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Neurology > Localising Lesions > Flashcards

Localising Lesions Flashcards

1
Q

what are movement disorder features arise from lesions in the corticospinal/ pyramidal tracts

A

pyramidal/ UMN features:

pyramidal weakness (corticospinal distribution: hemiparesis, quadriparesis, paraparesis, monoparesis, faciobrachial)
spascticity
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2
Q

what are the types of movement disorders that arise from lesion in the basal ganlgia

A 
(extrapyramidal)
hyperkinetic 
- dystonia
- tics
- myoclonus 
- chorea 
- tremor

hypokinetic (rigidity and bradykinesia)

  • parkinsonism
  • parkinson’s disease
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3
Q

what movement disorders arise from the cerebellum

A

ataxia

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4
Q

what makes up the peripheral nervous system

A

spinal nerve
root
plexus
peripheral nerves

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5
Q

what are the features of focal weakness

A

in distribution of peripheral nerve or spinal root
hemi-distribution (one side of body)
pyramidal distribution

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6
Q

what is pyramidal distribution weakness

A

where the extensors are weaker in the arms and the flexors are weaker in the legs

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7
Q

what are the features of non focal weakness

A

generalised
predominantly proximal or distal
if truely generalised will include bulbar motor function

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8
Q

UMN weakness:

distribution

A

corticospinal

  • hemiparesis
  • quadriparesis
  • paraparesis
  • monoparesis
  • faciobrachial
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9
Q

LMN weakness:

distribution

A

generalised
predominantly proximal, distal or focal
no preferential involvement of corticospinal innervated muscles

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10
Q

UMN weakness:

Sensory loss

A

central pattern

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11
Q

LMN weakness:

Sensory loss

A
  • can be none
  • glove
  • stocking
  • peripheral nerve or root distribution
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12
Q

UMN weakness:

  • deep tendon reflexes
  • superficial reflexes
  • pathological reflexes
A

deep- increased (unless very acute= flaccid)
superficial- decreased
pathological- increased

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13
Q

LMN weakness:

  • deep tendon reflexes
  • superficial reflexes
  • pathological reflexes
A

deep- normal/ decrease
superficial- normal
pathological- normal

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14
Q

what are the superficial reflexes

A

plantar
gag/ swallow
cremasteric
corneal

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15
Q

what are the pathological reflexes

A

babinski (upward plantar, fanning and hyperextension of the toes), hoffmans etc

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16
Q

UMN weakness:

sphincter function

A

sometimes impaired

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17
Q

LMN weakness:

sphincter function

A

usually normal (except in cauda equina)

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18
Q

UMN weakness:

muscle tone

A

increased

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19
Q

LMN weakness:

muscle tone

A

decreased/ normal

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20
Q

UMN weakness:

muscle bulk

A

sometimes hypertrophy

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21
Q

LMN weakness:

muscle bulk

A

wasting

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22
Q

UMN weakness:

other CNS signs?

A

possibly

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23
Q

LMN weakness:

other CNS signs?

A

no

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24
Q

increased tone, brisk reflexes, pyramidal/ corticospinal pattern of weakness (= weak extensors in the arm, weak flexors in the legs) = ?

A

upper motor neurone pattern

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25
Q

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

A

lower motor neurone pattern

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26
Q

what are the features of muscle disease

A

wasting (usually proximal)
decreased tone
decreased/ absent tendon reflexes

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27
Q

what are the features of NMJ weakness

A

fatiguable weakness
normal/ decreased tone
normal reflexes
NO SENSORY SYMPTOMS

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28
Q

what are the features of functional weakness

A 
no wasting 
normal tone 
normal reflexes 
erratic power 
non anatomical loss
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29
Q

what causes UMN weakness

A

acute stroke syndromes
space occupying lesions
spinal cord problems

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30
Q

what weakness results from a hemispheric lesion

A

contralateral pyramidal weakness in face, arm, leg

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31
Q

what results from a parasagittal frontal lobe lesion

A

paraparesis

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32
Q

what UMN weakness results from a spinal cord lesion

A

pyramidal weakness below the level of the lesion
if cervical spine- arms and legs
if thoracolumbar- legs

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33
Q

what part of spinal cord do lower motor neurones attach to

A

anterior horn

34
Q

what can cause a lower motor neurone lesion in the anterior horn cells

A

motor neurone disease
spinal muscular atrophy
lead poisoning, poliomyelitis etc

35
Q

what are the two patterns of lower motor lesions in peripheral nerves

A

symmetrical (often length dependant):
- polyneuropathy with weakness and sensory symptoms: can be complication of diabetes, alcohol, metabolic insults

mononeuropathy:

  • result of nerve compression (carpal, ulnar tunnel, radial neuropathy) or
  • mononeuritis multiplex (asymmetric polyneuropathy) (occurs in diabetes or vasculitis)
36
Q

what are the features of a median nerve mononeuropathy

A

thumb abduction paresis
thenar atrophy
sensory loss - thumb, second, third fingers, lateral 1 half of fourth finger

e.g. carpal tunnel syndrome

37
Q

what are the features of a ulnar nerve mononeuropathy

A

finger and thumb adduction paresis

sensory loss- fifth and medial one half of fourth finger

38
Q

what are the features of a radial nerve mononeuropathy

A

wrist, thumb and finger extension (wrist drop)
brachioradialis DTR lost
sensory loss on dorsum of hand

e.g. saturday night palsy

39
Q

what are the features of a femoral nerve mononeuropathy

A

knee extensor paresis
loss of quads DTR
sensory loss over anterior thigh and medial calf

40
Q

what are the features of a sciatic nerve mononeuropathy

A

ankle dorsiflexions and plantarfelxion paresis (flail ankle)
loss of achilles DTR
sensory loss on buttock, lateral calf, most of foot
e.g. caused by herniated disc

41
Q

what are the features of a fibular nerve mononeuropathy

A

ankle dorsiflexion and evertors paresis (foot drop)
sensory loss on dorsum of foot and lateral calf
e.g. foot drop

42
Q

what do NMJ disorder occur in

A

acetylecholine receptor antibodies mediated myasthenia gravis:
-ocular/ generalised

inhibition of acetylcholinesterase by organophosphate poisoning

lambert-eaton paraneoplastic syndrome
-interference with presynaptic calcium channel function

43
Q

what can cause muscle disorders

A 
inflammatory 
endocrine (e.g. hypothyroidism, cushings, electrolyte abnormalities)
metabolic disorders
durgs and toxins
infections 
rhabdomyelisis
44
Q 
shoulder abduction:
name the 
-muscle 
-nerve 
-nerve root
A

deltoid
axillary
C5

45
Q 
elbow extension:
name the 
-muscle 
-nerve 
-nerve root
A

triceps
radial
C7

46
Q 
finger extension:
name the 
-muscle 
-nerve 
-nerve root
A

extensor digitorum
posterior interossues (radial)
C7

47
Q 
index finger abduction:
name the 
-muscle 
-nerve 
-nerve root
A

first dorsal interosseus
ulnar
T1

48
Q 
hip flexion
name the 
-muscle 
-nerve 
-nerve root
A

iliopsoas
femoral
L1,2

49
Q 
knee flexion
name the 
-muscle 
-nerve 
-nerve root
A

hamstrings
sciatic
S1

50
Q 
ankle dorsiflexion
name the 
-muscle 
-nerve 
-nerve root
A

peroneals
common peroneal and sciatic
L4,5

51
Q 
great toe dorsiflexion
name the 
-muscle 
-nerve 
-nerve root
A

extensor hallucis longus
common peroneal
L5

52
Q

what roots innervate the ankle DTR

A

S1,2

53
Q

what roots innervate the knee DTR

A

L3,4

54
Q

what roots innervate the biceps DTR

A

C5,6

55
Q

what roots innervate the triceps DTR

A

C7,8

56
Q

what does stocking (and later glove) sensory loss suggest

A

length dependent neuropathy

57
Q

what is length dependent neuropathy

A

a polyneuropathy= it is the longest nerve-fibers that are most at risk, while the shorter
nerve-fibers are less affected. In brief, polyneuropathy is a “length-dependent” neuropathy. Because the
longest nerve-fibers in the body are those that run from the lower back to the feet, in typical cases of
polyneuropathy the first part of the body to become weak or numb is the feet.

58
Q

what does a sensory level loss suggest

A

spinal cord lesion

59
Q

what does hemianaesthesia suggest

A

contralateral cerebral lesion

60
Q

what does dissociated sensory loss suggest (loss of spinothalamic (temp and pain) but reserved dorsal column (vibration, light tough, proprioception)

A

hemi cord damage (anterior spinal artery syndrome, brown sequard, syringomyelia)

61
Q

what are the cerebellar signs

A

gait is broad-based and unsteady
Intention tremor / ataxia is assessed in the arms by finger-nose test and in the legs by knee-heel testing. Tremor gets exaggerated the nearer the target
Dysdiadochokinesis: clumsy fast alternating movements
Nystagmus and dysarthria are additional features of cerebellar disorders

62
Q

what are extrapyramidal symptoms/ parkisonism

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

63
Q

what is the role of the frontal lobe

A

generates novel strategies and has executive functions. It enables self-criticism and trying again

Orbitofrontal cortex: response to primitive stimuli (hunger, thirst, sexual function) damage causes disinhibition
Dorsolateral prefrontal cortex: response to external stimuli (executing work resposnibilities)
Cingulate gyrus and dorsomedial frontal lobe: motivation, damage causes abulia (lack of will) or even akinetic mutism

64
Q

what does the prefrontal cortex connect to

A

other association cortices, basal ganglia, limbic system, thalamus and hippocampus

65
Q

what symptoms can arise from damage to the frontal lobe

A

Personality dysfunction
Paraparesis
Paratonia
Grasp reflex
Frontal gait dysfunction (magnetic gait)
Cortical hand
Seizures
Incontinence
Visual field defects (anterior visual pathway incl optic chiasms are beneath frontal lobe)
Expressive dysphasia (Broca’s area is in the dominant frontal lobe)
Anosmia (olfactory pathway is beneath frontal lobes)

66
Q

what symptoms can arise from temporal lobe disorders

A

Memory dysfunction especially episodic memory
Agnosia (visual and sensory modalities in particular)
Language disorders receptive 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

67
Q

what symptoms can arise from damage to the parietal lobe

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

68
Q

what is the treatment protocol for parkinsons

A

Symptomatic treatment with Levodopa replacement or dopamine agonist
Multidisciplinary team management including Speech and language, OT, PT, exercise
For selected patients deep brain stimulation (subthalamic nucleus, globus pallidus int)

69
Q

how does levodopa work

A

crosses the blood brain barrier while dopamine does not. Levodopa is then converted to dopamine in the brain while peripheral break down is prevented by the addition of ‘inhibitors of aromatic amino acid decarboxylase (carbidopa). Thus a carbidopa/levodopa formulation is often prescribed.

70
Q

name some dopamine agonists used in PD

A

pramipexole, ropinirole, and bromocriptine

71
Q

what other drugs can be used in PD

A

MAO-B inhibitors such as selegiline and rasagiline can improve symptoms in patients with mild disease (as monotherapy) as well patients already on levodopa.
Anticholinergics such as trihexyphenidyl or diphenhydramine (Benadryl) aim to combat tremor, but usually cause severe side effects
Amantadine blocks NMDA receptors and has a mild attenuation of resting tremor and dystonia. May alleviate levodopa induced dyskinesias.

72
Q

is PD usually symmetrical or asymmetrical

A

asymmetrical

73
Q

what does failure to respond to even high doses of levodopa mean in PD

A

suggests it is not idiopathic PD

74
Q

what can levodopa cause in PD

A

dyskinesias

75
Q

what is primary lateral sclerosis

A

a presentation of MND

pure upper motor neurone syndrome

76
Q

what imaging for stroke

A

MRI T1/T2 and FLAIR images to identify old lesions and lesions of non-vascular origin
Diffusion weighted images (DWI) to identify new ischemic lesions (hyperintensities)

T2 to identify bleeds and microbleeds

Perfusion-weighted images (PWI) may be useful to identifies brain areas at risk of ischemia
CT brain: hyperintenisities – bleed, subtle ischemic signs in the acute phase of stroke (may be normal, early signs: loss of limits of lentiform nucleus, poor grey white matter differentiation, loss of insular ribbon)

77
Q

what are the features of a lacunar syndrome

A

No visual field defect
No new higher cortical or brainstem dysfunction
Pure motor hemiparesis, or pure sensory deficit of one side of the body, or 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

78
Q

what are the symptoms of a posterior circulation syndrome (stroke)

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
79
Q

what are the symptoms of a total anterior circulation syndrome (stroke)

A

Hemiplegia and homonymous hemianopia contralateral to the lesion, and
Either aphasia or visuospatial disturbances
+/- sensory deficit contralateral to the lesion

80
Q

what are the symptoms of a partial anterior circulation syndrome

A

One or more of unilateral motor or sensory deficit, aphasia or visuospatial neglect (with or without homonymous hemianopia)
Motor or sensory deficit may be less extensive than in lacunar syndromes

Neurology (35 decks)

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