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Charles Kennedy, one of the first child neurologists in the USA, passed away on October 6, 2015 in Maine at the age of 95 following a brief illness. Born in Buffalo, NY, he attended Nichols School and later Deerfield Academy. He graduated from Princeton University with honors in Chemistry in 1942.
At Princeton, in addition to preparing for medical school, he was also a member of the choir, glee club and the Princeton Nassoons (an all male a cappella group). He went on to receive his MD degree at the University of Rochester while in the Navy V-12 program. Internship was at Yale New Haven Hospital during which time World War II ended. After the war, he remained on active duty in the Navy where he was assigned to the Veterans Administration Psychiatric Hospital in Canandaigua, NY.
Following his 2 years of military service, he went through a pediatrics residency at the Childen’s Hospital of Buffalo. Neurology and Child Neurology training was with Sidney Carter at the Neurological Institute in New York. During this time, Kennedy and Carter published an article on optic neuritis in children and the risk for multiple sclerosis, a paper that spurned future research . Following his fellowship, Charles was appointed Chief of Neurology at the Children’s Hospital of Philadelphia.
Kennedy had a very strong interest in the cerebral blood flow and metabolic requirements of the developing brain. Very early in his career, he developed a close collaboration with Louis Sokoloff, also a physician scientist who never practiced medicine except during internship at Philadelphia General Hospital. As early as 1957, Kennedy et al. (J Clin Invest) used the Kety-Schmidt method (a modification of the Fick Principle) to show for the first time that children require higher cerebral blood flow and oxygen utilization than adults.
In 1967, Kennedy took a sabbatical at the Laboratory of Cerebral Metabolism at the NIH, working with Louis Sokoloff. That sabbatical was a life changing event for Kennedy who decided not to return to his position in Philadelphia but to pursue his research collaboration with Sokoloff at the NIH. He split his time between NIH and Georgetown University School of Medicine, where he was Professor and Chief of Child Neurology. The following years were highly productive and scientifically rewarding. Sokoloff and Kennedy became life-long friends and colleagues; they complemented each other with their skills. A series of experiments investigated the use of various carbon-14 labeled radiotracers and quantitative autoradiography to measure cerebral blood flow.
In 1977, Sokoloff, Reivich , Kennedy and the group published the seminal paper in Journal of Neurochemistry on the 14C-2-deoxyglucose method for the measurement of local cerebral glucose utilization in the rat brain. This method has been widely used in various experimental paradigms in a number of species. Importantly, the method provides the basis for the measurement of glucose metabolism in humans using positron emission tomography (PET), which is now routinely used in the clinical setting.
Lou Sokoloff (left) and Charles Kennedy (right) at the NIH
At Georgetown, Kennedy trained a number of child neurologists who went on to pursue academic careers, including Bennett Lavenstein, Harry Chugani, and Pauline Filippek. He demonstrated great skill clinically. Indeed, there are few who excel both in the clinic and in the laboratory. One of us (HC), as a medical student at Georgetown, was so impressed by his clinical/research activities that I took an elective with Dr. Kennedy at NIH after which I decided to pursue a career in child neurology with a similar area of research. For all those who came in contact with Charles Kennedy he embodied the characteristics of a physician scholar, gentleman, advisor, confidante and role model.
Charles maintained his humor even into his 90’s. He once said: “if you are my age, and you don’t have heart disease or cancer, I guess you just wait for organ failure!” Kennedy is survived by his wife, Eulsum Kennedy, a talented sculptor and painter (of North Korean descent). He joked about her as well by saying: “the reason I remain slim is that my wife has put me on a North Korean diet!” Kennedy is also survived by his sister Florence Davidsen of Iowa City, and 3 children from a previous marriage: Allen Kennedy of NYC, Jacqueline MacMillan of Sommerville, Mass, and Carol Radmer of Valley Park, Mo, and 2 grandchildren. We will miss you Charles.
Harry T. Chugani, MD (Wilmington, DE)
Bennett Lavenstein, MD (Washington, DC)
Cover photo: Charles Kennedy, MD at Children’s Hospital of Philadelphia
Citations: Sokoloff L, Reivich M, Kennedy C, Des Rosiers MH, Patlak CS, Pettigrew KD et al. (1977) The [14C]deoxyglucose method for the measurement of local cerebral glucose utilization: theory, procedure, and normal values in the conscious and anesthetized albino rat.J Neurochem 28 (5):897-916. PMID: 864466.
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The 2nd meeting of the Posterior Fossa Society will take place at the Convention Centre Liverpool on Sunday, June 12th 2016.
The Posterior Fossa Society is an international group of researchers and health care professionals (doctors, nurses, psychologists, speech pathologists, linguists, neuroscientists etc.) who are dedicated to research into the causes, features, treatment and prevention of the postoperative Cerebellar Mutism Syndrome (CMS) and Cerebellar Cognitive Affective Syndrome (CCAS) in children and adults. It reaches its goals by systematically gathering and exchanging information on the CMS and CCAS, both online and during international meetings and conferences.
In the first meeting in Reykjavik, Iceland in June 2015, the definition of postoperative Cerebellar Mutism Syndrome was addressed. In the meeting of the Posterior Fossa Society in Liverpool, the focus will be on prevention and treatment of symptoms. The meeting is open to members and non-members of the Society.
In addition to lectures of experts in the field, in the program, one session is reserved for free papers and opportunity for poster presentations.
Abstract submission for free paper session and posters: You are invited to submit abstracts on the topics of prevention of postoperative CMS and treatment of CMS symptoms. All abstracts are to be submitted on line and should be a maximum of 300 words. The abstract should mention:
'Abstract for PFS meeting'
Title of your abstract,
Author and Co-authors
Abstract text (maximum 300 words)
Presentation preference (platform or poster presentation)
Registration fee:
Early registration (1st of January to 25th of March- 2016) £75.00
Standard registration: (25th of March-13th of May 2016) £95.00
Late registration: (13th of May- 15th of June 2016) £125.00
Registration fees include conference material, lunch and refreshments. Participants of the PFS meeting are invited to the SIOP & PFS Dinner on the 11th June evening at 7.30pm – Maritime Museum Albert Dock - £35 per person.
Please note that the program of the Posterior Fossa Society meeting is specifically designed to compliment the 90 minute session on Cerebellar Mutism Syndrome in the main ISPNO meeting for which abstract submission is also welcome.
see http://www.ispno2016.com/pfs.php for more details
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Twelfth Göttingen Meeting of the German Neuroscience Society (March 22 – 25, 2017)
The Göttingen Meeting of the German Neuroscience Societies is one of the largest multi-disciplinary neuroscience meetings in Europe with around 1.700 participants. It covers a wide range of research fields in the neurosciences including vertebrate and invertebrate systems, molecular, cellular and systemic neurobiology, neuropharmacology, developmental, computational, behavioral, cognitive and clinical neuroscience.
The call for symposia for the 12th Göttingen Meeting of the German Neuroscience Society is open now. Symposia dealing with all areas of neuroscience research are invited. The application must be submitted via the meetings website. The meeting's language is English.
The deadline for submissions is Monday, February 15, 2016.
36 symposia (i.e. six symposia in six parallel sessions) with will be accepted.
- The symposium proposal must contain the following information:
- The title of the symposium
- The name of the organizer(s)
- A short description of the symposium
- The name and address of each of the four intended speakers
- The titles (tentative) of the talks
The organisers must adhere to the following rules:
- Organizers of a symposium in 2015 are not entitled to organize a symposium in 2017
- The title for the symposium should be succinctly worded and should not exceed 100 characters including spaces.
- The proposal should contain a short description in English not exceeding 5.000 characters including spaces.
- Members of the program committee can be invited speakers of a symposium but cannot be the sole organizer of a symposium.
- The duration of a symposium is 2 hours. The maximum number of speakers if four. The affiliation and the (tentative) title of each speaker must be provided.
- Two oral communications by young predoctoral students must be included in the symposium. These will be selected by the symposium organizer from the abstracts submitted in fall 2016.
Symposia are self-supporting, it is the obligation of the symposium organizer to raise the necessary funds for the symposium. The German Neuroscience Society cannot guarantee financial support. Both the organizers and the invited speakers of a symposium have to pay registration fee.
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There have been nearly 60 cases identified in California from 2012 - 2015 of acute flaccid myelitis, a rare syndrome described as polio-like, with most patients being children and young adults, according to a study in the December 22/29 issue of JAMA. The cause of the condition in these cases remains unknown.
With the elimination of wild poliovirus in populations throughout most of the world, the clinical syndrome of acute flaccid paralysis (characterized by weakness or paralysis and reduced muscle tone) due to spinal motor neuron injury has largely disappeared from North America. Despite occasional case reports, the absence of centralized public health surveillance for non-polio acute flaccid paralysis in the United States has precluded accurate incidence estimates. In the fall of 2012, the California Department of Public Health (CDPH) received 3 separate reports of acute flaccid paralysis cases with evidence of spinal motor neuron injury. No such cases had been reported to the program during the preceding 14 years. In response to these unusual case reports, the CDPH implemented enhanced surveillance for similar cases with the goal of characterizing observed cases and identifying possible causes.
Keith Van Haren, M.D., of Stanford University, Palo Alto, Calif., and colleagues summarized reported cases of acute flaccid myelitis, which encompasses a subset of acute flaccid paralysis cases, in patients with radiological or neurophysiological findings suggestive of spinal motor neuron involvement reported to the CDPH with symptom onset between June 2012 and July 2015. Cerebrospinal fluid, serum samples, nasopharyngeal swab specimens, and stool specimens were submitted to the state laboratory for infectious agent testing.
Fifty-nine cases were identified. Median age was 9 years (50 of the cases were younger than 21 years). Symptoms that preceded or were concurrent included respiratory or gastrointestinal illness (n = 54), fever (n = 47), and limb myalgia (n = 41; muscle pain). Among 45 patients with follow-up data, 38 had persistent weakness at a median follow-up of 9 months. Two patients, both immunocompromised adults, died within 60 days of symptom onset.
Enteroviruses were the most frequently detected pathogen in either nasopharynx swab specimens, stool specimens, serum samples (15 of 45 patients tested). No pathogens were isolated from the cerebrospinal fluid. The incidence of reported cases was significantly higher during a national enterovirus D68 outbreak occurring from August 2014 through January 2015 compared with other monitoring periods.
"The etiology of acute flaccid myelitis cases in our series remains undetermined. Although the syndrome described is largely indistinguishable from poliomyelitis on clinical grounds, epidemiological and laboratory studies have effectively excluded poliovirus as an etiology," the authors write.
The researchers note that "ongoing surveillance efforts are required to understand the full and potentially evolving levels of infectious agent-associated morbidity and mortality."
"To our knowledge, the California surveillance program for acute flaccid paralysis is the first to use specific case criteria and report subsequent incidence data for the subset of paralysis cases attributable solely to acute flaccid myelitis and may serve as a guide for similar surveillance efforts in the future."
Reference:
Van Haren K, Ayscue P, Waubant E, et al. Acute Flaccid Myelitis of Unknown Etiology in California, 2012-2015. JAMA. 2015;314(24):2663-2671. doi:10.1001/jama.2015.17275.
Cover image: Sagittal and Axial Magnetic Resonance Imaging (MRI) of the Spinal Cord From Representative Patients in This Case Series
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Researchers have discovered how immune cells triggered by recurrent Strep A infections enter the brain, causing inflammation that may lead to autoimmune neuropsychiatric disorders in children. The study, performed in mice, found that immune cells reach the brain by traveling along odor-sensing neurons that emerge from the nasal cavity, not by breaching the blood-brain barrier directly. The findings could lead to improved methods for diagnosing, monitoring, and treating these disorders.
The study, led by researchers at Columbia University Medical Center (CUMC) and the University of Minnesota, Minneapolis, was published today in the online edition of the Journal of Clinical Investigation.
Recurrent Group A streptococcus (S. pyogenes) infections, which cause "strep throat," have been linked to autoimmune neuropsychiatric disorders, notably Pediatric Autoimmune Neuropsychiatric Disorders associated with Streptococcal infections, or PANDAS. Children with PANDAS exhibit Tourette's syndrome-like motor and vocal tics or obsessive-compulsive behaviors that appear to happen "out of the blue."
The Strep A bacterial cell wall contains molecules similar to those found in human heart, kidney, or brain tissue, according to a co-leader of the study, Dritan Agalliu, PhD, Assistant Professor of Pathology and Cell Biology (in Neurology and Pharmacology) at CUMC. These "mimetic" molecules are recognized by the immune system, which responds by producing protective antibodies. But because of this molecular mimicry, the antibodies react not only to the bacteria but also to the host tissues, producing autoantibodies that attack the body's own tissues. Previously, scientists did not understand how these autoantibodies would gain access to the brain, because brain vessels form an extremely tight blood-brain barrier that prevents free movement of molecules, antibodies and immune cells from the blood into the brain.
A few years ago, researchers discovered that recurrent Strep A infections trigger the production of immune cells known as Th17 cells, a type of helper T cell, in the nasal cavity. But it was unclear how these Th17 cells lead to brain inflammation and symptoms such as those seen in children with PANDAS.
Studying the tissues of mice infected intranasally with Strep A, Drs. Agalliu and colleagues found that bacterial-specific Th17 cells move along the surface of olfactory, or odor-sensing, axons that extend from the nasal cavity through the cribriform plate, a sieve-like bone that separates the nasal cavity from the brain. From there, the cells reach the olfactory bulb in the brain, which processes information about odors.
"Once the Th17 cells enter the brain, they break down the blood-brain barrier, allowing autoantibodies and other Th17 cells to enter the brain and promote neuroinflammation," said Dr. Agalliu. "What's interesting is that we see abundant Group A Strep bacteria in the nose, but they never penetrate the brain," he added. "This is different from Group B Strep--the cause of bacterial meningitis--which causes neuroinflammation by entering the brain directly."
The findings may lead to a more definitive diagnostic test for PANDAS, which is currently diagnosed based on clinical symptoms and the presence of Strep A infection or autoantibodies against brain proteins. "We are also interested in exploring ways to treat the disorder by repairing the blood-brain barrier itself to prevent the entry of autoantibodies into the brain," said Dr. Agalliu.
Citation:
Group A Streptococcus intranasal infection promotes CNS infiltration by streptococcal-specific Th17 cells
Thamotharampillai Dileepan, Erica D. Smith2, Daniel Knowland, Martin Hsu, Maryann Platt, Peter Bittner-Eddy, Brenda Cohen, Peter Southern, Elizabeth Latimer, Earl Harley, Dritan Agalliu, and P. Patrick Cleary
Published December 14, 2015
J Clin Invest. 2015. doi:10.1172/JCI80792.
Cover image: Group A Streptococcus
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