Course:KIN366/ConceptLibrary/IllicitSubstanceAbuse

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Movement Experiences for Children
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KIN 366
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Instructor: Dr. Shannon S. D. Bredin
Email: shannon.bredin@ubc.ca
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Illicit substances include drugs such as cocaine, opiates, amphetamines, and cannabis. Usage of these drugs during pregnancy has been known to cross the placenta and cause negative consequences for the fetus that include cognitive, behavioral, and motor developmental delays. Substance use during pregnancy has also been linked to increased risk of various medical and obstetrical complications such as spontaneous abortions, premature labor and births, and postpartum hemorrhages among others (Finnegan, 2013). Though evidence for developmental restraints has increased dramatically over the past century, the rate of substance abuse has not decreased, but has even been on a rise (Finnegan, 2013).

Prevalence

According to a study done by Iqbal et al. (2002), out of the 4.1 million women of childbearing age who abuse drugs in the United States, approximately 3% continue their drug use during pregnancy. Based on estimates from the National Survey on Drug Use and Health (NSDUH), approximately 222,000 infants prenatally exposed to illegal drugs are born each year (National Institute on Drug Abuse, 2005). Though there is a significant decrease in rates of usage, the consequences and effects on the fetus are profound, making it imperative that the prevalence rate is lowered even further.

Confounding Factors and Limitations to Research

Studies with substance abuse in pregnant women show many limitations, where effects on the infant’s development is influenced by various factors such as the type of substance, frequency and exposure, as well as timing of usage during pregnancy (Carta et al., 2001; Covington et. al., 2002; Singer et. al., 2004).

Studies have also found that illicit substance abuse during pregnancy has dose-dependent effects on infant development – meaning the higher and longer the duration of exposure, the more severe the consequences (Singer et al., 2004; Lewis et al., 2004).

One major limitation is that most current academic research includes data from predominately African American woman from lower socioeconomic backgrounds (Covington et al., 2002; Singer et. al., 2004). A wide all-encompassing data of pregnant women from different socioeconomic and racial backgrounds is lacking, making it difficult to generalize research results with much certainty (Kim and Krall, 2006).

Women engaging in illicit drug abuse during pregnancy tend to be using more than one drug within the same period, increasing the limitations to understanding the effects and mechanisms of each individual drug (Kim and Krall, 2006; Finnegan, 2013; Wendell, 2013). Using a combination of drugs has been known to cause synergistic effects that could exacerbate the negative consequences in fetal development (Wendell, 2013). Mixing certain drugs such as heroin and cocaine during pregnancy shows increased developmental delay as well as increased withdrawal symptoms in the infant immediately after birth (Wendell, 2013).

Mechanism and Effects for Different Drugs

Cocaine

As one of the most extensively studied substances, cocaine has been infamously known to have negative effects, resulting in “brain damaged” infants and children “oblivious to affection” (Finnegan, 2013). Cocaine is a potent natural stimulant, which works in the body by blocking the central reuptake of dopamine, serotonin, and norepinephrine, as well as peripheral reuptake of norepinephrine (Komiskey et al., 1997; Pitts and Marwah, 1987). Due to its low molecular weight and high lipid solubility, cocaine is easily diffused across the placenta, blood-brain barrier, as well as transferred in breast milk, increasing the infant’s susceptibility (Simone et al., 1994). Cocaine has vasocontrictive properties, which may result in a variety of potentially detrimental effects including increased maternal blood pressure, increased uterine contractility, and decreased uterine blood flow (Nass and Frank, 2010). These effects could lead to increased risks of fetal hypoxia, spontaneous abortion, premature labor, low birth weight, and still birth (Finnegan, 2013; Nass and Frank, 2010). The relative risk for development delay is approximately 40 times higher for infants exposed to cocaine than for infants not exposed to drugs in utero (Schneider & Chasnoff, 1992). Infants prenatally exposed to cocaine usually exhibit motor developmental delays such as poor quality of movements, fine motor movement, increased muscle tone, poor primitive reflexes, and poor rotational movements (Finnegan, 2013; Nass and Frank, 2010; Schneider & Chasnoff, 1992). Cocaine exposure has also been linked to lower arousal, poor self-regulation, and poor executive functioning, potentially due to delayed brain development caused by neurological damage and decreased placental blood flow in the fetus (Schneider & Chasnoff, 1992; Behnke and Smith, 2013; Finnegan, 2013). A combination of physiological and cognitive effects such as increased muscle tonicity, persistence of primitive reflexes, and poorer control of attention may account for the infant’s delay in development of volitional motor movements (Schneider & Chasnoff, 1992; Behnke and Smith, 2013; Finnegan, 2013). Developmental delays, motor deficits, and other effects such as height deficits are still significant at 12 months and could persist until middle childhood (Finnegan, 2013; Beveren, Little, & Spence, 2000). These infants may also suffer from seizures, which could limit their ability to reach motor milestones (Beveren, Little, & Spence, 2000).

Amphetamines and Methamphetamines

Infants exposed to amphetamines prenatally showed higher risk for delays in cognitive development, gross motor development, as well as a longer timeline for reaching motor milestones (Rattue, 2012). Amphetamines such as ecstasy work in the body by depleting the level of serotonin, which is a neurotransmitter important for many brain functions, including gross motor control (Rattue, 2012). Serotonin is crucial for brain formation in early fetal development and regulating sleep cycles and mood states. Fluctuations in the level of serotonin can result in long-term effects on learning, memory, and motor development (Rattue, 2012; Finnegan, 2013). Amphetamines have been shown to inhibit the release of prolactin, which could potentially reduce and taint the mother’s supply of breast milk, increasing infants’ susceptibility of substance (Finnegan, 2013). Methamphetamines are an even more potent stimulant drug, with studies showing detrimental effects on the infant with as few as just one dose during pregnancy (Adlaf et al., 2005). Methamphetamines are also known to cause fetal growth restrictions such as reduced head circumference, length and birth weight, amongst other medical complications (Adlaf et al., 2005). The mechanism of these growth restrictions are thought to be caused by the constriction of blood vessels in both mother and fetus as a consequence of methamphetamines, which results in drastically decreasing nutrient delivery to the fetus and increased fetal blood pressure (Burchfield et al., 1991; Stek et al., 1995). These growth delays result in limitations and obstacles in the way of motor development of the child (Finnegan, 2013).

Opiates

Opiates are a broad umbrella term that refers to chemical substances derived from the opium poppy such as heroin, methadone, and oxycodone (Finnegan, 2013). Due to this drug’s pain relief properties, opiates are some of the most common drugs used during pregnancy, with prevalence rates increasing at alarming rates especially among teenagers and young adults (Finnegan, 2013). Heavy opiate abuse has been shown to result in severe neurological consequences including attention span, memory, and verbal fluency (Guerra et al., 1987; Kamboj et al., 2005). Opiate exposed infants also show increased rates of developmental delays such as shorter length and smaller head circumference at birth, with lower heights persisting through toddlerhood (Finnegan, 2013; Hunt et al., 2008). Height could present constraints and limitations to motor development and development of movement skills.

The most prominent medical issues in infants linked to heroin abuse are low birth weights and prematurity, though these deficiencies could be countered if the mother undergoes methadone maintenance treatment during pregnancy (Finnegan, 2013). Methadone is a synthetic opiate that is used for treatment, and works by preventing fluctuating of maternal drug use and minimizes repeated intoxication and withdrawal effects in drug-exposed infants (Kaltenbach et al., 1998). Untreated heroin-addicted pregnant women have been associated to higher rates of birth complications such as miscarriages as well as nutritional deficiencies that could be problematic for the developing fetus (Finnegan, 1976). This discrepancy in height may result in limitations and obstacles for motor development.

Cannabis

Maternal tobacco smoking can have a dose-response effect on reduced birth weight, increased rates of birth complications such as placenta previa and placental infarcts, and poor oxygen delivery response to the fetus (Godding et al., 2004). Infants exposed to tobacco prenatally also display higher rates of hypertonia, which severely disrupts motor development in children (Godding et al., 2004).

Marijuana smoking produces five times higher carbon monoxide levels, which increases the severity of consequences for the fetus compared to tobacco (Chiriboga, 2003). The higher carbon monoxide levels are also hypothesized to be the main driving mechanism for disrupting fetal development (Chiriboga, 2003). Cannabinoids, the principle psychoactive substance in cannabis, crosses the placenta while it circulates in the mother’s body for up to 30 days before excretion (Abel, 1985). Due to the longer period of time the drug stays in the mother’s body for, the severity of effects increases as a product of prolonged fetal exposure (Abel, 1985). Cannabinoids can also be transferred from the mother to the infant through breastfeeding (Abel, 1985; Finnegan, 2013). The development of dopamine pathways in the infant may also be altered by cannabis exposure, in turn lowering their coordination skills and ability to initiate movements (Rodriguez de Fonseca et al., 1991).

Infants exposed to marijuana prenatally have been linked to an increase in body motility, tremors, startles, and abnormal reflexes during the neonatal period (Fried and Makin, 1987). These factors could act as limitations and hindrances for developing fine and gross motor skills. These infants are also typically smaller in size, increasing its vulnerability to other medical issues (Finnegan, 2013; Fried and Makin, 1987).

Practical Application

Techniques for Working with Drug Exposed Infants

Drug-exposed infants and children may exhibit certain personality traits and characteristics such as having heightened reactions and emotions (Landdeck-Sisco, 1997). It is important to provide a calm and comfortable environment for these infants to learn: such as avoiding the use of loud voices, harsh lighting, as well as frequent and fast transitions between activities (Landdeck-Sisco, 1997). Being aware and conscious of fluctuations in the infant’s behavior and state is key to resolving distress or escalated emotions (Landdeck-Sisco, 1997). Predictive and regular use of special care techniques such as swaddling blankets around the infant, massaging, and holding the infant could promote developmental abilities and encourage the child to develop self-control and self-calming behaviors (Landdeck-Sisco, 1997). When facilitating learning in infants, it is beneficial to gradually increase the amount and time of daily developmental activities as opposed to overwhelming them with too many activities (Landdeck-Sisco, 1997). If the child displays frequent temper tantrums, it may be helpful to remain calm and encourage the child to use words to describe their emotions (Landdeck-Sisco, 1997). Offering supportive verbal reassurance, eye contact and physical comfort such as rubbing their back could be beneficial in helping the child gain control of their emotions and behaviors (Landdeck-Sisco, 1997).

Tremors when Stacking and Reaching

If the child exhibits tremors, it would be beneficial to observe the child and take note of the tremor onset, the duration, and ways in which the child compensates for them in order to track progress and understand behavior (Landdeck-Sisco, 1997). Providing the child with a variety of materials and objects such as stacking toys, large blocks, and puzzles to play with can enhance the development and refinement of their fine motor movement skills (Landdeck-Sisco, 1997).

Difficulty with Gross Motor Skills

Infants exposed to drugs prenatally exhibit atypical traits of motor development such as increased muscle tone, worsened reflexes and volitional moving, as well as poorer overall quality of movements (Nass and Frank, 2010; Schneider & Chasnoff, 1992; Finnegan, 2013). These biological predispositions heavily influence these infants’ ability to develop gross motor skills. With these difficulties, it is beneficial to provide infants with appropriate motor activities for practice through means of playing, accompanied with songs, or with equipment for motivation (Landdeck-Sisco, 1997). Offering guidance, verbal cues and scaffolding would also help the child gain and specialize motor movement skills (Landdeck-Sisco, 1997).

References

  1. Abel, E.L. (1985) Effects of prenatal exposure to cannabinoids. In T.M. Pinkert (ed) Current Research on the Consequences of Maternal Drug Abuse. National Institute on Drug Abuse Research Monograph No. 59. Rockville, MD: U.S. Department of Health and Human Services.
  2. Adlaf, E.M., Begin, P., & Sawka, E. (Eds.). (2005). Canadian Addiction Survey: A national survey of Canadians use of alcohol and other drugs: Prevalance and use and relative harms. Ottawa: Canadian Centre on Substance Abuse.
  3. Behnke, M., & Smith, V. (2013). Prenatal Substance Abuse: Short-Effects on the Exposed Fetus, 131 (3). American Academy of Pediatrics.
  4. Beveren, T. T., Little, B. B., & Spence, M. J. (2000). Effects of prenatal cocaine exposure and postnatal environment on child development. American Journal of Human Biology, 12, 417-428. doi:10.1002/(SICI)1520-6300(200005/06)12:3<417::AID-AJHB12>3.0.CO;2-C
  5. Burchfield, D.J., Lucas, V.W., Abrams, R.M., Miller, R.L., & DeVane, C.L. (1991). Disposition and pharmacodynamics of methamphetamine in pregnant sheep. Journal of the American Medical Association, 265, 1968–1973.
  6. Carta, J. J., Atwater, J. B., Greenwood, C. R., McConnell, S.R., McEvoy, M. A., & Williams, R. (2001). Effects of cumulative prenatal substance exposure and environmental risks on children’s developmental trajectories. Journal of Clinical Child Psychology, 30(3), 327-337.
  7. Chiriboga, C. (2003). Administration 101: Evaluation of a Professional Development Program. New Directions for Community Colleges, 2003(123), 73-81. doi:10.1002/cc.123
  8. Covington, C. Y., Nordstrom-Klee, B., Ager, J., Sokol, R., & Delaney-Black, V. (2002). Birth to age 7 growth of children prenatally exposed to drugs: A prospective cohort study. Neurotoxicology and Teratology, 24, 489-496.
  9. Finnegan, L. (2013). Licit and Illicit Drug Use During Pregnancy: Maternal, Neonatal and Early Childhood Consequences. Retrieved from Canadian Center on Substance Abuse website: http://www.ccsa.ca/Resource%20Library/CCSA-Drug-Use-during-Pregnancy-Report-2013-en.pdf
  10. Finnegan, L.P. (1976). Clinical effects of pharmacologic agents on pregnancy, the fetus and the neonate. Annals of the New York Academy of Sciences, 281, 74.
  11. Fried, P. A., & Makin, J. E. (1987). Neonatal behavioral correlates of prenatal exposure to marihuana, cigarettes and alcohol in a low risk population. Neurotoxicology and Teratology, 9(1), 1-7. doi:10.1016/0892-0362(87)90062-6
  12. Godding, V., Bonnier, C., Fiasse, L., Michel, M., Longueville, E., Lebecque, P., … Galanti, L. (2004). Does in utero exposure to heavy maternal smoking induce withdrawal symptoms in neonates? Pediatric Research, 55(4), 645–651.
  13. Guerra, D., Sole, A., Cami, J., & Tobena, A. (1987). Neuropsychological performance in opiate addicts after rapid detoxification. Drug and Alcohol Dependence, 20, 261–270.
  14. Hunt R.W., Tzioumi D., et al. (2008). Adverse neurodevelopmental outcome of infants exposed to opiate in-utero. Early Human Development 2008; 84(1):29-35
  15. Iqbal, M.M., Sobhan, T., & Ryals, T. (2002). Effects of commonly used benzodiazepines on the fetus, the neonate, and the nursing infant. Psychiatric Services, 53(1), 39–49.
  16. Kaltenbach K., Berghella V. et al. (1998). Opioid dependence during pregnancy. Effects and management. Obstetrics and Gynecology Clinics of North America 1998; 25(1): 139-151
  17. Kamboj, S.K., Tookman, A., Jones, L., & Curran, H.V. (2005). The effects of immediate-release morphine on cognitive functioning in patients receiving chronic opioid therapy in palliative care. PAIN, 117, 388–395.
  18. Kim, J., & Krall, J. (2006). Literature Review: Effects of Prenatal Substance Exposure on Infant and Early Childhood Outcomes. National Abandoned Infants Assistance Resource Center. Retrieved from http://aia.berkeley.edu/media/pdf/prenatal_substance_exposure_review.pdf
  19. Komiskey HL, Miller DD et al. (1997). The isomers of cocaine and tropacocaine: effect on 3H-catecholamine uptake by rat brain synaptosomes. Life Sciences 1977; 21(8): 1117-1122
  20. Landdeck-Sisco, J. (1997). Children with Prenatal Drug and/or Alcohol Exposure(Factsheet 49). Retrieved from ARCH National Resource Center for Respite and Crisis Care Services website: https://www.utdcfsadopt.org/arch_49.shtml
  21. Lewis, M. W., Misra, S., Johnson, H. L., & Rosen, T. S. (2004). Neurological and developmental outcomes of prenatally cocaine-exposed offspring from 12 to 36 months. The American Journal of Drug and Alcohol Abuse, 30(2), 299-320.
  22. Nass, R. D., & Frank, Y. (2010). Prenatal Drug Exposre. In Cognitive and behavioral abnormalities of pediatric diseases (pp. 588-597). New York: Oxford University Press.
  23. National Institute on Drug Abuse. (2005). NIDA InfoFacts: Pregnancy and drug use trends. Retrieved February 22, 2015, from http://www.nida.nih.gov/Infofacts/pregnancytrends.html
  24. Pitts D.K., Marwah J. (1987). Cocaine modulation of central monoaminergic neurotransmission. Pharmacology, Biochemistry, and Behavior 1987; 26(2): 267-277
  25. Rattue, P. (2012, March 2). Prenatal Exposure To Ecstasy Linked To Developmental Delays. Medical News Today. Retrieved February 26, 2015, from http://www.medicalnewstoday.com/articles/242438.php
  26. Rodiguez de Fonseca, F., & Hernandez, M. L. (1991). Early changes in the development of dopaminergic neurotransmission after maternal exposure to cannabinoids.Pharmacological, Biochemical, and Behavioral Science, 41(3), 469-474. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/1350099
  27. Schneider, J., & Chasnoff, I. (1992). Motor assessment of cocaine/polydrug exposed infants at age 4 months. Neurotoxicology and Teratology, 14(2), 97-101. doi:10.1016/0892-0362(92)90057-H
  28. Simone C., Derewlany L. O., et al. (1994). Transfer of cocaine and benzoylecgonine across the perfused human placental cotyledon. American Journal of Obstetrics and Gynecology 1994; 170(5 pt1_: 1404-1410.
  29. Singer, L. T., Minnes, S., Short, E., Arendt, R., Farkas, K., Lewis, B. et al. (2004). Cognitive outcomes of preschool children with prenatal cocaine exposure. JAMA, 291, 2448-2456.
  30. Stek, A.M., Baker, R.S., Fisher, B.K., Lang, U., & Clark, K.E. (1995). Fetal responses to maternal and fetal methamphetamine administration in sheep. American Journal of Obstetrics and Gynecology, 173, 1592–1598.
  31. Wendell, A. (2013). Overview and Epidemiology of Substance Abuse in Pregnancy.Clinical Obstetrics and Gynecology, 56(1), 91-96. doi:10.1097/GRF.0b013e31827feeb9
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