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PACES final > Neurology station > Flashcards

Neurology station Flashcards

(55 cards)

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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

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2
Q

UMN signs

A

increased tone, increased reflexes, clonus, upgoing plantars contralateral

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3
Q

LMN signs

A

decreased tone, decreased reflexes, fasiculations, ipsilateral

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4
Q

pseudobulbar involvement

A

UMN Cranial nerves 9,10,12

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5
Q

Bulbar involvement

A

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

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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.

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7
Q

how do you differentiate between bulbar vs pseudobulbar involvement

A

LMN would have fasciculations and wasting (bulbar)

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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.

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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
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10
Q

ACA

A

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

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11
Q

MCA

A

arm > leg

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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

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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)

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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

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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.

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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

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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

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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.

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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

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20
Q

Facial nerve palsy UMN

A

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

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21
Q

Facial nerve palsy LMN

A

facial nerve lesion = ipsilateral and frontalis weakness = FOREHEAD AFFECTED

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22
Q

what is bells phenomenon

A

eyeball up and out to protect cornea

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23
Q

causes of facial nerve palsy

Study These Flashcards
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

Study These Flashcards
A

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

25
unilateral facial palsy
Herpes zoster – Ramsey Hunt Diabetes mononeuropathy Tumour
26
signs of MS
young, female. Catheter, walking aids, increased reflexes and tone, internuclear ophthalmoplegia, optic atrophy and RAPD
27
management of MS
MDT Disease modifying drugs = interferon, alemtuzumab, natalizumab Methylprednisone for flare ups Baclofen for muscle spasms
28
cerebellar syndrome examination
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
DANISH
dysdiadokinesia Ataxia nystagmus intention tremor slurred speech hyporeflexia, hypotonia
30
causes of cerebellar syndrome
Multiple sclerosis = young female Stroke = older, AF, CABG, tar staining Alcohol = liver disease Phenytoin
31
what is Charcot Marie tooth disease and how to investigate
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
Contralateral superior quadrantopia
temporal superior
33
Contralateral inferior quad
Parietal inferior
34
what is 3rd nerve palsy
Down and out Ptosis Dilate palsy
35
causes of 3rd nerve palsy
uncal herination Cavernous sinus thrombosis, PICA, amyloid, DM, MS
36
horners
Ptosis, miosis, anhidrosis
37
horners causes
Stroke, sclerosis, tumour, carotid artery dissection
38
wernickes aphasia
receptive aphasia (temporal lobe) - comprehension is imparied
39
brocas apahsia
expressive aphasia (frontal lobe) - speech non fluent
40
Contralateral homonoymous hemianopia
optic tract
41
Bitemporal hemianopia
optic chiasm
42
LMN causes
polio, lead poison Alcoholic neuropathy Leprosy DM, EToH Vit b12 deficiency
43
causes of UMN
Abscess, cerebrovascular accident, tumour, demyelination, MS, cord compression, trauma, MND,
44
acute meningitis causes and treatment
Neonates = GBS, listeria, e.coli Adults = s.pneumo, n.meningitidis IV CEFTRIAZONE + IM BENZYLPENICILLIN ELDERLY = + AMOXICILLIN NEONATES = IV CEFOTAXIME + IV AMOXICILLIN
45
TIA treatment
Aspirin 300mg Review by specialist 1. Clopidogrel 75mg pO OD 2. Statin Surgery = carotid artery endarectomy
46
haemorrhagic stroke treatment
CT head if negative then LP with XANTHOCHROMIA 1. Nimodipine CCB 21d 2. First line = coiling 3. Second line = surgical clipping
47
ischaemic stroke treatment
1. Aspirin 300mg 2. No AF = clopidogrel 3. AF = apixaban
48
conductive hearing loss causes
Wax Pus Tympanic membrane perforation Ossicle defects e.g. otosclerosis
49
sensorineural hearing loss causes
idiopathic Drugs e.g. aminoglycosides or gentamicin Infective = meningitis, measles, mumps Meniere’s trauma, MS Presbycusis - age related hearing loss
50
normal lower limb examination presentation
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
normal cranial nerve exam presentation
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
Normal upper limb examination presentation
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
drugs causing Parkinsonism’?
! Chlorpromazine ! Metoclopramide ! Prochlorperazine ! Sodium valproate ! Methyldopa
54
what is parkinsons disease
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
what are parkinsons plus syndromes
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)

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