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The Ultimate Guide To Passing Clinical Medical Finals > Neurology > Flashcards

Neurology Flashcards

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USMLE® Step 1 flashcards
1
Q

What does clasp knife spasicity suggest?

A

Pyramidal disease in upper motor neurone lesion

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2
Q

What does cog wheel rigidity suggest?

A

Extrapyramidal disease

Elicited by slowly pronating and supinating the patient’s wrist.

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3
Q

What is the muscle tested in shoulder ABduction?

A

Supraspinatus and Deltoid

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4
Q

What is the muscle tested in Shoulder ADduction?

A

Petoralis Major, Latissimus Dorsi

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5
Q

What is the muscle tested in Elbow Flexion?

A

Biceps and brachioradialis

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6
Q

What is the muscle tested in Elbow Extension?

A

Triceps

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7
Q

What is the muscle tested in Finger ABduction?

A

interossei

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8
Q

What is the muscle tested in Finger ADduction?

A

Interossei

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9
Q

What is the nerve root tested in shoulder ABduction?

A

C5

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10
Q

What is the nerve root tested in Shoulder ADduction?

A

Multiple, mainly C7

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11
Q

What is the nerve root tested in Elbow Flexion?

A

C5, C6

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12
Q

What is the nerve root tested in Elbow Extension?

A

C7

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13
Q

What is the nerve root tested in Wrist Flexion?

A

C7 and C8

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14
Q

What is the nerve root tested in Wrist Extension?

A

C7

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15
Q

What is the nerve root tested in finger ABduction and ADduction?

A

T1

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16
Q

What is the grading scale for power?

A

Medical Research Council Muscle Strength Scale

0: No visible Movements
1: Flicker of Movement on Active Contraction
2: Active movement with gravity eliminated
3: Active Movement against gravity but not against resistance
4: Active movement against gravity and resistance, but not normal strength
5: Normal

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17
Q

What does difficulty with past pointing and intention tremor suggest?

A

Cerebellar Disease

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18
Q

What does difficulty in dysdiadocokinesis suggest?

A

Cerebellar Disease

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19
Q

What are you testing in supinator reflex?

A

C5 & C6

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20
Q

What are you looking for in supinator reflex?

A

The contraction of the brachioradialis muscles- finger and elbow flexion

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21
Q

What are you testing in bicep reflex?

A

C5 & C6

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22
Q

What are you looking for in bicep reflex?

A

Contraction of the bicep muscles

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23
Q

What are you testing in triceps reflex?

A

C7

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24
Q

What are you looking for in triceps reflex?

A

Contraction of the tricep muscle

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25
Q

Where do you test dermatomes?

A

Picture

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26
Q

What nerve tract are you testing with proprioception?

A

Dorsal Column

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27
Q

What tuning fork in Neuro vibration sense?

A

128-Hz

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28
Q

What sensory modality are you testing with tuning fork?

A

Vibration- Dorsal Column

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29
Q

What is the muscle tested in Hip Flexion?

A

Iliosoas

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30
Q

What is the muscle tested in Hip extension?

A

Gluteus Maximus

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31
Q

What is the muscle tested in Knee Flexion?

A

Hamstrings

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32
Q

What is the muscle tested in Knee Extension?

A

Quadriceps

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33
Q

What is the nerve root tested in Hip Flexion?

A

L1 & L2

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34
Q

What is the nerve root tested in Hip Extension?

A

L5 & S1

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35
Q

What is the nerve root tested in Knee Flexion?

A

L5 & S1

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36
Q

What is the nerve root tested in Knee Extension?

A

L3 & L4

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37
Q

What is the muscle tested in Dorsiflexion?

A

Tibialis Anterior

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38
Q

What is the muscle tested in Plantar flexion?

A

Calf Muscles

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39
Q

What is the nerve root tested in Dorsiflexion?

A

L4 & L5

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40
Q

What is the nerve root tested in Plantar Flexion?

A

S1

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41
Q

Where do you assess Sensation on lower limb?

A

PIC

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42
Q

What are you testing in knee reflex?

A

L3 & L4

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43
Q

What are you looking for in knee reflex?

A

Knee Extension and quadricep muscle contraction

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44
Q

What are you testing in Ankle reflex?

A

L5 &S1

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45
Q

What are you looking for in ankle reflex?

A

Plantar flexion and contraction of the calf muslce.

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46
Q

What is a normal Babinski response?

A

Down going plantars.

47
Q

What does the inability to tandem walk suggest?

A

Cerebellar disease

48
Q

What does Romberg’s Test test for?

A

Sensory Ataxia

49
Q

What are reflexes?

A

Monosynaptic responses to muscle fibre stretch, mediated via the spinal cord with inhibitary input from higher neurones.

In UMN lesions the inhibitory input from higher neurones is reduced and so reflexes are increased.

50
Q

Pattern of Signs in an UMN lesion

A

Tone- Increased tone or spasticity, clonus
Power- Reduced: Mainly in arm extensors and leg flexors
Pronator Drift
Reflexes: Hyperreflexia
Inspection: No muscle wasting or fasiculaitons

51
Q

Difference between Tone and Spasticity.

A

Spasticity is velocity dependent: tone decreases with velocity

52
Q

Where is the lesion in an UMN relative to the signs?

A

Contralateral Side

53
Q

Pattern of Signs in an LMN lesion

A

Tone: Hypotonia
Power: Reduced
Reflexes: Diminished/ Absent
Inspection: Muscle Wasting and fasiculaitons

54
Q

Where is the lesion in an LMN relative to the signs?

A

Ipsilateral side

55
Q

Differentials for UMN lesions

A

Stroke, MS

56
Q

DDx for LMN lesions

A

Radiculopathy, Peripheral Neuropathy, Mononeuropathies

57
Q

Features of Cerebellar Disease

A 
Dysdiadokinesia
Ataxia and Hypotonia
Horizontal Nystagmus
Intention Tremor with Pass Pointing
Staccato or Slurred Speech
Heel Shin Ataxia
Wide based, unsteady ataxic gait- pt falls to side of lesion
58
Q

How do you assess whether a tremor is an action tremor or not?

A

Rule out any muscle activation

Take the pts arms and support them in your arms.
A truley cerebellar tremor will disappear.

59
Q

What are the causes of cerebellar disease?

A
  1. Space Occupying Lesions ( Tumours, Abcescess, Bleeds)
  2. Multiple Sclerosis
  3. Chronic Alcohol Abuse
  4. Anti- Epileptic Drugs e.g Phenytoin
60
Q

What is the speed of a Parkinsonian Tremor?

A

4-7Hz

61
Q

What happens in Parkinsons to Speech and Handwritin?

A

There is a slowing down of speech and micrographia

62
Q

What is the extrapyramidal system?

A

The basal ganglia and it’s connections; especially those to do with movement.
The extrapyramidal system is charged with modulation and initiation of movement.

63
Q

What is Parkinson’s Disease?

A

Progressinve Neurodegenerative disorder characterised by Lewy Bodies, neuronal loss and degeneration of the substantia nigra

Diagnosis is clinical, but some patients have L-Dopa or apomorphine challenges.
PET of MRI scanning is sometimes done to exclude other diagnoses

64
Q

Causes of Parkinsonism

A

Parkinson’s Disease: Idiopathic

65
Q

Treatment of Parkinson

A

…

66
Q

How do you demonstrate Fatuigability in myasthenia Gravis?

A

Ask the patient to gaze upwards for a few minutes.

Pts with MG will get increased Ptosis

67
Q

How would you complete your exam in a patient with suspected myasthenia gravis?

A
  1. Look for Thymectomy Scar
  2. Assess for signs of other AI disease
  3. Assess speech (get dyarthria and poor swallowing due to weak bulbar muscles)
  4. Check eyes: Get Ophthalmoplegia, ptosis and diplopia due to weak eye muscles.
68
Q

How do pts with Myasthenia Gravis tend to present?

A

With diplopia, typically worse when tired.

69
Q

How do you diagnose Myasthenia Gravis?

A

Clinical Diagnosis

Can use tensolin test. Give edrophonium (short active ACh) and get a rapid improvement in symptoms

70
Q

What specialist investigations do you do for Myasthenia Gravis?

A

BLood test: Anti-Ach Antibodies
Tensolin Test
EMG- reduced amplitude of evoked potentials with repetative stimulation

71
Q

What is Myasthenia Gravis?

A

Auto Immune disorder affective the neuromuscular junction. Antibodies block the action of post-synaptic acetylcholine receptors

72
Q

What do you need to distinguish Myasthenia Gravis from?

A

Lambert-Eaton Syndrome

  • Occular and bulbar muscles are not affected
  • Second wind phenonemon
73
Q

How do you treat Myasthenia Gravis?

A

Medical: Cholinesterase Inhibitors, Immunosuppressants and corticosteroids (But be careful as pts are at risk of myasthenia crises if there is a coexisting infection-some crises are drug induced)
Surgical: Thymectomy for Thymomas

74
Q

Typical Examination Findings for Multiple Sclerosis.

A

UMN: Increased tone, Clonus, Brisk Reflexes, Weakness.. Bilateral.

Neuro-opthalmology:
Internuclear Ophthalmoplegia
Optic Nerve Damage

Cerebellar Signs: Ataxia, Dysarthria

Cranial Nerve Palsy: Facial Nerve

Sensation altered in a variable fashion. Altered temperature sensation, Trigeminal neuralgia, Lhermitts phenomenon-electric shock sensation down arms and legs on neck flexion.

May have catheter-neurogenic bladder dysfunction

75
Q

DDx in pt with suspected MS

A

Spinal Cord LEsion: Tumour or trauma causing spastic paraparesis

76
Q

Investigating Multiple Sclerosis

A

MRI Brian and Spinal Cord: First line investigation, reveals plaques or multiple white matter lesions, particularly in the brainstem and periventricular areas.
Electrophysiology: Prolonged Visual Evoked Potentials
CSF: High Protein, Raised WCC, Electrophoresis shows oligoclonal bands.

77
Q

What is Multiple Sclerosis?

A

Neurological Disorder of unknown cause resulting in multiple areas of plaques of demyelination in the brain and spinal cord, disseminated in time and space.
There is a female predominance.
Characteristically begins in early adult hood: Clinical course can be broadly broken down to progressive and relapsing remitting.

78
Q

What factors give poor prognosis in MS?

A

Male
Increased Age
Motor Symptoms
High Number of Relapses with incomplete remissions

79
Q

How would you treat MS

A

This patient will require an MDT approach
The focus of the treatment is to prevent disability and its progression.

High dose steroids: Aid recovery and promote remission during acute relapses but do not affect long term prognosis

Beta-Interferon has been shown to delay progress of disability, reduce relapse rates and reduce disease activity.

Urinary catheteriastion- neurogenic bladder dysfunction.

Physio and OT- aid mobility and limit disability.

Muscle relaxants: Baclofen for painful spasticity

Pt and Family Self Help group referral

80
Q

4 Groups of Cranial Nerves

A
  1. Olfactory
  2. Ophthalmology: II, III, IV, VI
  3. Cerebellopontine Angle Nerves: V, VII, VIII
  4. Bulbar Nerves: IX, X, XI, XII
81
Q

What is a turned out eyelid called?

A

Ectropion

82
Q

What is a turned in eyelid called?

A

Entropion

83
Q

Causes of Entropion

A
  1. Congenital
  2. Age related
  3. Infection
  4. Trauma
84
Q

Causes of Ectropion

A

Normally the Lower Lid

Styes (Hordeolum)- acute focal infection, usually staphyloccocal involving the glands of Zeis or meibomian glands

85
Q

SE of Entropion

A

Redness and irritation due to inversion of eyelashes with excessive lacrimation

86
Q

SE of ectropion

A

Corneal Exposure, lacrimation, scarring of the conjunctiva and eventually vision loss.

87
Q

What is the causes of proptosis?

A

Increased volume in the fixed volume orbital cavity forcing the orbit forward

88
Q

What are the causes of proptosis?

A
  1. Inflammatory
  2. Infection
  3. Vascular pathology

In Graves disease: AI reaction in orbital tissues which become infiltrated with inflammatory tissue and matter

89
Q

What does iritis look like?

A

Mudded iris, often with pupil constriction

90
Q

When do pupils constrict?

A
  1. Light
  2. Extremes in age: Old and infancy
  3. Sleep
91
Q

When do pupils dilate?

A
  1. Fear
  2. Excitement
  3. Poor light
92
Q

What happens in the accommodation reflex

A

Pupils constrict and converge

93
Q

Pathological cause of a Small Pupil.

A

Miosis

  1. Argyll Robinson
  2. Horner’s Syndrome
  3. Iritis
94
Q

Argyll Robinson pupil

A

Small, irregular pupil.

Doesn’t react to light but accommodates

95
Q

Horner’s Syndrome

A

Miosis
Ptosos
Anhydrosis on affected side

Due to lesion in the sympathetic chain.

Pupil reacts normally to light and accommodation

96
Q

Iritis

A

Poor reaction to light and accommodation

97
Q

Pathological cause of large pupil (Mydriasis)

A
  1. Holmes-Aidie Pupil

2. 3rd Nerve Palsy

98
Q

Holes-Adie Pupil

A

Congenital, Slow, incomplete reaction to light. Accommodation is slow/ Normal.

Holmes Adie Syndrome if loss of deep tendon reflexes

99
Q

CN3 Lesion

A

Interruption of parasympathetic chain, no reaction to light or accommodation. BUT normal side still reacts consensually

100
Q

Aeitiology of Arcuate Scotoma

A

Glaucoma

101
Q

Aeitiology of Central Scotoma

A

Macular Degeneration

102
Q

Aeitiology of Unilateral Deficit

A

PIC

Arterial Occulsion
Branch Retinal Vein Occlusion
Retinal Detachment

103
Q

Superior Homonomous L/R sided quadrantinopia

A

Right sided means left temporal lesion

104
Q

Inferior Homonomous L/R sided quadrantinopia

A

Right sided means left parietal lesion

105
Q

Homonomous Hemianopia

A

Right field deffect means Left OPtic radiation or visual cortex

106
Q

Bitemporal hemianopia

A

Lesion a optic Chiasm

107
Q

Loss of vision in one eye

A

Optic nerve lesion

Complicated lesion of Chiasm

108
Q

What are the branches of the Facial Nerve?

A

To Zanzibar by Motor Car

Temporal, Zygomatic, Buccal, Marginal Mandibular, Cervical

109
Q

Causes of facial nerve palsy

A
  1. Bells Palsy
  2. Infective: Ramsay Hunt Syndrome, Lyme Disease, TB
  3. Brain Lesons: in brainstem and cerebellopontine angle
  4. Others: ENT, Trauma, etc
  5. Bells Palsy: Classically described as idiopathic but can be viral. Typically Facial Weakness is the only sign.
  6. Ramsay-Hunt Syndrome: Reactivation of Herpes Zoster in the geniculate ganglion–> altered taste and vesicles in the external auditory meatus
  7. Brainstem= Tumours, MS, CVA
  8. Cerebellopontine Angle= Meningioma, Acoustic Neuromas
  9. ENT: Otitis Media, Cholesteatoma, Parotid Tumours
  10. Trauma: Base of skull fracture, barotrauma whilst diving

others include: DM, Guillain-Barre Syndrome

110
Q

What is Bells Phenomenon?

A

On attempted closure of the eye the eye rolls up

It is due to weak orbicularis oculi muscles resulting in difficulty in closing eyes

111
Q

Key features of Bells Palsy

A 
Unilateral- Facial Droop
Bells Phenomenon: Weak Orbicularis Oculi
Inability to raise eyebrow: Weak frontalis muscle
Inability to frown
Smooth Nasolabial Fold
112
Q

How do you localise a facial nerve palsy

A
  1. Ask about changes in hearing- Hyperacusis suggests lesion distal to the stapedius branch
  2. Ask about changes in lacrimaiton and taste- Major branch of facial nerve, Chorda Tympani goes through facial canal of petrous temporal bone.
113
Q

Treatment of Bells Palsy

A

Steroids- within 6 days
? Aciclovir

Eye protection

The Ultimate Guide To Passing Clinical Medical Finals (4 decks)

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