7 remarkable patients who determined the course of neuroscience

It is no exaggeration to say that most progress in medicine has been achieved one unfortunate patient after another. Either by accident, or by misguided design, our understanding of human physiology and pathology have frequently come at the expense of the misfortune of countless patients, and it continues to do so. Whilst large trials teach us a lot about the characteristics of diseases, it is however the single case study that often reveals the most defining insights. For example, it was the accidental gunshot injury sustained by Alexis St Martin that led to our understanding that the gastric phase of digestion depends on the acid produced by the stomach. The gory injury resulted in a permanent fistula between St Martin’s stomach and his skin, a veritable window through which the army doctor, William Beaumont, peered to see nature at work.

By Jesse Shire Myer – A book, Life and Letters of Dr. William Beaumont …, Public Domain, Link

But enough of other organs; our interest is of course the nervous system. Who then were the tragic heroes of neuroscience, the valiant who submitted their bodies in life, and their brains in death, for the advancement of science? Who are the famous, and the infamous, in the annals of the brain? Here is our run down of 7 remarkable patients who defined the history of neuroscience.

Brain with Hands. Michael Coglan on Flickr. https://www.flickr.com/photos/mikecogh/21837053882


7. Patient SM

Patient SM is one of the lesser known figures in neuroscience, but her contribution to the science of emotions is immense. As someone who simply did not know what it was to experience fear, she provided the clues to the anatomical foundations of our passions. It turned out that the source of her fearlessness were lesions in her amygdala. It is little wonder that her life was characterised by risky ventures and perilous experiences, as she was incapable of detecting and avoiding danger. The amygdala is now established as the command and control centre for the emotions. One could argue, albeit unoriginally, that to lose one amygdala may be an accident, but to lose both will have to be termed a disaster. And in the case of Patient SM, her catastrophe is a result of Urbach–Wiethe disease, a disorder which destroys both amygdalas…but mercifully spares the hippocampus.

By Images are generated by Life Science Databases(LSDB). – from Anatomography, website maintained by Life Science Databases(LSDB).You can get this image through URL below. 次のアドレスからこのファイルで使用している画像を取得できますURL., CC BY-SA 2.1 jp, Link

6. Anna ‘O’

By Original uploader was Kaesar at it.wikipediaLink

Bertha Pappenheim, better known by her nickname ‘Anna O‘, was the seminal hysterical patient reported by Josef Breuer and Sigmund Freud. It is probably to her singular credit that the concept of hysteria became a neuroscience curiosity, even if this was on the fringes. Her constellation of symptoms will however be familiar to every neurologist: limb paralysis, speech difficulties, visual impairment, hallucinations, and episodes of loss of consciousness. It is clear that this disorder lives on, and after several iterations, now comes under the remit of functional neurological disorders (FND). It is interesting that Freud had the largely correct insight that behind many cases of hysteria lies some form of trauma.

5. Blanche Wittman

By André Brouillet – Photo prise dans un couloir de l’université Paris V, Public Domain, https://commons.wikimedia.org/w/index.php?curid=3820726

The great French neurologist Jean-Martin Charcot is not a person to be outdone by other neuroscientists, and this applies to his one-time protege, Sigmund Freud. It is therefore not surprising that in studying hysteria, he outdid Freud by finding a more remarkable subject called Blanche Wittman. She became his star attraction in the demonstrations he held at the Pitié-Salpêtrière Hospital where she performed for the great and the good of French neurology. It is in this way that she achieved abiding fame in the iconic painting of Pierre Aristide André Brouillet. Her dramatic hysterical attacks earned her the sobriquet ‘The Queen of Hysterics‘, but her contribution to the actual science of the brain is rather underwhelming. There is however no denying that she is a lasting landmark in the history neuroscience.

4. Auguste Deter

By Unknown authorUnknown source, Public Domain, Link

Whilst the name Alois Alzheimer has gone down in history for describing the fearsome dementia that bears his name, the name of the patient who made it all possible is not a household one at all. Auguste Deter was the first person to be diagnosed with the horrendous disease which still ravages mankind, and without any cure in sight. After studying her illness in life, Alzheimer had the fortune of examining her brain after her death. It is his detailed examination that revealed what we now know as the hallmarks of the disease, senile plaques and neurofibrillary tangles. It is remarkable that a recent analysis of Alzheimer’s preserved histopathological slides revealed that Auguste Deter carried the classical presenilin 1 (PSEN1) gene mutation that is associated with the disease. Can neuroscience ever be any more satisfying than that!

3. Louis Victor Leborgne

By Polygon data were generated by Database Center for Life Science(DBCLS)[2]. – Polygon data are from BodyParts3D[1], CC BY-SA 2.1 jp, Link
Yet another watershed neuroscience patient whose name doesn’t often ring any bells, or flow easily off the tongue. Leborgne’s misfortune was to develop a curious inability to speak, now recognised as expressive aphasia. He was only able to communicate with a single word, tan, and this explains his nickname, Patient Tan. Paul Broca’s fortune, on the other hand, was to study Leborgne in life, and to examine his brain after death. This singular patient made Broca a household name because this type of speech difficulty is also known as Broca’s aphasia. Broca also localised the lesion responsible for Leborgne’s aphasia, and it was in a part of the dominant hemisphere now known as Broca’s area. Two eponyms for the price of one you may say. Leborgne is also probably the turning point for the contentious concept of cerebral localisation, resurrecting it from the ashes of phrenology.

2. Phineas Gage

By Author of underlying work unknown. – File:PhineasPGage.jpg, Public Domain, Link

Phineas Gage is remarkable for achieving what few other neuroscience patient have, entry into popular folklore. The victim of a work-related accident, Gage sustained a unique form of brain injury when he was impaled by a tamping rod whilst trying to set explosions as part of his work as a rail construction worker. The explosion was accidentally set off prematurely, and the rod was propelled through Gage’s left cheek bone, through his left eye socket, and it then penetrated both frontal lobes. It was remarkable that Gage was not physically inconvenienced immediately following the accident, but surviving the whole affair was just the beginning of his real misfortune; his personality, previously calm and dedicated, became volatile and disinhibited. In relating the story of Gage, there is no getting away from a famous quotation; those who knew him before his accident pithily remarked that Gage ‘was no longer Gage‘. It is to his misfortune that we owe our understanding of the important role the frontal lobes play in regulating personality and behaviour.


1. Henry Molaison

By Images are generated by Life Science Databases(LSDB). – from Anatomography, website maintained by Life Science Databases(LSDB).You can get this image through URL below. 次のアドレスからこのファイルで使用している画像を取得できますURL., CC BY-SA 2.1 jp, Link

Known only as Patient HM throughout his life, Henry Gustav Molaison is perhaps the most important patient to ever cross the path of neuroscience. He earned this distinction on account of the profound amnesia he developed after he underwent brain surgery to control his severe epilepsy. Very bravely, his neurosurgeon, William Beecher Scoville, removed large chunks of his temporal lobes on both sides, a previously unheard of procedure. His epilepsy became largely controlled, but the aftermath was a disaster; he lost the ability to form new memories. As it has become a familiar refrain by now, Henry’s misfortune became a boon for neuroscience. He became probably the most extensively studied patient in the history of brain science; he spent the rest of his life undergoing one neuropsychological test or the other until neuroscientists obtained a thorough understanding of the anatomical and functional foundations of memory formation. Whilst the key lesson from his case is the important role of the hippocampus in memory formation, there is so much more he contributed to brain science in life. And even after death, his brain is an object of fascination for neuroscientists; they opened up his skull as soon as he died, took out his brain, and cut it up into tiny slices for further study. Henry is therefore the ultimate neuroscience patient who keeps giving even after departing this mortal coil.

Over the next few weeks I will be reviewing three excellent books on Henry Molaison in my book review blog, The Doctors Bookshelf. Why not follow me there to find out more about the remarkable man.


Do you want to explore more interesting neuroscience patients?

Here are 9 to satisfy your urge!



Giovanni A

Jane Avril


Little Hans

Marquis de Dampierre

Patient JP

Patient NA

The emerging links between Alzheimer’s disease and infections

Alzheimer’s disease (AD) is one of the most fearsome and recalcitrant scourges of neurology. We think we know a lot about it; after all it has been a quite a while since Alois Alzheimer described amyloid plaques and neurofibrillary tangles in his index patient, Frau Deter. But the more neuroscientists study the disease, the murkier the field looks. For example, we are still not quite sure what the plaques and tangles really signify; for all we know, they may just be innocent bystanders, powerless by-products of a neurodegenerative process that defies understanding. We have accumulated an endlessly long list of AD risk factors, but we have singularly been unable to point a finger at the cause of AD.

By National Institute on Aging – http://www.nia.nih.gov/alzheimers/topics/alzheimers-basics, Public Domain, Link

This elusive void may however be a void no longer, if what superficially appears to be an outlandish theory turns out to be correct. And the theory is that AD is caused by infection! Just take a deep breathe, and allow yourself the space to make a giant leap of imagination. My attention was first drawn to the infective hypothesis of AD by a headline in Scientific American screaming Controversial New Push to Tie Microbes to Alzheimer’s Disease. The obvious key word here of course is controversial: is it possible that AD, this quintessential neurodegenerative disease, is…just another chronic infection?

Alzheomer’s at the microscopic level. Oak Ridge National Laboratory on Flickr. https://www.flickr.com/photos/oakridgelab/4071453587

To find the original source of the story, the trail of bread crumbs led to an editorial published in the Journal of Alzheimer’s Disease in 2016, plainly titled Microbes and Alzheimer’s Disease. But this is not a run-of-the-mill editorial at all because it was written by 33 senior scientists and clinicians from a dozen countries. And their reason for an alternative theory of AD is simple: amyloid, the long-suspected culprit for decades, has failed to live up to its billing. They point  out that amyloid exists harmlessly in the brains of many older people who never go on to develop dementia. They also cite studies which demonstrate that treating amyloid, by immunological means, does not improve the state of people suffering from AD. Amyloid, in other words, is not such a bad guy after all. But all the while we have been setting traps to ensnare it, the microbial villains have been running amok, having a field day.

Автор: own work – adapted from http://www.pdb.org/pdb/cgi/explore.cgi?pdbId=1IYT using PyMOL, Суспільне надбання (Public Domain), Посилання

But why should microbes succeed where amyloid, the ubiquitous protein, has woefully failed? The editorial gave 8 good reasons to argue that the infection theory is better than the amyloid hypothesis. One reason is that the brains of people with AD are often riddled with inflammation, a characteristic feature of infections. Another reason is the observation that AD can be transferred to primates when they are inoculated with the brain tissue of someone with AD.

194 001 001. US Department of Energy on Flickr. https://www.flickr.com/photos/departmentofenergy/14534273083

It may be hard to swallow, but if you are still maintaining your imaginative leap, just spare a thought for the microbes that are on the line-up of competing suspects. Take your pick, from helicobacter pylori to fungal infections, from spirochetes such as Lyme neuroborreliosis to chlamydia, from cytomegalovirus (CMV) to polymicrobial infections. But of all the potential suspects, one stands head and shoulders above the rest (no fungal pun intended-honest).

E. coli bacteria. NIAID on Flickr. https://www.flickr.com/photos/niaid/16578744517

And the culprit with the most number of index fingers pointing at it is herpes simplex virus type 1 (HSV1). The editorial tells us that there have been about 100 publications, by different groups, demonstrating that HSV1 is a ‘major factor‘ in the causation of AD. Some of these studies have shown that people with AD have immunological signs of significant HSV infection in their blood. The editorial goes further to review the possible mechanisms by which HSV1 may cause AD; one of these is the possibility that the virus lowers the risk of AD in people who possess the APOE ɛ4 allele genetic liability.

Von Thomas Splettstoesser (www.scistyle.com) – Eigenes Werk, CC BY-SA 4.0, Link

Just when you are getting your head round the idea, the infection theory takes a very sinister turn. And this relates to the perverse modus operandi of the microbes. The authors tell us that the microbes first gain access to the brains of their victims when they (the victims) were much younger. Like sleeper cells in their ghoulish crypts, the microbes hibernate, biding their time until their victims get older, and their immunity declines. The microbes then awaken, and like malevolent zombies, set out to wreak gory mayhem and cataclysmic destruction. And they do this either by causing direct damage to the brain, or indirectly by inducing inflammation.

Microbes. Quin Dombrowski on Flickr. https://www.flickr.com/photos/quinndombrowski/4067633894

You can now descend form your giant imaginative leap and start to wonder: if AD is indeed caused by microbes, what can we do about it? ‘Tis time for some down-to-earth deep thinking.

What are the new diseases emerging in neurology?

Medical futurists predict that scientific advances will lead to more precise definition of diseases. This will inevitably result in the emergence of more diseases and fewer syndromes. This case is made very eloquently in the book, The Innovators Prescription. Many neurological disorders currently wallow at the intuitive end of medical practice, and their journey towards precision medicine is painfully too slow. Neurology therefore has a great potential for the emergence of new disorders.


In the ‘good old days’, many diseases were discovered by individual observers working alone, and the diseases were named after them. In this way, famous diseases were named after people such as James Parkinson, Alois Alzheimer, and George Huntington. For diseases discovered by two or three people, it didn’t take a great stretch of the imagination to come up with double-barrelled names such as Guillain-Barre syndrome (GBS) or Lambert-Eaton myasthenic syndrome (LEMS).

By uncredited - Images from the History of Medicine (NLM) [1], Public Domain, https://commons.wikimedia.org/w/index.php?curid=11648572
By uncredited – Images from the History of Medicine (NLM) [1], Public Domain, https://commons.wikimedia.org/w/index.php?curid=11648572
Today, however, new diseases emerge as a result of advances made by large collaborations, working across continents. These new diseases are named after the pathological appearance or metabolic pathways involved (as it will require an act of genius to create eponymous syndromes to cater for all the scientists and clinicians involved in these multi-centre trials). This is unfortunately why new disorders now have very complex names and acronyms. Take, for examples, chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) and chronic relapsing inflammatory optic neuropathy (CRION). It is a sign that we should expect new neurological diseases to be baptised with more descriptive, but tongue-twisting, names.



New disease categories emerge in different ways. One is the emergence of a new disorder from scratch, with no antecedents whatsoever. Such was the case with autoimmune encephalitis, a category which has come from relative obscurity to occupy the centre stage of eminently treatable diseases. I have posted on this previously as What’s evolving at the cutting edge of autoimmune neurology and What are the dreadful autoimmune disorders that plague neurology? Other disease categories form when different diseases merge into a completely new disease category, or when a previously minor diseases mature and stand on their own feet. These are the stuff of my top 8 emerging neurological disorders.


By Photo (c)2007 Derek Ramsey (Ram-Man) - Self-photographed, CC BY-SA 2.5, Link
By Photo (c)2007 Derek Ramsey (Ram-Man) – Self-photographed, CC BY-SA 2.5, Link

1. mTORopathy

This huge monster is ‘threatening’ to bring together, under one roof, diverse disorders such as tuberous sclerosis complex, epilepsy, autism, traumatic brain injury, brain tumours, and dementia. You may explore this further in my previous blog post titled mTORopathy: an emerging buzzword for neurology.

Merging bubbles. Charlie Reece on Flikr. https://www.flickr.com/photos/charliereece/777487250
Merging bubbles. Charlie Reece on Flikr. https://www.flickr.com/photos/charliereece/777487250

2. IgG4-related autoimmune diseases

This new group of neurological diseases is threatening to disrupt the easy distinction between several neurological disorders such as myasthenia gravis (MG), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and Guillain Barre syndrome (GBS). It even includes the newly described IgLON 5 antibody disorder, something I blogged about as IgLON5: a new antibody disorder for neurologists. You may explore IgG4-related disorders in this paper titled The expanding field of IgG4-mediated neurological autoimmune disorders. 

By Aida Pitarch - Own work, CC BY-SA 4.0, Link
By Aida PitarchOwn work, CC BY-SA 4.0, Link

3. Anti-MOG antibody disorders

Now, neurologists have always known about MOG, mostly as a minor bit player, an extra, so to say. No more, it is now all grown up and matured. And the growth is fast and involves many inflammatory demyelinating disease of the CNS such as fulminant demyelinating encephalomyelitis and multiphasic disseminated encephalomyelitis. How far will it go?


4. Hepatitis E virus related neurological disorders

A field which is spurning new neurological disorders is neurological infections, and Hepatitis E virus (HEV) is in the forefront. We are now increasingly recognising diverse Hepatitis E related neurological disorders. HEV has now been linked to diseases such as Guillain Barre syndrome (GBS) and brachial neuritis. And the foremost researcher in this area is Harry Dalton, a hepatologist working from Cornwall, not far from me! And Harry will be presenting at the next WESAN conference in Exeter in November 2017.

By Transferred from en.wikipedia to Commons.This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #5605.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain, Link
By Transferred from en.wikipedia to Commons.This media comes from the Centers for Disease Control and Prevention‘s Public Health Image Library (PHIL), with identification number #5605.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers.English | Slovenščina | +/−, Public Domain, Link

5. Zika virus

Zika virus is another novel infection with prominent neurological manifestations. We are learning more about it every day, and you may check my previous blog post on this, titled 20 things we now know for certain about the Zika virus.

By Manuel Almagro Rivas - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=47941048
By Manuel Almagro RivasOwn work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=47941048

6. Multisystem proteinopathy

Multisystem proteinopathy is a genetic disorder which affects muscles and bone, in addition to the nervous system. It is associated with Paget’s disease of the bone and inclusion body myositis, with implications for motor neurone disease (MND) and frontotemporal dementia (FTD). Quite a hydra-headed monster it seems, all quite complex, and perhaps one strictly for the experts.

Hydra. Andrew Jian on Flikr. https://www.flickr.com/photos/andrew_jian/475479747
Hydra. Andrew Jian on Flikr. https://www.flickr.com/photos/andrew_jian/475479747

7. GLUT-1 deficiency syndromes

GLUT-1 stands for glucose transporter type 1. Deficiency of GLUT-1 results in impaired transportation of glucose into the brainGLUT-1 deficiency syndrome presents with a variety of neurological features such as dystonia, epilepsy, ataxia, chorea, and a host of epilepsy types. It starts in infancy and is characterised by a low level of glucose and lactic acid in the cerebrospinal fluid. Expect to hear more on this in the near future.

Sugar Cubes. David pacey on Flikr. https://www.flickr.com/photos/63723146@N08/7164573186
Sugar Cubes. David pacey on Flikr. https://www.flickr.com/photos/63723146@N08/7164573186

8. Progressive Solitary Sclerosis

And this is my favourite paradigm shifter. Neurologists often see people with brain inflammatory lesions and struggle to decide if they fulfil the criteria for multiple sclerosis (MS). The current threshold for concern is when there have been two clinical events consistent with inflammation of the nervous system, or their MRI scan shows involvement of at least two different sites of the nervous system. Well, dot counting may soon be over, going by this paper in Neurology titled Progressive solitary sclerosis: gradual motor impairment from a single CNS demyelinating lesion. The authors identified 30 people with progressive clinical impairment arising from a single inflammatory nervous system lesion. The authors were convinced enough to recommend the inclusion of this new entity, progressive solitary sclerosis, in future classifications of inflammatory disorders of the central nervous system. Move over progressive MS, here comes progressive SS. Neurologists will surely have their job cut out for them.

Solitary tree at Sunset. epcp on Flikr. https://www.flickr.com/photos/epcprince/3418260382
Solitary tree at Sunset. epcp on Flikr. https://www.flickr.com/photos/epcprince/3418260382

Do you have any suggestions of emerging neurological disorders? Please leave a comment


PS. These disorders are all covered in neurochecklists


Are these the all-time most influential Neurologists?

Who are the most influential neurologists in history? Not an easy task as the starting field is rather wide. Creating a ‘top list‘ of anything is potentially controversial because there are often no clear inclusion criteria, and justifications are often subjective.


"Alois Alzheimer 003" by uncredited - http://neurophilosophy.wordpress.com/2006/11/03/100-years-of-alzheimers-disease/. Licensed under Public Domain via Commons - https://commons.wikimedia.org/wiki/File:Alois_Alzheimer_003.jpg#/media/File:Alois_Alzheimer_003.jpg
“Alois Alzheimer 003” by uncredited – http://neurophilosophy.wordpress.com/2006/11/03/100-years-of-alzheimers-disease/. Licensed under Public Domain via Commons – https://commons.wikimedia.org/wiki/File:Alois_Alzheimer_003.jpg#/media/File:Alois_Alzheimer_003.jpg


I was initially swayed by the length of Wikipedia entries but cautioned myself when I noticed that the piece on Raymond Adams was very brief. Furthermore, there was no entry at all for C David Marsden! Sacrilege, I thought. I felt strongly enough about this that I registered as a Wikipedia editor, and now there is a Wikipedia page for David Marsden.

By Joaquín Sorolla (1863 - 1923) ([1]) [Public domain or Public domain], via Wikimedia Commons
Santiago Ramon y Cajal by Joaquín Sorolla (1863 – 1923) ([1]) [Public domain or Public domain], via Wikimedia Commons

Fame and celebrity are also significant influences on ‘top lists’. The debate that followed Gerald Stern‘s article, the world’s best known neurologist, shows the justifiable importance of fame, but I tried hard to discount ‘mere’ celebrity. By the way, Stern’s lecture on this subject is worth viewing.

Eponymous syndromes also tug at the heart, and I discovered that there is a book titled Neurological Eponyms. I have not read it, so I am unbiased in this regard. It is however difficult to avoid the influence of JMS Pearce who seems to have written on every neurology great!

To compose a credible list, I thought a set of criteria was essential and I guided myself with these:

  • Volume, significance, and variety of contribution to neurology
  • Influence on clinical practice
  • Longevity of contribution
  • Breaking new grounds
  • Influence on other Neurology greats
  • Receipt of a Nobel prize
  • Lasting legacy in terms of books 
Jean Marie Charcot by André Brouillet (see below) [Public domain], via Wikimedia Commons
Jean Marie Charcot by André Brouillet (see below) [Public domain], via Wikimedia Commons

I have been liberal with the term ‘neurologist’ in the context of making this list. I have considered any specialist who has made a significant contribution to neurological knowledge and practice (how else would Alois Alzheimer get on the list?) Did I forget to mention-each name on the list is not living!

George Huntington (c. 1908)
George Huntington (c. 1908)


Here then is my list of The Top 30 Most Influential Neurologists with links to their Wikipedia entries:

  1. Raymond ADAMS
  2. Alois ALZHEIMER
  3. Joseph BABINSKI
  4. Charles BELL
  5. Paul BROCA
  6. Santiago Ramón y CAJAL
  7. Jean-Martin CHARCOT
  8. Macdonald CRITCHLEY
  9. Guillaume DUCHENNE
  10. Charles Miller FISHER
  11. Nikolaus FRIEDREICH
  12. Norman GESCHWIND
  13. William Richard GOWERS
  14. Anita HARDING
  15. Gordon Morgan HOLMES
  16. George HUNTINGTON
  17. John Hughlings JACKSON
  18. Gheorghe MARINESCU
  20. Pierre MARIE
  21. C David MARSDEN
  22. H Houston MERRITT
  23. Antonio Egas MONIZ
  24. James PARKINSON
  25. Arnold PICK
  26. Heinrich Irenaeus QUINCKE
  27. Charles Scott SHERRINGTON
  28. Charles Putnam SYMONDS
  29. Thomas WILLIS
  30. Samuel Alexander Kinnier WILSON


"An unidentified man" by Unknown - http://www.tecnologiahechapalabra.com/img_noticias/@old/%7B6E28BB2F-B004-4354-865D-F275131FBEB2%7D_James_Parkinson.jpg. Licensed under Public Domain via Wikimedia Commons - https://commons.wikimedia.org/wiki/File:An_unidentified_man.jpg#/media/File:An_unidentified_man.jpg
“An unidentified man” by Unknown – http://www.tecnologiahechapalabra.com/img_noticias/@old/%7B6E28BB2F-B004-4354-865D-F275131FBEB2%7D_James_Parkinson.jpg. Licensed under Public Domain via Wikimedia Commons – https://commons.wikimedia.org/wiki/File:An_unidentified_man.jpg#/media/File:An_unidentified_man.jpg


There are however too many influential neurologists, and to do justice to more of them, here is The Neurology Lounge Top 100 Neurology Greats.

If you think there is a name that is not on this list, and you strongly feel that it should be, please let me know (but you must suggest which name on the list should be replaced!) And by the way, do you have a photo of C David Marsden for his Wikipedia entry?