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Unit 17 > Biomed from JKHALLER > Flashcards

Biomed from JKHALLER Flashcards

1
Q

What part of the embryo does the nervous system arise from?

A

Ectoderm

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2
Q

What region of the neural tube gives rise to the cerebrum?

A

Telecephalon

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3
Q

What region of the neural tube gives rise to the thalamus, hypothalamus, and epithalamus?

A

Diencephalon

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4
Q

What region of the neural tube gives rise to the midbrain?

A

Mesencephalon

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5
Q

What region of the neural tube gives rise to the pons and cerebellum?

A

Metencephalon

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6
Q

What region of the neural tube gives rise to the pons and myelencephalon?

A

Medulla oblongata

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7
Q

What are the 5 key steps in neural development?

A
  1. Patterning
  2. Neural Migration
  3. Axonal Migration
  4. Synaptogenesis
  5. Myelination
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8
Q

What drives neural patterning?

A

Signaling molecules like BMP4 (Bone morphogenic protein) and their concentration gradients

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9
Q

What are the structures that surround the closed neural tube and secrete signaling molecules to aid in patterning?

A

Notocord, Ventral, SHH

Neural Crest, Dorsal, BMP4

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10
Q

How do neurons migrate?

A

From inner surfaces to outer surfaces along glia “highways”

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11
Q

Does neuronal migration occur before or after patterning?

A

TRICKED YA. These occur in parallel with each other.

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12
Q

What are some potential consequences of improper neural migration?

A

Childhood epilepsy, mental retardation, and lack of sense of smell.

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13
Q

What are the 3 main processes in the migration of axons?

A

Pathway selection, target selection, address selection.

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14
Q

What are the 2 mechanisms by which guide cells can work to execute axonal migration?

A

Short and long range (both attraction and repulsion)

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15
Q

What is synaptic stabilization?

A

At birth, you have about 2500 synapses / neuron. By age 2 this triples. In adulthood these inactive synapses are eliminated.

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16
Q

One study utilized young animal models to mimic stroke. They created 5 groups: control, inactive, restraint, early training, and delayed training. What did they find?

A
  • training of any type leads to physiological reorganization of CST
  • early training but NOT delayed leads to behavioral change
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17
Q

We know that weeks 4-8 post-natal development the CST forms cholinergic interneurons. One study examined this finding. What did they find?

A

Lots more AcH secreted at the level of the SC with early training.

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18
Q

Early intervention/training has been shown to drive 3 main mechanisms of neural development. What are they?

A

Cortical reorganization, cortical spinal plasticity, increased cholinergic interneurons

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19
Q

Describe the process of myelination through development.

A
  1. Starts @ 28 weeks gestation
  2. Posterior limb or Internal Capsule @ 36 weeks
  3. Most of CST is completed at 2 years of age
  4. Continues through adolescence
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20
Q

Briefly describe patterns of myelination through development.

A
  • inferior > superior
  • posterior > anterior
  • proximal > distal
  • sensory before motor
  • projection before association
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21
Q

What are projection fibers?

A

Connect the brain to SC

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22
Q

What do association fibers connect?

A

Connect different parts of the same hemisphere

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23
Q

What is an ocular dominance column?

A

Columns in the lateral geniculate nucleus consisting of neurons that receive signals from the left eye only or the right eye only

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24
Q

What is cerebral palsy?

A

A group of permanent disorders of development of movement and posture caused by non-progressive (so, more acute episodes or lack of development) disturbances in the developing brain.

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25
Q

What is dystonia?

A

Uncontrollable muscle contraction (either from twisting and repetitive movements or abnormal fixed postures).

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26
Q

What is choreoathetosis?

A

Irregular movements in the combo of chorea (irregular contractions and athetosis (twisting/writhing)

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27
Q

Define the gross motor classification scheme (GMCS) for functional ability of individuals with CP?

A
  1. walks without limitations
  2. walks with limitations
  3. walks using device
  4. self-mobility with limitations, may use powered mobility
  5. transported
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28
Q

What is the incidence of CP?

A

2-3/1000 children

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29
Q

What is the most common type of CP seen?

A

Spastic (specifically diplegia)

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30
Q

What are some prenatal, perinatal, and postnatal etiologic risk factors of CP dev’pt?

A

Prenatal - infex, maternal diabetes/illness, abnormal placental attachment, clotting abnormalities, intrauterine growth restriction

Perinatal - prematurity, umbilical cord abnormalities, low birth weight, maternal illness

Postnatal - neonatal infex, trauma, CVA, acidosis

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31
Q

Pre-term babies are 30% more likely to develop CP. What is the main reason for this?

A

Structural and functional immaturity of blood vessels so that these kids are susceptible to ischemic and hemorrhagic injury.

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32
Q

Why is the germinal matrix so susceptible to CVA?

A

Poor blood flow (ischemia) and fragile walls of arterial vessels (hemorrhage)

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33
Q

In addition to structural and functional immaturity of cerebral vasculature, what are some additional risk factors of CP development for preterm infants?

A
  • less autoregulation of cerebral blood flow
  • ineffective myocardial fx
  • delayed ductus arteriosis and foramen ovale closure
  • oligodendrocytes still in pre-myelination phase
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34
Q

What is periventricular leukomalacia (PVL)?

A

Primary arterial ischemic injury to arterial end-zones affecting immature white matter

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35
Q

In what areas does periventricular leukomalacia (PVL) primarily occur?

A

bilaterally in frontal and/or parietal lobes

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36
Q

What is the grading system for intraventricular hemorrhage (IVH)?

A
  1. Bleed in geminal matrix
  2. Bleed into lat ventricles w/ no hydrocephalus
  3. Bleed into lat ventricles w hydrocephalus
  4. parenchymal hemorrhage / periventricular hemorrhagic infarction (PVHI)
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37
Q

Is PVHI typically unilateral or bilateral? What about PVL (Periventricular Leukomalacia)?

A

PVHI (unilateral)

PVL (bilateral)

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38
Q

What are the complications of intraventricular hemorrhage?

A

Obstructed drainage in terminal vein > ischemia / obstruction of CSF pathways > compression/ischemia of white matter

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39
Q

Describe the presentation of PVL.

A

bilateral, if frontal LE > UE spastic diplegia with spared cognition, parietal cognition and vision are affected and motor can be affected.

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40
Q

What is the presentation of a cerebellar injury?

A

Hypotonia/ataxia
Cognition/language affected
Behavioral challenges

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41
Q

What is the presentation of periventricular infarction?

A

severe unilateral impairment

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42
Q

Does posthemorrhagic hydrocephalus tend to affect LE or UE more?

A

LE

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43
Q

For infants who suffer full term brain injuries, what areas of the brain are most susceptible to ischemia? Why is this the case?

A

Developing neurons in deep grey matter of cortex and brainstem, due to high metabolic activity / demand of glu and O2

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44
Q

What are cerebrovascular injuries commonly experienced by full term infants?

A

global hypoxia/ischemia, ischemic infarct, hemorrhage

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45
Q

How can infants who experience global hypoxia/ischemia have no deficits?

A

“brain-sparing” blood flow diverts blood from major organs to supply areas of the brain in need of it.

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46
Q

Global hypoxia/ischemia can be brief/incomplete, prolonged/incomplete, or brief/complete. Describe what areas are damaged in each condition.

A

Brief/incomplete - no deficits

Prolonged/incomplete - white matter injury and end-organ damage

Brief/complete - deep gray matter

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47
Q

What are some causes of arterial ischemic strokes?

A

embolus (anything that gets to somewhere too small and can’t pass), thrombus (blood clot in a vein), clotting disease, narrow or damaged arteries

48
Q

What are some causes of cerebral sinovenous thrombosis?

A

Clotting in the venous system

49
Q

What are some causes of intracranial hemorrhage?

A

aneurysm, arteriovenous malformation, damaged or fragile blood vessels, clotting abnormality

50
Q

How is the dx of CP made?

A
  1. Document delay in neuro maturation
  2. ID UMN dysfx
  3. Rule out anything else
51
Q

What are some prenatal risk factors for CP development?

A

Exposure to toxins, infection, genetic syndromes, chromosomal abnormalities, maternal drug/alcohol abuse, rhesus incompatability (rh + vs. rh -)

52
Q

What are some perinatal risk factors for CP dev’t?

A

Birth trauma, nuchal cord (umbilical cord wrapped around neck), placental abruption, low birth weight.

53
Q

What are some postnatal risk factors for CP dev’pt?

A

Infex (meningitis and encephalitis), hypoxia, trauma, arterio-occlusive CVA

54
Q

After we dx CP, we classify it anatomically and neuropathically. What are some possible classifications in each category?

A

Anatomical (I know)

Neuropathic:

  • spastic
  • athetoid
  • ataxic
  • mixed
  • hypotonic
55
Q

When is the GMFC (gross motor classification system) most useful for us?

A

When kids are older than 6

56
Q

Patient presentation of children with CP gives us some indication about where in the CNS damage may have occurred. What are the possible locations and what do we see with each one?

A

CST: spasticity
Cerebellum: ataxia
Basal Ganglia: athetosis, chorea, choreoathetosis, ballismus, dystonia

57
Q

What are the large classifications of ortho problems we see in kids with CP?

A

spastic hip disease, spinal deformity, ankle/foot deformities

58
Q

In addition to MSK deformities, what are some other concerns/comorbidities we might see in individuals w/ CP?

A

CNS: seizures, mental retardation, visual

GI: speech, swallowing, reflux

Genitourinary: bladder dysfx, reflux, infex

59
Q

What are the major priorities (IN ORDER) we want to fix with surgical intervention for children with CP?

A

Communication, ADLs, Mobility, Walking

60
Q

What PRIMARY problems are seen in individuals with CP and what are ways to intervene for a surgeon?

A

Spasticity - drugs, neurosurgery, botox

Neurosurgery options: dorsal rhizotomy (nerves in lower SC leading to spasticity are cut), intrathecal baclofen

61
Q

What are SECONDARY problems seen in those with CP and ways to intervene surgically?

A

Muscle contracture and bony abnormailities - intervene w/ orthotics, PT, and ortho surgery: muscle lengthening, muscle transfer, osteotomy/arthrodesis

62
Q

The following drugs are commonly given to patients w/ CP. What are they and what is a major side effect? Diazepam, Baclofen, Tizanidine.

A

DECREASE TONE. Sedation is a major side effect (also weakness and hypotonia).

63
Q

How does Botox work for those with CP?

A

Blocks AcH release by nerves at motor end points (irreversible binding BUT reversible condition bc nerves regrow)

64
Q

What types of patients do well with botox injections in CP?

A

Those with dynamic muscle contracture with a limited (LESS THAN 4) number of muscles involved

65
Q

What does phenol/alcohol injection compare to botox injection for children with CP?

A

More painful, but lasts longer.

66
Q

How does a dorsal rhizotomy procedure work?

A

Cut afferent sensory rootlets to decrease stimulation from muscle spindle and weaken muscle. This works to prevent the need for ortho surgery.

67
Q

Patient selection is crucial for the success of a dorsal rhizotomy procedure. What kinds of patients are you looking for?

A

Pure spasticity, no fixed contractures, good selective motor control, 4-8 y.o., adequate cognition to be able to cooperate w/ rehab

68
Q

When is an intrathecal baclofen procedure indicated for children with CP?

A

Spasticity which interferes with function or ease of care, ambulatory patients where rhizotomy is contraindicated

69
Q

What types of patients do well w/ serial casting? How frequently should you be casting?

A

Mild spasticity/contractures (otherwise pointless), cast every 1-2 weeks for 6-8 weeks (but varies).

70
Q

What are some functions of orthotics as an intervention for children w/ CP?

A

Prevent deformity, stabilize joints, substitute for weak muscles, rarely go above knee

71
Q

When is muscle-tendon lengthening indicated?

A

For dynamic and static soft tissue contractures

72
Q

What are common procedures that occur at the hip for children with CP?

A

Psoas lengthening, derotational osteotomy (correct IR)

73
Q

Derotational osteotomy is used to correct femoral IR. How much do these kids frequently have and what is the normal range to get back down to?

A

They have about 60, normal is 15

74
Q

If a child exhibits impaired clearance during the swing phase of gait, what is one cause derived from spasticity?

A

Spastic rectus femoris

75
Q

Which hamstrings are commonly targeted in hamstring lengthening procedures?

A

Medial (worried about stiff gait if lengthening lateral hamstrings)

76
Q

What are the common procedures that occur at the knee for kids with CP?

A

Hamstring lengthening, tibial derotational osteotomy

77
Q

Why don’t you want to lengthen the soleus in children with equinus (PF)?

A

Very important for stance phase support

78
Q

In what classification of CP is equinovalgus most common?

A

diplegia

79
Q

How does a distal femoral extension osteotomy and patellar ligament advancement affect ROM?

A

It doesn’t, but it can change the arc of motion.

80
Q

What is a lateral column lengthening procedure used to treat?

A

Equinovalgus

81
Q

What are some procedures that can be used to treat flexible equinovarus? (can also be used for rigid/fixed)

A

Gastroc/Soleus Lengthening

Tib Posterior or Ant Lengthening

Split tendon transfer of tib ant or post

82
Q

What are some procedures that can be used to treat fixed equinovarus?

A

calcaneal osteotomy, closing wedge of cuboid, DF osteotomy of the medial column, triple arthrodesis

83
Q

What is the pathophysiology of spastic hip disease?

A

Spasticity / muscle imbalance leads to ADD>ABD and FLEX>EXT = displacement out of socket

84
Q

What clinical finding suggests that a child is particularly at risk for hip dislocation?

A

ADD > 45 deg passively

85
Q

What is a procedure commonly used as a preventative technique for hip dislocation?

A

Add Longus, Gracilis, Psoas lengthening

86
Q

What are some indications that would point towards managing scoliosis with a spinal arthrodesis procedure?

A

Curve > 40-50 deg, sitting imbalance, visceral problems or pain, degree of intellectual disability

87
Q

Define apraxia.

A

Disorder of learned skilled movement that CANNOT be attributed to sensorimotor dysfunction or comprehension deficits.

88
Q

Which hemisphere of the brain is particularly involved with praxis (and therefore more affected with apraxia)?

A

LEFT

89
Q

What portions of the LEFT hemisphere are particularly involved with praxis?

A

Inferior parietal lobe particularly the angular and supramarginal gyri

90
Q

What are the classifications of apraxia?

A

Ideational and ideomotor

91
Q

Define ideational and ideomotor apraxia.

A

Ideational - affects object use which is either inappropriate or in wrong sequence (man with pancakes uses spoon to cut)

Ideomotor - inability to correctly perform pantomimes and imitations (show me how to brush your teeth and they can’t, but just going to use a toothbrush not an issue).

92
Q

What are some clinical examples of ideomotor apraxia?

A

Awkward clumsy movements, difficulty sequencing, spatial orientation errors, difficulty coupling joints.

93
Q

List and define the ways that apraxia can be assessed.

A

TULIA - bottom up / dxing impairment out of functional task - but it is unclear how this may relate to real life.

Observational - Top Down, determines how apraxia interferes w/ occupational and motor performance, less reliable.

94
Q

What are the different approaches to treatment of apraxia?

A
  1. Strategy Training - compensation aimed at improving independence w/ ADLs
  2. Direct Training - task specific, errorless learning, whole task
  3. Exploration Training (vs. the above) - observe highlight difficulty, guided exploration, practice actions out of context
95
Q

What do gesture production exercises improve?

A

ability to pantomime but not ability to function in real life

96
Q

Define unilateral spatial neglect.

A

absence of awareness of failure to respond to stimuli on side OPPOSITE brain lesion

97
Q

Is unilateral spatial neglect more common s/p L or R hemisphere CVA?

A

R

98
Q

What is anosognosia?

A

Patient denies having hemiparesis on hemiparetic side

99
Q

How long does neglect take to solve?

A

3-6 mo

100
Q

What areas of the neuroanatomy are commonly affected in unilateral spatial neglect?

A

RIGHT temporo-parietaloccipital junction, parietal lobe, frontal lobe

Sometimes basal ganglia / thalamus

101
Q

How can we describe neglect?

A

Allocentric - in relation to an object (so no matter where the person is standing with relation to the object)

Egocentric - pt ignores one side of body and things in peripersonal space

102
Q

What are the types of neglect?

A

Perceptual, representational (memory oriented), motor

103
Q

Does prism adaptation assist with allo or ego neglect?

A

ego

104
Q

What is the dosage for eye patch wear schedule according to the research?

A

8 hrs/day/15days

105
Q

How does e-stim help w/ unilateral spatial neglect?

A

activates proprioceptive mapping

106
Q

How often do kids get no orthoses?

A

usually 1x/yr

107
Q

What type of patient would benefit from a cascade chipmunk or cricket foot orthosis?

A

flexible deformity (ex: hindfoot valgus)

108
Q

What patients might benefit from a supramalleolar orthosis?

A

Pronation, ligamentous laxity, mild gastroc spasticity, secondary laxity

109
Q

Who should you not recommend a supramalleolar orthosis for?

A

Anyone toe walking or w/ PF contracture

110
Q

Indications for a toe-off orthosis?

A

foot drop, mild crouch

precautions: insufficient ankle PROM, quad spasticity, knee hyperex, insufficient ML control

111
Q

Indications for posterior leaf spring orthoses?

A

foot drop, poor pushoff, hemiplegic CP, insufficient power

precautions: insufficient ML control, significant gastroc spasticity

112
Q

Indications for articulating AFOs in children?

A

insufficient DF in swing, gastroc spasticity, active DF present, idiopathic toe walking

precautions, PF contracture, severe proximal weakness

113
Q

How does limiting PF affect the knee joint?

A

Decreases recurvatum

114
Q

Indications and precautions for articulating (free DF w/ PF block) AFOs?

A

toe-heel gait, early heel rise, gastroc tone, knee hyperextension

precautions: toe walking gait pattern, gastroc contracture

115
Q

What does a ground reaction AFO/floor reaction AFO do?

A

corrects crouch / knee flexion / DF contracture

- it BLOCKS DF

Unit 17 (4 decks)

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