Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PACES > Neurology > Flashcards

Neurology Flashcards

1
Q

Differentials for bilateral ptosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

differentials for bilateral LMN facial weakness

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which drugs can exacerbate myasthenia gravis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what conditions are associated with MG

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

botulism, miller fisher syndrome, LEMS, mitochondrial myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

causes of a peripheral motor neuropathy

A

motor polyneuropathy
GBS
lead toxicity
porphyria
HSMN
chronic inflammatory demyelinating polyneuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the features of autonomic neuropathy

A

postural hypotension
urinary retention
impotence
ileus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the inheritence of HSMN

A

autosomal dominant inheritence pattern
mutation of PMP22 gene on chromosome 17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are the diagnostic criteria of MS

A

CNS demyelinating plaques causing neurological impairements seperated by time and place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how does multiple sclerosis affect pregnancy
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
26
causes of a spastic paraperesis myelopathy
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
27
what classification of stroke do you know
Bamford classification a) contralateral hemiplegia b) contralateral homonomous hemianopia c) higher cortical dysfunction (dysphagia, dyspraxia, neglect) 3/3 TACS, 2/3 PACS
28
what is a lacunar circulation stroke
purely hemi-motor or sensory loss
29
what would you expect to see in a parietal lobe lesion
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
what would you expect to find from an occipital lobe lesion
homonymous hemianopia (with macula sparing) cortical blindness visual agnosia
31
what would you expect to find from a temporal lobe lesion
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
what would you expect to find from a frontal lobes lesion
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
what would you expect to find from a cerebellum lesion
midline lesions: gait and truncal ataxia hemisphere lesions: intention tremor, past pointing, dysdiadokinesis, nystagmus
34
how would you treat a cord compression
emergency involve the neurosurgical team for urgent decompression in instance of malignancy can also consider chemo/ radiotherapy high dose steroids can be used
35
management of MND
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
what is the classification of MND
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
what are the causes of generalised wasting of hand muscles
anterior horn cells- MND, syringmyelia, cervical cord compression, polio brachial plexus- cervical rib, pancoast tumours, trauma muscle disuse atrophy- rheumatoid arthritis
38
differentials for parkinsonisms
idiopathic parkinsons disease drugs- chlorpromazine, metoclopramide, sodium valproate tumours at the basal ganglia lewy body dementia - visual hallucinations PSP/ MSA wilsons disease
39
investigations for parkinsons
clinical diagnosis serum caeruloplasmin L/S BP cognitive testing DAT/ SPECT testing- shows impaired dopamine transporter binding
40
what is the pathology of parkinsons disease
degeneration of the dopaminergic neurones between the substantia nigra and basal ganglia
41
what are some non-motor symptoms of PD
mood disorders, REM sleep disorder, anosmia, constipation, cognitive impairment, visual hallucinations, pain, autonomic disturbance
42
what are the medical treatment options for PD
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
Cerebellar signs
D: Dysdiadochokinesia A: Ataxia N: Nystagmus I: Intention tremor S: Slurred or scanning speech or syllables H: Hypotonia
44
Causes of cerebellar lesion
Paraneoplastic syndrome Abscess/atrophy Stroke/sclerosis (multiple sclerosis) Trauma Raised ICP Infection Ethanol and poisons Spinocerebellar ataxia (progressive degenerative genetic disease)
45
what is rombergs test
romberg's is ataxia when the visual stimulus is removed. Instability suggests a sensory ataxia
46
what is spinocerebellar ataxia
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
What is Miller Fisher syndrome
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
with which cancers are paraneoplastic cerebellar syndromes most frequently associated
small cell lung, breast, gynaecological, testicular and lymphomas
49
which side would you see signs from a unilateral cerebellar lesions
limb symptoms are ipsilateral to a cerebellar lesion nystagmus would have the fast phase maximum on looking towards the side of the lesion
50
what symptoms are associated with Freiderichs ataxia
kyphoscoliosis, optic atrophy, sensory neuropathy, cardiomyopathy, diabetes
51
what is myotonic dystrophy
autosomal dominant genetic muscle disorder of which there are 2 types. It affects smooth muscle, cardiac muscle and skeletal muscle
52
what are the complications/ associations of myotonic dystrophy
diabetes, cardiomyopathy, tachy/ bradyarrhythmia (hence PPM), respiratory compromise from diaphragm weakness, dysphagia, PEG feeding, testicular atrophy
53
differentials for a distal myopathy
inclusion body myositis myotonic dystrophy fascio-scapulohumeral dystrophy GBS
54
differentials for proximal myopathy
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
differentials for chorea
syndeham's chorea- rhematic fever drug induced- anti convulsants cerebral infarction wilson's disease huntingtons disease
56
macula sparing defect
57
cerebellar vs sensory ataxia signs
cerebellar ataxia- eye signs + dysarthria + other cerebellar signs sensory ataxia- JPS + vibration
58
causes of cerebellar ataxia
acute: vascular- haemorrhage vs infarct cerebellitis- varicella demyelination chronic alcohol nutritional deficiencies surgery previous trauma
59
types of sensory ataxia
central- spinal cord esp dorsal column damage peripheral- peipheral neuropathy- large myelinated nerve fibres
60
Multifocal motor neuropathy
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
management of MND
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
investigation of MND
neurophysiology- deenervation of peripheral nerves, no sensory changes
63
causes of chorea
acute: stroke, hypoglycaemia inflammatory: sydenhams chorea, SLE chronic: huntingtons disease
64
atrophy- calf hypertrophy muscle weakness, reduced reflexes types
muscular dystrophy Duchenne/ Beckers dystrophy limb girdle dystrophy fascioscapulohumeral dystrophy spinobular muscular atrophy progressive muscular atrophy
65
limb girdle
inherited muscular dystrophy raised CK EMG- myopathic changes
66
management of muscular dystrophy
MDT - therapists to aid with any physical impairement - ECG/ echo - swalloe impairement

PACES (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions