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Neuro Boards > Neuro Peds Pathology > Flashcards

Neuro Peds Pathology Flashcards

1
Q

Arthrogryposis Multiplex Congenita (AMC)

A
  • non-progressive

- restriction of movement in utero => fibrosis of muscles and joint structures

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2
Q

Arthrogryposis Multiplex Congenita (AMC) Etiology

A
  • most cases unknown cause; small genetic link to autosomal dominant trait
  • A causative factor is lack of movement inutero in early development
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3
Q

Athrogryposis Multiplex Congenita (AMC) s/sx (4)

A
  • Cylindrical extremities with minimal definition
  • Muscle atrophy
  • Dislocation of joints
  • Significant and multiple contractures**
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4
Q

Arthrogryposis Multiplex Congenita (AMC) treatment

A
  • Attain maximal level of developmental skills; stretching, positioning, strengthening, splinting, use of adaptive equipment
  • Family/caregiver education
  • Possible surgical intervention
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5
Q

Autism Spectrum Disorder (ASD)

A
  • Umbrella term for group of brain development disorders

- Characterized by difficulty with social interaction and communication, as well as repetitive behaviors

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6
Q

Autism Spectrum Disorder (ASD) Etiology

A

Multifactorial cause including genetics and environmental factors

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7
Q

ASD s/sx

A
  • Emerge at age 2 or 3
  • nonpurposeful/no speech
  • awkwardness in social interactions
  • inability to understand body language
  • lack of empathy
  • defensiveness or indifference toward sensory stimulation
  • repetitive self-stimulating behaviors
  • perseverations
  • preoccupations with routines/rituals
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8
Q

ASD Treatment

A
  • focuses on improving social communication/decreaseing non-purposeful movements and vocalizations
  • Possible sensory integration therapy
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9
Q

Cerebral Palsy (CP)

A
  • Umbrella term to desribe non-progressive movement disorders due to brain damage acquired in utero, during birth, or in infancy
  • Brain damages decreases the brain’s ability to monitor/control nerve/voluntary muscle activity
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10
Q

CP etiology

A
  • Can occur in utero or secondary to hypoxia, maternal infections, drug/alcohol abuse, placental abnormalities, toxemia, prolonged labor, prematurity, and Rh incompatiability
  • Cases vary in severity and intellectual disability may be seen in severe cases
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11
Q

Causes of Acquired CP (3)

A

meningitis, CVA, seizures, and brain injury

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12
Q

CP motor patterns (mix patterns exist!) (2)

A

1) Spastic CP

2) Athetoid CP

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13
Q

Spastic CP

A

UMN lesion in motor cortex

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14
Q

Athetoid CP

A

Basal ganlia lesion

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15
Q

Possible distrubtions of CP involvement (4)

A

1) Monoplegia: one extremity
2) Diplegia: Bilateral lower extremity involvement
3) Hemiplegia: unilateral UE/LE involvement
4) Quadraplegia: entire body involved

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16
Q

CP Treatment

A
  • Lifelong process
  • Normalization of tone
  • stretching
  • strengthening
  • motor learning
  • developmental milestones
  • positioning
  • weight bearing activities
  • mobility skills
  • splinting/AD/specialized seating
  • possible surgical intervention to reduce spasticity
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17
Q

Down Syndrome

A

Extra third 21st chromosome (trisomy 21)

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18
Q

Down Syndrome Etiology

A

incomplete cell division at 21st pair of chormosomes due to nondisjunction, translocation, or mosaic classification

19
Q

Down Syndrome s/sx (8)

A
  • intellectual disability
  • hyoptonia/joint hypermobility
  • flattened facial features
  • almond-shaped eyes
  • flat feet
  • scoliosis
  • congenital heart disease**
  • visual/hearing loss
20
Q

Down Syndrome treatment

A
  • emphasize exercise and fitness, stability
  • maximize respiratory function
  • family/caregiver education
  • possible surgical intervention for cardiac abnormalities
21
Q

Duchenne Muscular Dystrophy (DMD)

A
  • progressive disorder caused by absence of gene required to produce muscle proteins (dystrophin and nebuilin)
  • Fat/CT eventually replace muscle
  • Typically die in teens due to cardiopulmonary failure
22
Q

DMD etiology

A
  • Genetic disorder**- x-linked recessive trait

- mother is “silent carrier” and only males will manifest the disease

23
Q

DMD s/sx

A
  • Symptoms usually manifest between 2-5 years old
  • progessive weakness
  • Falling
  • toe walking
  • excessive lordosis
  • pseudohypertophy of muscle groups (calf)**
  • Progressive impairment with ADLs and mobility around age 5 => eventual inability to walk
24
Q

DMD PT treatment

A
  • respiratory function
  • submax exercise**
  • mobility skills
  • splinting
  • orthotics
  • adaptive equipment
  • family/caregiver education
  • med management: immunsuppresants, steroids
25
Q

Prader-Willi Syndrome diagnosis

A

Diagnosed by physical attributes and behavior patterns

26
Q

Prader-Willi Syndrome Etiology

A

Partial deletion of chromosome 135

27
Q

Prader-Willi Syndrome s/sx (physical and behavioral)

A
  • Physical characteristics: small hands, feet, and sex organs, hyotonia, almond-shaped eyes, obesity, incoordination, intellectual disability
  • Behavioral characteristics: constant desire for food*
28
Q

Prader-Willi Syndrome Treatment

A
  • Postural control
  • Exercise and fitness
  • Gross and fine motor skills training
29
Q

Spina Bifida

A

Developmental abnormality d/t failure of neural tube closing by 28th day of gestation

30
Q

Spina Bifida Etiology

A

Multiple factors, but attributed to insufficient folic acid intake by mother

31
Q

Spina Bifida Classfications (2)

A

1) Spina Bifida Occulta

2) Spina Bifida Cystica

32
Q

Spina Bifida Occulta

A
  • Non-fusion of the spinous processes of vertebrae, but spinal cord and meninges stay intact
  • No associated disability
33
Q

Spina Bifida Cystica

A
  • Cyst-like protrusion through the unfused vertebrae

- Results in impairment; worse prognosis than SB Oculta

34
Q

Forms of Spina Bifida Cystica (2)

A

1) Spina Bifida Cystica Meningocele

2) Spina Bifida Cystica Myelomeningocele

35
Q

Spina Bifida Cysta: Meningocele

A
  • Herniation of meninges and CSF and meninges into a sac that protrudes through the vertebral defect
  • Spinal cord remains within the canal
36
Q

Spina Bifida Cystica: Myelomeningocele

A
  • Severe form
  • Herniation of meninges, CSF, and spinal cord extending through defect in the vertebrae
  • Cyst may or may not be covered in skin
37
Q

Spina Bifida Cystica: Myelomeningocele s/sx

A
  • motor loss bleow level of defect in spinal cord
  • sensory deficits
  • hydrocephalus**
  • Arnold-Chiari Type II malformation
  • osteoporosis
  • clubfoot**
  • scoliosis
  • tethered cord syndrome
  • latex allergy**
  • bowel/bladder dysfunction
  • learning disabilities
38
Q

Spina Bifida Treatment

A
  • Family education
  • Facilitation of developmental milestones
  • Skin care
  • Strengthening
  • Balance and mobility training
  • Adaptive Equipment
  • Splinting
  • Orthotic prescription
  • Wheelchair prescription
39
Q

Spinal Muscular Atrophy (SMA)

A

Progressive degeneration of the anterior horn cells

40
Q

SMA Etiology

A

Autosomal recessive inheritance (mutation of chromosome 5)

41
Q

Types of SMA (3)

A

1) Acute Infntile SMA: life expectancy < 1 year
2) Chronic Childhood SMA: Steady impairment, though child can survive into adulthood
3) Juvenile SMA: Occurs later in childhood (4-17), typically survive into adulthood

42
Q

SMA s/sx (same regardless of type)

A
  • Vary in onset/speed of progression
  • Progressive muscle weakness and atrophy
  • Diminished/absent DTRs
  • End-stage respiratory compromise**
  • Sensation and cognition unimpaired**
43
Q

SMA treatment

A
  • Sesnsory stimulation

- Supportive care: family education, mobility training, use of AD/equipment

Neuro Boards (18 decks)

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