Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PACES final > Neurology station > Flashcards

Neurology station Flashcards

1
Q

stroke signs

A

Signs on inspection = circumducting gait, strong flexors in arms, strong extensors in legs, fixed flexed arm = pyramidal weakness, walking aids, wasted on affected side, increased tone/clonus, clasp knife spasticity, brisk reflexes and upgoing plantars

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

UMN signs

A

increased tone, increased reflexes, clonus, upgoing plantars contralateral

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

LMN signs

A

decreased tone, decreased reflexes, fasiculations, ipsilateral

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

pseudobulbar involvement

A

UMN Cranial nerves 9,10,12

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

Bulbar involvement

A

CN 9,10,11 = swallow and speech - aspiration and nutrition = PEG or NGT
LMN

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

What do you need to assess for in query stroke

A

Assess visual fields for Bamford classification
Assess pulse for AF and carotids for bruits.

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

how do you differentiate between bulbar vs pseudobulbar involvement

A

LMN would have fasciculations and wasting (bulbar)

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

stroke presentation

A

Today I performed a neurological examination on this gentleman. On general inspection he looked alert. He showed a circumducting gait on walking on the right with a flexed arm and extended leg. There was associated clasp knife spasticity, and hyperreflexia on the right. Clonus was present on the right, and plantars were upgoing. Power was 4/5 on the right. His left side was normal with power 5/5. These findings are consistent with a left sided partial anterior circulation infarct. I would like to take a full history, and feel his pulse for AF, listen to his carotids for bruits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bamford classification

A
  1. TACS = total anterior circulation stroke = hemiplegia, homonymous hemianopia, higher cortical dysfunction
  2. PACS = partial anterior circulation stroke = 2/3 of above
  3. Lacunar stroke = hemi-motor or hemi-sensory stroke only
  4. Posterior circulation stroke = visual field defects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ACA

A

leg > arm
so may have fixed extended leg but normal arm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MCA

A

arm > leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

parkinsonism signs

A

Gait = shuffling, slow turn, asymmetrical limited arm swing
Face = expressionless, slow monotonous speech
Other = asymmetrical, pill rolling resting tremor, bradykinesia, rigidity, cogwheel rigidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

causes of parkinsonism

A

Idiopathic Parkinson’s disease
Lewy Body dementia (early dementia signs)
Multisystem atropy (if postural hypotension)
Supranuclear palsy (if palsy of eye movement)
Drug induced (if antipsychotics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

treatment of parkinsons

A

Conservative = carers, MDT, management of other comorbidities, optimising housing
Medical = Levodopa, co-carelodopa = reduced peripheral breakdown of dopa
Surgical = deep brain stimulation

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

Parkinsons presentation

A

Today I examined this gentleman’s neurological system. He was slow to start and slow to turn on walking. He had a shuffling gait with reduced arm swing on the left. He had a resting tremor in his left hand and there was marked rigidity on the left arm. Power and reflexes were normal. There was bradykinesia on examination of repeated movements. These findings are consistent with Parkinsonism. I would like to measure his lying and standing blood pressure, examine the eye movements, and perform an examination of his higher cognitive function to assess for the cause of his parkinsonism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

motor neurone disease signs

A

Mixed upper and lower motor signs
Fasciculations, increased tone, absent and brisk reflexes, upgoing plantars, bulbar or pseudobulbar tongue and speech
Normal sensory examination

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

motor neurone disease signs

A

Mixed upper and lower motor signs
Fasciculations, increased tone, absent and brisk reflexes, upgoing plantars, bulbar or pseudobulbar tongue and speech
Normal sensory examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MND presentation

A

Today I examined this gentleman’s neurological system. He had reduced muscle bulk in all limbs and fasciculations. Tone was increased with brisk reflexes in the upper limbs but the knee and ankle jerk reflexes could not be elicited. Plantars were upgoing. There was globally reduced power in all limb at 4/5. Sensory examination was normal. These findings are consistent with a diagnosis of motor neuron disease. I would like to examine for bulbar involvement and take a full history.

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

DDx for mixed upper and lower signs

A

Motor neuron disease
Dual pathology e.g. peripheral neuropathy and stroke
Conus medullaris
B12 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Facial nerve palsy UMN

A

stroke = cerebral hemisphere lesion = contralateral + preservation of frontalis muscles FOREHEAD SPARED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Facial nerve palsy LMN

A

facial nerve lesion = ipsilateral and frontalis weakness = FOREHEAD AFFECTED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is bells phenomenon

A

eyeball up and out to protect cornea

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

causes of facial nerve palsy

A

Stroke/MS = Pons = corticospinal tract signs
Acoustic neuroma = cerebello-pontine angle = 5, 6 , 7 palsies
Cholesteatoma = inner ear lesion = 8th nerve palsy
Parotid tumour = facial nerve = parotid scar/swelling
ramsey hunt syndrome
lyme disease

24
Q

management of bells palsy

A

Prednisolone if <72 hours
Eye protection
Anti-virals not usually used

25
Q

unilateral facial palsy

A

Herpes zoster – Ramsey Hunt
Diabetes mononeuropathy
Tumour

26
Q

signs of MS

A

young, female. Catheter, walking aids, increased reflexes and tone, internuclear ophthalmoplegia, optic atrophy and RAPD

27
Q

management of MS

A

MDT
Disease modifying drugs = interferon, alemtuzumab, natalizumab
Methylprednisone for flare ups
Baclofen for muscle spasms

28
Q

cerebellar syndrome examination

A
  1. Gait = broad and unsteady, ataxia worse when heel-toe walk
  2. Arms = decreased tone, decreased reflexes, dysdiadokinesia, past pointing and intention tremor, rebound overshoot
  3. Eyes = nystagmus = cerebellar nystagmus = fast towards the lesion and worse towards affected side
  4. Speech = british constitution, west register street
29
Q

DANISH

A

dysdiadokinesia
Ataxia
nystagmus
intention tremor
slurred speech
hyporeflexia, hypotonia

30
Q

causes of cerebellar syndrome

A

Multiple sclerosis = young female
Stroke = older, AF, CABG, tar staining
Alcohol = liver disease
Phenytoin

31
Q

what is Charcot Marie tooth disease and how to investigate

A

Muscle wasting
Thickened nerves
BL, symmetrical LMN  foot drop, high step gait, absent ankle jerk
Stocking distribution loss of sensation
Ix via Nerve conduction studies and Genetic testing

32
Q

Contralateral superior quadrantopia

A

temporal superior

33
Q

Contralateral inferior quad

A

Parietal inferior

34
Q

what is 3rd nerve palsy

A

Down and out
Ptosis
Dilate palsy

35
Q

causes of 3rd nerve palsy

A

uncal herination
Cavernous sinus thrombosis,
PICA,
amyloid,
DM,
MS

36
Q

horners

A

Ptosis, miosis, anhidrosis

37
Q

horners causes

A

Stroke, sclerosis, tumour, carotid artery dissection

38
Q

wernickes aphasia

A

receptive aphasia (temporal lobe) - comprehension is imparied

39
Q

brocas apahsia

A

expressive aphasia (frontal lobe) - speech non fluent

40
Q

Contralateral homonoymous hemianopia

A

optic tract

41
Q

Bitemporal hemianopia

A

optic chiasm

42
Q

LMN causes

A

polio,
lead poison
Alcoholic neuropathy
Leprosy
DM,
EToH
Vit b12 deficiency

43
Q

causes of UMN

A

Abscess, cerebrovascular accident, tumour, demyelination, MS, cord compression, trauma, MND,

44
Q

acute meningitis causes and treatment

A

Neonates = GBS, listeria, e.coli
Adults = s.pneumo, n.meningitidis

IV CEFTRIAZONE + IM BENZYLPENICILLIN
ELDERLY = + AMOXICILLIN
NEONATES = IV CEFOTAXIME + IV AMOXICILLIN

45
Q

TIA treatment

A

Aspirin 300mg
Review by specialist

  1. Clopidogrel 75mg pO OD
  2. Statin

Surgery = carotid artery endarectomy

46
Q

haemorrhagic stroke treatment

A

CT head if negative then LP with XANTHOCHROMIA

  1. Nimodipine CCB 21d
  2. First line = coiling
  3. Second line = surgical clipping
47
Q

ischaemic stroke treatment

A
  1. Aspirin 300mg
  2. No AF = clopidogrel
  3. AF = apixaban
48
Q

conductive hearing loss causes

A

Wax
Pus
Tympanic membrane perforation
Ossicle defects e.g. otosclerosis

49
Q

sensorineural hearing loss causes

A

idiopathic
Drugs e.g. aminoglycosides or gentamicin
Infective = meningitis, measles, mumps
Meniere’s trauma, MS
Presbycusis - age related hearing loss

50
Q

normal lower limb examination presentation

A

Today I performed a lower limb neurological examination of X year old Y.
On general inspection the patient was comfortable at rest, did not have any walking aids and had no bedside paraphernalia of neurological disease.
On closer inspection of the legs, the patient did not exhibit any stigmata of neurological disease such as scars or muscle wasting.
Tone was normal and no spasticity was noted.
Power was 5/5 in all muscle tested.
Reflexes, sensation, proprioception and coordination were normal in all modalities tested.
Gait was normal, and Romberg’s test was negative.
In conclusion this was a normal neurological examination of the lower limb.
To complete my examination, I would like to take full history and perform a cranial and upper limb examination.
I would like to take a full set of observations, perform a capillary blood glucose and take bloods, including FBC, U&Es and LFTs for baseline.
No further invasive tests are required at this point.

51
Q

normal cranial nerve exam presentation

A

Today I performed a cranial nerve examination of X year old Y.
On general inspection the patient was comfortable at rest, did not have any walking aids and had no bedside paraphernalia of neurological disease.
On closer inspection of the face, the patient did not exhibit any stigmata of neurological disease such as face drooping or eye deviation.
Pupils were equal and reactive. There was no visual field abnormality and no pain on eye movement.
No abnormality was identified when testing cranial nerves 1 through 12.
In conclusion this was a normal neurological examination of the cranial nerves.
To complete my examination, I would like to take full history and perform an upper and lower limb examination.
I would like to take a full set of observations, perform otoscopy and fundoscopy exams, and take bloods, including FBC, U&Es and LFTs for baseline.
No further invasive tests are required at this point.

52
Q

Normal upper limb examination presentation

A

Today I performed an upper limb neurological examination of X year old Y.
On general inspection the patient was comfortable at rest, did not have any walking aids and had no bedside paraphernalia of neurological disease.
On closer inspection of the arms, the patient did not exhibit any stigmata of neurological disease such as scars or muscle wasting.
Tone was normal and no spasticity was noted.
Power was 5/5 in all muscle tested.
Reflexes, sensation, proprioception and coordination were normal in all modalities tested.
There was not pronator drift or intention tremor noted.
In conclusion this was a normal neurological examination of the upper limb.
To complete my examination, I would like to take full history and perform a cranial and lower limb examination.
I would like to take a full set of observations, perform a capillary blood glucose and take bloods, including FBC, U&Es and LFTs for baseline.
No further invasive tests are required at this point.

53
Q

drugs causing Parkinsonism’?

A

! Chlorpromazine
! Metoclopramide
! Prochlorperazine
! Sodium valproate
! Methyldopa

54
Q

what is parkinsons disease

A

Parkinson’s disease is a neurodegenerative disease caused by disruption of dopaminergic
neurotransmission in the basal ganglia. The loss of dopaminergic neurones occurs most prominently
in the ventral lateral substantia nigra. Approximately 60–80% of dopaminergic neurons are lost
before the motor signs of Parkinson’s disease emerge.

55
Q

what are parkinsons plus syndromes

A

Parkinson-Plus conditions are neurodegenerative conditions with Parkinsonian characteristics but
with additional features that distinguish them from idiopathic Parkinson’s disease. examples:
- Multiple systems atrophy
- Progressive supranuclear palsy
- Corticobasal degeneration

PACES final (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions