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Spring 2015 > Block 4 neuro part 3 > Flashcards

Block 4 neuro part 3 Flashcards

1
Q

Global developmental delay-

A

children under the age of 5 who are >2 standard deviations below the mean on age related, standardized developmental assessments

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2
Q 
IQ:
Mild mental retardation-
Moderate mental retardation-
Severe mental retardation-
Profound mental retardation-
A

-50-69
-35-49
-20-34
-

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3
Q

Big developmental milestone of 4 months-

A

head control

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4
Q

Big developmental milestone of 6 months-

A

sits up

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5
Q

Big developmental milestone of 9 months-

A

crawls

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6
Q

Big developmental milestone of 1 year-

A

walks, first words

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7
Q

Big developmental milestone of 2 years-

A

2 word phrases

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8
Q

Big developmental milestone of 3 years-

A

3 word phrases

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9
Q

Which of these developmental screening tools is NOT recommended? Ages and Stages, Parental evaluation of developmental status, Brignance screen, Denver II

A

Brignance Screen

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10
Q

Static encephalopathy-

A

developmental milestones reached, just at slower pace

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11
Q

Neurodegenerative disease effect on development-

A

development starts off normal but you reach a plateu and possible regression

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12
Q

Pervasive developmental delay-

A

motor skills intact, but delay in social/behavioral delays

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13
Q

Pervasive developmental delay-

A

motor skills intact, but delay in social/behavioral delays

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14
Q

the TORCH infections-

A

Toxoplasmosis, Rubella, CMV, HSV

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15
Q

most common cause of hydrocephalus in premature babies-

A

intraventricular hemorrhage

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16
Q

We used to thing that all CP was caused by ___________ due to a mistake by doctor. Since then, we have found that this is the case only _____% of the time, and it is usually not the doctor’s fault.

A
  • Hypoxic Ischemic Encephalopathy

- 20%

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17
Q 
Timing of hypoxic Ischemic Encephalopathy (percentages) for term infants
Antepartum-
Intrapartum-
Intrapartum/Antepartum-
Postnatal-
A
  • 20%
  • 35%
  • 35%
  • 10%
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18
Q

Kwashiorkor is caused by a _____ deficiency

A

protein

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19
Q

kernicterus-

A

a buildup of bilirubin from postnatal liver failure/insufficiency

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20
Q

Adenoma sebaceum, cortical tubers, ash leaf macule, and giant cell astrocytoma are consistent with a diagnosis of

A

Tuberous sclerosis

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21
Q

cafe-au-lait macules, lisch nodules, optic nerve gliomas and fibroma molluscum are consistent with a diagnosis of:

A

neurofibromatosis type I

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22
Q

Sturge Weber Syndrome-

A

contralateral hemiparesis, seizures, cognitive delays, due to meninges stealing blood from brain, leading to cortical calcifications and whatnot

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23
Q

Sturge Weber Syndrome-

A

contralateral hemiparesis, seizures, cognitive delays, due to meninges stealing blood from brain, leading to cortical calcifications and whatnot

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24
Q

Consciousness has 2 components:

A

level of alertness and content of consciousness

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25
Q

If someone has decreased consciousness, think of damage to ______ or ______

A

bilateral cortical hemispheres or RAS

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26
Q

with delirium, ____ is intact but person has disturbed content of consciousness

A

alertness

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27
Q

Delerium is caused by generalized or multifocal process affecting _______

A

both hemispheres

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28
Q

all patients in coma will change after _____ weeks, for better or worse

A

2-4

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29
Q

Patients who have survived the coma state without gaining higher cognitive function =

A

vegetative state

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30
Q

person is considered to be in a persistent vegetative state if they are in vegetative state for longer than _____

A

3 months

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31
Q

difference between vegetative state and minimally conscious state =

A

minimally conscious person has definite behavioral evidence of awarenenss of self and environment. Pt is able to follow simple commands, verbalize intelligibly, responses to stimuli are not just reflexes

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32
Q

what eye movements can occur in locked in state?

A

blinking and vertical eye movements

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33
Q

will a vegetative person respond to noxious stimuli?

A

yes

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34
Q

Subfalcine herniation will damage _____, leading to coma

A

RAS

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35
Q

first sign of an uncal herniation:

A

blown pupil from CN III damage

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36
Q

triad of uncal herniation:

A

blown pupil, contralateral hemiparesis, altered mental status

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37
Q

the same signs are observed in bilateral uncal herniation and ______ herniation

A

central

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38
Q

Duret Hemorrhages result from:

A

tearing of penetrating arteries of teh basilar artery that innervate the brainstem

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39
Q

Mass effect-

A

a growing mass which results in secondary pathological effects like herniation, midline shift, or increased intracranial pressure

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40
Q

important parts of History when evaluating a coma patient (after stabilizing them of course). 6 things

A

duration, onset, trauma, past medical Hx, Family Hx, Medications

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41
Q

Glasgow Coma Scale: Eye Opening

A

spontaneous 4
to speech 3
to pain 2
none 1

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42
Q

Glasgow Coma Scale: Verbal Response

A 
oriented and converses 5
confused conversation 4
inappropriate words 3
incomprehensible sounds 2
none 1
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43
Q

Glasgow Coma Scale: Motor Response

A 
obeys commands 6
localizes pain 5
withdraws to pain 4
decorticate posture 3
decerebrate posture 2
none 1
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44
Q

Glasgow Coma Scale (infants): Verbal Response

A 
coos/babbles 5
irritable 4
cries to pain 3
moans to pain 2
none 1
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45
Q

Glasgow Coma Scale (infants): motor response

A 
normal spontaneous movements 6
withdraws to touch 5
withdraws to pain 4
abnormal flexion 3
abnormal extension 2
none 1
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46
Q

oculocephalic reflex/Dolls eye tests connection between CN ____ and CN’s ___, ____, and ____

A
  • VIII

- III, IV, VI

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47
Q

If Pt responds to cold caloric test, cortex is out but ____ is intact

A

brainstem (vestibulocular reflex)

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48
Q

If only abducens works in cold calorics test, then there is a disease process of ______

A

MLF

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49
Q

afferent and efferent nerves of gag reflex are

A

IX and X

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50
Q

Cheyne-Strokes breathing-

A

hyperventilation followed by hypoventilation bec. CO2 receptors are dissociated

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51
Q

Apea Test-

A

ventilate with 100% O2, then disconnect ventilator but continue with O2, monitor ABG to check for signs of ventilation

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52
Q

when testing for pain and thermal sensation in coma patient, watch for changes in _______ while eliciting deep painful stimulation

A

pulse or blood pressure

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53
Q

4 steps in assessing brain death:

A
  • determine lack of cortical functioning by exam
  • lack of brainstem function by exam (includes apnea test)
  • observation period (varies based on age and whether mechanism of brain death is known)
  • Ancillary testing (EEG, cerebral blood flow, evoked potentials)
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54
Q

4 steps in assessing brain death:

A
  • determine lack of cortical functioning by exam
  • lack of brainstem function by exam (includes apnea test)
  • observation period (varies based on age and whether mechanism of brain death is known)
  • Ancillary testing (EEG, cerebral blood flow, evoked potentials)
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55
Q

4 steps in assessing brain death:

A
  • determine lack of cortical functioning by exam
  • lack of brainstem function by exam (includes apnea test)
  • observation period (varies based on age and whether mechanism of brain death is known)
  • Ancillary testing (EEG, cerebral blood flow, evoked potentials)
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56
Q

attention selectivity is highest in ____ arousal stage

A

medium

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57
Q

attentional stream paradigm-

A

two or more segregated series of stimuli are presented and subjects selectively attend to one over the other to perform a task

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58
Q

the 2 hypotheses between selective attention

A

early selection and late selection

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59
Q

early selection-

A

filter out irrelevant information before completion of perceptual and sensory analysis (short term storage of info, then info is bottlenecked and only certain things pass through)

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60
Q

late selection-

A

all stimuli are processed through completion of sensory and perceptual processing before selection occurs (Executive function decides what to filter)

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61
Q

Result of late selection is that signals from higher order cortical areas flow back down to sensory cortical areas to facilitate ______________

A

the sensory representation of the attended stimulus

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62
Q

Result of late selection is that signals from higher order cortical areas flow back down to sensory cortical areas to facilitate ______________

A

the sensory representation of the attended stimulus

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63
Q

Attentional Blink-

A

when target and probe are presented either very close or very far temporally from each other, they are are more accurately responded to, than when they are an intermediate amount of time apart (100-300 ms)

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64
Q

endogenous attention-

A

ability to voluntarily direct attention to specific aspects of the environment, typically based on an individuals goals.

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65
Q

exogenous attention-

A

stimuli arising from the environment attract our attention involuntarily

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66
Q

Locations of endogenous attention (2):

A

parietal areas (intraparietal sulcus) and frontal areas (including FEF and lateral prefrontal cortex)

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67
Q

Locations of exogenous attention (2):

A

temporo-parietal junction and right ventral frontal cortex

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68
Q

in a visual spatial attention test, unattended stimuli peak at P100, which correlates with the ______ cortex, while attended stimuli peak at N100 which correlates with the _______ areas

A
  • extrastriate visual

- parietal visual

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69
Q

Gist of the visual attention test is that the same stimulus elicits different neural responses due to _____

A

attention differences

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70
Q

recent evidence indicates that when there is no cue, arbitrarily stimuli elicit activity in the ____ and _____

A

LGN and thalamus

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71
Q

Balint’s syndrome-

A

bilateral damage to the posterior parietal/lateral occipital cortex. leads to simultanagnosia, optic ataxia, oculomotor apraxia, inability to respond to exogenous stimuli

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72
Q

simultanagnosia-

A

inability to attend to more than 1 object at a time

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73
Q

optic ataxia-

A

inability to reach for an object under visual guidance

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74
Q

oculomotor apraxia-

A

difficulty looking at objects using saccades

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75
Q

______ cortex dominates visual attention

A

right parietal

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76
Q

difference in neglect between right and left parietal lesion-

A

right parietal lesion leads to total left sided neglect, whereas left parietal lesion leads to only partial neglect because you still have representation from the right parietal

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77
Q

difference in neglect between right and left parietal lesion-

A

right parietal lesion leads to total left sided neglect, whereas left parietal lesion leads to only partial neglect because you still have representation from the right parietal

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78
Q

damage to supramarginal gyrus leads to

A

conduction aphasia

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79
Q

If wernicke’s area is spared but there is damage to angular gyrus, symptoms include-

A

alexia, anomia, constructional apraxia, agraphia, finger agnosia, confusion of left and right personal space

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80
Q

angular gyrus is BA ___

A

39

81
Q

Gertsmann syndrome-

A

damage in BA 39 that includes acalculia, finger agnosia, right/left disorientation

82
Q

during endogenous attentional tasks, ____ cortex organizes attentional control, and ______ cortex carries out attentional modulation

A
  • Frontal

- Parietal

83
Q

When you tell someone to look left, ___ lobe makes decision to look left and ____ lobe mediates the attention being paid to the left

A
  • frontal

- parietal

84
Q

The ______ cortex exerts top down regulation of attention and behavior

A

prefrontal

85
Q

too much catecholamine = _______ attention. Too little = ______ attention

A
  • disorganized

- distracted

86
Q

Attention modulation is a balance between NE acting on ____ receptors and dopamine acting on _____ receptors

A
  • alpha 2A

- D1

87
Q

Attention modulation is a balance between NE acting on ____ receptors and dopamine acting on _____ receptors

A
  • alpha 2A

- D1

88
Q

how does methylpheidate (ritalin work)

A

DA reuptake inhibitor

89
Q

how does Adderall work?

A

enhances DA release

90
Q

schizophrenics have poor mismatch negativity, meaning

A

they are unable to distinguish btw common and rare stimuli. Everything is sensed as background noise

91
Q

schizophrenics have poor mismatch negativity, meaning

A

they are unable to distinguish btw common and rare stimuli. Everything is sensed as background noise

92
Q

3 kinds of focal seizures-

A

simple partial, complex partial, secondary generalized convulsive

93
Q

simple partial seizure-

A

no impairment of consciousness, sometimes aura or sensory phenom. before seizure

94
Q

complex partial seizure-

A

with aura and some degree of LOC/bilateral involvement

95
Q

secondary generalized convulsive seizure-

A

complex partial spreads to involve all of the bilateral cortical hemispheres

96
Q

6 types of generalized seizures-

A

absence, tonic, clonic, atonic, myoclonic, and generalized convulsive

97
Q

absence seizure-

A

very short and can occur frequently and repeatedly if unrecognized

98
Q

tonic seizures-

A

characterized by stiffness and non-responsiveness

99
Q

clonic seizures-

A

jerking, noted amplitude vs frequency changes

100
Q

atonic seizure-

A

body goes limp

101
Q

myoclonic seizure-

A

jerky movements

102
Q

generalized convulsive seizure-

A

rare; no aura; all over happens suddenly

103
Q

first step in the diagnostic work up of a seizure is to:

A

check to make sure it isn’t provoked. If so, treat the cause

104
Q

If patient has returned to baseline neuro. status after a seizure, diagnostic workup is pretty minimal. Includes these 5 things:
*you are checking for provoked cause of seizure before you classify as epilepsy

A

comprehensive metabolic panel, urine tox, LP, neuroimaging, EEG

105
Q

If someone has had a seizure, do emergent CT scan in these 5 cases:

A
  1. someone has altered mental status w/o improvement
  2. focal neurological deficits
  3. kids under 2 yrs age (to rule out shaken baby)
  4. head trauma
  5. metastatic brain cancer (if person already diagnosed with cancer)
106
Q

If Pt is a young, otherwise healthy person, do an MRI to pick up on subtleties such as: (3)

A

low grade glioma, developmental brain malformation, small vascular malformation

107
Q

Outpatient MRI is done when there’s: (3)

A

historical evidence of a focal SZ, focality is detected on EEG, or after a second unprovoked seizure

108
Q

____ must be done on everyone following first unprovoked seizure

A

EEG

109
Q

important not to get EEG too early because:

A

transient, post-ictal changes can occur after a seizure that may show up on the EEG

110
Q

3 reasons to do an EEG

A

method of diagnosing grand mal seizure, determines focality, checks for epilepsy syndrome

111
Q

If Pt is determined to be having unprovokes seizures, they are diagnosed with ______, then the next decision to be made is:

A
  • epilepsy

- whether to give them AED’s or not

112
Q

If Pt is determined to be having unprovokes seizures, they are diagnosed with ______, then the next decision to be made is:

A
  • epilepsy

- whether to give them AED’s or not

113
Q

AED should only be used for ______ seizures

A

unprovoked

114
Q

AED should only be used for ______ seizures

A

unprovoked

115
Q

risk of having first unprovoked seizure is 10%, second is ___, third is ____

A

30%

80%

116
Q

Stevens-Johnson Syndrome can be a side effect of

A

anticonvulsant drugs

117
Q

seizure kindling-

A

if seizures start early in life, there is evidence that you can have secondary changes to the hippocampus that make it epileptogenic

118
Q

The difficult treatment balance to figure out for children with epilepsy is:

A

treating the seizures without causing cognitive hindrance/decline/slowing down

119
Q

Febrile Seizure-

A

A Sz occurring between 6 months and 6 years of age associated with fever but without evidence of intracranial infection or other defined cause

120
Q

Doctors must differentiate benign febrile seizures from seizures triggered in the setting of:

A

a febrile illness

121
Q

febrile seizures are considered provoked/unprovoked?

A

provoked

122
Q

risk of developing epilepsy after a febrile seizure is

A

3%

123
Q

3 things that increase risk of developing epilepsy in Pt that has had febrile seizure:

A
  1. baseline neurological deficits
  2. family history of epilepsy
  3. complex febrile seizures
124
Q

The biggest thing to determine with a febrile seizure is:

A

whether or not it could be meningitis

125
Q

Do we do an EEG for a febrile seizure?

A

no, it is a provoked seizure.

126
Q

How do we rule out meningitis for a febrile seizure?

A

Do a CT then LP

127
Q

Why are AED’s not recommended to treat febrile seizures?

A

bc it will mess with cognitive development

128
Q

Status epilepticus-

A

a condition characterized by an epileptic seizure that is sufficiently prolonged or repeated at sufficiently brief intervals so as to produce an unvarying and enduring epileptic condition

129
Q

Status epilepticus-

A

a condition characterized by an epileptic seizure that is sufficiently prolonged or repeated at sufficiently brief intervals so as to produce an unvarying and enduring epileptic condition

130
Q

working definition of status epilepticus is a seizure lasting more than ____ minutes. Any longer than this, you can reasonably assume it isn’t going to resolve on its own and could lead to brain damage

A

10

131
Q

4 kinds of status epilepticus seizures

A
  • generalized convulsive (grand mal)
  • generalized non-convulsive (absence)
  • focal non convulsive (this one is tricky, as ppl can be diagnosed with psichiatric disorder bec. their focal seizure went on for days)
  • and epilepsia partialis continua (focal, usually in motor cortex)
132
Q

Lifetime risk among epilepsy patients: for SE:

A

15%

133
Q

risk of SE among epileptics whose seizures start under 1 year of age

A

70%

134
Q

risk of first time seizures going into status epilepticus

A

10%

135
Q

highest recurrent risk of status epilepticus-

A

remote symptomatic (brain injury a few months ago) or neurodegenerative etiologies

136
Q

lowest risk of recurrent status epilepticus-

A

idiopathic or febrile etiology

137
Q

most important etiology of status epilepticus-

A

acute symptomatic, because you need to treat the underlying provocation

138
Q

Pathophysiology of status epilepticus brain injury:
cardiac output increases 3 fold to meet increased fuel demands. Over time, metabolic demand will outstrip supply and ________ damage will ensue, leading to _______, _______, _______. The excessive release of glutamate from the seizure will cause excess Ca++ influx that leads to ________ neuronal damage including the activation of _______ and _______ that cause cell breakdown.

A

Pathophysiology of status epilepticus brain injury:
cardiac output increases 3 fold to meet increased fuel demands. Over time, metabolic demand will outstrip supply and mitochondrial damage will ensue, leading to lactic acidosis, impaired cerebral autoregulation, and cerebral edema. The excessive release of glutamate from the seizure will cause excess Ca++ influx that leads to excitotoxic neuronal damage including the activation of proteases and lipases that cause cell breakdown.

139
Q

Pathophysiology of status epilepticus brain injury:
cardiac output increases 3 fold to meet increased fuel demands. Over time, metabolic demand will outstrip supply and ________ damage will ensue, leading to _______, _______, _______. The excessive release of glutamate from the seizure will cause excess Ca++ influx that leads to ________ neuronal damage including the activation of _______ and _______ that cause cell breakdown.

A

Pathophysiology of status epilepticus brain injury:
cardiac output increases 3 fold to meet increased fuel demands. Over time, metabolic demand will outstrip supply and mitochondrial damage will ensue, leading to lactic acidosis, impaired cerebral autoregulation, and cerebral edema. The excessive release of glutamate from the seizure will cause excess Ca++ influx that leads to excitotoxic neuronal damage including the activation of proteases and lipases that cause cell breakdown.

140
Q

3 layers most susceptible to to excitotoxic injury during SE-

A

purkinje cell layer of cerebellum, thalamic neurons, and CA1 neurons of the hippocampus

141
Q

Management of SE- what do the ABCD’s stand for?

A

Airway, Breathing, Cardiovascular, Dextrose (for hypoglycemia)

142
Q

After doing the ABCD’s for SE, do a medical history that looks for: (4)

A

prior epilepsy, use of AED’s, infection, trauma

143
Q

After doing a medical history for SE, do a physical exam that looks for: (3)

A

trauma, meningitis, focal seizures

144
Q

first round of drugs for SE

A

Fast acting; give within 10 minutes; Benzodiazepines

145
Q

2 examples of benzodiazepines

A

lorazepam and diazepam

146
Q

second round of drugs for SE are given if:

A

still seizing after 2x admin of benzos

147
Q

3 examples of second round drugs for SE

A

Pheytoin, fosphenytoin, phenobarbital

148
Q

what must you watch for if you choose to do second round drugs for SE?

A

respiratory distress, since you mixed with benzos

149
Q

what must you watch for if you choose to do second round drugs for SE?

A

respiratory distress, since you mixed with benzos

150
Q

what must you watch for if you choose to do second round drugs for SE?

A

respiratory distress, since you mixed with benzos

151
Q

reticulospinal tract controls

A

breathing and urination

152
Q

brown-sequard syndrome-

A

spinal cord hemisection; loss of fine touch and vibration on ipsilateral side of lesion, pain and temp on contralateral side, and movement ipsilateral side

153
Q

plegia-

A

complete lesion, no function below that level

154
Q

paresis-

A

some muscle strength preserved

155
Q

tetraplegia or quadriplegia-

A

injury of the cervical spinal cord anywhere above C8

156
Q

paraplegia-

A

injury of the thoracic, lumbo-sacral cord or cauda equina

157
Q

hemiplegia-

A

paralysis of one half of the body

158
Q

hemiplegia-

A

paralysis of one half of the body

159
Q

match the muscle to spinal cord segment: C5

A

deltoid or biceps

160
Q

match the muscle to spinal cord segment: C6

A

wrist extensors

161
Q

match the muscle to spinal cord segment: C7

A

triceps

162
Q

match the muscle to spinal cord segment: C8

A

flexor digitorum profundus

163
Q

match the muscle to spinal cord segment: T1

A

hand intrinsics

164
Q

match the muscle to spinal cord segment: L2

A

iliopsoas

165
Q

match the muscle to spinal cord segment: L3

A

quadriceps

166
Q

match the muscle to spinal cord segment: L4

A

tibialis anterior

167
Q

match the muscle to spinal cord segment: L5

A

EHL

168
Q

match the muscle to spinal cord segment: S1

A

gastrocnemius

169
Q 
ASIA strength scoring breakdown
Grade 0-
1-
2-
3-
4-
5-
A 
0- no contraction
1- contraction without movement
2- movement with gravity eliminated
3- movement against gravity
4- movement close to normal but when you compare left to right there is a difference
5- normal strength
170
Q 
Deep tendon reflexes spinal segment
Arm-
Styloradial-
Triceps-
patellar-
achilles-
A 
C5
C6
C7
L3
S1
171
Q

Hoffman reflex-

A

tap of the nail on patients middle or fourth finger and thumb flexes. should not happen normally

172
Q

clonus-

A

series of involuntary muscular contractions and relaxations. test by rapidly flexing the foot upward. only sustained clonus is considered abnormal

173
Q

level of motor injury is graded as last level with ____ strength

A

3/5

174
Q

sensory level of injury is measured as

A

last level with preserved sensation

175
Q

as long as ___ spinal segment is intact, can still shrug shoulders

A

C2

176
Q

inability to breath means spinal injury is above ___

A

C3

177
Q

if a patient can breathe but needs to be intubated later on, what does that tell us about spinal cord lesion?

A

it is below C5

178
Q

why would someone with a spinal cord injury be able to breathe but then later not be able to?

A

edema/swelling of the spinal cord

179
Q

Midcervical injuries result in:

A

varying degrees of diaphragm dysfunction and neurogenic and spinal shock

180
Q

spinal shock-

A

just the los of reflexes after an injury before UMN signs take over

181
Q

Neurogenic shock-

A

loss of sympathetic tone; seen in cervical injuries; due to interruption of the sympathetic input from the hypothalamus to the cardiovascular centers

182
Q

hypotension due to neurogenic shock is associated with _____cardia due to inability to convey information to vasomotor centers of spinal cord

A

brady

183
Q

hypovolemic shock-

A

hypotension with tachycardia

184
Q

4 things to expect with a cervical lesion-

A

quadriplegia, bowel/bladder retention, breathing difficulties, neurogenic/spinal shock

185
Q

after a thoracic spinal injury, you will see UMN signs in affected muscles with the exception of:

A

if there is spinal shock, you will initially see areflexia

186
Q

central cord lesion-

A

type of lesion where arms are more affected than legs

187
Q

cervical traction-

A

stretching of neck to realign it

188
Q

cauda equina syndrome-

A

LMN paralysis

189
Q

C-spine myelopathy-

A

UMN paralysis

190
Q

lumbar herniation localization:
Big toe pain
Heel/little toe pain-
little finger pain-

A
  • L5
  • S1
  • L4
191
Q 
Cervical herniation localization:
Shoulder pain-
thumb pain-
middle finger pain-
little finger pain-
A
  • C5
  • C6
  • C7
  • C8
192
Q

T2 MRI what color are CSF and water?

A

white

193
Q

osteophytes-

A

bony spurs that form to counteract and stabilize area of disc degeneration

194
Q

spinal claudication-

A

pain after walking for certain distances

195
Q

MILD procedure stands for

A

minimally invasive lumbar decompression

196
Q

how do you treat an osteoporotic vertebrae?

A

inflate a balloon in the body of the vertebra and fill it with cement

197
Q

in reference to spinal problems, when pt has leg pain, think _____. When they have back pain think _______

A
  • disc herniation

- disc degeneration

198
Q

posterior approach to surgical correction of cervical spinal pain is reserved for:

A

extensive spinal stenosis

Spring 2015 (9 decks)

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