You are leaving Medscape Education
Cancel Continue
Log in to save activities Your saved activities will show here so that you can easily access them whenever you're ready. Log in here CME & Education Log in to keep track of your credits.
 

Table 1.  

right brain regions – medial PFC, DLPFC and ventrolateral PFC
Age† Cohort‡ Category Results/outcomes Exposure
details
Ref.
Fetus
17–22 GW Growth Reduced foot length and bodyweight ≥0.4 J/day [48]
18–22 GW Dopamine signaling Decreased D2 mRNA in amygdala of males only ≥0.4 J/day [152]
18–22 GW Endorphin signaling Decreased opioid peptide (PENK) and receptor (κ) in caudal putamen and thalamus, respectively;
increased opioid receptor (µ) in the amygdala
[74]
Neonatal
Neonatal OPPS Neurobehavior Increased tremors, exaggerated startles and diminished responsiveness to light [46]
Neonatal MHPCD Growth Decreased body length ≥1 J/day, first
Trim
[49]
Neonatal Growth
Neurobehavior
No effect on birthweight, length or gestational age
No effect

[54]
Neonatal VIPS Growth No effect on birthweight, preterm delivery or abruptio placentae [35]
Neonatal Growth
Behavior
No effect on birthweight, length or gestational age
More irritable, less responsive to calming, increased jitters and startles

[52]
Neonatal NBDPS Growth No effect on birthweight, gestational age or preterm delivery [40]
1 mo Behavior Less irritable, more alert, more robust autonomic and motor systems, more autonomically stable and
increased orientation
≥2.86 J/day [54]
Toddler
8 mo MHPCD Growth No effect [49]
9 mo MHPCD Mental/motor skills Delayed mental development ≥1 J/day, third
Trim
[26]
1 y OPPS Mental/motor skills No effect [55]
1 y Mental/motor skills Decreased motor scores, no effect on mental development ≥0.5 J/day, first
Trim
[149]
19 mo MHPCD Mental/motor skills No effect [26]
2 y OPPS Mental/motor skills No effect [55]
3 y MHPCD Intelligence
Cognition
No effect on overall IQ for entire cohort
For African–Americans: decrease in short-term memory and verbal reasoning

≥1 J/day,
first/second Trim
[57]
3 y MHPCD Sleep and arousal Lowered sleep efficiency, more nocturnal arousals and more awake time after sleep onset [153]
Childhood
4 y Sustained attention Increased number of omission errors First Trim [45]
4 y MHPCD Motor skills No effect on balance and coordination skills [154]
5–6 y OPPS Cognition and
language
No effect [155]
6 y MHPCD Growth No effect [156]
6 y OPPS Memory
Attention
Behavior
No effect
Increased number of omission errors
Described as more impulsive and hyperactive
≥0.86 J/day [58]
6 y MHPCD Impulsivity
Sustained attention
Decrease in errors of omission
Lower overall composite score
Second Trim [60]
6 y MHPCD Intelligence
Cognition
Lower overall composite score
Lower verbal reasoning, quantitative reasoning and short-term memory
≥1 J/day,
first/second Trim
[59]
9–12 y OPPS Reading and language No effect in regards to reading or language [68]
9–12 y OPPS Intelligence
Executive function
No effect in terms of full scale IQ
Impulse control and visual hypothesis aspects are negatively impacted

> 0.86 J/day
[63]
Adolescence
10 y MHPCD Behavior and emotion
Behavior and emotion
Fewer internalizing problems, although not correlated with teacher’s report
Predicted lower scores in design memory and screening index
≥0.4 J/day
second Trim
≥0.89 J/day,
first Trim
[47]
10 y MHPCD Learning and memory
Sustained attention
Predicted lower scores in design memory and screening index
Increase in errors of commission
≥0.89 J/day,
first Trim
≥0.89 J/day,
second Trim
[47]
10 y MHPCD Depression Increased levels of depressive symptoms >0.89 J/day,
first/third Trim
[64]
12 y Psychotic symptoms No effect [66]
10–14 y Volumetric MRI No effect on cortical gray matter volume, white matter volume, cerebral spinal fluid or
parenchymal volume
[69]
10 y

14 y
MHPCD Behavior and
cognition
Delinquent behaviors
Negatively associated with depressive symptoms, IQ, learning and memory

Increased delinquent behaviors
≥0.89 J/day,
first/second Trim
≥0.89 J/day
[61]
13–16 y OPPS Sustained attention Decreased stability of attention over time ≥0.86 J/day [71]
13–16 y OPPS Growth No changes in weight, height or puberty symptoms [157]
13–16 y OPPS Visual memory Lower scores in abstract designs and Peabody spelling ≥0.86 J/day [27]
16 y MHPCD Fine motor
coordination
Visual–motor
coordination
Various light deficits in processing speed and interhemispheric motor coordination

Slight increase in visual–motor coordination
≥2 J/mo [158]
Young adult
18–22 y OPPS Response inhibition
Response inhibition
by fMRI
Intelligence
Working memory
by fMRI
Slightly more errors of commission
Increased bilateral PFC activity, right premotor cortex activity; decreased activity in left cerebellum

No effect
Increased activity in left medial PFC, inferior frontal gyrus and left cerebellum; decreased activity in




[72]



[73]

Prenatal Marijuana Exposure Studies in Humans

†Exposed offspring study age.
‡Specified conditions of prenatal exposure.
DLPFC: Dorsolateral prefrontal cortex; GW: Gestation week(s); J: Joint; MHPCD: Maternal Health Practices and Child Development Project; mo: Month(s); NBDPS: National Birth Defects Prevention Study; OPPS: Ottawa Prenatal Prospective Study; PENK: Proenkephalin; PFC: Prefrontal cortex; Trim: Trimester; VIPS: Vaginal Infections and Prematurity Study; y: Year(s).

CME

Lasting Impacts of Prenatal Cannabis Exposure and the Role of Endogenous Cannabinoids in the Developing Brain

  • Authors: Chia-Shan Wu, PhD; Christopher P. Jew; Hui-Chen Lu, PhD
  • CME Released: 7/1/2011
  • THIS ACTIVITY HAS EXPIRED FOR CREDIT
  • Valid for credit through: 7/1/2012, 11:59 PM EST
Start Activity


Target Audience and Goal Statement

This activity is intended for primary care clinicians, obstetricians, neurologists, psychiatrists, pediatricians, and other healthcare providers advising pregnant women regarding the effects of prenatal marijuana exposure and/or caring for their offspring.

The goal of this activity is to review the interaction of prenatal exposure to marijuana with endocannabinoid effects on neural development.

Upon completion of this activity, participants will be able to:

  1. Describe the epidemiology of prenatal exposure to marijuana, based on a review
  2. Describe the neurodevelopmental effects of prenatal exposure to marijuana
  3. Describe the effects of endocannabinoids on neural development and how prenatal exposure to marijuana influences these effects


Disclosures

As an organization accredited by the ACCME, Medscape, LLC, requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest.

Medscape, LLC, encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.


Author(s)

  • Chia-Shan Wu, PhD

    The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital

    Disclosures

    Disclosure: Chia-Shan Wu, PhD, has disclosed no relevant financial relationships.

  • Christopher P. Jew

    The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital; Program in Developmental Biology, Baylor College of Medicine, Houston, Texas

    Disclosures

    Disclosure: Christopher P. Jew has disclosed no relevant financial relationships.

  • Hui-Chen Lu, PhD

    The Cain Foundation Laboratories, Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital; Department of Pediatrics; Program in Developmental Biology; Department of Neuroscience, Baylor College of Medicine, Houston, Texas

    Disclosures

    Disclosure: Hui-Chen Lu, PhD, is supported by NIH grants: NS048884 (NINDS), DA029381 (NIDA) and HD065561 (NICHD).

Editor(s)

  • Elisa Manzotti

    Editorial Director, Future Science Group, London, United Kingdom

    Disclosures

    Disclosure: Elisa Manzotti has disclosed no relevant financial relationships.

CME Author(s)

  • Laurie Barclay, MD

    Freelance writer and reviewer, Medscape, LLC

    Disclosures

    Disclosure: Laurie Barclay, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

  • Nafeez Zawahir, MD

    CME Clinical Director, Medscape, LLC

    Disclosures

    Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

  • Sarah Fleischman

    CME Program Manager, Medscape, LLC

    Disclosures

    Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.


Accreditation Statements

    For Physicians

  • This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Medscape, LLC and Future Medicine Ltd. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians.

    Medscape, LLC designates this Journal-based CME activity for a maximum of 1.00 AMA PRA Category 1 Credit(s)™ . Physicians should claim only the credit commensurate with the extent of their participation in the activity.

    Medscape, LLC staff have disclosed that they have no relevant financial relationships.

    Contact This Provider

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]


Instructions for Participation and Credit

There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page. To receive AMA PRA Category 1 Credit™, you must receive a minimum score of 70% on the post-test.

Follow these steps to earn CME/CE credit*:

  1. Read the target audience, learning objectives, and author disclosures.
  2. Study the educational content online or printed out.
  3. Online, choose the best answer to each test question. To receive a certificate, you must receive a passing score as designated at the top of the test. Medscape Education encourages you to complete the Activity Evaluation to provide feedback for future programming.

You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it. Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print out the tally as well as the certificates by accessing "Edit Your Profile" at the top of your Medscape homepage.

*The credit that you receive is based on your user profile.

CME

Lasting Impacts of Prenatal Cannabis Exposure and the Role of Endogenous Cannabinoids in the Developing Brain: Conclusion

processing....

Conclusion

Marijuana abuse during pregnancy and adolescence represents a major health problem owing to its potential consequences on neural development. Prenatally cannabis-exposed children display cognitive deficits, suggesting that maternal consumption has interfered with the proper maturation of the brain. Several pharmacological effects of THC, the active principle of Cannabis sativa preparations such as hashish and marijuana, are mimicked by the endogenous eCBs, 2-AG and AEA. On the other hand, pharmacological inhibition or genetic deletion of either FAAH or MAGL to elevate endogenous levels of AEA and 2-AG, respectively, does not reproduce the full spectrum of responses observed with THC. Interestingly, a recently developed dual FAAH/MAGL inhibitor (JZL195) induced THC-like drug discrimination responses, which were not observed with disruption of either FAAH or MAGL alone.[149] The observation that the THC-like additive effects of dual FAAH/MAGL blockade can be reversed by CB1R antagonists suggests that most, if not all, acute cognitive responses to THC are mediated through the CB1R.[150] Whether THC produces effect by partially activating CB1R or antagonizing the action of 2-AG and AEA at this receptor remains an open question.[151]

2-AG is the most abundant eCB in the brain. Basal 2-AG levels in the adult brain are approximately 200 times those of AEA,[83] while an approximately 1000-fold excess of tissue 2-AG concentrations over those of AEA exists in the fetal brain.[102] The relative contribution of the two arms of eCB signaling in regulating neurogenesis, axonal growth and guidance, and synaptogenesis during development is not well understood. The data from dual blockade of FAAH/MAGL indicate that AEA and 2-AG signaling pathways interact to regulate specific behavioral processes in vivo, including those relevant to drug abuse.[150] Hence, future studies employing novel pharmacological and genetic tools may help to dissect out specific eCB signaling pathways in regulating neural developmental processes.