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Neurology > General neurology [29/10/20] > Flashcards

General neurology [29/10/20] Flashcards

1
Q

4 key features of Parkinson’s disease

A

Bradykinesia, rigidity, postural instability, tremor

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2
Q

Parkinsonism cauases

A
  • idiopathic PD
  • vascular Parkinsonism
  • normal pressure hydrocephalus
  • Parkinson’s plus syndrome [PPS]
  • iatrogenic
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3
Q

Typical preparation of L-dopa for PD

A
  • Co-careldopa/ co-beneldopa [L-dopa given with a dopa-decarboxylase]
  • CR prep
  • dispersable prep [rescue/morn.]
  • can have Statevo which is co-careldopa plus etacapone [etacapone helps stop breakdfown of L-dopa and is a COMT inhibitor]
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4
Q

Dopamine agonists available, and their advantage over L-dopa

A
  • non-ergot [Ropinirole, Pramiexole, Rotigotine]
  • ergot [Bromotcriptine etc.]
  • adv: less dyskinesia, longer acting
  • dis: higher risk hallucinations, compulsive behaviour, postural hypotension, daytime sleepiness, specific ergot SE like fibrosis lungs/chest so need constant monitoring ECG/CT
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5
Q

Examples of MAOI and cautions related to them

A
  • Selegiline, Rasagiline.
  • Serotonin syndrome: pyrexia, agitation, sweating, diarrhoea
  • Tramadol, Dethidine, MTX are CI
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6
Q

When to start drug treatment for PD?

A

No disadvantage starting early, generally for Sx control [esp. L-dopa best for that]

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7
Q

Non-motor Sx of PD

A

Mood, sleep [esp. REM sleep], cognitive, impulse control disorder, autonomic dysfunction, anosmia [pts can have Sx for 20y without Dx]
REM sleep disorder: pts acting out their dreams.
Insomnia due to stiffness/restlessness

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8
Q

Psychotic PD Tx

A
  • assess provoking factors [could be illness, metabolic, infection]
  • refer to neuro
  • disconintue meds like MAOI
  • intitiate clozapine, quitiepine [consider acetylcholine esterase inhibitors]
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9
Q

Autonomic Sx PD

A

orthostatic hypotnesion, N and vomiting, hypersalivation, nocturia, sweating etc.

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10
Q

When can DBS be used for PD and what is the benefit?

A

used in the subthalamic nucleus, lowers requirement for L-dopa [by about half its dose]
- only for pts with motor fluctutations

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11
Q

Sx of a third nerve palsy

A

Parasympethic fibres
Apex petrous part temporal bone
Fixed dilated pupil

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12
Q

Sx of cerebellar syndrome

A

Ataxia, nystagmus
ipsilateral
Midraib, pons, medulla

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13
Q

What is above and below the brain stem?

A

Above: thalamus, internal capsule
Below: spinal cord

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14
Q

Describe the reticulating activating system and its function

A

Peri-aqueductal grey matter/ floor of the 4th ventricle
->
alertness, sleep/awake, REM/nonREM sleep, resp control, CV drive

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15
Q

Disorders affecting the brainstem

A

Tumour [meningioma, schwanomma, mets etc,], inflammation [MS], metabolic, trauma, Haemorrhage [AVM, aneurysm], infarct [vertebral artery infarct], infection [cerebellar in ear]

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16
Q

What is compensated type 2 respiratory failure?

A

High CO2, normal or low O2, high bicarb [to compensate]

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17
Q

Mx of acute neuromuscular respiratory weakness

A
  • ABCD
  • ABG
  • ECG
  • supportive Mx respiratory and autonomic instability
  • early anaesthetic call
  • consider infection
  • Tx underlying condition
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18
Q

How to investigate MG?

A
  • consider culprit [drugs like Mebeverine]
  • bloods for ACh receptor antibodies [MuSK]: 85% positive [though takes 3w]
  • thyroid function [autoimmune coexistence]
  • CT chest [possible thymoma]
  • if antibodies there: simple fibre EMG [NM] dysfunction
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19
Q

Mx of generalised MG

A
  • assess severity
  • caution Rx [stop Mebeverine]
  • Pyridostigmine 30mg qid inc. to 60 qid and higher [max 450mg per day]
  • steroids 10mg al days increasing by 10mg after 3rd dose aiming for 100mg alt days [quicker if IP, beware dips]
  • bone protection, PPI
  • IVIg
  • Tx infections early, aggressively and care with antibiotics
  • LARGE list of drugs CI in MG patients
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20
Q

What is a typical pyramidal [or UMN] pattern of weakness?

A
  • Flexors > extensors in UL
  • Extensors > flexors in LL
  • consequently, pt circumducts leg to walk as cannot flex hip properly to take step
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21
Q

Ix for pt with back pain, difficulty walking, pyramidal weakness

A
  • MRI cervical spine [possible compression], LP, admit and observe = DONE IMMEDIATELY
  • [NCS, anti-glioside antibodies, infection serology for cause]
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22
Q

Mx of GBS

A

IVIg, monitor pulse and BP, monitor FVC

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23
Q

Autonomic instability Mx for GBS

A
  • tachycardia: drugs/DC cardioversion
  • bradycardia: drugs/pacing
  • HTN: labetolol
  • hypotension: fluids, inotropics
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24
Q

Mx of respiratory failure in MND

A

Care with O2, consider infection, NIV on ward, ITU usually not appropriate

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25
Q

Origin and function of the pyramidal and extrapyramidal tracts

A

Pyramidal

  • origin: cerebral cortex
  • function: voluntary control of muscles and face

Extrapyramidal

  • origin: brainstem
  • function: involuntary and autonomic control muscles such as tone, balance, posture, locomotion
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26
Q

Functionally, how are pyramidal tracts split?

A
  • Corticospinal tracts: lateral [90%, decussate medulla and terminate ventral horn] and anterior [ipsilateral then decussates cervical and thoracic segmental levels]
  • Corticobulbar
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27
Q

Functionally, how are the extrapyramidal tracts split?

A

Originate brainstem, motor fibres spinal cord
Four tracts:
- vestibulospinal and reitculospinal do not decussaate, ipsilateral innervation
- rubrospinal and tectospinal contralteral

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28
Q

How many somatic pairs of nerve in the NS?

A

31 pairs

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29
Q

UMN vs LMN features

A

UMN
- bulk: normal, tone: increased, strength: decreased, fasciculations: absent, reflexes: increased
LMN
- bulk: reduced [wasting], tone: normal or decreased, strength: decreased, fasciculations: may be present, reflexes: decreased or absent

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30
Q

Causes of weakness

A 
Neuropathies
- peripheral neuropathy
- GBS
- MEI
- MND
Myopathies
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31
Q

Compare three main types peripheral nerve damage

A

Polyneuropathy [peripheral neuropathy]
Mononeuropathy multiplex [at least 2 neurones]
Mononeuropathy

32
Q

Predominantly motor loss peripheral neuropathy

A
  • GBS
  • chronic inflammatory demyleinating polymuerhpathy [CIDP] i.e. chronic GBS
  • hereditary sensorimotor neuroapthies [HSMN] e.g. Charcot Marie Tooth Disease
  • DIptheria
  • Pomphoria? or something
33
Q

Predominantly sensory loss peripheral neuropathy

A
  • deficiency states [B12/folate]
  • DM
  • alcohol/toxins/drugs
  • metabolic abn. e.g. uraemia
  • leprosy
  • amyloidosis
34
Q

Define mononeuritis multiplex

A
  • Painful, asymmetrical sensory and motor neuropathy
35
Q

Features and causes of mononeuritis multiplex

A
  • Subacute presentation
  • Inflammatory/immune mediated
  • Causes: vasculitides e.g. Churg-Strauss, CT disorders [like sarcoid]
36
Q

Mononeuropathy exmaples

A

Median nerve [Carpal Tunnel]
Ulnar elbow
Radial axilla
Common peroneal nerve leg

37
Q

Neuropathy Ix

A 
history and exam
- neurpathy screen
vasculitic screen
- EMG/NCS
-CSF study
- imaging/nerve biopsty

[all after Hx optional]

38
Q

neuropathy Tx

A

20% idiopathic with no Tx [just give analgesic]
treat underlying cause [e.g. deficiency/DM]
inflammatory like CIDP then prrednisolone with steroids sparing agents like azathioprine
vasculitic neurpathy give prednisolone with immunosuppreant like cyclophosphamide

39
Q

Features of GBS [incl. on LP]

A 
AI response causing demyelination
Post infectious e.g. resp or GI
Subacute [<6w] ascending paralysis/numbness/areflexia
NCS: demyleinating
LP: raised CSF protein
40
Q

Tx for GBS

A

IVIg or plasmapharesis, support, monoitor, FVC, ITU review

41
Q

How long recorvry GBS?

A

Weeks to years

42
Q

Features of MG

A

AID; antibodies against nicotinic acetylchline receptors
Common, potentially fatal
Thymus dysfunction common [hyperplasia, thymoma]
Generalised weakness:
- proximal limbs
- neck and face [head drop, ptosis]
- extraocular [complex diplopia]
bublar Sx [speech and swallow] pareticularly in elderly
ocular in 10-25% pts
risk other AID like thyroid, PA

43
Q

Ix for MG

A

Tensilon test [allow accumulation of ACh in the NMJ]

  • AChR antibodies
  • EMG [look at NMJ]
  • CT thorax
44
Q

Tx for MG

A
  • acetylcholine esterase inhibitors [Pyridostigmine]: in symptomatic
  • immunosuppresants [steroids start slwoly, azathioprine/MTX/mycophenolate]
  • thymomectomy
45
Q

What is a myasthenic crisis?

A
  • Severe weakness incl. respiraotry muscles
  • High risk of death
  • Cause: infection, natural disease cycel, under/overdosing
46
Q

Mx for myasthenic crisis?

A

Take change in myasthenic condition seriously
urgent revierw neurologist
Think about breathing and monitor
Anaesthetic review

47
Q

Simple definition of MND

A

Slelective degeneration of motor neurones in the motor cortex and anterior horn of the spinal cord [also CN]. presents with LMN and UMN signs.

48
Q

Ix for MND

A

LP, NCS/EMG, MRI [to r/o]

49
Q

Clinical features of MND

A

No sensory, visual, or B/B involvement
Asymmetrical weakness
Bulbar and limb onset
Survival typically 2-5y

50
Q

Common muscle disorders

A
  • steroid myopathy
  • statin myopathy
  • metabolic and endocrine myopathies
  • myotonic dystrophy
51
Q

List some uncommon muscle disorders

A 
Most muscular dystrophies
- Duchenne, FSHD
Inflammatory muscle disorders
- polymyositis, dermatomyositis
Mitochondrial disorders
52
Q

Features of muscle disroders

A

Stairs, chair, hair
wasting is common
Facial weakness occurs in some [FSMD]
Neck weakness and contractures can occur
Scoliosis often feature especially in Duchenne
Eye movements disorders are rare [seen in mitochrondrial]

53
Q

Muscle Ix

A

CK, EMG, ESR/CRP,

+/- genetics [like DMD], biopsy

54
Q

General rule, nerve compared to muscle disease?

A 
Nerve = distal weakness
Muscle = proximal weakness
55
Q

Aetiology of MND

A

Sporadic [unknown], or familial [SODL, C9ORF2]

56
Q

Types of MND

A
  • ALS [50]: LMN and UMN. Worse bulbar onset.
  • PLS: motor cortex only, so UMN
  • PMA: LMN, best prognosis
  • PBP: CNs 9 to 12, palsy tongue, chewing and swallowing. Worse prognosis.
57
Q

Features of MND

A

Sx: weakness, bublar Sx [dysarthria, dysphagia, siarrlorrhoea]
Sx: assymetrical pattern weakness, ALS both UMn and LMN signs
Ix: no Dx test, neurophysioogy/EMG may detect denervation, MEI helps excl, LP to r/o

58
Q

Mx for MND

A

Riluzole, NIV, gastrostomy

59
Q

What are PD associated with?

A

Lewy bodies [tangles alpha-synuclein and ibiquitin]

60
Q

Ix for PD

A

usually clincial Dx, MRi and CT to r/o, PET and SPECt scans [alsdo DaTSCAn]

61
Q

Define Huntington’s Disease

A

Inherited neurodegenerative disease characterised by chorea, dystonia, incoordination, cognitive decline and benhioural difficulties

62
Q

Aetiology of HD

A

AD [complete penetrance], gene chromosoem 4 encodes for Huntingtin, degneration of cholinergic and GABAnergic neurones. CAG nucleotides need over 35 repeats.

63
Q

Features of HD

A

after 35 y.o, chorea, personality changes, intellectual impairment, dystonia, saccadic eyes, rigidity, dementia, bulbar Sx, sleep problems

64
Q

Ix for HD [incl. part of brain looked at]

A

genetic testing, CT/MRI can show atrophy of caudate nucleus

65
Q

Mx and prognosis for HD

A

No DMT, 15-20 years life

66
Q

Define dementia

A

Syndrome deteriorating memory, thinking, behaivour, and ability for ADLs

67
Q

Types of dementia

A

AD [50%], vascular [25%], LBD [15%], FTD [5%], mixed dementia, PD+ genetic causes dementia
Also, potentially Tx causes dementia

68
Q

potentially Tx causes of dementia

A

Substance abuse, hypothyroidism, SOL, NPH, syhpilis, vit. B12 defi, pellagra

69
Q

Dx of dementia

A

histor yna dexam, screen impairment with e.g, MMSE

70
Q

Ix for dementia

A

dementia screem, r/o other causes confusion like FBC, LFTs, U and E, EST, TFT, syphilis, cvortisol, glucose, CT head, EEG, LP [CJD]

71
Q

Mx of dementia

A

acetyolcholinesterase inhibotres [e.g. donepezil] for mild to mod AD
NMDA [memantine] for 2nd line where ACHe doesn;t work

72
Q

What is PSP?

A

Supranuclear palsy or Parkinson plus syndrome;

impairments vertical gaze [hard stairs], parkinsons, falls, speech, cognitive impairment

73
Q

Mx of PSP

A

poor repsonse to L-dopa

74
Q

What is TGA~?

A

Loss transient memory
anxious and repeat questions
no recall events

75
Q

Chorea cause

A

daamge basal ganglia

- HD, RFs, drugs [l-dopa antipsychotics], thyrotoxicoiss, PRV, poison, ataxis trelangactasia etc.

76
Q

Lewy body dementia Sx

A 
Progressive cognitive decline:
- attention and EF decline first compared to memory loss
cognitive fluctutating
- usually CD before Parkinsons
- visual hallucinations
77
Q

Cx of stroke

A 
raised ICP [cerebral oedema, haemorrhage, [signs HTN, new neurology, GCS]
- aspiration
pressure sores
depression
cognitiv e impariemtn
othert medical problems]

Neurology (13 decks)

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