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Neurology > Pediatrics > Flashcards

Pediatrics Flashcards

1
Q

primitive/spinal reflexes

A
  • Flexor withdrawal
  • Crossed extension
  • Traction
  • Moro
  • Startle
  • Grasp
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2
Q

Flexor withdrawal

A

Stimulus: noxious stimulus (pinprick) to the sole of the foot. Tested in supine or sitting position.

Response: toes extend, foot DF, entire leg flexes uncontrollably

Onset: 28 weeks gestation

Integrated: 1-2 months

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3
Q

Crossed extension

A

Stimulus: noxious stimuli to the ball of foot of extremity fixed in extension; tested in supine.

Response: opposite LE flexes, then adducts and extends

Onset: 28 weeks gestation

Integrated: 1-2 months

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4
Q

Traction

A

Stimulus: grasp forearm and pull up from supine into sitting

Response: grasp and total flexion of the UE

Onset: 28 weeks gestation

Integrated: 2-5 months

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5
Q

Moro

A

Stimulus: sudden change in position of head in relation to trunk; drop patient backward from sitting position

Response: extension, abduction of UEs, hand opening, and crying followed by flexion, adduction of arms across chest

Onset: 28 weeks gestation

Integrated: 5-6 months

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6
Q

Startle

A

Stimulus: sudden loud or harsh noise

Response: sudden extension or abduction of arms, crying

Onset: birth

Integrated: persists

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7
Q

Grasp

A

Stimulus: maintained pressure to palm of hand (palmar grasp) or to ball of foot under toes (plantar grasp)

Response: maintained flexion of fingers or toes

Onset: palmar at birth; plantar at 28 weeks gestation

Integrated: palmar- 4-6 months; plantar- 9 months

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8
Q

tonic/brainstem reflexes

A
  • asymmetrical tonic neck (ATNR)
  • symmetrical tonic neck (STNR)
  • symmetrical tonic labyrinthe (TLR or STLR)
  • positive supporting
  • associated reactions
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9
Q

Asymmetrical tonic neck (ATNR)

A

Stimulus: rotation of the head to one side

Response: flexion of skull limbs, extension of the jaw limbs, “bow and arrow” or “fencing” posture

Onset: birth

Integrated: 4-6 months

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10
Q

Symmetrical tonic neck

A

Stimulus: flexion or extension of the head

Response: with head flexion: flexion of the arms, and extension of the legs
with head extension: extension of the arms, and flexion of the legs

Onset: 4-6 months

Integrated: 8-12 months

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11
Q

Symmetrical tonic labyrinthine (TLR or STLR)

A

Stimulus: prone or supine position

Response: with prone position: increased flexor tone/flexion of all limbs
with supine position: increased extensor tone/extension of all limbs

Onset: birth

Integrated: 6 months

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12
Q

Positive supporting

A

Stimulus: contact to the ball of the foot in upright standing position

Response: rigid extension (co-contraction) of the LEs

Onset: birth

Integrated: 6 months

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13
Q

Associated reactions

A

Stimulus: resisted voluntary movement in any part of the body

Response: involuntary movement in resting extremity
(homolateral synkinesis and Ramestes)

Onset: birth-3 months

Integrated: 8-9 years

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14
Q

Midbrain/Cortical reflexes

A
  • neck righting action on the body (NOB)
  • body righting acting on the body (BOB)
  • labyrinthine head righting (LR)
  • optical righting (OR)
  • protective extension (PE)
  • equilibrium reactions- tilting (ER)
  • equilibrium reactions postural fixation
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15
Q

Neck righting action on the body (NOB)

A

Stimulus: passively turn head to one side; tested in supine

Response: body rotates as a whole (log rolls) to align the body wit the head

Onset: 4-6 months

Integrated: 5 years

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16
Q

Body righting acting on the body (BOB)

A

Stimulus: passively rotate upper or lower trunk segment; tested in supine

Response: body segment not rotated follows to align the body segments

Onset: 4-6 months

Integrated: 5 years

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17
Q

Labyrinthine head righting (LR)

A

Stimulus: occlude vision; alter body position by tipping body in all directions

Response: head orients to vertical position with mouth horizontal

Onset: birth to 2 months

Integrated: persists

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18
Q

Optical righting (OR)

A

Stimulus: alter body position by tipping body in all directions

Response: head orients to vertical position with mouth horizontal

Onset: birth to 2 months

Integrated: persists

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19
Q

Body righting acting on head (BOH)

A

Stimulus: place in prone or supine position

Response: head orients to vertical position with mouth horizontal

Onset: birth to 2 months

Integrated: 5 years

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20
Q

Protective extension (PE)

A

Stimulus: displace COG outside of BOS

Response: arms or legs extend and abduct to support and to protect the body against falling.

Onset: arms 4-6 months, legs 6-9 months

Integrated: persists

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21
Q

Equilibrium reactions (ER)

A

Stimulus: displace the COG by tilting or moving the support surface (e.g. with a moveable object such as an equilibrium board or ball)

Response: curvature of the trunk toward the upward side along with extension and abduction of the extremities on that side; protective extension on the opposite (downward) side

Onset: prone 6 months, supine 7-8 months, sitting 7-8 months, quadruped 9-12 months, standing 12-21 months

Integrated: persists

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22
Q

Equilibrium reactions- postural fixation

A

Stimulus: apply a displacing force to the body , altering the COG in its relation to the BOS; can also be observed during voluntary activity

Response: curvature of the trunk towards the external force with extension and abduction of the extremities on the side to which the force was applied

Onset: prone 6 months, supine 7-8 months, sitting 7-8 months, quadruped 9-12 months, standing 12-21 months

Integrated: persists

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23
Q

Special associated reactions

A
  • homolateral synkinesis
  • Raimeste’s phenomenon
  • Souque’s phenomenon
  • Imitation synkinesis
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24
Q

Associated reaction general

A

resist flexion normal UE = get flexion involved UE
resist extension normal UE = get extension involved UE
resist flexion normal LE = get extension involved LE
resist extension normal LE = get flexion involved LE

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25
Q

Homolateral synkinesis

A
  • resist flexion involved UE = get flexion involved LE

* resist extension involved UE = get extension involved LE

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26
Q

Raimeste’s phenomenon

A
  • resist adduction normal extremity get adduction involved extremity
  • resist abduction normal extremity get abduction involved extremity
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27
Q

Souque’s phenomenon

A

•elevation of the involved arm above horizontal may elicit an extension and abduction response of the fingers

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28
Q

Imitation synkinesis

A

as involved extremity is performing a task it also takes place in the normal extremity i.e thumb to finger

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29
Q

Apgar

A

•performed at 1 minute then again at 5 minutes
•graded on 5 criteria: activity (muscle tone), pulse, grimace (reflex irritability), appearance (skin color), respiration
•each criteria is graded on a scale of 0 to 2
1) Activity (muscle tone): 0=absent, 1=UE and LE flexion, 2=active movement
2) Pulse: 0=absent, 1= <100 bpm, 2= >100 bpm
3) Grimace (reflex irritability): 0=flaccid, 1=some flexion of extremities, 2=active motion (cough, sneeze, withdrawal)
4) Appearance (skin color): 0=blue, pale, 1=pink body, blue extremities, 2=pink
5) Respiration: 0=absent, 1=slow, irregular, 2=vigorous, cry
•Total points are then added:
- 0-3: severely depressed
- 4-6: moderately depressed
- 7-10: excellent condition

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30
Q

Developmental phases

A
  • Neonate: 0-10 days
  • Infantile: 0-3 months
  • Preparation: 4-6 months
  • Modification: 7-9 months
  • Refinement: 10-12 months
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31
Q

Infantile phase 1 month

A

1 Month:
Important notes:
•decreased physiological flexion

Standing/ Walking:
•automatic walking reflex

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32
Q

Infantile phase: 2 months

A

2 Months:
Important notes:
• hypotonia/asymmetry

Prone/ Supine:
• (P) head turning/lifting improved, cannot yet hold in midline
• (S) head rotates further to the side through asymmetrical extensor pull, which stimulates ATNR, leads to improved lateral vision

Sitting/ Other:
• (sit) head bobbing (due to lack of neck flexor strength)

Standing/ Walking:
• automatic walking no longer present

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33
Q

Infantile phase: 3 months

A

3 Months:
Important notes:
• symmetry- midline orientation of hands, eyes, and head

Prone/ Supine:
• (P) puppy position- forearm WB, foor on foot desensitization contact
• (S) head can be held in midline. Hands to chest for increased body awareness

Sitting/ Other:
• can sustain head elevation- develops a “neck”

Standing/ Walking:
• takes weight on feet again, LEs abd/ knees stiffly extend

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34
Q

Infantile phase: Neonate 0-10 days

A

Neonate 0-10 days:
Important notes:
• physiological flexion

Standing/ Walking:
• automatic walking reflex (continues through 1 month)

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35
Q

Preparation phase: 4 months

A

4 months:
Important notes:
•lateral neck flexion

Prone/ Supine:
• (P) start to roll from prone to sidelying and able to achieve prone on elbow position
•(S) start to roll from supine to sidelying, which is helped by hands on knees position. Also able to put hands together in space

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36
Q

Preparation phase: 5 months

A

5 months:
Prone/ Supine:
• (P) elbow extension in prone position + weight shift and reach while prone on elbows. Start to roll from prone to supine
• (S) feet to mouth leads to increased desensitization

Sitting/ Other:
(sit) when pulled to sitting by their head no longer lags. Can also ring sit with arms forward.

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37
Q

Preparation phase: 6 months

A

6 months:
Important notes:
• Landau reflex (superman position when held horizontal in air in prone) complete
• may say first word (often dada)

Prone/ Supine:
(S) able to roll from supine to prone with LEs out in space and able to transfer objects from one hand to the other.

Sitting/ Other:
• (sit) nice and erect sitting posture with protective extension forward

Standing/ Walking:
• bounce

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38
Q

Modification phase: 7 months

A

7 months:
Important notes:
•equilibrium reactions present in supine and starting in sitting

Prone/ Supine:
•(P) baby can pivot in a circle

Sitting/ Other:
• (sit) sits unsupported with protective extension sideways
•(O) can go from prone to quadruped then rock to sit

Standing/ Walking:
•from quadruped may pull to stand

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39
Q

Modification phase: 8 months

A

8 months:
Important notes:
• equilibrium reactions in sitting beginning in quadruped

Prone/ Supine:
• (P) creeping

Sitting/ Other:
• (O) goes from sitting to quadruped to kneeling to standing

Standing/ Walking:
• must “plop” to get down. Cruises sideways on furniture, needs both UEs

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40
Q

Modification phase: 9 months

A

9 months:
Important notes:
• feed themselves “pinch” with fingers
• constant movement

Sitting/ Other:
• (sit) able to side, and w sit. Protective extension backwards begins.
• (O) crawling over objects

Standing/ Walking:
• cruising semi-turned

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41
Q

Refinement phase: 10 months

A

10 months:
Sitting/ Other:
•(sit) protective extension backwards

Standing/ Walking:
•cruise with one UE and can lower to sit slowly

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42
Q

Refinement phase: 11 months

A

11 months:
Sitting/ Other:
• (sit) long sit
• (O) half kneeling more functional

Standing/ Walking:
• can stand by leg extension rather than UE extension
• reach for objects, which leads to falls in standing
• high guard appearance

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43
Q

Refinement phase: 12 months

A

12 months:
Important notes:
• roll ball
• say 2 words

Standing/ Walking:
• able to weight shift and lift one leg

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44
Q

Important landmarks: 11-14 months

A

walking

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45
Q

Important landmarks: 14 months

A

drink out a cup

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46
Q

Important landmarks: 18 months

A

starts climbing, walks sideways and backwards, ascends and descends stairs and small elevations, turns pages

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47
Q

Important landmarks: 24 months

A

kick ball, running, feed self with spoon

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48
Q

Important landmarks: 14-32 months

A

talk in sentences

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49
Q

Important landmarks: 3 years

A

stand on one foot, jump in place, ride tricycle, walks heel to toe

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50
Q

Important landmarks: 4 years

A

skips, alternate feet up and down stairs, throw overhead, put shoes on correct feet, brush hair and teeth

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51
Q

Important landmarks: 5 years

A

hop, catch a ball, jump off object and land on 2 feet

52
Q

Important landmarks: school age

A

handedness established

53
Q

Cerebral palsy

A

due to non-progressive damage to the CNS before age 3 in single or multiple locations of the immature brain. Can be prenatal (before birth), perinatal (during birth), or postnatal (after birth) in origin. Usually results from lack of oxygenation but may also result from infection, trauma, cranial hypoxia, consanguinity (inbreeding=genetic issue), or baby’s blood is just not compatible with the mother’s.
•Frequently associated with placental insufficiency, prematurity, grade III or IV intraventricular hemmorrhage, or periventricular leukomalacia (the death of small areas of brain tissue around fluid-filled areas called ventricles. A major cause is thought to be changes in blood flow to the area around the ventricles of the brain).
•difficult to diagnose during infancy, often diagnosed between 8-12 months of age

54
Q

CP clinical picture

A

• impaired voluntary muscle control and coordination may be accompanied by or associated with:

  • mental retardation
  • learning disabilities
  • speech disorders
  • auditory impairments, seizures, and abnormalities of vision
55
Q

Classifications for CP based on area(s) of body impairment

A
  • Monoplegia
  • Diplegia
  • Triplegic
  • Hemiplegic
  • Quadraplegic
56
Q

CP Monoplegia

A

one limb involved

*trunk and face may also be involved

57
Q

CP Diplegia

A

2 limbs involved- usually the LEs and you may see a scissor gait
*trunk and face may also be involved

58
Q

CP Triplegia

A

3 extremities involved

*trunk and face may also be involved

59
Q

CP Hemiplegia

A

1 UE and 1 LE on the same side of the body involved (just like with CVA)
*trunk and face may also be involved

60
Q

CP Quadraplagia

A

4 extremities and the trunk involved

*trunk and face may also be involved

61
Q

CP classifications are based on…

A

areas of the brain affected and tone

62
Q

CP tone classifications

A
  • Spastic
  • Dyskinetic/Athetoid
  • Ataxic
63
Q

CP spastic tone

A

most common due to involvement of motor cortex or white matter -corticospinal tract- to and from cortical sensorimotor sections of the brain

64
Q

CP dyskinetic/athetoid tone

A

due to involvement of the basal ganglia

65
Q

CP ataxic tone

A

due to involvement of the cerebellum

66
Q

Motor syndromes of CP: Spastic Diplegia

A
  • spastic diplegia is the most common classification (35%)
  • UMN s/s: spasticity, (+) Babinski, clonus, hyperreflexia
  • location of the lesion: corticospinal tracts (pyramidal tracts)
  • etiology: periventricular leukomalacia
  • presentation: scissor gait- increased hip adductor tone, commando crawl (legs drag behind due to weakness)
67
Q

Motor syndromes of CP: Spastic hemiplegia

A
  • spastic hemiplegia is the second most common CP classification (25%)
  • UMN s/s
  • location of the lesion: corticospinal tracts
  • etiology: CVA, IVH
  • presentation: cirumductive gait (on weak side), early handedness (decreased use of affected side)
68
Q

Motor syndromes of CP: Spastic Quadraplegia

A
  • spastic quadraplegia is the third most common type of CP (20%)
  • location of the lesion: corticospinal tract
  • etiology: PVL
  • presentation: most severe form of CP, affects all limbs and often impacts swallowing, high likelihood of seizures and cognitive impairment
69
Q

Motor syndromes of CP: athetoid/extrapyramidal

A
  • 4th most common CP classification (15%)
  • no UMN s/s: hypotonia with increased tone later in life
  • location of the lesion: extrapyramidal tracts (basal ganglia)
  • etiology: birth asphyxia
  • presentation: involuntary contraction of all muscle groups. Difficulty with speech and swallowing, normal intelligence and low risk of seizures, upper body slightly more affected than lower body
70
Q

CP secondary conditions

A
  • mental retardation: (30%)
  • seizures: 1/3, tegrotol, dilantin, phenobarbitol
  • vision impairments
  • ortho issues: decreased ROM
  • oral motor dysfunction
  • dental problems
  • hearing loss
  • decreased spatial awareness
71
Q

CP therapeutic interventions

A
  • address impairments (ROM, normalized movement, sensory deficits) and functional limitations (mobility, weight shift, rolling, WB, transitional movements, walking)
  • decrease tone
  • increase ROM (with precautions if orthopedic issues present)
  • increase strength
  • increase functional motor skills and mobility
  • educate caregivers- feeding, ROM, dressing, influencing, tone, facilitating normal movement
  • identify barriers and recommend medications- AD, adaptive equipment
72
Q

Modified Ashworth scale

A
  • scale for spasticity
  • 0: no increase in muscle tone
  • 1: slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of ROM when the affected part is moved into flexion or extension
  • 1+: slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remaining (less than 1/2) of the ROM
  • 2: more marked increase in muscle tone through most of the ROM, but affected part moves easily
  • 3: considerable increase in muscle tone; passive movement difficult
  • 4: affected part(s) rigid in flexion or extension
73
Q

CP treatment (meds and surgery)

A
  • meds: baclofen, valium, dantrolene sodium, clonidine, zanaflex
  • surgery: rhizotomy (nerve roots cut)
  • hippotherapy= horse back riding
74
Q

Spina bifida main facts

A
  • birth defect 1/1,000 babies
  • bones of spine form improperly (when the neural tube doesn’t close)
  • malformation, or opening in the spine
  • spinal cord exposed (in severe cases)
  • 3 types: spina bifida occulta, meningocele, myelomeningocele
75
Q

3 types of spina bifida

A
  • spina bifida occulta
  • meningocele
  • myelomeningocele
76
Q

Spina bifida clinical picture

A

congenital condition caused when the neural tube doesn’t fully close, forming at approx 4 weeks gestation
•the skin over the involved area may be closed (occulta) or open (aperta) with a cyst (cystica)

77
Q

Spina bifida occulta

A
  • neural arches do not connect but there is no neural material outside of the spinal canal
  • most commonly occurs in the lower lumbar spine
  • most benign with no neuro effects (pt doesn’t even know)
  • clinical s/s: skin depression or dimple, dark tufts of hair, telangiextasis (dilated blood vessels), soft subcutaneous lipomas (fatty tumors)
  • asymptomatic in 40% of cases
78
Q

Meningocele SB

A
  • neural arches do not connect and the meningeal membranes protrude through the opening in the child’s spinal column.
  • the cord is not trapped so the child often doesn’t exhibit any neuro s/s
  • may possibly have bowel and bladder dysfunction
79
Q

Myelo (SC) meningocele

A
  • both the SC and the meninges protrude through the vertebral defect into a sac or open area in the back
  • the SC and surrounding tissue may be visible and exposed to the environment, which places the child at high risk for infection
  • the SC is malformed and the child exhibits atypical development including flaccid LEs and loss of sensation below the level of the myelomeningocele
  • possible bowel and bladder dysfunction
  • the defect can occur at any spinal level, but is often seen in the L/S area spinal level
  • accompanying the myelomeningocele are abnormalities of the brain such as Arnold-Chiari malformation (type II) in which the cerebellum, pons, and medulla, are elongated and protrude into the foramen magnum
  • hydrocephalus (obstructed CSF and head enlargement) is seen in 80% due to obstructed flow of CSF
  • can be prevented (up to 72%) if women take folic acid
80
Q

Treatment for SB

A
  • meningocele can be treated surgically to restore normal SC function
  • myelomeningocele spina bifida is operated on within 48 hours after birth to prevent infection. Surgeons place the SC back in the canal and cover with muscle and skin. Paralysis and bowel problems still persist after surgery.
81
Q

Hydrocephalus

A

•the enlargement of the ventricular system (which produces CSF) in the brain due to an increase in CSF
•could be the result of Arnold-Chiari malformation
•hydrocephalus requires immediate treatment and correction in the form of a ventriculoperitineal (VP) shunt (goes from ventricles to under the skin behind the ear, under the clavicle, to the peritoneal abdominal area), with an extra length of tubing for growth (could also do an atrioventricular shunt, brain to atrium)
• Caregivers must be taught to watch for shunt malfunction including:
-irritability
-increased sleepiness
-personality changes
-sunset eyes, downward gaze
-HA

82
Q

SB associated impairments

A
  • bowel and bladder dysfunction- children may need to self cath
  • latex allergy present in 73% of children with spina bifida
  • tethered cord occurs when the SC is fixed caudally because of pathology. The tethered cord becomes stretched (especially as the child grows), distorted, and ischemic and may show atypical neuro signs such as decreased strength, and increased LE spasticity, changing urologic patterns. Surgery to free the cord is usually performed.
  • PI’s due to decreased sensation below lesion level and incontinence
  • contractures due to muscular imbalances
  • osteoporosis due to decreased WB and decreased muscle pull
83
Q

SB interventions

A
  • address functional deficits and capitalize on the child’s strengths
  • family education on: optimal positioning, importance of WB and upright positioning, shunt care and signs of malfunction and infection, skin check, ROM, orthotics, AD, and adaptive equipment
  • static and dynamic balance training
  • independence in functional skills
  • mobility training
84
Q

Muscular dystrophy

A
  • a group of genetic diseases in which muscle fibers are unusually susceptible to damage. These damaged muscles become progressively weaker. Most people who have muscular dystrophy will eventually use a w/c
  • there are many different kinds of MD. Symptoms of the most common variety begin in childhood. Occurs primarily in boys. Other types of MD don’t surface until adulthood.
  • people with MD may have respiratory issues (this is often an eventual fatality) and trouble with swallowing. Also contractures and organ problems.
  • there is no cure but meds and therapy can slow it down
85
Q

MD traits

A
  • all forms are due to a genetic disorder
  • progressive loss of muscle contractility due to destruction of myofibrils
  • diagnosis made with clinical exam, EMG, muscle biopsy, DNA analysis, enzyme lab
  • primary impairments include insidious weakness: scoliosis, winging of the scapula, increased lordosis
  • secondary impairments = decreased respiratory capacity, easy fatigability, occasional obesity
  • PT used to prolong pt independence with increased use of AD, w/c, and adaptive equipment as the disease progresses
86
Q

Duchenne MD

A

•4-5 y/o onset of classic clinical features
•psuedohypertrophy of calves and possibly also delts, quads, and forearm extensors- not actually hypertrophy but rather deposits of fat as the muscle breaks down.
• tightness of gastroc and TFL
•initial s/s: clumsiness (muscle weakness), falling, inability to keep up with peers
• Trendelenburg and toe walking with shoulder retraction, and decreased UE swing
* (+) Gowers sign- use of UE’s to push up on thighs to attain standing from the floor
• ambulation frequently impossible by age 12

87
Q

treatment muscular dystrophy

A
  • function (anything to keep them participating in the community)
  • aquatics
88
Q

Sickle-cell anemia

A

• genetic life-long disorder characterized by RBC that assume abnormal, rigid, sickle shape
•prevalence in US is approx. 1 in 5,000 mostly affecting black people
•sickle shaped RBC obstruct capillaries and restrict blood flow, resulting in clotting, ischemia, pain, and often organ damage
•hand and foot swelling
•painful crises are treated with hydration and analgesics, NSAIDs -> opiod -> PCA devices
•complications include: CVA, cholelithiasis, avascular necrosis, osteomyelitis, leg ulcers, retinopathy, jaundice, decreased immune reactions, due to hyposplenism, pneumonia, pulmonary hypotension, chronic renal failure, chronic pain
TX: children- folic acid, penicillin, bone marrow transplants

89
Q

Osteogenesis imperfecta

A
  • group of heritable disorders characterized by impairment of collagen maturation (gene mutation)
  • collagen forms a major portion of bone, dentin (teeth), sclerae (eyes), ligaments and skin
  • genetic (autosomal dominant defect) bone disorder. Pt’s are born with defective CT or without the ability to make CT
  • 8 different types of OI
90
Q

Characteristics of OI

A

•bones fx easily, short stature, spinal curvature, barrel-shaped rib cage, bone deformity mild to mod, early loss of hearing, poor muscle tone, discoloration of sclera (blue grey)

91
Q

Treatment for OI

A
  • increase overall bone strength to prevent bone fx, while maintaining mobility. PT used to strengthen muscles and improve mobility in a gentle manner while minimizing risk of fx.
  • often involves hydrotherapy, support cushions for improved posture
  • pt’s encouraged to change positions frequently to change pressure on bones
  • use of assistive and adaptive devices, meds, biphosphonates, surgery- metal rods, spinal fusions
92
Q

Prader-Willi

A

•genetic diagnosis made by physical and behavioral characteristics rather than genetic testing
•causative factor- partial deletion of chromosome 15
• characteristics: small hands, feet, and sex organs, hypotonia, almond-shaped eyes, obesity, and a constant desire for food, coordination impairments and mental retardation
Tx: posture control, exercise, fitness, gross and fine motor skills

93
Q

Down’s syndrome

A

•genetic abnormality with an extra 21st chromosome
• advanced maternal age increases risk
•characteristics: mental retardation, hypotonia, joint hypermobility, flattened nasal bridge, narrow eyelids, epicanthial folds (skin fold of the upper eyelid covering the inner corner of the eye), small mouth, feeding impairments, flat feet, scoliosis, congenital heart disease, visual and hearing loss.
Tx: exercise, fitness, stability, maximizing respiratory function, caregiver ed, may need heart surgery
*Downs children tend to have atlanto-axial subluxation in the neck

94
Q

Arthrogryposis Multiplex Congenita

A

• literally means joint many at birth fused
•multiple, non-progressive joint contractures are noted at birth. The cause is unknown; may be an underlying neuropathy or myopathy. The limbs appear atrophic, with waxy skin lacking normal joint creases (caused they’re fused). The elbows are extended, the wrists flexed and ulnarly deviated, the thumb adducted and clasped and the fingers flexed.
TX: treatment is difficult. Serial splinting is started soon after birth, however, correction is often inadequate

95
Q

Arthrogryposis Multiplex Congenita additional

A

•non-progressive muscular disorder
• causative factors include: poor movement in utero due to myopathic, neuropathic, or joint abnormalities allowing fibrosis of muscles and structures within the joints, for a small percentage there is an autosomal dominant trait.
•characteristics include: cylinder-like extremities, muscle contractures, joint dislocation, and atrophy
TX: attain max level of development skills through positioning, stretching, strengthening, splinting, and adaptive equipment, surgery may be needed

96
Q

Ortonloni’s test

A

*opposite of Barlow’s test
Purpose: assess for congenital hip dislocation

Position: supine fix hips and knees @ 90° of flexion; clinician’s thumbs are on the infant’s medial thighs and fingers on the lateral thigh

Technique: firmly traction the thigh while gently abducting the leg so that femoral head is translated anterior into the acetabulum

Interpretation: (+) test = reduction of the hip; an audible “clunk” may be heard

97
Q

Barlow’s test

A

*opposite of Ortolani test
Purpose: assess for hip dysplasia

Position: supine 90/90; clinician’s thumbs are on the infant’s medial thigh and fingers on the lateral thigh

Technique: apply a posterior force thru the femur as the thigh is gently adducted

Interpretation: (+) test = the examiner’s finger that is on the greater trochanter will detect a palpable dislocation.

98
Q

Key development: 1 month

A
  • turns head to side

* holds head up in prone position

99
Q

Key development: 2 months

A
  • turns from side to back
  • sits with complete support
  • holds objects placed in the hand
100
Q

Key development: 4 months

A
  • able to hold head erect
  • reaches for objects with both hands
  • starts hand to mouth activities
101
Q

Key development: 5 months

A
  • can turn over

* rolls supine to prone

102
Q

Key development: 6 months

A
  • reaches for objects with one hand

* completes turning and rolling

103
Q

Key development: 7 months

A

•sits unsupported

104
Q

Key development: 9 months

A

•locomotion through crawling

105
Q

Key development: 10 months

A
  • cruises

* gets to standing position

106
Q

Key development: 11-14 months

A
  • walks but very unsteady

* stands without support

107
Q

Key development: 15 months

A

• walks more steadily but with a wide BOS

108
Q

Key development: 18 months

A
  • continues to improve balance when walking but still poor

* starts climbing

109
Q

Key development: 2 years

A
  • starts running

* improves balance

110
Q

Key development: 3 years

A

•stands on one foot

111
Q

Key development: 4 years

A
  • skips on one foot

* alternating feet when going up and down stairs

112
Q

Apgar behaviors: motor development is directed and dependent upon…

A

1) maturation of the nervous system
2) individual genetic coding
3) handling
4) environmental experiences (feedback)

113
Q

Apgar behaviors: development proceeds…

A
  • cephalo -> caudally
  • prox -> distal
  • gross movement -> fine movement
114
Q

Apgar behaviors: motor development better named sensory motor development because of considerable sensory input which contributes to development. All sensory systems are involved

A
  • tactile
  • proprioceptive
  • kinesthetic
  • visual
  • vestibular
115
Q

Apgar behaviors: characteristics of movement

A
  • every movement involves a weight shift
  • weight shift is the stimulus for righting reactions and righting reactions are automatic background for all movements. Righting reactions are also the basis for equilibrium reactions
  • weight shift -> righting reactions -> equilibrium reactions (and all other movements)
116
Q

early signs of recognizing CP

A

Neonatal:
•weak or absent sucking/swallowing
• episodes of bradycardia or apnea
•signs of cerebral irritation such as a high pitched cry or jitteriness
•tone may be decreased
•primitive reflexes (Moro, stepping) may be difficult to elicit

3 months:
•difficulty feeding, tongue thrust may be present
•irritability
•tone usually hypotonic
• brisk DTR
•persistent or obligatory primitive reflexes
•child keeps on or both hands fisted
• strabismus (one eye going in different direction)
•advanced head control- usually better in prone due to increased extensor control, difficulty maintaining head in midline in supine

6 months:
•delayed motor milestones or abnormal patterns (rolls by spinal extension rather than segmental)
•preferential unilateral hand use or fisting
• little spontaneous movements, inability to bring hands to midline, reach
•persistence of primitive reflexes
•arching or strong tendency to stand (without sitting)
• infant feels stiff on handling
•difficult to dress

9 months:
•delayed developmental/atypical movement
•crawling- arm movements only, nonreciprocal, asymmetrical movement
•reaching- splaying of fingers and extended wrist, tremor
•kicking- nonreciprocal
•holding arms flexed

12 months:
• scissoring, toe-walking, athetoid movement, handedness

117
Q

anencephaly

A

exposed, open, underdeveloped cerebrum. Brain stem and its functions preserved.

118
Q

SB in more proximal locations: cranial meningocele

A

meninges and CSF in herniating cyst in upper cervical/lower cranial region

119
Q

SB in more proximal locations: meningoencephalocoele

A

brain in an external cyst

120
Q

Talipes/equinovarus/clubfoot

A

foot twisted into extreme inversion so that the sole of the foot cannot touch the ground

121
Q

Spinal muscular atrophy

A
  • autosomal recessive genetic inheritance
  • certain types have mutation on chromosome 5
  • there is progressive muscular weakness, atrophy, decreased DTRs, normal intelligence, intact sensation, and end stage respiratory compromise
  • Tx: positioning, vestibular and visual stimulation, access to play. Educate caregivers on use of AD and adaptive equipment
122
Q

Hemophelia

A
  • group of hereditary genetic disorders that impair the body’s ability to control blood clotting or coagulation
  • the hemophiliac does not bleed more intensely than the regular person but can bleed for much longer
  • in areas such as the brain or inside the joints, this can be fatal or permanently disabling
123
Q

turner syndrome

A

•encompasses several conditions of which absence of an entire sex chromosome is most common
•characteristics: short stature, lymphedema, broad chest, low hairline, low-set ears, webbed necks, gonadal dysfunction, amenorrhea-> sterility; congenital heart disease, hypothyroidism (Hashimoto’s thyroiditis), DM, vision and hearing issues, many autoimmune diseases; and specific pattern of cognitive defecits especially visuospatial, mathematical, and memory areas
TX: growth hormone and extrogen replacement therapy, complications as appearing

124
Q

Klinefelter’s syndrome

A

•a condition in which males have an extra X sex chromosome
•affected individuals have at least two X chromosomes and one Y
•exists in 1 out of every 1,000 males
•characteristics: small testicles, reduced fertility, some degree of language learning impairments, deficits in executive functions. Severely involved may have germ cell tumors, breast cancer, osteoporosis. Co-existing conditions include: pulmonary disease, varicose veins, DM, RA
TX: testosterone, other tx per complications

125
Q

Ehlers-danos syndrome

A
  • group of inherited CT disorders caused by defect in the synthesis of collagen
  • collagen helps tissues to resist deformation, in the skin, muscles, and ligaments, blood vessels, and visceral organs- insufficiency causes increased elasticity in these tissues which may vary from mild to life threatening issues.
  • major signs and symptoms: highly flexible fingers, toes, loose and unstable joints that are prone to dislocation, sprains, subluxations, flat feet, easy bruising, fragile blood vessels, abnormal wound healing, low muscle tone, muscle weakness, early onset OA, cardiac effects, dysautonomia, valvular heart disease
  • Other less common signs and symptoms: osteopenia, talipes equinovarus, scoliosis, kyphosis, tethered spinal cord syndrome: OA hypermobility, Arnold-Chiari malformation, nerve compression syndromes, fibromyalgia, delayed developmental skills due to hypotonia, Raynaud’s, irritable bowel syndrome, etc…
126
Q

Fetal alcohol syndrome

A
  • maternal alcohol use during pregnancy
  • growth deficiencies
  • permanent brain damage, neurological abnormalities, developmental delay, learning/behavior disorders
  • abnormal facial features including short eye opening, short nose, flat midface, thin upper lip, and small chin

Neurology (9 decks)

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