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PACES > Neurology > Flashcards

Neurology Flashcards

1
Q

Differentials for bilateral ptosis

A

congenital
bilateral horner’s (syringomyelia)
myotonic dystrophy
myasthaenia gravis

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2
Q

differentials for bilateral LMN facial weakness

A

bilateral bells pallsy, sarcoidosis, GBS, Facioscapulohumeral (FSH) dystrophy, myotonic dystrophy

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3
Q

how to investigate myasthenia gravis

A

bloods including looking for antibodies to acetylcholine receptors, striated muscle, muscle sensitive tyrosine kinase
electrophysiology- repetitive stimulation and single fibre electromyography

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4
Q

pathophysiology of myasthenia gravis

A

a disorder characterised by antibodies targetting the nicotinic acetylcholine receptors on the post synaptic membrane of the neuromuscular junction.

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5
Q

antibodies in MG

A

85-90% of patients have anti nicotinic acetylcholine receptor antibodies, other antibodies are muscle specific tyrosine kinase receptors and striated muscle antibodies

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6
Q

which drugs can exacerbate myasthenia gravis

A

aminoglycosides, pencillamine, fluroquinolones, macrolides, beta blockers, phenytoin

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7
Q

what conditions are associated with MG

A

diabetes, hypo/hyperthyroidism, pernicious anaemia, RA, pemphigus

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8
Q

What other conditions present in a similar fashion to MG/ what are differentials

A

botulism, miller fisher syndrome, LEMS, mitochondrial myopathy

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9
Q

what is the difference between MG and LEMS

A

LEMS caused by antibodies directed at pre synaptic voltage gated calcium channels.
Contrary to MG, there is no fatiguability with repetitive movement.

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10
Q

what are the treatment options for MG

A

1st line are long-acting acetylcholinesterase inhibitors such as pyridostigmine
The majority of patients eventually require additional immunosuppression:
prednisolone initially
azathioprine, cyclosporine, mycophenolate mofetil may also be used
thymectomy

Management of myasthenic crisis
plasmapheresis
intravenous immunoglobulins

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11
Q

what are the side effects from acetylcholinesterase inhibitors

A

e.g. pyridostigmine
side effects are incresed muscarinic activity which can result in excessive lacrimation, salivation, N+V, diarrhoea

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12
Q

what is the role of thymectomy in patients with myasthenia gravis

A

T lymphocyte tolerance to autoantigens develops in the thymus. Patient with thymomas have more severe weakness and higher antibody titres. Thymectomy can result in medication free remission. It may also be considered in the absence of thymoma to improve symptoms and induce remission.

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13
Q

what are some of the causes of peripheral sensorineuropathy

A

sensory polyneuropathy:
metabolic- diabetes, hypothyroid,
nutritional deficiencies: vitamin B12 deficiency, thiamine B1 deficiency, B6
toxins- alcohol, vincristine, isoniazid
immune- RA/SLE
vasculitis- GPA
neurological cause- CIDP
infections- HIV

nerve conduction studies- demyelinating (more immune mediated and require specialist input) / axonal

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14
Q

how to investigate causes of peripheral neuropathy

A

Bloods: FBC
ESR- inflammatory disorders
CTD screen
renal profile, LFT
immunoglobulins, electrophoresis

nerve conduction studies- most are axonal vs demyelinating (CIDP/ GBS)

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15
Q

causes of a peripheral motor neuropathy

A

motor polyneuropathy
GBS
lead toxicity
porphyria
HSMN
chronic inflammatory demyelinating polyneuropathy

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16
Q

if you suspect GBS what investigations would you do

management

A

I would take an ABCDE approach
FVC to assess respiratory involvement- <1.5L would warrant ITU involvement
ECG for arrythmia risk
history of diarrhoea- stool sample to look for campylobacter

IVIG, plasma exhange

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17
Q

What are the features of autonomic neuropathy

A

postural hypotension
urinary retention
impotence
ileus

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18
Q

what are other causes of pes cavus

A

unilateral: malunion of fractures, burns, polio spinal trauma, spinal cord tumour, congenital/idiopathic

bilateral: freiderichs/ muscular dystrophies, spinal muscular atrophy, cerebral palsy, hereditary spastic paraperesis, spinal cord tumours

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19
Q

what is the inheritence of HSMN

A

autosomal dominant inheritence pattern
mutation of PMP22 gene on chromosome 17

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20
Q

why are pain and temperature inaffected in patients with HSMN

A

pain and temperature sensation is carried in the unmyelinated fibres therefore these sensations are unaffected

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21
Q

management of multiple sclerosis

A

MDT approach
physiotherapy for mobility
OT for walking aids

in acute deterioration- high dose corticosteroids, and counsel about long term steroid use

long term medical management- disease modifying treatments such as IFN B and glatiramer
monoclonal abs such as alemtuzumab and natalizumab can also be used

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22
Q

what are the cranial nerve signs associated with MS

A

Intranuclear opthalmaplegia - failure of one eye to adduct and nystagmus of other eye on abduction suggests lesion of medial longitudinal fasiculus
RAPD
optic atrophy
reduced visual acuity

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23
Q

what are the diagnostic criteria of MS

A

CNS demyelinating plaques causing neurological impairements seperated by time and place

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24
Q

What clinical features may be present with MS

A

autonomic dysfunction- urinary incontinence, impotence, bowel problems
Uthoff’s phenomenon- worsening of symptoms after a hot bath or exercise
lhermittes syndrome- lightening pains down the spine on flexion of neck due to cervical cord plaques

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25
Q

how does multiple sclerosis affect pregnancy

A

reduced relapse rate during pregnancy but an increased risk of relapse in the post partum period
generally safe for foetus although there is a possible reduction in birth weightc

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26
Q

causes of a spastic paraperesis
myelopathy

A

compressive- degeneration e.g. disc herniation/ vertebral disc disease.
tumour- primary or metastatic
trauma
infection- epidural abscess, spinal TB, viral (polio, CMV, EBV)
Potts, vertebral osteomyelitis
haematoma
congenital
vascular- spinal infarcts, arteriovenous malformation
inflammatory- MS (transverse myelitis), sarcoid, CTD SLE
metabolic- B12 deficiency
degenerative- MND, HSMN, hereditary spastic paraparesis

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27
Q

what classification of stroke do you know

A

Bamford classification
a) contralateral hemiplegia b) contralateral homonomous hemianopia c) higher cortical dysfunction (dysphagia, dyspraxia, neglect)
3/3 TACS, 2/3 PACS

28
Q

what is a lacunar circulation stroke

A

purely hemi-motor or sensory loss

29
Q

what would you expect to see in a parietal lobe lesion

A

sensory inattention
apraxias
astereognosis (tactile agnosia)
inferior homonymous quadrantanopia
Gerstmann’s syndrome (lesion of dominant parietal): agraphia, acalculia, finger agnosia and right-left disorientation

30
Q

what would you expect to find from an occipital lobe lesion

A

homonymous hemianopia (with macula sparing)
cortical blindness
visual agnosia

31
Q

what would you expect to find from a temporal lobe lesion

A

Wernicke’s aphasia: this area ‘forms’ the speech before ‘sending it’ to Brocas area. Lesions result in word substituion, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)

32
Q

what would you expect to find from a frontal lobes lesion

A

expressive (Broca’s) aphasia: located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus. Speech is non-fluent, laboured, and halting
disinhibition
perseveration
anosmia
inability to generate a list

33
Q

what would you expect to find from a cerebellum lesion

A

midline lesions: gait and truncal ataxia
hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus

34
Q

how would you treat a cord compression

A

emergency
involve the neurosurgical team for urgent decompression
in instance of malignancy can also consider chemo/ radiotherapy
high dose steroids can be used

35
Q

management of MND

A

MDT approach
specialist neurology clinic and MND nurses
PT/OT for rehabilitation and aids
SALT team for swallow safety
dieticians and consideration of PEG feeding
check respiratory function (FVC) as patients can develop T2RF and may require NIV at night
cognitive screening as an association with fronto-temporal dementia
consider riluzole (glutamate antagonist) which may slow down progression (does not improve QOL)

36
Q

what is the classification of MND

A

3 types but often overlapping
1) ALS (50%)- affects corticospinal tracts predominantly, causing a spastic para/tetraparesis
2) progressive muscular atrophy (25%)- affects anterior horn cell producing wasting, fasciculations and wasting (best prognosis)
3) progressive bulbar palsy (25%)- affects lower cranial nerves and supra-bulbar nuclei producing speech and swallow problems (worst)

37
Q

what are the causes of generalised wasting of hand muscles

A

anterior horn cells- MND, syringmyelia, cervical cord compression, polio

brachial plexus- cervical rib, pancoast tumours, trauma

muscle disuse atrophy- rheumatoid arthritis

38
Q

differentials for parkinsonisms

A

idiopathic parkinsons disease
drugs- chlorpromazine, metoclopramide, sodium valproate
tumours at the basal ganglia
lewy body dementia - visual hallucinations
PSP/ MSA
wilsons disease

39
Q

investigations for parkinsons

A

clinical diagnosis
serum caeruloplasmin
L/S BP
cognitive testing
DAT/ SPECT testing- shows impaired dopamine transporter binding

40
Q

what is the pathology of parkinsons disease

A

degeneration of the dopaminergic neurones between the substantia nigra and basal ganglia

41
Q

what are some non-motor symptoms of PD

A

mood disorders, REM sleep disorder, anosmia, constipation, cognitive impairment, visual hallucinations, pain, autonomic disturbance

42
Q

what are the medical treatment options for PD

A

delay medical management for as long as possible as effects wear off/
1) Levadopa with a peripheral decarboxyl inhibitors e.g. madopar/ co-beneldopa
- can cause nausea, dyskinesia, on/off phenomenon
impulsivity and increased spending
2) dopamine agonists e.g. pergolide- used in younger patients, has fewer side effects, delays use of L-dopa
3) anticholinergics e.g. procyclidine can help with tremors, particularly if drug related
4) MOA-B inhibitors e.g. selegilline, inhibit breakdown of dopamine

43
Q

Cerebellar signs

A

D: Dysdiadochokinesia
A: Ataxia
N: Nystagmus
I: Intention tremor
S: Slurred or scanning speech
or syllables
H: Hypotonia

44
Q

Causes of cerebellar lesion

A

Paraneoplastic syndrome
Abscess/atrophy
Stroke/sclerosis (multiple sclerosis)
Trauma
Raised ICP
Infection
Ethanol and poisons
Spinocerebellar ataxia (progressive degenerative genetic disease)

45
Q

what is rombergs test

A

romberg’s is ataxia when the visual stimulus is removed. Instability suggests a sensory ataxia

46
Q

what is spinocerebellar ataxia

A

SCA is a group of AD genetic conditions which cause degenerative cerebellar syndrome. They are due to a trinucleotide repeat and shows genetic anticipation, presenting earlier and more severely in successive generations

47
Q

What is Miller Fisher syndrome

A

this is an autoimmune condition which presents usually post infection, that causes opthalmoplegia, ataxia, loss of lower limb reflexes. It can overlap with GBS

48
Q

with which cancers are paraneoplastic cerebellar syndromes most frequently associated

A

small cell lung, breast, gynaecological, testicular and lymphomas

49
Q

which side would you see signs from a unilateral cerebellar lesions

A

limb symptoms are ipsilateral to a cerebellar lesion
nystagmus would have the fast phase maximum on looking towards the side of the lesion

50
Q

what symptoms are associated with Freiderichs ataxia

A

kyphoscoliosis, optic atrophy, sensory neuropathy, cardiomyopathy, diabetes

51
Q

what is myotonic dystrophy

A

autosomal dominant genetic muscle disorder of which there are 2 types. It affects smooth muscle, cardiac muscle and skeletal muscle

52
Q

what are the complications/ associations of myotonic dystrophy

A

diabetes, cardiomyopathy, tachy/ bradyarrhythmia (hence PPM), respiratory compromise from diaphragm weakness, dysphagia, PEG feeding, testicular atrophy

53
Q

differentials for a distal myopathy

A

inclusion body myositis
myotonic dystrophy
fascio-scapulohumeral dystrophy
GBS

54
Q

differentials for proximal myopathy

A

1) infective/ post-infective
a) viral- HIV, CMV, EBV
b) bacterial- lymes disease, TB
c) parasitic- nematodes

2) toxins
statins, steroids

3) endocrinological
thyroid disease
cushings disease
acromegaly

4) systemic disease
SLE
vasculitis
sarcoidosis

55
Q

differentials for chorea

A

syndeham’s chorea- rhematic fever
drug induced- anti convulsants
cerebral infarction
wilson’s disease
huntingtons disease

56
Q

macula sparing defect

A
57
Q

cerebellar vs sensory ataxia signs

A

cerebellar ataxia- eye signs + dysarthria + other cerebellar signs
sensory ataxia- JPS + vibration

58
Q

causes of cerebellar ataxia

A

acute:
vascular- haemorrhage vs infarct
cerebellitis- varicella
demyelination

chronic
alcohol
nutritional deficiencies
surgery
previous trauma

59
Q

types of sensory ataxia

A

central- spinal cord esp dorsal column damage
peripheral- peipheral neuropathy- large myelinated nerve fibres

60
Q

Multifocal motor neuropathy

A

Acquired autoimmune demyelinating motor neuropathy

Associated with motor conduction block

Slowly progressive, distal motor neuropathy which progresses over many years

Anti-GM1 antibodies frequently raised

61
Q

management of MND

A

specialist neurology clinic- specialist neurologist and the motor neurone disease specialist nurses.

drug treatment- Riluzole. This is the only
drug treatment available and confers a very small increase in overall survival

multidisciplinary team approach physios and
occupational therapists as they may be able to provide supportand adaptations in the home and
workplace.

speech and language team, we might want to consider non-oral feeding in the form of a PEG tube
communication aids

screening this patient’s respiratory function
I would do an early morning blood gas, FVC as well.
Patients with motor neurone disease can develop problems with type 2 respiratory failure and may go on to needing NIV, especially at night.

screen for are cognitive and behavioral changes that
could be suggestive of frontotemporal dementia.

62
Q

investigation of MND

A

neurophysiology- deenervation of peripheral nerves, no sensory changes

63
Q

causes of chorea

A

acute: stroke, hypoglycaemia
inflammatory: sydenhams chorea, SLE
chronic: huntingtons disease

64
Q

atrophy- calf hypertrophy
muscle weakness, reduced reflexes

types

A

muscular dystrophy
Duchenne/ Beckers dystrophy
limb girdle dystrophy
fascioscapulohumeral dystrophy
spinobular muscular atrophy
progressive muscular atrophy

65
Q

limb girdle

A

inherited muscular dystrophy
raised CK
EMG- myopathic changes

66
Q

management of muscular dystrophy

A

MDT
- therapists to aid with any physical impairement
- ECG/ echo
- swalloe impairement

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