used in some cases of Lewy body dementia, frontotemporal dementia and Parkinson’s disease
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95
Q

example cholinesterase inhibitors

A

donepezil, rivastigmine, galantamine

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96
Q

side effects of cholinesterase inhibitors

A

nausea, dizziness, insomnia, cholinergic crisis

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97
Q

when is donepezil CI

A

relatively CI in patients with bradycardia

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98
Q

What is memantine and when is it used?

A
  • Used in moderate to advanced Alzheimer’s disease & vascular dementia
  • Can be used in combination with cholinesterase inhibitors
  • An NMDA antagonist = results in decreased glutamate-induced calcium-mediated excitotoxicity
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99
Q

Side effects of memantine

A
  • Side effects = headaches, dizziness, confusion, hallucinations, seizures
100
Q

What features make a patient more likely to have delirium than dementia?

A
  • Impairment of consciousness
  • Fluctuation of symptoms e.g., worse at night, periods of normality
  • Abnormal perception – illusions and hallucinations
  • Agitation, fear
  • Delusions
101
Q

What features make a patient more likely to have depression than dementia?

A
  • Short history, rapid onset
  • Biological symptoms e.g., weight loss, sleep disturbance
  • Patient worried about poor memory
  • Reluctant to take tests, disappointed with results
  • MMSE – variable
  • Global memory loss – dementia typically causes recent memory loss
102
Q

Causes of delirium

A 
Pain
Infection
Nutrition 
Constipation
Hydration
Medication/Metabolic
Environment
103
Q

Symptoms of delirium

A 
memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention
104
Q

Mx of delirium

A

tx cause
modify environment
1st line sedative = haloperidol 0.5mg
2nd line = olanzapine

105
Q

what neurological changes does diabetes typically cause?

A

peripheral neuropathy
Sensory loss, not motor loss
glove and stocking distribution

106
Q

mx of diabetic neuropathy

A

Do the following when diabetic neuropathy is painful:

1st line = amitriptyline, duloxetine, gabapentin or pregablin

2nd line = try one of the other 3 drugs above

Rescue therapy for exacerbations = tramadol

pain management clinics

107
Q

What are the neurological GI affects of diabetes?

A

Gastrointestinal autonomic neuropathy.

Get gastroparesis, chronic diarrhoea or GORD

108
Q

what are the symptoms and mx of gastroparesis seen in diabetic gastrointestinal autonomic neuropathy?

A

symptoms = erratic BM control, bloating and vomiting

mx = metoclopramide, domperidone or erythromycin

109
Q

what is encephalitis?

A

inflammation of the brain

110
Q

causes of encephalitis

A

autoimmune

Most common = viral

  • herpes simplex virus
  • varicella zoster virus
  • EBV
  • enterovirus
  • adenovirus
  • influenza virus
  • polio, mumps, rubella and measles

bacterial & fungal

111
Q

presentation of encephalitis

A 
Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
Fever
112
Q

diagnosis of encephalitis

A

LP - CSF for viral PCR
CT scan if LP is CI (GCS below 9, harm-dynamically unstable, active seizures or post-ictal)
MRI scan after LP
EEG
Swabs - throat and vesicle swabs to find cause
HIV testing

113
Q

mx of encephalitis

A

IV acyclovir for HSV or VZV

IV ganciclovir for CMV

Repeat LP to ensure successful tx before stopping antivirals

114
Q

complications of encephalitis

A 
Lasting fatigue and prolonged recovery
Change in personality or mood
Changes to memory and cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance
115
Q

what is epilepsy and what are seizures?

A

umbrella term for a condition where there is a tendency to have seizures.

Seizures are transient episodes of abnormal electrical activity in the brain.

116
Q

Ix for epilepsy

A

EEG
MRI brain - to diagnose structural problems & tumours
ECG

117
Q

What are the types of generalised seizures?

A 
tonic-clonic (grand mal)
tonic
clonic
typical absence (petit mal)
myoclonic: brief, rapid muscle jerks
atonic
118
Q

What type of seizures involve a complete LOC?

A

Generalised seizures

119
Q

What happens during a generalised tonic clonic seizure?

A 
LOC almost immediately 
Tonic - muscle tensing 
clonic - muscle jerking 
tongue biting
incontinence
groaning
irregular breathing 
post-ictal period
120
Q

Mx for generalised seizures

A

1st line = sodium valproate

121
Q

mx for tonic clonic seizures

A

1st line = sodium valproate

2nd line = lamotrigine or carbamazepine

122
Q

symptoms of absence seizure and what type of seizure is it?

A

generalised seizure

patient becomes blank, stares into space and abruptly returns to normal
unaware of surroundings
won’t respond
last 10-20 seconds

usually in children and they grow out of it

123
Q

mx of absence seizures

A

First line: sodium valproate or ethosuximide

124
Q

What are focal seizures?

A

previously termed partial seizures
these start in a specific area, on one side of the brain
usually start in the temporal lobes

125
Q

what level of consciousness is expected in focal seizures?

A

the level of awareness can vary in focal seizures:

1) Focal aware (previously termed ‘simple partial’)
2) focal impaired awareness (previously termed ‘complex partial’)
3) Awareness unknown

126
Q

What are the types of focal seizures?

A

motor (e.g. Jacksonian march)

non-motor (e.g. déjà vu, jamais vu; )

other features such as aura

127
Q

mx for focal seizures

A

First line: carbamazepine or lamotrigine

Second line: sodium valproate or levetiracetam

128
Q

What are atonic seizures?

A

Generalised seizures
Also known as drop attacks

characterised by brief lapses in muscle tone.
<3 minutes

Typically begin in childhood

can indicate lennox-gastaut syndrome

129
Q

mx for atonic seizures

A

First line: sodium valproate

Second line: lamotrigine

130
Q

What are myoclonic seizures?

A

Generalised seizures

Sudden brief muscle contractions, like a sudden jump
Usually patient is awake

Can happen in infancy as part of juvenile myoclonic epilepsy = Janz syndrome

131
Q

mx of myoclonic seizures

A

First line: sodium valproate

Other options: lamotrigine, levetiracetam or topiramate

132
Q

Who gets juvenile myoclonic epilepsy (Janz syndrome)?

A

teens, more common in girls

133
Q

Features of juvenile myoclonic epilepsy (Janz syndrome)

A
  1. Infrequent generalized seizures, often in morning
  2. Daytime absences
  3. Sudden, shock like myoclonic seizure
    usually good response to sodium valproate
134
Q

When do patients get alcohol withdrawal seizures?

A

occur in patients with a history of alcohol excess who suddenly stop drinking

the peak incidence of seizures is at around 36 hours following cessation of drinking

135
Q

why do patients get alcohol withdrawal seizures

A

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

136
Q

what are psychogenic non-epileptic seizures?

A

previously termed pseudoseizures, this term describes patients who present with epileptic-like seizures but do not have characteristic electrical discharges

patients may have a history of mental health problems or a personality disorder

137
Q

What are the key facts about infantile spasms (West syndrome)?

A

Brief spasms beginning in first few months of life
1. Flexion of head, trunk, limbs → extension of arms (Salaam attack); last 1-2 secs, repeat up to 50 times
2. Progressive mental handicap
3. EEG: hypsarrhythmia
usually 2nd to serious neurological abnormality (e.g. TS, encephalitis, birth asphyxia) or may be cryptogenic
poor prognosis

138
Q

What happens in benign rolandic epilepsy?

A

paraesthesia (e.g. unilateral face), usually on waking up

139
Q

Important considerations for prescribing anti-epileptics

A

Prescribe by brand

antiepileptics can induce/inhibit the P450 system resulting in varied metabolism of other medications, for example warfarin

anti epileptics are generally teratogenic - advice women to take advice from a neurologist prior to conception

Breastfeeding is generally considered safe for mothers taking antiepileptics with the possible exception of the barbiturates

140
Q

Driving rules following a seizure

A

generally patients cannot drive for 6 months following a seizure.

For patients with established epilepsy they must be fit free for 12 months before being able to drive

141
Q

How does sodium valproate work and what is it used for?

A

Increases GABA activity

1st line for generalised seizures

142
Q

Side effects of sodium valproate

A 
ncreased appetite and weight gain
alopecia: regrowth may be curly
P450 enzyme inhibitor
ataxia
tremor
hepatitis
pancreatitis
thrombocytopaenia
teratogenic (neural tube defects)
143
Q

How does carbamazepine work and what is it used for?

A

Binds to sodium channels increasing their refractory period

First line for focal seizures

144
Q

Side effects of carbamazepine

A 
P450 enzyme inducer
dizziness and ataxia
drowsiness
leucopenia and agranulocytosis
SiADH
visual disturbances (especially diplopia)
145
Q

How does lamotrigine work and what is it used for?

A

Sodium channel blocker

2nd line for generalised and focal seizures

146
Q

Side effect of lamotrigine

A

Stevens-Johnson syndrome

147
Q

How does phenytoin work and what is it used for?

A

Binds to sodium channels increasing their refractory period

Used as an IV infusion in refractory status

148
Q

Side effects of phenytoin

A 
P450 enzyme inducer
dizziness and ataxia
drowsiness
gingival hyperplasia, hirsutism, coarsening of facial features
megaloblastic anaemia
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
149
Q

What is status epilepticus

A

defined as seizures lasting more than 5 minutes or more than 3 seizures in one hour or or 2 or more seizures in a 5 minutes period without the person returning to normal between the,

150
Q

Mx of status epilepticus

A 
ABC
Airway protection
O2
Assess cardiac function 
Check BMs

IV lorazepam 4mg, repeat after 10 mins
In community - buccal midazolam or rectal diazepam

If seizures persist = IV phenytoin or phenobarbital

No response within 45 minutes = induction of GA

151
Q

What is essential tremor?

A

an autosomal dominant condition which usually affects both upper limbs

152
Q

What are the symptoms of essential tremor?

A

postural tremor: worse if arms outstretched
improved by alcohol and rest
most common cause of titubation (head tremor)

153
Q

Mx of essential tremor

A

propranolol is first-line

primidone is sometimes used

154
Q

What are the types of tremors?

A

1 Rest tremor

2 Action tremor

  • Postural tremor (when in a specific position)
  • Kinetic tremor = simple (uniformly throughout a voluntary movement), task specific or intention (worse as the body part approaches the target, associated with the cerebellum)
  • Isometric tremor
155
Q

What is an extra dural haemorrhage and where is the bleed coming from?

A

Bleed between the skull and the dura mater.

usually caused by rupture of the middle meningeal artery in the temporo-parietal region

156
Q

What causes extra dural haemorrhages?

A

Fracture of the temporal bone e.g. from traumatic brain injury

Rarely:

  • Atriovenous abnormalities
  • bleeding disorders
157
Q

what does an extra dural haemorrhage look like on CT?

A

Bi-convex lemon shaped mass limited by the cranial sutures

Secondary features - midline shift and brainstem herniation

158
Q

symptoms of an extra dural haemorrhage

A

ongoing headache following traumatic head injury

LOC then a period of improved neurological symptoms and consciousness (lucidity) followed by a rapid decline over hours as the haematoma gets larger

159
Q

mx of extra dural haemorrhage

A

ABCDE
Coagulation bloods and reverse any anticoagulation
Prophylactic abx if open skull fracture
Antiepileptics to reduce seizure risk
Mannitol/barbiturates to reduce ICP
Definitive management = Burr hole craniotomy to remove the haematoma, may need hemicraniotomy if there’s lots of blood/oedema to prevent brain stem herniation

160
Q

what is the anatomical landmark of the middle meningeal artery?

A

MMA lies underneath the pterion

Its where the parietal, frontal, sphenoid and temporal bones fuse

161
Q

Ix for extradural haemorrhage

A

BMs to rule out hypoglycaemic cause of reduced GCS
ECG to rule out heart block causing reduced GCS
Coagulation
Group and save
CT head
Skull xray
Cerebral angiography - to look for atriovenous malformation

162
Q

complications of extra dural haemorrhage

A

Infection: due to skull fracture or as a result of operative intervention
Cerebral ischaemia: typically occurs adjacent to the haematoma
Seizures
Cognitive impairment
Hemiparesis
Hydrocephalus due to obstruction of the ventricles
Brainstem injury: due to significantly raised ICP

163
Q

Signs of extradural haemorrhage

A 
Reduced GCS
Confusion
Cranial nerve deficits - oculomotor nerve palsy = fixed and dilated ipsilateral pupil
Motor/sensory deficits in limbs
Hyperreflexia 
Spasticity 
Upping plantar reflex 
Cushing's triad = bradycardia, HTN and deep/irregular breathing
164
Q

What is cushings triad?

A

A physiological response to raised ICP to attempt to improve perfusion

HTN
Bradycardia
Irregular breathing pattern

165
Q

what causes malaria?

A

caused by Plasmodium protozoa which is spread by the female Anopheles mosquito.

There are four different species which cause disease in man:
Plasmodium falciparum (causes nearly all episodes of severe malaria)
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae

166
Q

Protective factors against malaria

A

Sickle cell trait
G6PD deficiency
HLA-B53
absence of Duffy antigens

167
Q

Features of severe malaria caused by plasmodium falciparum

A 
schizonts on a blood film
parasitaemia > 2%
hypoglycaemia
acidosis
temperature > 39 °C
severe anaemia
complications as below
168
Q

Complications of severe malaria caused by plasmodium falciparum

A

cerebral malaria: seizures, coma

acute renal failure: blackwater fever, secondary to intravascular haemolysis, mechanism unknown

acute respiratory distress syndrome (ARDS)

hypoglycaemia

DIC

169
Q

symptoms of non-falciparum malaria

A

general features of malaria: fever, headache, splenomegaly
Plasmodium vivax/ovale: cyclical fever every 48 hours. Plasmodium malariae: cyclical fever every 72 hours
Plasmodium malariae: is associated with nephrotic syndrome.

170
Q

General symptoms and signs of malaria

A

Suspect malaria in someone who lives or has travelled to an area of malaria.
The incubation period is 1-4 weeks after infection with malaria although it can lie dormant for years.

Fever, sweats and rigors
Malaise
Myalgia
Headache
Vomiting

Pallor due to the haemolytic anaemia
Hepatosplenomegaly
Jaundice as bilirubin is released during the rupture of red blood cells

171
Q

Diagnosis of malaria

A

Malaria blood film - in EDTA bottle. Send 3 samples over 3 consecutive days (48 hour cycle of malaria released into blood from blood cells)

172
Q

Mx of malaria

A

Oral options in uncomplicated malaria:

  • Artemether with lumefantrine (Riamet)
  • Proguanil and atovaquone (Malarone)
  • Quinine sulphate
  • Doxycycline

Intravenous options in severe or complicated malaria:

  • Artesunate. This is the most effective treatment but is not licensed.
  • Quinine dihydrochloride
173
Q

Advice for malaria prophylaxis

A

Be aware of locations that are high risk
No method is 100% effective alone
Use mosquito spray (e.g. 50% DEET spray) in mosquito exposed areas
Use mosquito nets and barriers in sleeping areas
Seek medical advice if symptoms develop
Take antimalarial medication as recommended

174
Q

What are options for antimalarial medications?

A

Proguanil and atovaquone (Malarone)

Taken daily 2 days before, during and 1 week after being in endemic area
Most expensive (around £1 per tablet)
Best side effect profile

Mefloquine

Taken once weekly 2 weeks before, during and 4 weeks after being in endemic area
Can cause bad dreams and rarely psychotic disorders or seizures

Doxycycline

Taken daily 2 days before, during and 4 weeks after being in endemic area
Broad-spectrum antibiotic therefore it causes side effects like diarrhoea and thrush
Makes patients sensitive to the sun causing a rash and sunburn

175
Q

What causes meningitis in adults?

A

bacterial causes:

  • neisseria meningitides (meningococcus)
  • Streptococcus pneumoniae (pneumococcus)

If over 60/immunosuppressed, consider listeria monocytogenes

viral causes:

  • coxsackie virus
  • echovirus
  • mumps
  • HSV
  • CMV
  • HZV
  • HIV
  • measles
176
Q

Symptoms of meningitis

A 
Fever
Neck stiffness
Vomiting 
Headache
Photophobia
Altered consciousness
Seizures

If there’s meningoccocal septicaemia = non-blanching rash

Kernig’s test - lift leg and straighten knee
Brudzinski’s test - lift neck/head

177
Q

CSF findings in bacterial meningitis

A

cloudy appearance
Low glucose
High protein
10-5000 white cells (polymorphs - neutrophils)

178
Q

CSF findings in viral meningitis

A

Clear appearance
60-80% of plasma glucose
normal/raised proteins
15-1000 white cells (lymphocytes)

179
Q

CSF findings in TB meningitis

A

slightly cloudy, fibrin web appearance
Low gluocse
High protein
10-1000 lymphocytes

Use Ziehl-Neelsen stain & PCR

180
Q

Ix for meningitis

A 
FBC
CRP
Coagulation screen
Blood culture
Whole blood PCR
Blood glucose
Blood gas
LP - if no signs of raised ICP
181
Q

Mx of meningitis

A

IM benzylpenicillin in the community if meningococcal disease is suspected

Initial empirical therapy for adults <50 = IV cefotaxime

Add on amoxicillin if aged >50

Meningococcal meningitis = IV benzylpenicillin or cefotaxime

Pneumococcal meningitis = IV cefotaxime

Meningitis caused by haemophilus influenzae = IV cefotaxime

Meningitis caused by listeria = IV amoxicillin + gentamicin

Penicillin allergic = chloramphenicol

AND GIVE IV DEXAMETHASONE

  • To reduce risk of neurological sequelae
  • don’t give if: septic shock, meningococcal septicaemia, immunocompromised or its following surgery
182
Q

Post exposure prophylaxis for meningococcal meningitis contacts

A

prophylaxis needs to be offered to household and close contacts of patients affected with meningococcal meningitis & people who been exposed to respiratory secretion, regardless of the closeness of contact - within 7 days of symptom onset

Give oral ciprofloxacin or rifampicin

183
Q

What causes brain mets?

A 
Lung cancer (most common)
Breast ca
Malignant melanoma
Renal cell carcinoma
Colorectal ca
Pancreatic ca
Testicular ca
184
Q

symptoms of brain mets

A

Seizures
Focal neurological deficits
cognitive deficits
Headaches

185
Q

Ix for brain mets

A

CT +/- PET to find primary

186
Q

Mx of brain mets

A

Surgical resection
radiotherapy
glucocorticoids to reduce tumor oedema
Palliative care

187
Q

Symptoms of migraines

A

a severe, unilateral, throbbing headache
associated with nausea, photophobia & phonophobia
attacks may last up to 72 hours
patients characteristically go to a darkened, quiet room during an attack
‘classic’ migraine attacks precipitated by an aura (1/3 of patients)
typical aura are visual, progressive, last 5-60 minutes and are characterised by transient hemianopic disturbance or a spreading scintillating scotoma

188
Q

Common triggers for migraines

A 
tiredness, stress
alcohol
combined oral contraceptive pill
lack of food or dehydration
cheese, chocolate, red wines, citrus fruits
menstruation
bright lights
189
Q

What is the diagnostic criteria for migraines?

A

International Headache Society

Must have at least 5 attacks that fulfill the following criteria:

1) Lasts 4-72 hours
2) headache with 2 of the following: unilateral, pulsatile, moderate/severe pain, aggravation by physical activity
3) during headache 1 of the following: nausea/vomiting, photophobia/phonophobia
4) not attributed to another disorder

190
Q

Mx for migraines

A

ACUTE TX:

1) oral triptan (sumatriptan) + NSAID/paracetamol
2) metoclopramide/prochlorperazine + NSAID/triptan

PROPHYLAXIS:

1) topiramate / propranolol (give propranolol to women of child bearing age - topiramate is teratogenic & reduces effectiveness of hormonal contraception)
2) acupuncture
3) riboflavin
4) menstrual migraine = frovatriptan / zolmitriptan

Pizotifen is no longer recommended - weight gain and drowsiness

191
Q

types of migraine

A

migraine without aura
migraine with aura
silent migraine - aura but no headache
hemiplegic migraine

192
Q

Symptoms of hemiplegic migraine

A 
Typical migraine symptoms
Sudden or gradual onset
Hemiplegia (unilateral weakness of the limbs)
Ataxia
Changes in consciousness
193
Q

what are triptans and when are they used?

A

5HT receptor agonists - serotonin receptor agonists

used to abort migraines when they develop

194
Q

mx of migraines in pregnancy

A

1st line = paracetamol
2nd line = NSAIDs in 1st and 2nd trimester
Avoid aspirin and codeine during pregnancy

195
Q

what is contraindicated in migraines with aura?

A

The COCP

196
Q

what is motor neurone disease?

A

an umbrella term that encompasses a variety of specific diagnoses. Motor neurone disease is a progressive, ultimately fatal condition where the motor neurones stop functioning. There is no effect on the sensory neurones and patients should not experience any sensory symptoms.

197
Q

What are some types of MND?

A

Amyotrophic lateral sclerosis (ALS) - most common type

Progressive bulbar palsy (affects talking and swallowing)

progressive muscular atrophy

primary lateral sclerosis

198
Q

pathophysiology of MND

A

progressive degeneration of both upper and lower motor neurones. The sensory neurones are spared.

199
Q

risk factors for MND

A

family hx
smoking
heavy metals
certain pesticides

200
Q

presentation of MND

A

Late middle aged man
insidious progressive weakness of muscles throughout body affecting limbs, trunk, face and speech

increasing fatigue
clumsiness
dysarthria (slurred speech)
Wasting of small hand muscles/tibialis anterior

LMN signs -

  • muscle wasting
  • reduced tone
  • fasciculations
  • reduced reflexes

UMN signs -

  • increased tone/spasticity
  • brisk reflexes
  • pogoing plantar responses

Doesn’t affect

  • external ocular muscles
  • no cerebellar signs
  • abdominal reflexes preserved
  • loss of sphincter function = late feature
201
Q

diagnosis of MND

A

by specialist
diagnosis of exclusion

nerve conduction studies = normal motor conduction

electromyography = reduced action potentials with increased amplitude

MRI to exclude cervical cord compression and myelopathy

202
Q

management of MND

A

Riluzole - slows disease progression, extends survival by a few months

Edaravone - used in US not UK, slows disease progression

NIV - especially at night

MDT
Advanced directives
End of life care

203
Q

Main causes of death in MND

A

Respiratory failure

Pneumonia

204
Q

Characteristics of amyotrophic lateral sclerosis (ALS)

A

typically LMN signs in arms and UMN signs in legs

in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

205
Q

Characteristics of primary lateral sclerosis

A

UMN signs only

206
Q

Characteristics of progressive muscular atrophy

A

LMN signs only
affects distal muscles before proximal
carries best prognosis

207
Q

characteristics of progressive bulbar palsy

A

palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

208
Q

Prognosis of MND

A

50% of patients die within 3 years

209
Q

What is multiple sclerosis?

A

chronic progressive cell-mediated autoimmune disorder characterised by demyelination in the central nervous system

210
Q

who gets MS?

A

3 times more common in women
most commonly diagnosed in people aged 20-40 years
much more common at higher latitudes (5 times more common than in tropics)

Symptoms improve in pregnancy and the post part period

211
Q

types of MS

A

Clinically isolated syndrome

Relapsing remitting disease

Secondary progressive disease

Primary progressive disease

212
Q

pathology of MS

A

oligodendrocytes around neurones that produce myelin sheath in the CNS are affected

there is activation of immune cells against the myelin

in early disease, re-myelination can occur and symptoms can resolve

MS lesions are disseminated in time and space

213
Q

Causes of MS

A 
Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity
214
Q

Symptoms of MS

A

Symptoms usually progress over more than 24 hours.

At the first presentation, symptoms tend to last days to weeks and then improve.

OPTIC NEURITIS:

  • Demyelination of optic nerve
  • Loss of vision in one eye

EYE MOVEMENT ABNORMALITIES:

  • 6th CN lesion
  • Internuclear ophthalmoplegia
  • Conjugate lateral gase disorder

FOCAL WEAKNESS:

  • Bells palsy
  • Horners syndrome
  • Limb paralysis
  • Incontinence

FOCAL SENSORY SYMPTOMS:

  • Trigeminal neuralgia
  • Numbness
  • Paraesthesia
  • Lhermitte’s sign: electric shock sensation down the spine when flexing the neck

ATAXIA

  • sensory ataxia (Romberg’s test)
  • cerebellar ataxia
215
Q

what happens in a clinically isolated syndrome of MS

A

the first episode of demyelination and neurological signs and symptoms

MS cannot be diagnosed on one episode as the lesions have not been “disseminated in time and space”.

May never have another episode or develop MS

Lesions on MRI = more likely to progress to MS

216
Q

What happens in relapsing-remitting MS?

A

It is characterised by episodes of disease and neurological symptoms followed by recovery.

217
Q

What happens in secondary progressive MS?

A

there was relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions

Symptoms become more and more permanent

218
Q

what is primary progressive MS?

A

a worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions

Symptoms have to be progressive over a period of 1 year to diagnose primary progressive MS.

219
Q

Diagnosis of MS

A

Neurologist - clinical diagnosis

MRI scans - to show demyelinating lesions
LP = oligocloncal bands in CSF

220
Q

What do oligoclonal bands in CSF demonstrate?

A

Multiple sclerosis

221
Q

Symptoms of optic neuritis

A

Central scotoma. This is an enlarged blind spot.

Pain on eye movement

Impaired colour vision

Relative afferent pupillary defect: pupil dilates on swinging a light from the unaffected to affected eye

222
Q

Causes of optic neuritis

A 
MS
Sarcoidosis
Systemic lupus erythematosus
Diabetes
Syphilis
Measles
Mumps
Lyme disease
223
Q

Mx for optic neuritis

A

Urgent ophthalmology review
Steroids
50% with single episode of optic neuritis go on to develop MS in next 15 years

224
Q

Mx of MS

A

MDT

Disease modifying drugs and biologic therapies

Methylprednisolone in relapses

Exercise
Neuropathic pain = amitriptyline or gabapentin
Urge incontinence = oxybutynin
Spasticity = baclofen, gabapentin and physiotherapy

225
Q

What is myasthenia Gravis?

A

an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.

226
Q

who gets myasthenia Gravis?

A

women <40 yo

men >60 yo

227
Q

What is associated with myasthenia Gravis?

A

thymoma (tumour of the thymus gland)

228
Q

what antibodies are seen in myasthenia Gravis?

A

acetylcholine receptor antibodies

Rarer antibodies:

  • muscle specific kinase antibodies
  • low density lipoprotein receptor related protein 4 (LRP4) antibodies
229
Q

Symptoms of myasthenia Gravis

A

weakness that gets worse with muscle use and improves with rest

symptoms better in the morning and worse at the end of the day

symptoms affect the proximal muscles and small muscles of the head and neck

diplopia - due to extra ocular muscle weakness

ptosis - eyelid weakness causing drooping of the eyelids

weakness in facial movements

difficulty with swallowing

fatigue in the jaw when chewing

slurred speech

progressive weakness with repetitive movements

230
Q

how to elicit muscle fatiguability seen in myasthenia Gravis on examination

A

Repeated blinking will exacerbate ptosis

Prolonged upward gazing will exacerbate diplopia on further eye movement testing

Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

Check for a thymectomy scar.

Forced vital capacity

231
Q

Diagnosis of myasthenia Gravis

A

Test for the antibodies:

1) Acetylcholine receptor (ACh-R) antibodies (85% of patients)
2) Muscle-specific kinase (MuSK) antibodies (10% of patients)
3) LRP4 (low-density lipoprotein receptor-related protein 4) antibodies (less than 5%)

CT/MRI thymus for thymoma

Edrophonium test - give IV edrophonium chloride (neostigmine) - in MG will give a brief and temporary relief of muscle weakness

232
Q

Mx of myasthenia Gravis

A

Reversible acetylcholinesterase inhibitors (pyridostigmine or neostigmine)

Immunosuppression with prednisolone or azathioprine

Thymectomy

Monoclonal antibodies: rituximab / eculizumab

233
Q

What is a myasthenic crisis?

A

a severe complication of myasthenia gravis
life threatening
acute worsening of symptoms

can lead to respiratory failure as a result of weakness in the respiratory muscles

234
Q

Mx of myasthenic crisis

A

BiPAP / intubation and ventilation

IV immunoglobulins

plasma exchange

235
Q

What is Parkinson’s disease?

A

a condition where there is a progressive reduction of dopamine in the basal ganglia (specifically the substantia nigra) of the brain, leading to disorders of movement.

The symptoms are characteristically asymmetrical, with one side affected more than the other.

236
Q

What is the classic triad of symptoms seen in Parkinson’s disease?

A

Resting tremor
Rigidity
Bradykinesia

237
Q

symptoms of parkinsons disease

A

unilateral pill rolling tremor (worse on rest/when distracted, improves with movement)

cogwheel rigidity

handwriting gets smaller and smaller

shuffling gait

difficulty initiating movements e.g. standing to walking

difficulty in turning when standing

hypomimia - reduced facial movements and expressions

Depression
sleep disturbance/insomnia
anosmia
postural instability
cognitive impairment/memory problems
238
Q

name some Parkinson’s-plus syndromes

A

Multiple system atrophy
dementia with leeway bodies
progressive supra nuclear palsy
corticobasal degeneration

239
Q

What is multi system atrophy?

A

a rare condition where the neurones of multiple systems in the brain degenerate.

affects the basal ganglia & multiple other areas

degeneration of the basal ganglia = Parkinson’s presentation.

degeneration in other areas = autonomic dysfunction (causing postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (causing ataxia).

240
Q

What is dementia with Lewy bodies?

A

a type of dementia associated with features of Parkinsonism

causes a progressive cognitive decline

associated symptoms: visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness.

241
Q

How is parkinsons disease diagnosed?

A

clinical diagnosis by specialist

242
Q

Mx of parkinsons disease

A

Levodopa:

  • co-benyldopa (levodopa + benserazide)
  • co-careldopa (levodopa + carbidopa)

+ COMT inhibitors - entacapone (to slow the breakdown of levodopa)

Dopamine agonists - bromocrytopine/carbergoline

MOA-B inhibitors - selegiline/rasagiline

243
Q

How is levodopa used to treat Parkinson’s disease?

A

levodopa = synthetic dopamine

must be combined with a drug that stops levodopa being broken down by the body = carbidopa or benserazide

levodopa is the most effective parkinsons drug but it becomes less effective over time - reserved for when other treatments aren’t controlling symptoms

244
Q

Side effects of levodopa

A

when doses are too high patients get dyskinesias:

  • dystonia
  • chorea
  • athetosis
245
Q

How do dopamine agonists work in parkinsons, name some and what are the side effects?

A

Mimic dopamine in the brain

bromocryptine, pergolide, carbergoline

SE: pulmonary fibrosis

246
Q

How do MAO-B inhibitors work in parkinsons and name some?

A

they stop the break down neurotransmitters like dopamine, serotonin and adrenalin

Selegiline, rasagiline

247
Q

Test to see if fluid draining from ears/nose is CSF

A

Test glucose - would be positive in CSF but not in mucus

Beta-2-transferrin is gold standard

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