What Is Echophenomenon?

Echophenomenon is the involuntary repetition of another person’s words or actions. When words are imitated, this may be defined as echolalia. When a person compulsively repeats the actions of someone else, it is called echopraxia. People can suffer from either echolalia and echopraxia, or both.

It should be understood that there is a very big distinction between willfully repeating another person’s actions or words, and doing it without conscious purpose. In the former, it’s an annoying, often teasing gesture that frequently occurs among school children, particularly siblings. In the latter, the movement or sounds being repeated aren’t on purpose and certainly aren’t meant to tease or annoy others.

The distinction is valuable because there are some people who suffer from echopraxia, or more generally echopathy, that may live in very mainstreamed environments. People with Tourette syndrome may suffer this condition, and in a school setting, the movements of others student might be picked up on by the child and reproduced in an echopractic fashion. Obviously teaching other students in a class not to mind this behavior would be important for mainstreaming success.

It shouldn’t be assumed that echopraxia is only suffered by people with Tourette syndrome, and all people with Tourette’s do not suffer it. There are many illnesses or conditions where echopraxia may occur. Some people with autism are echopractic, and the condition occasionally presents in people with schizophrenia. Other illnesses that are associated with echopathy include Ganser Disorder and occasionally major depressive disorder. From time to time, medical literature presents information about others who have suffered from echopraxia, and this includes those who have suffered brain tumors and some types of seizure disorders.

Due to the variety of conditions associated with echopraxia, it’s hard to say exactly what causes it in all cases or how it is best treated. Most times treating the underlying disease is the best way to minimize echopathy. Parents may find it particularly challenging to help children with this condition when they talk to doctors. Any demonstration of new movements or behaviors by the parent could result in new tics on the part of the echopractic child.

Children, mostly to their benefit, are also extremely observant, and may note small movements in others that might easily be turned into a repetitive movement by self. Of course it can be said that, for anyone, the condition of having unwanted repetitious movements is extremely difficult. This is especially the case, since many times people with this condition are quite cognizant that the behavior is unusual, possibly uncomfortable, and very often draws unwanted attention.

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Michigan medical marijuana panel looks to add PTSD to law but rejects autism, other conditions

Marijuana (AP File Photo)

 A state panel appointed to review Michigan's medical marijuana law gave preliminary approval on Tuesday to a citizen petition seeking to add post-traumatic stress disorder to the list of debilitating conditions that can qualify a patient for participation in the program.

The Michigan Marihuana Act Review Panel, in a 7-2 vote, recommended adding PTSD to the list. The preliminary vote will be followed by a public hearing, which must be scheduled within 60 days under state rules, before the panel reconvenes to make a formal recommendation.

The head of the Michigan Department of Licensing and Regulatory Affairs, the state agency responsible for appointing the panel and administering the medical marijuana program, will have final say on whether to add PTSD to the list of debilitating conditions.

LARA disbanded a previous iteration of the panel in April after acknowledging failure to appoint members in a manner consistent with administrative rules. The original panel had recommended adding PTSD, and the new-look group, whose members were appointed in June, followed suit in Tuesday's preliminary vote.

"In my opinion, marijuana is one of the best medications for people with PTSD," said appointee David Crocker, a medical doctor from Kalamazoo who serves as president of Michigan Holistic Health. "…We have a lot of veterans with PTSD in our clinics. Many of them will tell you they think marijuana saved their lives, and many of their families will tell you the same thing."

Jeanne Lewandowski of Detroit, a panel member who works as director of palliative medicine at St. John Hospital and Medical Center, spoke out against the petition and was one of two appointees to vote against it. She argued that marijuana could impair the ability of military veterans to reintegrate into society and said she was concerned about social isolation.

PTSD petitioner John EvansJohn Evans of Ann Arbor, a military veteran and medical marijuana user, explains why he filed a petition seeking to add PTSD to Michigan's law.

In a series of separate votes, the panel rejected petitions seeking to add insomnia, asthma and autism to the list of debilitating conditions under the law. The insomnia vote was preliminary, meaning it will also be subject to a public hearing followed by another vote.

The asthma and autism votes, however, were considered final because the previous iteration of the panel had already considered the petitions and LARA had organized public hearings, frustrating some members who felt the agency was employing a double standard.

"I didn't feel it was appropriate," said David Brogren of Bloomfield Hills, a non-physician panelist who serves as president of Cannabis Patients United. "They disbanded the original panel because it was put together in error. I don't believe the errors were malicious or anything like that -- it wasn't a conspiracy, they just made a mistake -- but I think what they should do was go back to square one on all (the petitions). That would be the most fair thing."

During a public comment section of Tuesday's panel meeting, several marijuana advocates criticized the state for its handling of the review panel, which was envisioned in the 2008 law, mandated by administrative rules established in 2009, but did not meet for the first time until 2012.

A number of advocates questioned whether LARA had again violated the administrative rules by appointing only six members to the panel who also serve on the state's Advisory Committee on Symptom Management. Seven are required.

But Carole Engle, director of LARA's bureau of health care services, expressed confidence that the panel was properly constituted and convened, noting that Michigan Gov. Rick Snyder is expected to appoint another member to the committee who would then serve on the panel moving forward.

"We are convinced that we are not wasting our time," Engle said in response to a question from a panel member. "…We're still missing one member from the advisory committee, but we do have a quorum of appropriately appointed members here today, and that should not impede the panel's ability to make decisions at all."

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A Link Between Autism and Cannabinoids

A neuron affected by an NL3 mutation.NEURON, FOLDY ET AL.Two autism-related mutations in a synapse-adhesion protein lead to deficits in prolonged endocannabinoid signaling in mice. It’s a surprising connection that suggests such signaling problems could be implicated in autism spectrum disorders, according to a paper published today (April 11) in Neuron.

Tonic endocannabinoid signaling is long-lasting and contrasts with the brief pulses characteristic of phasic signaling. Endocannabinoid signaling in general affects memory formation, learning, pain, and other important processes, but the distinctions between tonic and phasic signaling have been poorly understood.

“It’s a very stimulating finding which could be a real turning point in understanding tonic endocannabinoids and how this otherwise mysterious lipid signaling really works,” said Bradley Alger, a neuroscientist at the University of Maryland School of Medicine who was not involved in the study. But he warned that the paper, while tantalizing, did not even definitively show that endocannabinoid signaling deficits could lead to autistic behaviors in mice, let alone in humans.

The researchers studied two mutations in neuroligin-3 (NL3), a gene encoding a protein involved in building and maintaining synapses. One mutation is a deletion of the entire gene, while the other, called R451, involves a single amino acid substitution. “These two mutations both have been associated with autism in humans,” said coauthor Thomas Südhof, a cellular physiologist at Stanford University.

Südhof and colleagues sought to understand what physiological effects the mutations had in common, assuming that if they could find a shared effect it might explain how they both led to autism. Using mice with each of the mutations, they made electrophysiological recordings of the interactions between pairs of cells in the hippocampal areas of the mouse brains. They compared recordings in the two types of mutant mouse brain cells to recordings done in normal mouse brains.

While synaptic changes often differed depending on the mutation, one type of cell containing cannabinoid type-1 (CB1) receptors showed similar alterations in its patterns of excitation for both types of mutant mice. Further investigation showed that tonic endocannabinoid signaling had been disrupted in these cells. “By this comparative physiology we were able to point out differences that pointed to this endocannabinoid signaling,” said Csaba Földy, also a cell physiologist at Stanford and an author of the paper.

The mechanism for how mutations in NL3 lead to endocannabinoid signaling deficits remains unclear. Could lacking properly functioning NL3 be interfering with endocannabinoid secretory machinery? Could it be somehow causing degradation of endocannabinoid signaling ligands? “We’re left without a really good idea of what it’s doing in single synapses or whether it’s effective behaviorally,” Alger said. Moreover, it is not yet clear how endocannabinoid signaling deficits would be involved in autistic symptoms, the authors said.

Alger added that, if the endocannabinoid system does turn out to be connected to autism in humans, medical marijuana could turn out to hold possibility for treating autism. But Südhof said that he did not know at this point whether marijuana would intensify or ameliorate autistic symptoms.

More immediately, said Alger, the findings will spur research into NL3 and other neuroligins, molecules he had never dreamed might have an effect on endocannabinoid signaling.  “We’re really just starting to understand how this works,” he said. “In terms of autism, we’ll have to refer to future research.

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A Link Between Autism and Cannabinoids

A neuron affected by an NL3 mutation.NEURON, FOLDY ET AL.Two autism-related mutations in a synapse-adhesion protein lead to deficits in prolonged endocannabinoid signaling in mice. It’s a surprising connection that suggests such signaling problems could be implicated in autism spectrum disorders, according to a paper published today (April 11) in Neuron.

Tonic endocannabinoid signaling is long-lasting and contrasts with the brief pulses characteristic of phasic signaling. Endocannabinoid signaling in general affects memory formation, learning, pain, and other important processes, but the distinctions between tonic and phasic signaling have been poorly understood.

“It’s a very stimulating finding which could be a real turning point in understanding tonic endocannabinoids and how this otherwise mysterious lipid signaling really works,” said Bradley Alger, a neuroscientist at the University of Maryland School of Medicine who was not involved in the study. But he warned that the paper, while tantalizing, did not even definitively show that endocannabinoid signaling deficits could lead to autistic behaviors in mice, let alone in humans.

The researchers studied two mutations in neuroligin-3 (NL3), a gene encoding a protein involved in building and maintaining synapses. One mutation is a deletion of the entire gene, while the other, called R451, involves a single amino acid substitution. “These two mutations both have been associated with autism in humans,” said coauthor Thomas Südhof, a cellular physiologist at Stanford University.

Südhof and colleagues sought to understand what physiological effects the mutations had in common, assuming that if they could find a shared effect it might explain how they both led to autism. Using mice with each of the mutations, they made electrophysiological recordings of the interactions between pairs of cells in the hippocampal areas of the mouse brains. They compared recordings in the two types of mutant mouse brain cells to recordings done in normal mouse brains.

While synaptic changes often differed depending on the mutation, one type of cell containing cannabinoid type-1 (CB1) receptors showed similar alterations in its patterns of excitation for both types of mutant mice. Further investigation showed that tonic endocannabinoid signaling had been disrupted in these cells. “By this comparative physiology we were able to point out differences that pointed to this endocannabinoid signaling,” said Csaba Földy, also a cell physiologist at Stanford and an author of the paper.

The mechanism for how mutations in NL3 lead to endocannabinoid signaling deficits remains unclear. Could lacking properly functioning NL3 be interfering with endocannabinoid secretory machinery? Could it be somehow causing degradation of endocannabinoid signaling ligands? “We’re left without a really good idea of what it’s doing in single synapses or whether it’s effective behaviorally,” Alger said. Moreover, it is not yet clear how endocannabinoid signaling deficits would be involved in autistic symptoms, the authors said.

Alger added that, if the endocannabinoid system does turn out to be connected to autism in humans, medical marijuana could turn out to hold possibility for treating autism. But Südhof said that he did not know at this point whether marijuana would intensify or ameliorate autistic symptoms.

More immediately, said Alger, the findings will spur research into NL3 and other neuroligins, molecules he had never dreamed might have an effect on endocannabinoid signaling.  “We’re really just starting to understand how this works,” he said. “In terms of autism, we’ll have to refer to future research.”

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Family uses medical marijuana to treat severely autistic son

FoxNews.com Medical marijuana is a controversial treatment option for adults – let alone children.

FoxNews.com But Jeremy Echols, of Oregon, says that that the drug is helping his autistic – and severely self-destructive – 11-year-old son, Alex.

By the time Alex was 5, he demonstrated severe self-destructive rage – such as head-butting walls until his face was black and blue. But after enrolling Alex in the state’s medical marijuana program, the family saw a dramatic improvements in Alex’s behavior. “He went from hitting himself, bloodying his face, to within an hour or hour-and-a-half, he would be playing with toys, which at that time was almost unheard of,” Echols said.

Alex’s parents give him a liquid form of the drug three times a week.

The American Academy of Pediatrics is against the use of medical marijuana in children, and a doctor told My Fox New York that the drug can be toxic to children’s developing brains. Also, there isn’t enough known about marijuana’s long-term side effects. But for the Echols family, the benefits significantly outweigh the risks.

“For us the long term side effects that are unknown, for something that can’t kill him, are a lot better than the long term side effects of him beating himself bloody,” Echols said.


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