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Neurology > Pattern recognition in Neurology > Flashcards

Pattern recognition in Neurology Flashcards

1
Q

What is focal weakness?

A
  • Weakness in distribution of peripheral nerve or spinal root
  • Hemi-distribution
  • Pyramidal distribution
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2
Q

What is non-focal weakness?

A
  • generalised
  • predominantly proximal or distal
  • if truly generalised: including bulbar motor function otherwise quadri- or tetraparesis
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3
Q

UMN weakness will be in what distribution?

A

Corticospinal distribution;

hemiparesis, quadriparesis,

paraparesis, monoparesis,

faciobrachial

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4
Q

LMN weakness will be in what distribution?

A

Generalised, predominantly proximal, distal or focal.

No preferential involvement of corticospinal innervated muscles.

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5
Q

Sensory loss in UMN weakness will be in a _____ pattern

A

Sensory loss in UMN weakness will be in a central pattern

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6
Q

Deep tendon reflexes are ______ (unless very acute: ____) in UMN weakness

A

Deep tendon reflexes are increased (unless very acute: flaccid) in UMN weakness

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7
Q

Superficial reflexes are ______ in UMN weakness?

A

Superficial reflexes are decreased in UMN weakness?

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8
Q

Pathological reflexes are ______ in UMN weakness, sphincter dunction is ______ impaired, muscle tone is ______. There may be some muscle ________.

A

Pathological reflexes are increased in UMN weakness, sphincter dunction is sometimes impaired, muscle tone is increased. There may be some muscle hypertrophy.

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9
Q

LMN sensory loss will be;

A

None, glove, stocking, peripheral nerve or root distribution

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10
Q

Deep tendon reflexes are ______ or ______ in LMN pathology, superficial reflexes are _____ along with pathological reflexes.

Sphincter function is ______ ______ (unless for example; _____ _____ ______)

Muscle tone is _______ or _______ and muscles may show signs of ______.

A

Deep tendon reflexes are normal or decreased in LMN pathology, superficial reflexes are normal along with pathological reflexes.

Sphincter function is usually normal (unless for example; cauda equina lesion)

Muscle tone is normal or decreased and muscles may show signs of wasting.

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11
Q

What is a pyramidal/corticospinal pattern of weakness?

A

Weak extensors in the arm, weak flexor in the leg

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12
Q

What is a lower motor neurone pattern of disease?

A

wasting, fasciculation, decreased tone, decreased or absent reflexes, flexor plantars

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13
Q

How does muscle disease present?

A

Wasting (usually proximal), decreased tone, decreased or absent tendon reflexes

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14
Q

How does NMJ disease present?

A

Fatiguable weakness, normal or decreased tone, normal tendon reflexes. No sensory symptoms.

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15
Q

How does functional weakness present?

A

No wasting, normal tone, normal reflexes, erratic power, non-anatomical loss

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16
Q

When does UMN disease occur?

A

Acute stroke syndromes, SOL, spinal cord problems

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17
Q

How can UMN lesions be located?

A

Determined by body segments involved and accompanying signs

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18
Q

How does a hemispheric UMN lesion present?

A

Contralateral pyramidal weakness in face, arm , leg- homunculus

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19
Q

How does a parasagittal frontal lobe UMN lesion present?

A

Paraparesis

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20
Q

How does a spinal cord UMN lesion present?

A

Pyramidal weakness below the level of the lesion

  • cervical: arms and legs
  • thoracolumbar: legs
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21
Q

What is a LMN lesion presentation?

A

wasting, fasciculation, decreased tone, decreased or

absent reflexes, flexor plantars

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22
Q

What causes LMN anterior horn cell lesions?

A

MND, spinal muscular atrophy, lead poisoning, poliomyelitis

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23
Q

How does peripheral nerve involvement present

A
  • Symmetrical (often length dependent) polyneuropathy with weakness and sensory symptoms: frequent complication of diabetes. Other aetiologies include a variety of toxic (alcohol) or metabolic insults as well as heritable disorders (often young onset and skeletal deformities)
  • Mononeuropathy as a result of nerve compression (carpal or tarsal tunnel syndrome, ulnar neuropathy, radial neuropathy) or mononeuritis multiplex (asymmetric polyneuropathy), which occurs in the context of diabetes or vasculitis
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24
Q

How does median nerve mononeuropathy present?

A

Motor pareses of thumb abduction with thenar atrophy

Thumb, secon, third fingers and lateral fourth finger- pain or sensory loss

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25
Q

What causes median nerve mononeuropathy?

A

Carpal tunnel

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26
Q

How does ulnar nerve mononeuropathy present?

A

Claw hand

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27
Q

Where is the pain/sensory loss in ulnar mononeuropathy?

A

Fifth and medial one-half of fourth finger

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28
Q

How does radial nerve mononeuropathy present?

A

Wrist drop

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29
Q

Which DTR is lost in radial nerve mononeuropathy?

A

Brachioradialis- compression of the radial nerve in the spiral groove of the humerus spares the triceps DTR

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30
Q

Where is the pain/sensory loss in radial nerve mononeuropathy?

A

Dorsum of hand

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31
Q

What is a common cause of radial nerve palsy?

A

Saturday night palsy

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32
Q

What is affected in femoral nerve mononeuropathy?

A

Knee extensors

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33
Q

Which DTR is lost in femoral nerve mononeuropathy?

A

Quadriceps

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34
Q

Where is the pain/sensory loss in femoral nerve mononeuropathy?

A

Anterior thigh, medial calf

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35
Q

What is affected by sciatic nerve mononeuropathies?

A

Ankle dorsiflexors and plantarflexors (flail ankle)

36
Q

Which DTR is lost in sciatic nerve palsy?

A

Achilles

37
Q

Where is pain/sensory loss in sciatic nerve palsy?

A

Buttock, lateral calf and most of foot

38
Q

What is a common cause of sciatic nerve mononeuropathy?

A

Sciatica from a herniated disk

39
Q

What is affected by fibular nerve mononeuropathy?

A

Ankle dorsiflexors and evertors (foot drop)

40
Q

Where is the pain and sensory loss in fibular nerve mononeuropathy?

A

Dorsum of foot and lateral calf

41
Q

When does NMJ weakness occur?

A
  • acetylcholine-receptor (Musk) antibody mediated myasthenia gravis- ocular or generalised
  • inhibition of acetylcholinesterase by organophosphate poisining
  • interference with presynaptic calcium channel function in lambert-eaton paraneoplastic syndrome
42
Q

Limb movement Muscle Nerve Nerve root

Shoulder abduction ______ _______ ________

Elbow extension ______ _______ ________

Finger extension ______ _______ ________

Index finger abduction ______ _______ ________

Hip Flexion ______ _______ ________

Knee Flexion ______ _______ ________

Ankle Dorsiflexion ______ _______ ________

Great Toe Dorsiflexion ______ _______ ________

A

Limb movement Muscle Nerve Nerve root

Shoulder abduction DeltoidAxillaryC5

Elbow extension TricepsRadialC7

Finger extension Extensor DigitorumPost. interosseusC7

Index finger abduction first dorsal interosseusUlnarT1

Hip Flexion IliopsoasFemoralL1, 2

Knee Flexion HamtringsSciaticS1

Ankle Dorsiflexion PeronealsCommon peroneal and sciaticL4, 5

Great Toe Dorsiflexion Extensor hallucis longusCommon PeronealL5

43
Q

What is the root innervation/deep tendon reflex of the ankle?

A

S 1,2

44
Q

What is the root innervation/deep tendon reflex of the knee?

A

L3, 4

45
Q

What is the root innervation/deep tendon reflex of the biceps?

A

C5, 6

46
Q

What is the root innervation/deep tendon reflex of the triceps?

A

C7, 8

47
Q

Stocking (and later glove) sensory loss implies _____ _______ _______

A

Stocking (and later glove) sensory loss implies length dependant neuropathy

48
Q

Dermatomal sensory loss can point towards _________, _______ or ______ lesion

A

Dermatomal sensory loss can point towards mononeuropathy, radicular or plexus lesion

49
Q

Sensory level loss of sensation implies a ______ ____ lesion

A

Sensory level loss of sensation implies a spinal cord lesion

50
Q

Hemianaesthesia suggests contralateral _______ lesion, or with no other signs a ___________ disorder

A

Hemianaesthesia suggests contralateral cerebral lesion, or with no other signs a non-organic disorder

51
Q

Dissociated sensory loss with lost ____________ (temperature/pain) but preserved ______ ______ (vibration, light touch, proprioception) suggests _______ damage (anterior spinal artery syndrome, brown-sequard syndrome, syringomyelia)

A

Dissociated sensory loss with lost spinothalamic (temperature/pain) but preserved dorsal colums (vibration, light touch, proprioception) suggests hemicord damage (anterior spinal artery syndrome, brown-sequard syndrome, syringomyelia)

52
Q

Describe a cerebellar gait

A

Broad-based and unsteady

53
Q

What ar the cerebellar signs?

A
  • broad-based gait and unsteadiness
  • intention tremor/ataxia
  • dysdiadochokinesis
  • Nystagmus
  • Dysarthria
54
Q

How is intention tremor/ataxia assessed in the arms and legs?

A

arms- By a finger nose test

legs- knee-heel testing

Tremor is exaggerated near the target

55
Q

What is dysdiadochokinesis?

A

Clumsy fast alternating movements

56
Q

What are the motor extrapyramidal symptoms?

A

Bradykinesia, Rigidity, resting tremor, impaired gait and posture

Hypomimia

Hypophonia

Reduced arm swing, stooped posture, small steps, festination, turning en bloc

Impaired postural reflexes

Asymmetry in PD, symmetry in drug induced or atypical PD

57
Q

What is the function of the frontal lobe?

A

Generates novel strategies and has executive functions. Enables self-criticism and trying again. The prefrontal cortex connects extensively to other association cortices; basal ganglia, limbic system, thalamus and hippocampus.

58
Q

What is the role of orbitofrontal cortex?

A

Response to primitive stimuli (hunger, thirst, sexual funciton)

59
Q

Damage of orbitofrontal cortex results in what?

A

Disinhibiiton

60
Q

What is the role of the dorsolateral prefrontal cortex?

A

Response to external stimuli (executing work responsibilities)

61
Q

What is the role of the cingulate gyrus and dorsomedial frontal lobe?

A

Motivation

62
Q

Damage to the cingulate gyrus and dorsomedial frontal lobe causes what?

A

abulia (lack of will) or even akinetic mutism

63
Q

Pathology in the temporal lobe can cause

A
  • Memory dysfunction especially episodic memory
  • Agnosia (visual and sensory modalities in particular)
  • Language disorders eceptive dysphasia (Wernicke, dominant hemisphere)
  • Visual field defects (congruous upper homonymous quadrantanopia)
  • Auditory dysfunction (Heschel’s gyrus, as hearing is represented bilaterally, deafness is not a cerebral feature)
  • Limbic dysfunction
  • Temporal lobe epilepsy
64
Q

Damage to parietal lobe can cause?

A
  • Visual field defect (congruous lower homonymous quadrantanopia)
  • Sensory dysfunction (visual and sensory modalities in particular)
  • Gerstmann’s syndrome (disease of the dominant angular gyrus, part of the inferior parietal lobe): Dysgraphia, left-right disorientation, finger agnosia, acalculia
  • Dyspraxia
  • Inattention (non-dominant angular gyrus)
  • Denial
65
Q

Can levodopa cross the BBB

A

yes

66
Q

Does dopamine cross the BBB

A

no

67
Q

what prevents the peripheral breakdown of levodopa?

A

inhibitors of aromatic amino acid decarboxylase

68
Q

Levodopa can be broken down by what enzyme and how can this be prevented?

A

atechol-O-methyltransferase (COMT), so COMT inhibitors such as entacapone and tolcapone are often employed

69
Q

How do dopamine agonists work?

A

Cross the BBB and act directly as D2- type receptors

70
Q

Name dopamine agonists

A

pramipexole, ropinirole, and bromocriptine

71
Q

How can MAO-B inhibitors be useful in PD?

A

selegiline and rasagiline can improve symptoms in patients with mild disease (as monotherapy) as well patients already on levodopa

72
Q

How can anticholinergics be used in PD?

A

trihexyphenidyl or diphenhydramine (Benadryl) aim to combat tremor, but usually cause severe side effects

73
Q

How does amantadine work in PD?

A

blocks NMDA receptors and has a mild attenuation of resting tremor and dystonia. May alleviate levodopa induced dyskinesias

74
Q

What are frequent presenting symptoms in MS?

A

Visual compromise, stiffness, and weakness

75
Q

How can symptoms of MS be made acutely worse?

A

With fever or higher temperatures

76
Q

What imaging is used to identify old stroke lesions and lesions of non-vascular origin?

A

MRIT1/T2 and FLAIR

77
Q

When is diffusion weighted imaging used?

A

to identify new ischemic lesions (hyperintensities) and a decrease in signal on the apparent diffusion coefficient of water (ADC map)

78
Q

What is T2 weighted imaging used for

A

to identify bleeds and microbleeds

79
Q

What are Time-of-flight sequences used to identify

A

Occulsions of the extra and intracranial arteries

80
Q

What are perfusion-weighted images used to identify?

A

identifies brain areas at risk of ischemia

81
Q

What is not found in lacunar stroke syndrome?

A

Visual defect

new higher or cortical brainstem dysfunction

82
Q

What is seen in lacunar stroke

A
  • Pure motor hemiparesis
  • pure sensory deficit of one side of the body
  • sensorimotor hemiparesis or ataxic hemiparesis (dysarthric clumsy hand syndrome or ipsilateral ataxia with crural hemiparesis)

– At least 2 of the 3 areas (face,arm,leg) should be involved in its entity

83
Q

How does posterior circulation syndrome present?

A

(any one of):

  • Cranial nerve palsy
  • Unilateral or bilateral motor or sensory deficit
  • Disorder of conjugate eye movements
  • Cerebellar dysfunction
  • Homonymous hemianopia
  • Cortical blindness
84
Q

How does total anterior circulation syndrome present?

A
  • hemiplegia and homonymous hemianopia contralateral to the lesion

AND

  • either aphasia or visuospatial disturbances
  • +/- sensory deficit contralateral to the lesion
85
Q

How does partial anterior circulation syndrome present?

A
  • one or more of;
    • unilateral motor or sensory deficit
    • aphasia
    • visuospatial neglect (with or without homonymous hemianopia)

Motor or sensory deficit may be less extensive than in lacunar syndromes

Neurology (41 decks)

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