Medical Writer: WE MOVE (Worldwide Education and Awareness for Movement Disorders)
Medical writer for this movement disorders education group, whose audience
includes both professionals and patients. Expertise in the etiologies and treatments of Parkinson's
disease, Huntington's disease, dystonia, and other movement disorders. Responsible for
booklets, slide lecture kits, manuscript editing, web pages, and current research news briefs.
Read issues of E-Move, my electronic newsletter of new research for movement disorder professionals.
Medical Editor: Parkinson's Disease: A Teaching Slide Set for Neurologists New York: WE MOVE, 2003
Medical Editor: Spasticity: Etiology, Evaluation, Management, and the Role of Botulinum ToxinWE MOVE, 2002
Editor and project coordinator for this 15-chapter, multi-authored, 250-page supplement on
spasticity and the role of botulinum toxin in its management. Responsible for all phases of editing;
research and rewriting to include recent findings; illustration planning and coordination. Originally published as Muscle & Nerve, Supplement 6 1997.
Writer: "Mechanical Ventilation for Neuromusculoskeletal Disease: A Video for Medical Professionals" Muscular Dystrophy Association, 1998
Writer: Medical news reports for Doctor’s Guide
Writer: Articles for Neurology Today, the monthly news magazine for practicing neurologists from the American Academy of Neurology
"Normal Alpha-synuclein is Triple Threat in Parkinson Disease," January 2004
In the drama of Parkinson’s disease etiology, alpha-synuclein made its spectacular debut in 1997, with the discovery that two gene mutations were linked to rare familial cases, and shortly thereafter that the protein was the major component of Lewy bodies, the pathological hallmark of PD. But whether normal alpha-synuclein (AS) is villain or victim in this play, and whether its role is closer to star or supporting player is still unknown.
Now, a team of researchers has found that possessing extra copies of the normal AS gene can cause familial Parkinson’s disease. This dramatic discovery at once moves alpha-synuclein closer to center stage, and focuses the spotlight even more brightly on protein accumulation as a true malefactor in the pathology of neurodegenerative diseases.
"Evidence Aggregates Against Alpha-synuclein in Varied Neurologic Disorders,"
January 2004
Alpha-synuclein is well-known for its key role in Parkinson’s disease. But it is also found in the brain pathology of Alzheimer’s disease and half a dozen other neurological disorders. Alpha-synuclein deposits may occur by themselves, but also frequently co-localize with deposits of tau and A-beta. What are the pathological features of these “alpha-synucleinopathies,” and what can their common features tell us about neurodegenerative disease? John Trojanowski, MD, PhD, untangled these issues and more in his lecture at the 33rd Annual Meeting of the Society for Neuroscience, held in New Orleans November 8-12, 2003.
"News from the Society for Neuroscience:
Your Brain on Drugs: What Research Suggests,"
January 2004
Drug abuse, like the poor, seems always to be with us. The problem has so far largely resisted any approach-- moral, criminalistic, or psychological--brought to bear on it, and as a consequence, progress against drug addiction has been limited. But new a understanding of the profound alterations of reward and inhibitory control that occur in the addicted brain at least offers insight into the powerful hold that drugs of abuse have on their victims, and why “just saying no” is so difficult for the addicted person.
"Neuroplasticity in the Transition to Addiction,"
January 2004
In explaining the difficulty of changing habitual behavior, the psychologist William James rebutted the drunken Rip Van Winkle’s excuse for every new fall from the wagon: “I won’t count this time!” “He may not count it,” James said in 1892, “but it is being counted none the less. Down among his nerve-cells and fibres the molecules are counting it, registering and storing it up to be used against him when the next temptation comes.”
One of the key questions in drug addiction research is what the nature of that “counting” is: what changes among the nerve cells to make the transition from using drugs to being addicted to them? In an exegesis on James’s formulation that drew on psychology, neuroanatomy, and molecular genetics, Terry Robinson, PhD, explored the role of neuroplasticity in the development of addiction in a lecture at the 33rd Annual Meeting of the Society for Neuroscience.
"ALS: It Takes a Neighborhood,"
December 2003
Amyotrophic lateral sclerosis is due to the progressive death of a single type of cell, the motor neuron. But while many have assumed its demise is largely due to factors acting within the motor neuron itself, the evidence to support that assumption has never been strong. Now, a new study shows that in a mouse model of ALS, the health of nonneuronal cells, not of the neurons themselves, is the key determinant of whether motor neurons live or die. As well as shedding light on the fundamental pathogenic events of ALS, these results have significant, and hopeful, implications for ALS therapy.
"RNA Repeats Its Role in New Disease,"
December 2003
When it was first described in 2001, fragile X-associated tremor/ataxia syndrome (FXTAS) seemed a bit hard to believe. The syndrome appeared in some elderly male relatives of boys with fragile X syndrome, but its manifestations were entirely different: instead of mental retardation, it was characterized by a movement disorder, and there was an underlying neurodegenerative process not seen in fragile X syndrome.
Now, a fly model of FXTAS, which displays the same expanded RNA repeat found in FXTAS patients, has quashed any lingering doubts about the reality of the syndrome, and at the same time strengthened the case for a particular model of its etiology—that the RNA, rather than being a mere intermediary, is itself the toxic entity. With this discovery, FXTAS joins a small but growing list of neurological diseases in which aberrant RNA plays a direct pathogenic role.
"Closing in on 10q: Is a Major New Alzheimer Gene in Sight?"
November 2003
In the hunt for the genetic basis of Alzheimer’s disease, chromosome 10q has become a tantalizing target. Several groups have independently shown that a small region on it influences age of onset for AD, and as more linkage studies are done, the target region has shrunk ever smaller. The gene or genes, however, remain elusive. Several candidate genes in the region have been proposed, but, without strong genetic evidence to support them, none has yet garnered much enthusiasm from the Alzheimer’s research community at large.
Now, a group from the Karolinska Institute thinks it has scored a bulls-eye. If they are right, the discovery not only identifies a clinically important gene but also may significantly advance the understanding of Alzheimer’s disease pathogenesis. Have they found the elusive quarry? Or might they have missed the target?
"Restless Legs Syndrome: Quality of Life is Impaired, Dopamine Agonist Effective," September 2003
Restless legs syndrome (RLS) affects as many as 10% of Americans, making it one of the most common of all neurological disorders. While in some patients the symptoms are only mildly bothersome, in others the unpleasant sensations and urge to move can have a significant impact on quality of life. Exactly how significant was made clear recently in a study led by Richard Allen, MD. At the same time, dopamine agonists have recently emerged as a highly effective form of treatment for RLS symptoms, and a recent study led by Charles Adler, MD, indicates the potential of one such agent, ropinirole. Both studies were presented here at the 55th Annual Meeting of the American Academy of Neurology.
"CMT: A Ubiquitous Gene, Delimited Disease, and Surprising Discovery," July 2003
More than a century passed between the first description of Charcot-Marie-Tooth disease in 1886, and the discovery of the first gene for the disease in 1991. Since then, more than two-dozen CMT genes have been identified, and the number is growing even higher. While this finding has clinical importance, its real importance might be the insight it could offer into the function of peripheral nerves, and what makes them so vulnerable to such varied genetic defects.
"Slowed Axonal Transport Identified in Motor Neuron Disease," June 2003
"Parkinson Trials: Neuroimaging Data, Often at Odds with Clinical Evidence, Deserves a Closer Look," March 2003
"Levodopa: Is it Neurotoxic, Neuroprotective - Or None of the Above?," February 2003
"Deep Brain Stimulation: Experts Debate Related Neuropsychological Risks," February 2003
"Fetal Transplant Study Results Prompt Call for Halt to Future Trials," January 2003
"American Academy of Cerebral Palsy and Developmental Medicine Annual Meeting:
The Best Surgery Options for Cerebral Palsy Spur Heated Debate," January 2003
"Rapid-Paced Genetic Discoveries Help Unravel the Pathogenesis of Myotonic Dystrophy, January 2003
"Higher Dose, Higher Frequency Improves Interferon Treatment for MS," August 2002
"Studies Confirm Promise of Deep Brain Stimulation for Parkinson Disease," July 2002
"New Data in on Detection, Progression, and Treatment of Huntington Disease," July 2002
"On Biochemical Terrorism:
Neurologists on the Front Lines Need to be Prepared," June 2002
"Clinical Applications of Stem Cells are Nearing Reality, Says Leading Neuroscientist," June 2002
"Age-at-Onset Gene Linked for Parkinson Disease and Alzheimer Disease," June 2002
"Town Hall Forum:
Panelists Debate Medical Privacy in the Information Age," June Supplement 2002
"Fetal Transplantation Found Risky for Huntington Disease," March 2002
"How to Deal With Somnolence and Sleep Attacks in Parkinson Patients," March 2002
"The Neurobiology of Emotion: Feeling the Way Toward a Map of the Emotions," January 2002
"Atypical Antipsychotics Useful for Treating Symptoms in Parkinson Disease," November/December 2001
"Stroke Strikes as a Global Burden, November/December 2001
"Viral Factors Explored in Etiology of Parkinson Disease," September/October 2001
"Gene Therapy is Evolving as Approach to Peripheral Neuropathies," September/October 2001
"Muscular Dystrophies: New Findings Signal a Greater Complexity, "September/October 2001
Writer: Articles for Neurology
Reviews, the monthly news magazine for practicing neurologists
"Tremor, Ataxia, and Dementia: An Expanding Role for FMR1 in Neurological Disease" 2003 A new movement disorder syndrome is due to an old and familiar gene mutation, according to a growing body of research. The disorder, which primarily affects older men, is called Fragile X-associated Tremor Ataxia Syndrome, or FXTAS (“fax-tass”). The mutation is a shorter version of the triplet repeat responsible for fragile X syndrome, the most common heritable cause of mental retardation. And some cases of yet another neurologic disorder, multiple system atrophy, may also be linked to this mutation.
"Lowering the Risk of Tardive Dyskinesia with Atypical Antipsychotics" 2003 Choosing the right neuroleptic medication can be a devil’s bargain, in which antipsychotic efficacy must be balanced against the risks of serious adverse effects. Of these, the abnormal movements of tardive dyskinesia (TD) have rated as among the most serious. The promise of “atypical” neuroleptics has been that they reduce the likelihood of development of tardive dyskinesia compared to the older drugs. Until now, however, no study has examined the relative risk of typical versus atypical agents in those patients most at risk for TD: older patients who have already started to develop abnormal movements. Dilip Jeste, MD, and Christian Dolder, MD, addressed this issue in a new study of patients with borderline tardive dyskinesia.
"Imaging
May Be the Best Means of Tracking Neuroprotection" January 2000 Neuroprotection--the
ability to protect neurons from degeneration in the face of a toxic threat-- has
long been the Holy Grail of Parkinson's disease treatment. But, as outlined
recently by Ira Shoulson of the University of Rochester Medical Center, although
the search is on, "a sobering look will conclude that we do not yet have
neuroprotective therapy for Parkinson's disease, at least not the type of
intervention of sufficient magnitude and duration that we can yet confident
about." "Yesterday's
Toxin, Today's Treatment--A Host of New Uses?" January 2000 Within
the past decade, botulinum toxin has undergone an extraordinary transformation,
moving from the therapeutic fringe to center stage as a treatment for a large
and growing number of neuromuscular disorders characterized by muscle
overactivity. "How Clinically Meaningful
Are Surgical Benefits for Patients with Parkinson's Disease?" November 1998 When
William Weiner and William Koller met recently in a "Crossfire" on the
merits of surgery for Parkinson's disease, they found little enough to agree on
that the lively program lived up to its name. Koller, of the University of
Kansas Medical School, was enthusiastic about the efficacy and safety of current
procedures, and optimistic about new ones. On the other hand, Weiner, of the
University of Miami School of Medicine, was highly skeptical, portraying most
procedures as risky, barely effective, unproven, or all three. The debate
occurred at the Annual Meeting of the American Academy of Neurology in
Minneapolis. "The Complexity of Complex
Regional Pain Syndrome" June 1999 Complex
regional pain syndrome (CRPS) is one of the most difficult pain disorders to
diagnose and treat. The difficulty stems in part from poor understanding of the
underlying pathophysiology, and in part from the wide variety of possible
presentations in the disorder, even within a single patient and in the course of
a single day. Leading figures in the field tried to untangle this complex
disorder at a recent symposium, held in San Diego at the 17th annual meeting of
the American Pain Society, in November, 1998. "The Persistent Biological
Consequences of Early Untoward Life Events" September 1999 "There
is no doubt in my mind that early trauma is associated with persistent changes
in the brain," said Charles Nemeroff, Professor and Chairman of the
Department of Psychiatry and Behavioral Sciences at the Emory School of
Medicine, in a speech before the 52nd Annual Meeting of the American Psychiatric
Association in May of 1999 in Washington, D.C. "New Strategies for Delaying
Motor Complications in Parkinson's Disease" November 1999 Motor
complications—dyskinesias, wearing off, and unpredictable "off"
periods—are among the most troubling and difficult-to-treat complications of
long- term Parkinson's disease therapy…New research, presented at the XIIIth
International Congress on Parkinson's Disease, now suggests that early
monotherapy with dopamine agonists may delay the onset of dyskinesias and other
motor complications in many patients. Furthermore, basic research into the
cellular changes accompanying motor fluctuations is providing the rationale for
new classes of drugs with potential benefit in Parkinson's disease. The Congress
was held in Vancouver July 24-28, 1999. "Cannabinoids in Movement
Disorders" November 1999 Will
Parkinson's disease be the next target for medical marijuana? It is too soon to
tell, but a spate of recent reports have begun to shed light on the importance
of cannabinoid receptors in the control of movement, and even to suggest their
manipulation may have significant therapeutic potential for parkinsonism and
other movement disorders. "Huntington's Disease: Do the
Benefits of Genetic Testing Outweigh the Risks?" October 1998 "New Research on the
Ketogenic Diet" December 1998 "Is the Time Right for
Transplantation in Huntington's Disease?" February 1999 "Institutionalization and
Mortality in Parkinson's Disease" February 1999 "Neuroleptics are Often the
Suspects in HIV Movement Disorders" April 1999 "New Directions in Magnetic
Resonance Imaging Methods" May 1999 "Neural Plasticity Following
Brain Injury" September, 1999 "Dementia and Normal Aging in
the Very Old" October 1999 "Inflammation in Parkinson's
Disease" December 1999
Back to my main page.
Also visit us at Hopestill Farm
rrobinson@nasw.org
117 Mill St.
Sherborn, MA 01770
508-653-5421