Taken from the webpage of
Dr. Thomas Armstrong
The theory of multiple intelligences was developed in 1983 by Dr. Howard Gardner, professor of education at Harvard University. It suggests that the traditional notion of intelligence, based on I.Q. testing, is far too limited. Instead, Dr. Gardner proposes eight different intelligences to account for a broader range of human potential in children and adults. These intelligences are:
•Linguistic intelligence ("word smart")
•Logical-mathematical intelligence ("number/reasoning smart")
•Spatial intelligence ("picture smart")
•Bodily-Kinesthetic intelligence ("body smart")
•Musical intelligence ("music smart")
•Interpersonal intelligence ("people smart")
•Intrapersonal intelligence ("self smart")
•Naturalist intelligence ("nature smart")
Dr. Gardner says that our schools and culture focus most of their attention on linguistic and logical-mathematical intelligence. We esteem the highly articulate or logical people of our culture. However, Dr. Gardner says that we should also place equal attention on individuals who show gifts in the other intelligences: the artists, architects, musicians, naturalists, designers, dancers, therapists, entrepreneurs, and others who enrich the world in which we live. Unfortunately, many children who have these gifts don’t receive much reinforcement for them in school. Many of these kids, in fact, end up being labeled "learning disabled," "ADD (attention deficit disorder," or simply underachievers, when their unique ways of thinking and learning aren’t addressed by a heavily linguistic or logical-mathematical classroom. The theory of multiple intelligences proposes a major transformation in the way our schools are run. It suggests that teachers be trained to present their lessons in a wide variety of ways using music, cooperative learning, art activities, role play, multimedia, field trips, inner reflection, and much more (see Multiple Intelligences in the Classroom). The good news is that the theory of multiple intelligences has grabbed the attention of many educators around the country, and hundreds of schools are currently using its philosophy to redesign the way it educates children. The bad news is that there are thousands of schools still out there that teach in the same old dull way, through dry lectures, and boring worksheets and textbooks. The challenge is to get this information out to many more teachers, school administrators, and others who work with children, so that each child has the opportunity to learn in ways harmonious with their unique minds (see In Their Own Way).
The theory of multiple intelligences also has strong implications for adult learning and development. Many adults find themselves in jobs that do not make optimal use of their most highly developed intelligences (for example, the highly bodily-kinesthetic individual who is stuck in a linguistic or logical desk-job when he or she would be much happier in a job where they could move around, such as a recreational leader, a forest ranger, or physical therapist). The theory of multiple intelligences gives adults a whole new way to look at their lives, examining potentials that they left behind in their childhood (such as a love for art or drama) but now have the opportunity to develop through courses, hobbies, or other programs of self-development (see 7 Kinds of Smart).
How to Teach or Learn Anything 8 Different Ways
One of the most remarkable features of the theory of multiple intelligences is how it provides eight different potential pathways to learning. If a teacher is having difficulty reaching a student in the more traditional linguistic or logical ways of instruction, the theory of multiple intelligences suggests several other ways in which the material might be presented to facilitate effective learning. Whether you are a kindergarten teacher, a graduate school instructor, or an adult learner seeking better ways of pursuing self-study on any subject of interest, the same basic guidelines apply. Whatever you are teaching or learning, see how you might connect it with
•words (linguistic intelligence)
•numbers or logic (logical-mathematical intelligence)
•pictures (spatial intelligence)
•music (musical intelligence)
•self-reflection (intrapersonal intelligence)
•a physical experience (bodily-kinesthetic intelligence)
•a social experience (interpersonal intelligence), and/or
•an experience in the natural world. (naturalist intelligence)
For example, if you’re teaching or learning about the law of supply and demand in economics, you might read about it (linguistic), study mathematical formulas that express it (logical-mathematical), examine a graphic chart that illustrates the principle (spatial), observe the law in the natural world (naturalist) or in the human world of commerce (interpersonal); examine the law in terms of your own body [e.g. when you supply your body with lots of food, the hunger demand goes down; when there's very little supply, your stomach's demand for food goes way up and you get hungry] (bodily-kinesthetic and intrapersonal); and/or write a song (or find an existing song) that demonstrates the law (perhaps Dylan's "Too Much of Nothing?").
You don’t have to teach or learn something in all eight ways, just see what the possibilities are, and then decide which particular pathways interest you the most, or seem to be the most effective teaching or learning tools. The theory of multiple intelligences is so intriguing because it expands our horizon of available teaching/learning tools beyond the conventional linguistic and logical methods used in most schools (e.g. lecture, textbooks, writing assignments, formulas, etc.). To get started, put the topic of whatever you’re interested in teaching or learning about in the center of a blank sheet of paper, and draw eight straight lines or "spokes" radiating out from this topic. Label each line with a different intelligence. Then start brainstorming ideas for teaching or learning that topic and write down ideas next to each intelligence (this is a spatial-linguistic approach of brainstorming; you might want to do this in other ways as well, using a tape-recorder, having a group brainstorming session, etc.). Have fun!
Thursday, February 10, 2011
Monday, February 7, 2011
Testing Autism Drugs in Human Brain Cells
A Method Involving Pluripotent Stem Cells Could Lead to Personalized Treatment of the Disease
By Jennifer Chu
Technology Review
November 11, 2010
Autism is a highly complex disorder affecting one in every 110 children born in the United States. The disease's genetic profile and behavioral symptoms fluctuate widely from case to case, and this variability has frustrated scientists' efforts to identify effective treatments. A new study suggests that autism could eventually be a target for personalized treatment, targeted to a patient's own neurons.
A team from the University of California, San Diego, and the Salk Institute for Biological Studies devised a way to study brain cells from patients with autism, and found a way reverse cellular abnormalities in neurons that have been associated with autism.
The researchers took skin biopsies from patients with a severe form of autism called Rett syndrome, and genetically reprogrammed those cells into pluripotent stem cells. Pluripotent stem cells have the power to differentiate into any kind of cell in the body, depending on environmental cues during early development. The team differentiated the stem cells into fully functioning neurons, and then studied their functioning. They found that neurons derived from patients with Rett syndrome showed certain abnormalities, including markedly smaller cell bodies, dendrite connections, and decreased cell-to-cell communication.
By treating these patient-derived neurons with an experimental drug, the researchers could reverse the cellular abnormalities. The findings, published today in the journal Cell, could give scientists a powerful tool for pinpointing the causes of autism and other brain disorders, and a way to choose targeted treatments.
"It took us two years to finish this project, and personalized medicine might not be that far off," says Carol Marchetto, first author of the paper and a postdoctoral researcher at the Salk Institute. "In the lifetime of a patient, you could go from his skin sample to a reprogrammed cell, to differentiating into a neuron, and find drugs that could be used on that patient."
Rett syndrome, which mostly affects girls, can cause highly impaired social and communication skills, which become apparent soon after a child learns to walk and talk. Patients with Rett can experience increased difficulty breathing and controlling their movements, and can develop repetitive and compulsive behaviors similar to other forms of autism.
Marchetto sees Rett syndrome as a gateway to the broader study of autism, since many other forms of autism share behavioral and genetic similarities with Rett syndrome.
Most cases of autism seem to stem from a combination of genetic abnormalities, but Rett arises from a single gene mutation, found on the MeCP2 gene on the X chromosome. In girls, one of two X chromosomes carries the mutation, and during fetal brain development, one chromosome is activated within each brain cell, seemingly at random. Rett patients can exhibit varying percentages of brain cells carrying the mutation, which can manifest as varying levels of severity of the disorder.
To understand how this genetic mutation plays out at a cellular level, Marchetto and her colleague Alysson Muotri, an assistant professor in the department of Molecular and Cellular Medicine at the UCSD's School of Medicine, took skin biopsies from four patients with Rett syndrome, reprogrammed them into pluripotent stem cells and experimented with a number of different conditions before they found a combination of growth factors that differentiated the stem cells into functioning human neurons.
They saw that each patient-derived stem-cell line generated a different percentage of neurons carrying the gene mutation. The defective neurons looked and acted differently from their normal counterparts, exhibiting smaller cell bodies, less dendrite connections, and impaired cell-to-cell communication.
The researchers treated neuron cultures with insulin-like growth factor (iGF1), which has been shown to reverse behavioral symptoms of Rett in mice. The drug reversed the biological symptoms of the disorder in the neurons, restoring dendrite connections and cell-to-cell signaling in defective neurons. The researchers plan to use the same process to generate neurons from more patients with both Rett syndrome and other forms of autism.
Jeffrey Neul, assistant professor of molecular and human genetics at Baylor College of Medicine, who studies Rett syndrome in mice, says animal models allow scientists to observe the behavioral effects of the disease, but this is a time- and labor-intensive process.
"The field really has been in desperate need of cellular-based assays that can be used to test therapeutic compounds," says Neul. "And it's really hard to push drug discovery if you don't have something you can do in a more rapid fashion."
The process Marchetto and Muotri have developed takes three months to generate fully functioning human neurons. While this is similar to the time frame of normal brain development, the researchers are looking for ways to speed the process up so they can rapidly generate brain cells and expose them to a variety of molecular factors and drug compounds.
The team also plans to move beyond the Petri dish once they've differentiated neurons from human skin cells, to see how the neurons work in a living brain. "What we can do is transplant human neurons in mouse brains and generate chimeric [hybrid human-animal] models," says Muotri. "We can then expose these animals to different environments, and see how they will affect the human neuron."
James Ellis, professor of molecular genetics at the University of Toronto, is doing similar work in reprogramming patients' skin cells into brain cells. He says that Muotri and Marchetto's findings open up a new testing ground for autism and other neurological disorders. "That's clearly what's going to be required of autism, where different people are going to have different mutations and mechanisms, in how they ended up with that outcome," he says.
By Jennifer Chu
Technology Review
November 11, 2010
Autism is a highly complex disorder affecting one in every 110 children born in the United States. The disease's genetic profile and behavioral symptoms fluctuate widely from case to case, and this variability has frustrated scientists' efforts to identify effective treatments. A new study suggests that autism could eventually be a target for personalized treatment, targeted to a patient's own neurons.
A team from the University of California, San Diego, and the Salk Institute for Biological Studies devised a way to study brain cells from patients with autism, and found a way reverse cellular abnormalities in neurons that have been associated with autism.
The researchers took skin biopsies from patients with a severe form of autism called Rett syndrome, and genetically reprogrammed those cells into pluripotent stem cells. Pluripotent stem cells have the power to differentiate into any kind of cell in the body, depending on environmental cues during early development. The team differentiated the stem cells into fully functioning neurons, and then studied their functioning. They found that neurons derived from patients with Rett syndrome showed certain abnormalities, including markedly smaller cell bodies, dendrite connections, and decreased cell-to-cell communication.
By treating these patient-derived neurons with an experimental drug, the researchers could reverse the cellular abnormalities. The findings, published today in the journal Cell, could give scientists a powerful tool for pinpointing the causes of autism and other brain disorders, and a way to choose targeted treatments.
"It took us two years to finish this project, and personalized medicine might not be that far off," says Carol Marchetto, first author of the paper and a postdoctoral researcher at the Salk Institute. "In the lifetime of a patient, you could go from his skin sample to a reprogrammed cell, to differentiating into a neuron, and find drugs that could be used on that patient."
Rett syndrome, which mostly affects girls, can cause highly impaired social and communication skills, which become apparent soon after a child learns to walk and talk. Patients with Rett can experience increased difficulty breathing and controlling their movements, and can develop repetitive and compulsive behaviors similar to other forms of autism.
Marchetto sees Rett syndrome as a gateway to the broader study of autism, since many other forms of autism share behavioral and genetic similarities with Rett syndrome.
Most cases of autism seem to stem from a combination of genetic abnormalities, but Rett arises from a single gene mutation, found on the MeCP2 gene on the X chromosome. In girls, one of two X chromosomes carries the mutation, and during fetal brain development, one chromosome is activated within each brain cell, seemingly at random. Rett patients can exhibit varying percentages of brain cells carrying the mutation, which can manifest as varying levels of severity of the disorder.
To understand how this genetic mutation plays out at a cellular level, Marchetto and her colleague Alysson Muotri, an assistant professor in the department of Molecular and Cellular Medicine at the UCSD's School of Medicine, took skin biopsies from four patients with Rett syndrome, reprogrammed them into pluripotent stem cells and experimented with a number of different conditions before they found a combination of growth factors that differentiated the stem cells into functioning human neurons.
They saw that each patient-derived stem-cell line generated a different percentage of neurons carrying the gene mutation. The defective neurons looked and acted differently from their normal counterparts, exhibiting smaller cell bodies, less dendrite connections, and impaired cell-to-cell communication.
The researchers treated neuron cultures with insulin-like growth factor (iGF1), which has been shown to reverse behavioral symptoms of Rett in mice. The drug reversed the biological symptoms of the disorder in the neurons, restoring dendrite connections and cell-to-cell signaling in defective neurons. The researchers plan to use the same process to generate neurons from more patients with both Rett syndrome and other forms of autism.
Jeffrey Neul, assistant professor of molecular and human genetics at Baylor College of Medicine, who studies Rett syndrome in mice, says animal models allow scientists to observe the behavioral effects of the disease, but this is a time- and labor-intensive process.
"The field really has been in desperate need of cellular-based assays that can be used to test therapeutic compounds," says Neul. "And it's really hard to push drug discovery if you don't have something you can do in a more rapid fashion."
The process Marchetto and Muotri have developed takes three months to generate fully functioning human neurons. While this is similar to the time frame of normal brain development, the researchers are looking for ways to speed the process up so they can rapidly generate brain cells and expose them to a variety of molecular factors and drug compounds.
The team also plans to move beyond the Petri dish once they've differentiated neurons from human skin cells, to see how the neurons work in a living brain. "What we can do is transplant human neurons in mouse brains and generate chimeric [hybrid human-animal] models," says Muotri. "We can then expose these animals to different environments, and see how they will affect the human neuron."
James Ellis, professor of molecular genetics at the University of Toronto, is doing similar work in reprogramming patients' skin cells into brain cells. He says that Muotri and Marchetto's findings open up a new testing ground for autism and other neurological disorders. "That's clearly what's going to be required of autism, where different people are going to have different mutations and mechanisms, in how they ended up with that outcome," he says.
Saturday, February 5, 2011
Cytomegalovirus Tied to Hearing Loss in Kids
CalorieLab Lab Notes
Cytomegalovirus (CMV), a common virus that usually does not make most people sick, may be associated with hearing loss in kids if mom is infected while pregnant according to a new study. In this study, 354 kids who were 4 years of age and up who had been tested for CMV and had hearing loss were examined. Thirty-four contracted CMV from their mothers and it was observed that kids who were CMV-positive at birth had more severe hearing loss than kids who were not and were more likely to have hearing loss in only one ear. Researchers did not have any clear answers as to why contracting CMV in utero may cause hearing problems. CMV is known to cause serious problems in babies if the mother contracts it during pregnancy. The next step will be to investigate how CMV causes hearing loss.
Cytomegalovirus (CMV), a common virus that usually does not make most people sick, may be associated with hearing loss in kids if mom is infected while pregnant according to a new study. In this study, 354 kids who were 4 years of age and up who had been tested for CMV and had hearing loss were examined. Thirty-four contracted CMV from their mothers and it was observed that kids who were CMV-positive at birth had more severe hearing loss than kids who were not and were more likely to have hearing loss in only one ear. Researchers did not have any clear answers as to why contracting CMV in utero may cause hearing problems. CMV is known to cause serious problems in babies if the mother contracts it during pregnancy. The next step will be to investigate how CMV causes hearing loss.
Wednesday, December 29, 2010
Younger Brains are Easier to Rewire
Study of blind patients supports the idea that there is a period early in a person’s development when brain regions can switch functions.
By Anne Trafton
MIT News Office
About a decade ago, scientists studying the brains of blind people made a surprising discovery: A brain region normally devoted to processing images had been rewired to interpret tactile information, such as input from the fingertips as they trace Braille letters. Subsequent experiments revealed a similar phenomenon in other brain regions. However, these studies didn’t answer the question of whether the brain can rewire itself at any time, or only very early in life.
A new paper from MIT neuroscientists, in collaboration with Alvaro Pascual-Leone at Beth Israel Deaconess Medical Center, offers evidence that it is easier to rewire the brain early in life. The researchers found that a small part of the brain’s visual cortex that processes motion became reorganized only in the brains of subjects who had been born blind, not those who became blind later in life.
The new findings, described in the Oct. 14 issue of the journal Current Biology, shed light on how the brain wires itself during the first few years of life, and could help scientists understand how to optimize the brain’s ability to be rewired later in life. That could become increasingly important as medical advances make it possible for congenitally blind people to have their sight restored, said MIT postdoctoral associate Marina Bedny, lead author of the paper.
Brain rewiring
In the 1950s and ’60s, scientists began to think that certain brain functions develop normally only if an individual is exposed to relevant information, such as language or visual information, within a specific time period early in life. After that, they theorized, the brain loses the ability to change in response to new input.
Animal studies supported this theory. For example, cats blindfolded during the first months of life are unable to see normally after the blindfolds are removed. Similar periods of blindfolding in adulthood have no effect on vision.
However, there have been indications in recent years that there is more wiggle room than previously thought, said Bedny, who works in the laboratory of MIT assistant professor Rebecca Saxe, also an author of the Current Biology paper. Many neuroscientists now support the idea of a period early in life after which it is difficult, but not impossible, to rewire the brain.
Bedny, Saxe and their colleagues wanted to determine if a part of the brain known as the middle temporal complex (MT/MST) can be rewired at any time or only early in life. They chose to study MT/MST in part because it is one of the most studied visual areas. In sighted people, the MT region is specialized for motion vision.
In the few rare cases where patients have lost MT function in both hemispheres of the brain, they were unable to sense motion in a visual scene. For example, if someone poured water into a glass, they would see only a standing, frozen stream of water.
Previous studies have shown that in blind people, MT is taken over by sound processing, but those studies didn’t distinguish between people who became blind early and late in life.
Early versus late
In the new MIT study, the researchers studied three groups of subjects — sighted, congenitally blind, and those who became blind later in life (age nine or older). Using functional magnetic resonance imaging (fMRI), they tested whether MT in these subjects responded to moving sounds — for example, approaching footsteps.
The results were clear, said Bedny. MT reacted to moving sounds in congenitally blind people, but not in sighted people or people who became blind at a later age.
This suggests that in late-blind individuals, the visual input they received in early years allowed the MT complex to develop its typical visual function, and it couldn’t be remade to process sound after the person lost sight. Congenitally blind people never received any visual input, so the region was taken over by auditory input after birth.
“We need to think of early life as a window of opportunity to shape how the brain works,” said Bedny. “That’s not to say that later experience can’t alter things, but it’s easier to get organized early on.”
Another important aspect of the work is the finding that in the congenitally blind, there is enhanced communication between the MT complex and the brain’s prefrontal cortex, said Ione Fine, associate professor of psychology at the University of Washington. That enhanced connection could help explain how the brain remodels the MT region to process auditory information. Previous studies have looked for enlarged nerve bundles, with no success. “People have been looking for bigger roads, but what she’s seeing is more traffic on the same-size road,” said Fine, who was not involved in the study.
Although this work supports the idea that brain regions can switch functions early in a person’s development, Bedny believes that by better understanding how the brain is wired during this period, scientists may be able to learn how to rewire it later in life. There are now very few cases of sight restoration, but if it becomes more common, scientists will need to figure out how to retrain the patient’s brain so it can process the new visual input.
“The unresolved question is whether the brain can relearn, and how that learning differs in an adult brain versus a child’s brain,” said Bedny.
Bedny hopes to study the behavioral consequences of the MT switch in future studies. Those would include whether blind people have an advantage over sighted people in auditory motion processing, and if they have a disadvantage if sight is restored.
By Anne Trafton
MIT News Office
About a decade ago, scientists studying the brains of blind people made a surprising discovery: A brain region normally devoted to processing images had been rewired to interpret tactile information, such as input from the fingertips as they trace Braille letters. Subsequent experiments revealed a similar phenomenon in other brain regions. However, these studies didn’t answer the question of whether the brain can rewire itself at any time, or only very early in life.
A new paper from MIT neuroscientists, in collaboration with Alvaro Pascual-Leone at Beth Israel Deaconess Medical Center, offers evidence that it is easier to rewire the brain early in life. The researchers found that a small part of the brain’s visual cortex that processes motion became reorganized only in the brains of subjects who had been born blind, not those who became blind later in life.
The new findings, described in the Oct. 14 issue of the journal Current Biology, shed light on how the brain wires itself during the first few years of life, and could help scientists understand how to optimize the brain’s ability to be rewired later in life. That could become increasingly important as medical advances make it possible for congenitally blind people to have their sight restored, said MIT postdoctoral associate Marina Bedny, lead author of the paper.
Brain rewiring
In the 1950s and ’60s, scientists began to think that certain brain functions develop normally only if an individual is exposed to relevant information, such as language or visual information, within a specific time period early in life. After that, they theorized, the brain loses the ability to change in response to new input.
Animal studies supported this theory. For example, cats blindfolded during the first months of life are unable to see normally after the blindfolds are removed. Similar periods of blindfolding in adulthood have no effect on vision.
However, there have been indications in recent years that there is more wiggle room than previously thought, said Bedny, who works in the laboratory of MIT assistant professor Rebecca Saxe, also an author of the Current Biology paper. Many neuroscientists now support the idea of a period early in life after which it is difficult, but not impossible, to rewire the brain.
Bedny, Saxe and their colleagues wanted to determine if a part of the brain known as the middle temporal complex (MT/MST) can be rewired at any time or only early in life. They chose to study MT/MST in part because it is one of the most studied visual areas. In sighted people, the MT region is specialized for motion vision.
In the few rare cases where patients have lost MT function in both hemispheres of the brain, they were unable to sense motion in a visual scene. For example, if someone poured water into a glass, they would see only a standing, frozen stream of water.
Previous studies have shown that in blind people, MT is taken over by sound processing, but those studies didn’t distinguish between people who became blind early and late in life.
Early versus late
In the new MIT study, the researchers studied three groups of subjects — sighted, congenitally blind, and those who became blind later in life (age nine or older). Using functional magnetic resonance imaging (fMRI), they tested whether MT in these subjects responded to moving sounds — for example, approaching footsteps.
The results were clear, said Bedny. MT reacted to moving sounds in congenitally blind people, but not in sighted people or people who became blind at a later age.
This suggests that in late-blind individuals, the visual input they received in early years allowed the MT complex to develop its typical visual function, and it couldn’t be remade to process sound after the person lost sight. Congenitally blind people never received any visual input, so the region was taken over by auditory input after birth.
“We need to think of early life as a window of opportunity to shape how the brain works,” said Bedny. “That’s not to say that later experience can’t alter things, but it’s easier to get organized early on.”
Another important aspect of the work is the finding that in the congenitally blind, there is enhanced communication between the MT complex and the brain’s prefrontal cortex, said Ione Fine, associate professor of psychology at the University of Washington. That enhanced connection could help explain how the brain remodels the MT region to process auditory information. Previous studies have looked for enlarged nerve bundles, with no success. “People have been looking for bigger roads, but what she’s seeing is more traffic on the same-size road,” said Fine, who was not involved in the study.
Although this work supports the idea that brain regions can switch functions early in a person’s development, Bedny believes that by better understanding how the brain is wired during this period, scientists may be able to learn how to rewire it later in life. There are now very few cases of sight restoration, but if it becomes more common, scientists will need to figure out how to retrain the patient’s brain so it can process the new visual input.
“The unresolved question is whether the brain can relearn, and how that learning differs in an adult brain versus a child’s brain,” said Bedny.
Bedny hopes to study the behavioral consequences of the MT switch in future studies. Those would include whether blind people have an advantage over sighted people in auditory motion processing, and if they have a disadvantage if sight is restored.
Friday, December 24, 2010
Christmas in Heaven
By Wanda Bencke
bencke@ponyexpress.net
I see the countless Christmas trees
around the world below
With tiny light, like Heaven's stars
reflecting on the snow.
The sight is so spectacular,
please wipe away that tear,
For I am spending Christmas
with Jesus Christ this year.
I hear the many Christmas songs
that people hold so dear
But the sounds of music can't compare
with the Christmas choir up here.
I have no words to tell you
of the joy their voices bring
For it is beyond description
to hear the angels sing.
I know how much you miss me,
I see the pain inside your heart
for I am spending Christmas
with Jesus Christ this year.
I can't tell you of the splendor
or the peace here in this place
Can you just imagine Christmas
with our Savior face to face?
I'll ask Him to lift your spirit
as I tell Him of your love
so then pray for one another
as you lift your eyes above.
Please let your hearts be joyful
and let your spirit sing
for I am spending Christmas in Heaven
and I'm walking with the King.
bencke@ponyexpress.net
Lysandra Kay Bencke was my thirteen year old handicapped daughter. On Christmas day 1997, Lysandra had a seizure and was in a coma for five days before she died. During those five days I wrote the poem "Christmas in Heaven". I sent it out in a belated Christmas cards to friends and relatives that year. They also sent it on to other friends and relatives, thus the poem and the story behind it have been changed.
See the story at http://www.christmasinheaven.net/story.html
I see the countless Christmas trees
around the world below
With tiny light, like Heaven's stars
reflecting on the snow.
The sight is so spectacular,
please wipe away that tear,
For I am spending Christmas
with Jesus Christ this year.
I hear the many Christmas songs
that people hold so dear
But the sounds of music can't compare
with the Christmas choir up here.
I have no words to tell you
of the joy their voices bring
For it is beyond description
to hear the angels sing.
I know how much you miss me,
I see the pain inside your heart
for I am spending Christmas
with Jesus Christ this year.
I can't tell you of the splendor
or the peace here in this place
Can you just imagine Christmas
with our Savior face to face?
I'll ask Him to lift your spirit
as I tell Him of your love
so then pray for one another
as you lift your eyes above.
Please let your hearts be joyful
and let your spirit sing
for I am spending Christmas in Heaven
and I'm walking with the King.
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