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Neurology > Revisin > Flashcards

Revisin Flashcards

1
Q

what are 2 possible side effects of a statin

A

muscle pain and weakness

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2
Q

what do you worry about with night pain

A

cancer

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3
Q

what are spinal red flags

A

back pain (worse at night, new pain in old patient)
bilateral sciatica, urinary incontinence
impotence
saddle anaesthesia

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4
Q

what is cauda equina syndrome

A

Compression/ irritation of lumbosacral nerve roots below conus medullaris

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5
Q

what are the common causes of cauda equina syndrome

A

herniated disc, spinal stenosis, vertebral fracture, tumour

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6
Q

what are the clinical features of cauda equina syndrome

A 
usually acute (<24hrs), rarely subacute or chronic. 
Motor signs - LMN signs → weakness in multiple root distribution, reduced tendon reflexes
Sensory signs - low back pain radiating to legs aggravated by sitting, relieved by lying down.  Saddle anaesthesia (S2-5)
Autonomic signs - urinary retention/ overflow incontinence, loss of anal tone (faecal incontinence).
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7
Q

treatment for cauda equina

A

PR
MRI of lumbar spine
decompression within 48 hrs

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8
Q

what reflexes are usually absent in cauda equina

A

ankle

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9
Q

where does the conus medullaris end

A

L1/2

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10
Q

what is degenerative cervical myelopathy

A

spinal cord dysfunction from compression in the neck.1 Patients report neurological symptoms such as pain and numbness in limbs, poor coordination, imbalance, and bladder problems. Owing to its mobility, the vertebral column of the neck is particularly prone to degenerative changes such as disc herniation, ligament hypertrophy or ossification, and osteophyte formation

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11
Q

what are the common symptoms of degernative cervical myelopathy

A

Neck pain/stiffness
Unilateral or bilateral limb/body pain
Upper limb weakness, numbness, or loss of dexterity
Lower limb stiffness, weakness, or sensory loss
Paraesthesia (tingling or pins and needles sensations)
Autonomic symptoms such as bowel or bladder incontinence, erectile dysfunction, or difficulty passing urine
Imbalance/unsteadiness
Falls

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12
Q

what are the motor signs of degenerative cervical myelopathy

A

o Pyramidal weakness (Upper limb; extensors more than flexors. Lower limb: flexors more than extensors)
o Limb hyperreflexia
o Spasticity (eg, clasp knife sign)
o Clonus, especially Achilles tendon
o Hoffman’s sign (thumb adduction/flexion +/− finger flexion after forced flexion and sudden release of a finger, distally)
o Babinski’s sign (upgoing plantar)
o Segmental weakness (corresponding to the level of compression)

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13
Q

what are the features of an upper motor neurone lesion

A 
paralyses affects movement rather than muscles 
slight muscle wasting 
spasticity 
hyperreflexia 
hypertonia 
normal power
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14
Q

what are the features of a lower motor neurone lesion

A 
flaccid paralysis (of muscle or muscle group)
severe atrophy 
hypotonia 
absent reflexes 
may have fasciculation and fibrillation
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15
Q

what is the most likely benign tumour of the brain

A

meningioma

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16
Q

what is foster kennedy syndrome

A

when a slow growing frontal lobe tumour compresses optic nerve causing it to atrophy

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17
Q

what level in spinal cord do sensory afferent from bladder enter

A

S2-4

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18
Q

what is danish

A

how to examine to cerebellum

  • dyskensia
  • ataxia
  • nystagmus
  • intention tremor
  • staccato speech
  • hypotonia
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19
Q

what tract will an upper motor neurone be in

A

pyramidal tracts

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20
Q

is parkinsons an UMN lesion

A

no as not within the pyramidal tract

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21
Q

are tremors pyramidal or extrapyramidal

A

extra pyramidal (involuntary movements)

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22
Q

where are LMNs

A

anywhere below L1/2 or out with the CNS

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23
Q

what is a tremor

A

involuntary movement in which there is rhythmicity, is a regular movement

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24
Q

what movements tend to develop in extrapyramidal disorders

A

involuntary- tremors

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25
Q

what are the types of tremors

A

resting- when sitting and relaxed
postural- holding arms in certain postitions
intention- when trying to complete an action

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26
Q

where must a lesion be if it affects the leg and arm

A

cervical spin or above

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27
Q

weakness is a symptoms of a lesion affecting which tract

A

pyramidal

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28
Q

why is there not weakness in parkinsons

A

as extrapyramidal

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29
Q

what are the hallmarks of parkinsons

A

SLOWNESS (bradykinesia- only symptoms seen in everyone)
tremor
tone (stiffness and rigidity)

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30
Q

what are the other symptoms of parkinsons

A 
can 'freeze' and struggle to initiate and stop movements 
shuffling gate 
stooped posture
changes in mood
handwriting gets smaller (micrographia)
balance problems 
depression and anxiety 
sleeping problems 
loose paralysis in dreams so cant act out what they are dreaming 
REM sleep disorder 
loose sense of smell and taste (before motor symptoms)
memory changes 
voice gets quieter 
constipation 
bladder problems
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31
Q

where is the lesion in parkinsons

A

substantia nigra in the basal ganglia (produces dopamine)

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32
Q

why is cerebrovascular pmhx important in parkinsons

A

as type of vascular parkinsons

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33
Q

what diseases are related to parkinsons

A

cerebrovascular disease, psychiatric problems (anti dopamine drugs)

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34
Q

what drugs are related to parkinsons

A

antihistamines, anti emetics (block dopamine), some anti psychotics

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35
Q

what are the risk factor for parkinsons

A

family Hx
risk factors for cardiovascular disease- alcohol, diet etc
NOT SMOKING - smoking protects you from parkinsons

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36
Q

what occupations have increased risk of parkinsons

A

agriculture, manganese minors, general exposure to chemicals

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37
Q

what is the commonest form of parkinsons

A

idiopathic

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38
Q

what type of movement do you loose in parkinsons

A

spontaneous

  • facial
  • adjusting position
  • rolling over in bed
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39
Q

are cranial nerves affected in parkinsons

A

no

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40
Q

how is tone affected in parkinsons

A

increased (not in same way as UMN lesion)
= rigidity (high tone but velocity independant)
also get cog wheel rigidity

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41
Q

what type of tone changes in UMN lesion

A

velocity dependent
spactity
hypertonic

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42
Q

what type of tone changes in LMN lesion

A

hypotonia

flaccidity

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43
Q

does parkinsons affect one or both sides

A

affects both sides of the brain but to different degrees so usually have one side affected in early stages then becomes more symmetrical

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44
Q

how is power affected in parkinsons

A

isnt as extrapyramidal

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45
Q

are reflexes affected in parkinsons

A

no as reflexes are pyramidal

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46
Q

is coordination affected in parkinsons

A

no as cerebellum fine

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47
Q

what do yuo get a resting tremor in

A

parkinsons

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48
Q

what do you get a postural tremor in

A

drugs, dystolic tremor, anxiety

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49
Q

what do you get an intention tremor in

A

cerebellar disease

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50
Q

what is a holmes tremor

A

a resting, postural and intentional tremor all at the same time

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51
Q

what is bradykinesia

A

slowness with decrement and degradation of repetitive movements (“fatigue”)

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52
Q

what are is affected in a central nervous system lesion

A

hemiplegia/ paraplegia/ whole limb

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53
Q

what type of weakness in a central nervous system lesion

A

heaviness

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54
Q

what are the additional features of a central nervous system lesion

A

spasms/ jerks

cognitive/ sphincter involvement

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55
Q

can you get sensory symptoms in a central nervous system lesion

A

yes

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56
Q

what area will be affected in a peripheral nervous system lesion

A

may be peripheral or localised areas

can be whole limb if affects plexus

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57
Q

what type of weakness in a peripheral nervous system lesion

A

positional/ with sleep

ascending

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58
Q

what additional features can exists in a peripheral nervous system lesion

A 
cramp 
twitching (fasciculations)
loss of grip 
tripping up 
unsteady with eyes closed
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59
Q

can you get sensory symptoms in a peripheral nervous system lesion

A

yes

pain may be prominent

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60
Q

where might be affected in NMJ lesion

A

ocular/ bulbar/ proximal limb

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61
Q

what is the weakness like in a NMJ lesion

A

fatiguable - worse after use

diurnal variations- worse towards end of day

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62
Q

what additional features can be seen in a NMJ lesion

A

bulbar- swallowing, speaking, loss of chewing/ talking
ocular- diplopia, ptosis, prolonged gaze hard
resp- orthopnoea

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63
Q

can you get sensory symption in a NMJ lesion

A

no

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64
Q

where might be affected in muscular lesion

A

proximal

symmetrical

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65
Q

what is the weakness like in a muscle lesion

A

may be aching
may be insidious
proximal weakness
symmetrical

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66
Q

what additional features can you get in a muscle lesion

A

myalgia
cramping
hard to get up from low chairs/ hang out washing

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67
Q

can you get sensory symptoms in a muscle lesion

A

no

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68
Q

what might be seen on inspection in a CNS lesion

A

abnormal limb posture

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69
Q

what might be seen on inspection in a PNS lesion

A

wasting/ fasciculations

pes cavus

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70
Q

what might be seen on inspection in a NMJ lesion

A

ptosis

ophthalmoplegia

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71
Q

what might be seen on inspection in a muscle lesion

A

proximal wasting

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72
Q

what happens to tone in a CNS lesion

A

increased

spacticity/ clonus

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73
Q

what happens to tone in a PNS lesion

A

decreased

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74
Q

what happens to tone in a NMJ lesion

A

normal or decreased

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75
Q

what happens to tone in a muscle lesion

A

normal or decreased

76
Q

what is the pattern of weakness like in peripheral neuropathy

A

distal weakness

77
Q

what is a pyramidal pattern of weakness

A

arm: extensors weaker than flexors
leg: flexors weaker than extensors
if brain affected= contralaterla
if cord affected= ipsilateral side

78
Q

what are reflexes like in a CNS lesion

A

increased

79
Q

what are reflexes like in a PNS lesion

A

decreased

80
Q

what are reflexes like in a NMJ lesion

A

normal or decreased

81
Q

what are reflexes like in a muscle lesion

A

normal or decreased

82
Q

what are reflexes like in a CNS lesion

A

extensor

83
Q

what are reflexes like in a PNS lesion

A

flexor/ mute

84
Q

what are reflexes like in a NMJ lesion

A

flexor

85
Q

what are reflexes like in a muscle lesion

A

flexor

86
Q

what distribution of sensory symptoms in a CNS lesion

A

brain- hemi sensory (one side for body, other side for face (trigeminal nerve))
cord- at sensory level

87
Q

what distribution of sensory symptoms the PNS lesion: sensory neuropathy

A

glove and stocking

88
Q

what distribution of sensory symptoms the PNS lesion: root/ plexus/ mononeuropathy lesion

A

depends on dermatome/ nerve

89
Q

what does velocity dependant increased tone mean

A

involves pyramidal tract

90
Q

where will see the effects of a lesion in the internal capsule

A

leg, arm, face and trunk

91
Q

what is the general pattern of an inflammatory lesion in the brain

A

relapsing and remitting

92
Q

what are the types of NMJ pathology and how can you differentiate them

A

lambert eaton= diminshed/ adbscence deep tendon reflex, autonomic features (is a pre synaptic problem)

myaestenia gravis - has ocular problems (post synaptic problem)

93
Q

how do you demonstrate NMJ pathologies

A 
bulbar- counting out loud
ocular- fixed horizontal gaze 
ptosis- fixed upward gaze
limb- repetitive movements 
(fatiguing weakness)
94
Q

what results from an L4/5 L5 impingement

A

weak toe dorsiflexion

95
Q

what results from an L5/S1 S1 impingement

A

weak knee flexion

decreased knee jerk

96
Q

what happens in a lesion on the brachial plexus

A

extensive arm weakness

97
Q

what happens in a lesion on the lumbosacral plexus

A

extensive leg weakness

98
Q

what results from a median nerve neuropathy

A

weak thumb abduction

99
Q

what results from a ulnar nerve neuropathy

A

weak finger abduction

100
Q

what are 2 features and common causes of peripheral neuropathy

A

is distal and sensory more than weakness

if acute- guillane barre syndrome
if chronic- diabetes/ alcohol

101
Q

what test do you always do in epilepsy

A

ECG!!!!!

102
Q

what does rigidity occur in

A

extrapyramidal conditions affecting the basal ganglia (e.g. parkinsons)

103
Q

is rigidity associated with weakness

A

no

but can have slow developing muscle contractions (bradykinesia)

104
Q

is there usually a change in tendon reflexes in rigidity

A

no

105
Q

what is spasticity dependent on

A

(velocity)

input to the spinal cord produced by the passive movement of the limb

106
Q

which muscles is spasticity predominantly found in

A

flexor muscles and forearm pronators inarm
extensor muscles in the legs
(think opposite to pyramidal weakness)

107
Q

what is the clasp knife phenomonenum

A

where spasticity builds up soon after the start of the passive movement, then melts away

108
Q

how is spasticity most easily elicited in the arm and leg

A

rapid extension of the elbow or supination of
the forearm

in the leg by rapid flexion of the knee

109
Q

will a slow movement meet resistance in spasticity

A

no

110
Q

what are the features of rigidity that distinguish it from spasticity

A

not velocity dependent
present equally in flexors and extensors
present throughout the range of movement
can have cog wheel or led pipe quality

111
Q

how is rigidity best elicited

A

relatively slow passive movements
In the arm by flexion-extension of the wrist and elbow, and by supination-pronation of
the elbow.

In the lower limb flexion-extension of the knee and ankle are tested

112
Q

what is the MRC power scale

A

0= No contraction
1= Flicker of contraction without movement
2= Slight movement with gravity eliminated*
3= Movement against gravity only
4= Movement against resistance
(can expand grade 4 to: 4+, 4 and 4-)
5= Normal power

113
Q

why do tendon reflexes change

A

Reflexes are very sensitive to pathology affecting the afferent side of the reflex arc. If
conduction is blocked in only a few muscle spindle primary afferents, then the
compound action potential elicited in all the motorneurones will be smaller, and the
reflex will be less brisk or absent.
Reflexes are also sensitive to “upper motorneurone lesions” affecting the descending
motor pathways in the cerebral hemispheres, brainstem and spinal cord. The
excitability of the alpha motorneurones increases and the reflexes become brisker.

114
Q

when is clonus abnormal

A

when it is sustained

115
Q

what is reinforcement when testing a reflex

A

e.g.to link the fingers of each

hand and attempt to pull them apart to test lower limb reflexes

116
Q

what is clonus

A

the rhythmic contraction of a muscle group elicited by a rapid passive stretch of it

117
Q

what is the triceps surae

A

pair of muscles located at the calf - the two-headed

gastrocnemius and the soleus- ankle extensors- common to get clonus here

118
Q

what is clonus a sign of

A

UMN lesions

always associated with brisk ankle jerks

119
Q

when are reflexes abnormal

A

when they are absent (with reinforcement).
when they are asymmetrical (right v left).
when there is a marked discrepancy between different reflexes (eg between those
in the arms and those in the legs).
when there is sustained clonus.

120
Q

what is a positive babinski response

A

big toe extends and the other toes fan- sign of UMN lesion

121
Q

what is a spastic gait

A

due to UMN lesion

affected limbs appear very stiff

122
Q

what causes a parkinonian gait

A

basal ganglia pathology

123
Q

what causes a truncal ataxia (widebase, unsteady)

A

cerebellar disease
hydrocephalus
proprioceptive loss (neuropathy/ myelopathy)

124
Q

what causes a high stepping gate

A 
biltaeral= peripheral neuropathy 
unilateral= peroneal nerve or L4 root lesion
125
Q

what causes a waddling gait

A

proximal leg weakness

126
Q

what are the types of tremor

A

Rest: Present when the subject is relaxed, and decreasing on
maintaining a posture or during movement
Postural/Action: Present on maintaining a posture and during movement, but
disappearing at rest.
Intention: Present towards the end of a movement to a target, causing
overshoot (dysmetria).

127
Q

what are the causes for resting tremor

A

parkinsons

128
Q

what are the causes for postural/ action tremor

A

Physiological
Essential tremor, drugs
Anxiety, Thyrotoxicosis

129
Q

what are the causes for intention tremor

A

cerebellar disease

130
Q

what happens to rapid supination/ pronation movements in parkinsons

A

In extrapyramidal diseases (Parkinsonian syndromes) there is a reduction in
the amplitude and speed of supination/pronation movements.

131
Q

what happens to rapid supination/ pronation movements in cerebellar disease

A

irregularity of the movements as well as slowing

and reduction in amplitude.

132
Q

how do different pathologies affect fine finger movement

A

impaired in upper motor neurone lesions affecting the hand,
particularly with cortical lesions when the hand may be clumsy with little
weakness.

Fine finger movements are also impaired in extrapyramidal
diseases and cervical myelopathy.

133
Q

what type of taste do the CN VII an IX nerves carry

A

sourness
sweetness
bitterness
saltiness

134
Q

what vision loss in optic neuritis

A

central scrotoma

135
Q

what causes red vision to be lost

A

optic nerve dysfunction

136
Q

where is a defect if vision loss is homonymous

A

behind the chiasm

137
Q

what is a hippus

A

oscillation in pupillary size

138
Q

what is the pupil like in horners syndrome

A

miotic (constricted)

will also have lack of upward gaze

139
Q

what is bells phenomenon

A

the upward deviation of the eyes on closure

140
Q

what causes diplopia when only one eye is open

A

refractive error or cerebellar problem

141
Q

what causes vertical upbeat nystagmus

A

most commonly seen as a side-effect of anticonvulsants but it may also occur in cerebellar and pontomedullary abnormalities and in Wernicke’s encephalopathy

142
Q

what causes down beat vertical nysatgmus (fast downward phase)

A

abnormality at the craniocervical junction
cerebellar degeneration and drug intoxication
Wernicke’s encephalopathy, demyelination, brain stem encephalitis, tumours at the foramen magnum and hydrocephalus.

143
Q

is there diplopia in long standing strabismus

A

no

144
Q

what does the medial longitudinal fasciculus connect

A

CN III, IV and VI

145
Q

in the trigeminal nerve, what are the central connection for touch and pain/ temperature afferents

A

touch = main sensory nucleus

pain/ temp= spinal nucleus

146
Q

where does UMN facial weakness tend to spare

A

the upper half of the face

147
Q

what nerve supplies taste to the anterior 2/3rds of the tongue

A

CN VII (facial)

148
Q

what does a corrective saccade in the head thrust test mean

A

a peripheral cause of vestobular problems

149
Q

does the spinal accessory nerve originate from cord or brain stem

A

both hehe

150
Q

what s a bulbar palsy

A

(bulbar= medulla)

caused by diseases affecting the lower cranial nerves e.g. a LMN lesion, NMJ or muscle problem

151
Q

what causes a pseudobulbar palsy

A

when a UMN lesion affects the lower cranial nerves (a disease of the corticobulbar tracts)

152
Q

what can a bulbar palsy with a LMN lesion cause

A

-impaired voluntary palatal movement
 impaired palatal movement on eliciting the gag reflex or loss of the gag reflex
 wasting and fasciculation of the tongue
 slurring dysarthria and dysphagia

153
Q

what does a pseudobulbar palsy cause

A 
 a brisk jaw jerk
 a brisk gag reflex
 a spastic tongue (with difficulty protruding the tongue and impaired rapid tongue
movements)
 a spastic dysarthria and dysphagia
154
Q

how do you test each occular muscle and nerve (movements)

A

III -superior rectus (looks laterally and upwards), inferior rectus (looks laterally and
downwards), medial rectus (looks medially), inferior oblique (looks medially and
upwards)
 IV -superior oblique (looks medially and downwards)
 VI - lateral rectus (looks laterally)

155
Q

what are the different types of articulation

A

Palatal articulation – “KA”,
Guttural articulation – “GO”,
Labial articulation – “PA”

156
Q

what level does should abduction test

A

C5

157
Q

what level does elbow flexion and wrist extension test

A

C6

158
Q

what level does elbow extension and wrist flexion test

A

C7

159
Q

what level does thumb extension test

A

C8

160
Q

what level does finger abduction test

A

T1

161
Q

what level does hip flexion test

A

L1,2

162
Q

what level does knee extension test

A

L3

163
Q

what level does ankle dorsiflexion test

A

L4

164
Q

what level does great toe extension

A

L5

165
Q

what level does ankle plantar flexion test

A

S1

166
Q

what is a glioblastoma

A

a high grade (grade 4) astrocytoma

167
Q

what is coning

A

where the brainstem and cerebellum get pushed through the foramen magnum (tonsillar herniation

168
Q

what is cushings triad

A

reduced respiratory, high BP and bradycardia

happens in coning

169
Q

what can cause too much CSF to be produced

A

choroid plexus malignancies

170
Q

who gets medulloblastomas

A

children

171
Q

what is seen pathologically in an acute infarct

A

oedema
discolouration (grey/ brown)
loss of normal architecture

172
Q

what happens to old strokes

A

gliosis, liqudification by macrophages

173
Q

what o watershed infarctions look like

A

wedge shape infarct on the peripheries of the brain

174
Q

what does global hypoxia look like pathologically

A

mottling

loss of differentiation between grey and white matter

175
Q

what are the RF for a subarachnoid haemorrhage

A

ADPKD
HPTx
obesity
smoking

176
Q

what increases and decreases in atrophy

A 
increase sulcus (depression- think in a sulc) 
decreased gyrus (bumps- think gyrating, bump and grind)
177
Q

what does MS look like pathologically

A

dark grey spots mainly affecting white matter, periventricular

178
Q

what is the lateral horn of the spinal cord

A

a triangular projection between the dorsal and ventral horns

it is present only in the thoracic and upper lumbar segment of the spinal cord

contains autonomic neurones (sympathetic system T1-L2)

179
Q

what is the path of the dorsal column medial leminiscus pathway

A

primary sensory fibres travel via the posterior root ganglion
up spinal cord
synapse with 2ndary order in medulla (nucleus cuneatus if above T6, nucleus gracilis if below T6)

fibres decussate to the contralateral medial leminiscus and travel upwards to synapse in the thalamus

relayed to the ipsilateral somatosensory cortex

180
Q

what is the path of the spinothalamic tract

A

The primary sensory axons enters the spinal cord, via the posterior root ganglion, then travel upwards for one or two segments at the periphery of the spinal cord through the tract of Lissauer to synapse in the dorsal horn.
They then cross to the contralateral side of the spinal cord to ascend to synapse in the thalamus.
Sensory signal are then relayed from the thalamus to the ipsilateral somatosensory cortex.

181
Q

what is the function of the spinocerebellar pathways

A

provides unconscious proprioceptive information to the cerebellum, in order to coordinate posture and the movement of the lower limb and upper limb musculature.

182
Q

what are the three spinocerebellar pathways and their functions

A

Dorsal/posterior spinocerebellar: carries unconscious proprioceptive information (from muscle spindles mainly) from the lower limbs, synapses in the dorsal nucleus of Clarke.

Cuneocerebellar: carries unconscious proprioceptive information from the upper limbs.

Ventral/anterior spinocerebellar: carries unconscious proprioceptive information (golgi tendon organs mainly) from the lower limbs then decussate twice to reach the ipsilateral cerebellum.

183
Q

do the spinocerebellar tracts travel to the contra or ipsilateral cerebellum

A

ipsilateral

184
Q

what is the role of the corticospinal tract

A

voluntary movements

185
Q

where do the anterior corticospinal tracts decussate

A

the anterior white commissure

186
Q

what does the anterior corticospinal tract mainly supply

A

proximal and axial muscles

Neurology (35 decks)

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