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ABCN Clinical Neuropsychology > In-utero Toxic Exposure > Flashcards

In-utero Toxic Exposure Flashcards

1
Q

FASD structural brain anomalies

A
  • Microcephaly
  • Migrational anomalies
  • Reductions in frontal, parietal, and temporal lobes volumes
  • White matter hypoplasia > gray matter hypoplasia.
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2
Q

The following four criteria must be met for a medical FAS diagnosis…

A

Growth Deficiency - below average height and/or weight

Craniofacial Features:
- short palpebral fissures (eye width decreases with increased prenatal alcohol
exposure)
-flat midface
- a short upturned nose
- smooth or long philtrum
(the ridges running between the nose and the lip)
- thin vermilion (the upper lip thins with increased prenatal alcohol exposure)

Central Nervous System Dysfunction:
- Structural abnormalities
- Hard neurologic signs (e.g., seizures)
- Functional abnormalities (e.g., cognitive, EF/attention, memory)

Prenatal Alcohol Exposure - confirmed or unknown prenatal alcohol exposure

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3
Q

FAS prevalence

A

global prevalence - 10%
US <1%

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4
Q

Risk of FAS in each trimester

A

First trimester drinking increases the likelihood of FASD 12x; drinking during the first and second trimester increases the likelihood of FASD 61x, and drinking in all three trimesters increases the likelihood of FASD 65x.

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5
Q

FAS neuropsychological expectations

A

ID (25%) FAS and (10%) ARND

ADHD (60–95%)

Verbal learning and memory deficits

Behavior: impulsive, disruptive, aggressive, delinquent, poor social judgement (increased ODD, CD, and OCD)

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6
Q

In utero exposure to cocaine may lead to abnormalities in the…

A

frontocingulate cortex, including the anterior cingulate gyrus.

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7
Q

Cocaine exposure: neuro expectations

A

Lower IQ
Attention/processing speed/EF
Verbal > visuospatial
Behavior: impulsive and display poor emotional control.

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8
Q

Prenatal cannabis exposure (PCE) has been found to be associated with…

A

fetal growth restriction and lower birthweight.

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9
Q

Neuropathology of regular marijuana use

A
  • reduced visual maturation and visual attentiveness
  • heightened tremors
  • exaggerated startle and visual responses
  • poor habituation to novel stimuli,
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10
Q

common drug use during pregnancy

A

alcohol > tobacco > cannabis

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11
Q

Marijuana use: neuro expectation

A
  • No IQ but academic underperformance
  • Attention/EF deficits
  • Verbal > visual
  • Behavior: delinquency, mood, and behavior dysregulation
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12
Q

Mercury’s harmful effects to the fetus include …

A

brain damage, intellectual disability, poor motor coordination, blindness, seizures, and inability to speak.

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13
Q

Lead exposure neuro expectation

A

EF
visuospatial skills
Increased: ADHD, ODD

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14
Q

Nicotine/Tobacco exposure neuro expectation

A

Increased ADHD

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15
Q

Amphetamine neuro expectation

A
  • Motor deficits during infancy
  • Deficits in executive functions during childhood
  • Poor emotional regulation
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16
Q

Opiates neuro expectation

A

Motor deficits during infancy with later deficits in executive functions and ADHD symptoms during childhood.

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17
Q

Antiepileptic meds (Valproic acid)

A

1st trimester - major anatomical birth defects
3rd trimester - cognitive and behavioral deficits

Exposure to Valproic acid has been linked to verbal deficits, as well as increased risk for ADHD and ASD.

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18
Q

In utero exposure to many toxic substances, namely lead and cocaine, appears to affect the developing CNS via its actions on what neurotransmitter?

A

Dopamine

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19
Q

Prenatal alcohol consumption affect on brain development in utero

A

during the first and second trimester interferes with neuronal migration and proliferation,

third trimester leads to structural damage to the cerebellum, hippocampus, and prefrontal cortex

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20
Q

In utero Exposures associated with visual/spatial deficits

A

Cocaine
Lead
Marijuana

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21
Q

Likely MRI finding from child with severe in-utero exposure to alcohol:

A

greater white matter than gray matter hypoplasia. Temporal lobes were more affected than temporal or occipital lobes.

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22
Q

Neuropathology of Prenatal Alcohol Exposure

A
  • Alterations in size and structure in brain regions.
  • During 1st and 2nd trimester, interferes with migration, proliferation, and organization of brain cells –> results in craniofacial and brain malformations.

-During 3rd trimester–> damage to cerebellum, hippocampus, and prefrontal cortex.

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23
Q

Neurochemical effects of alcohol

A
  1. Increased turnover of norepinephrine and dopamine
  2. Decreased transmission in acetylcholine systems
  3. Increased transmission in gamma-aminobutyric acid (GABA) systems
  4. Increased production of beta-endorphin in the hypothalamus
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24
Q

Structural brain anomalies associated with FASD

A

microcephaly

Migrational anomalies (e.g., heterotopias)

Disproportionate reductions in gray and white matter volumes, particularly in frontal, parietal, and temporal lobes.

White matter hypoplasia > gray matter hypoplasia.

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25
Q

General incidence of FAS

A

2x higher in the U.S. than other countries.

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26
Q

Facial Dysmorphology Characteristic of FAS

A

Associated features:
-Low nasal bridge
-Minor ear anomalies
-Epicanthal folds
-Small jaw

Discriminating Features:
- short palpebral fissures
- Short nose
- Flat mid-face
-indistinct philtrum
- thin upper lip

27
Q

Diagnostic criteria for FASD

A
28
Q

Alcohol Related Effects

A
29
Q

Determinants of Severity of FAS

A
  1. Quantity (Dose) Consumed –> High risk (> 100 mg/DL delivered at least weekly in early pregnancy or 6-8 beers in one sitting), some risk, unknown risk, or no risk.
  2. Pattern of Exposure –> Chronic consumption (4-5 drinks daily, binge drinking)
  3. Timing of Exposure –> 1st trimester increases the likelihood of FASD by 12x; drinking in the 2nd trimester increased by 61x; drinking in 3rd trimester increased by 65x
  4. Additional Risk factors:
    - polydrug use
    - higher maternal age
    - maternal mental health issues
    - lower education level
    - reduced access to prenatal and postnatal care and services
    - inadequate nutrition
    - environment that includes stress, abuse, and/or neglect.
30
Q

What are the lifelong neurocognitive and behavioral problems with FASD?

A
  • School failure/greater likelihood to drop out of school
  • inability to secure and hold employment
  • mental health issues
  • delinquency
31
Q

Comorbid diagnosis with FASD

A

ADHD

Conduct Disorder

ODD

OCD

32
Q

What are the main protective factors from FASD?

A

Early diagnosis – UNIVERSAL protective factors.

Services

Living in a stable home

Protection from violence (e.g., witnessing or being victimized).

33
Q

Neuropsychological Profile of FASD

A

Intelligence
- IQ ranges from 20 to 120, with average between 65-72.
- children w/dysmorphic features = lower IQ
- learning difficulties, poor judgment, and behavioral problems are common with and/or without ID
- Deficits in reading, spelling, and math

Attention/concentration
- 60-95% meet criteria for ADHD
- sig. deficits in sustained visual and auditory attention

Processing Speed
- slower reaction time
- reduced cognitive efficiency, esp. on more complex tasks

Speech/language
- deficits in oral-motor function and speech production due to facial abnormalities
- difficulties with naming, expressive + receptive language, and comprehension of complex language

Visuospatial
- difficulty analyzing hierarchical visual stimuli, and associated with motor deficits

Memory
- verbal learning and memory are impaired, mainly due to issues with acquiring new information rather than retaining it
- visual memory findings are inconsistent
- impaired spatial recall

EF
- wide spread

Sensorimotor
- delayed motor development and fine motor deficits, including tremors, poor coordination (linked to cerebellar dysfunction)
- sensory integration problems and issues with balance.

Emotion/personality
- impulsive
- disruptive
- socially disinhibited behaviors with poor social judgement
- higher rates of internalizing and externalizing behaviors
- sleep disturbance

34
Q

Neuropathological effects of cocaine in utero

A

effects on the monoamine system, esp. dopamine.

Early exposure effects gestation –> neural proliferation migration

Later exposure –> neural maturation and synpatomgenesis.

Abnormalities in the frontocingulate cortex, including the ACC.

35
Q

Cocaine in utero Epidemiology

A

~0.5 to 3% women use cocaine while pregnant.

born will small head circumference and low birthweight.

36
Q

Neurobehavioral abnormalities with in utero cocaine exposure

A

poor sleep cycles

abnormal startle response

abnormal brainstem evoked potentials

toddlers/preschoolers show impulsivity and emotional lability

37
Q

Neuropsychological profile of in utero cocaine exposure

A

Intelligence:
- lower IQ overall
- deficits in academic achievement due to environmental variables

Attention/concentration
- sustained attention and selected attention

Processing Speed
- slower reaction times on continuous performance tasks, but could be due to poor attention regulation

Language
- expressive language delay

visuospatial
- perceptual organization

Memory
- deficits in working memory

EF
- perseveration, disinhibition, and poor task orientation

Emotion/personality
- impulsive
- display poor emotional control
- frustrated in novel setting

38
Q

What is the primary target for THC in the brain?

A

Cannabinoid Receptor Type I

Associated with the mesocorticolimbic dopamine

39
Q

Endocannabinoid System

A

Exists at all stages of pregnancy, and therefore have many vulnerability points.

Prenatal cannabis exposure (PCE) –> associated with fetal growth restriction in mid and late pregnancy, lower birthweight, increase birth defects, increased stillbirth, altered sleep patterns, cause delay in infant visual maturation and visual attentiveness.

40
Q

Most consistent and visible consequences of prenatal cannabis exposure

A

heightened tremors
exaggerated startle response
poor habituation to novel stimuli
exaggerated moro reflex
increased athetoid movements
disinhibition in number of motor tests

41
Q

Determinants of severity in Marijuana use

A

poly drug use
low SES
maternal mental health
exposure to violence
limited access to medical and social services

42
Q

Neuropsychological profile of prenatal marijuana exposure

A

intelligence
- does not affect IQ
- lower performance in reading, math, and spelling (esp. with heavy exposure during 1st trimester)

Attention/concentration
- increased hyperactivity
- inattention
- impulsivity (esp. in the 1st and 3rd trimester)

EF
- deficits in top-down processing including issues with WM, attention, inhibition, self-regulation, and cognitive flexibility

Visuospatial skills
- Altered neural functioning in visuospatial WM
- deficits in visual memory, abstract reasoning, and visual-perceptual functioning

sensorimotor
- decreased visual habituation
- increased tremors
- no long term sensorimotor deficits by age 1

Emotion/personality
- increased risk for delinquent behaviors
- heightened vulnerability to neuropsychiatric disorder (e.g., schizophrenia)
- mood dysregulation, impulsivity, hyperactivity, and behavioral problems

43
Q

What are the common sources of mercury?

A

fungicides
pesticides
cosmetics
dental fillings
commercial thermometers
high efficiency compact fluorescent lightbulbs (CFL)

44
Q

What is the largest man-made source of mercury?

A

coal fired power plants

45
Q

What is the primary human exposure of mercury?

A

Eating fish with methylmercury

46
Q

Mercury is absorbed commonly in what body systems?

A

Neurologic

GI

renal systems

47
Q

What is the deadliest mercury compound?

A

dimethylmercury

Easily permeates into the skin, gets into the blood stream, deposited into the brain, kidneys, and other organs –> results in mercury poisoning.

Symptoms:
paresthesia
deterioration in fine motor coordination
restriction of the visual fields
progress to severe ataxia, dementia, and death

48
Q

Common exposures to Mercury

A

Consumptions of fish & shellfish

Vaccines –> Thimerosal

Dental Amalgams –> although recently concluded that it does not pose a serious health risk.

49
Q

Determinants of severity for Mercury

A

Linear dose-response relationship exists

Fetuses have greatest risk because of their inability to excrete mercury.

50
Q

What areas are most commonly affected in mercury exposure?

A

Cerebellum and occipital cortex.

Offspring of women with sig. mercury exposure have –> progressive cortical degenerative diseases, CP, ID, severe sensory deficits, microcephaly, and limb malformations.

51
Q

Polychlorinated Biphenyls (PCBs)

A

family or man-made organic chemicals of chlorinated hydrocarbons.

Commonly used in transformers, adhesives, tapes, plastic, rubber, oil - based pain, electrical devises, and carbonless paper.

52
Q

What is the principal route of exposure in PCBs?

A

maternal consumption of seafood before and during pregnancy.

Endocrine disruptors.

53
Q

Determinants of Severity in PCBs

A

Dose dependent associations exist between PCB level and neurobehavioral impairment.

Neurotoxic effects of PCBs on dopamine activity are potentiated by methylmercury.

54
Q

Neuropsychological profile for PCBs

A

Limited

reduced verbal abilities
deficits in EF

55
Q

Neuropathological effects from Lead (Pb)

A

Passes through the blood-brain into the CNS –> interferes with neurulation, migration, synaptogeneis, and neurotransmission.

May affect the dopamine system.

Decreased cerebral volume in the frontal gray matter, ACC, and prefrontal cortex.

decreased in N-acetylaspartate - to -creatine ratio (could be an indicator of neuronal loss).

56
Q

Signs of elevated Lead levels

A

headaches
irritability
abdominal pain
vomiting
weight loss
attention problems
hyperactivity
learning problems
slowed speech development

57
Q

Chelation Treatment

A

Used when lead levels are more than 44 μg/dL

uses dimercaptosuccinic acid to trap lead in the body and remove the lead through urine. This treatment is effective in reducing blood lead levels but is likely not effective in reversing cognitive or behavioral deficits.

58
Q

Neuropsychological profile of Lead exposure

A

Declines in IQ

EF (most common) > visuospatial

impulsive, inattentive, aggressive, internalizing + externalizing behaviors.

increased rates of ADHD and ODD.

59
Q

Effects of nicotine/tobacco exposure

A

lead to reduced fetal oxygen supply, fetal undernourishment, and vasoconstrictor effects on the placenta and umbilical cord.

Externalizing behaviors are common, esp. ADHD

60
Q

Amphetamines exposure

A

motor deficits in infancy

deficits in EF

poor emotion regulation.

61
Q

Opiate exposure in utero

A

predominately heroin –> can lead to decreases in neural plasticity and increased cell death. There is also an increased risk for lower birth weight.

Motor deficits > EF then ADHD

62
Q

Medication exposure prenatally

A

Anti-epileptic drugs –> In 1st trimester, will have major anatomical brith defects; in 3rd trimester, will have cognitive and behavioral defects.
*Valproic acid and polytherapy = significant risk

Blood thinners – developmental delay and Dandy-walker syndrome (congenital hydrocephalus)

Acne (accurate) –> birth defects and ID

SSRIs –> neonatal abstinence syndrome (NAS)

63
Q

Acrodynia

A

(“painful extremities”) is a rare disease that primarily affects young children exposed to mercury. It is often misdiagnosed in children as measles, other viral exanthems, or Kawasaki disease. Symptoms include irritability, photophobia, pink discoloration and edema of the hands and feet, hair loss, irritability, anorexia, insomnia, poor muscle tone, profuse sweating, and polyneuritis.

64
Q

Neonatal abstinence syndrome (NAS)

A

A nonspecific group of symptoms that can be displayed by some newborns whose mothers used illicit or prescription drugs during pregnancy.

Symptoms are variable –> excessive crying, irritability, hyperactive reflexes, seizures, and increased muscle tone.

ABCN Clinical Neuropsychology (34 decks)

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