Early clinicopathologic description of nodoparanodopathy in the 19th century.

Nodoparanodopathy is a recent concept in the field of peripheral neuropathy, corresponding to peripheral nerve disorders stemming from an autoimmune attack directed and limited to the nodal region. This concept was identified using modern techniques of electrophysiology, immunology, and pathology (including electron microscopy). We present here what we believe to be the earlier well-documented case of nodoparanodopathy in the medical literature, based on an article written by Samuel Gilbert Webber (1838-1926) in 1884.

William Barnett Warrington (1869-1919).

William Barnett Warrington (1869-1919) was a physician and physiologist working in Liverpool, United Kingdom, at the end of the 19th and beginning of the 20th centuries. His training included periods at the National Hospital for the Paralysed and Epileptic, Queen Square, London, and in the Liverpool laboratory of Charles Scott Sherrington. He investigated structural alterations in nerve cells following various nerve lesions and helped to develop laboratory facilities to support clinical practice through the Pathological Diagnosis Society of Liverpool. His clinical interests were broad, but his main focus seems to have been in disorders of the peripheral nervous system. He published many papers, encompassing descriptions of Charcot-Marie-Tooth disease, brachial plexus paralyses (possibly including neuralgic amyotrophy), and, in the context of the First World War, traumatic peripheral nerve injuries. He may have described cases of Guillain-Barré syndrome prior to the eponymous description but despite being familiar with the technique of lumbar puncture, he did not report cerebrospinal fluid findings in these patients.

Lack of historical evidence to support folic acid exacerbation of the neuropathy caused by vitamin B12 deficiency.

In 1998 a Tolerable Upper Intake Level (UL) for folic acid was established based on case reports from the 1940s suggesting that high-dosage folic acid intake, used to treat patients with pernicious anemia, had the potential to precipitate or speed-up the development of neurological problems. This UL has been employed in the decision-making process used by more than 80 countries to establish programs to fortify staple foods with folic acid to prevent neural tube birth defects. Some have claimed that this UL is flawed and has become an obstacle to the wider adoption of neural tube defect prevention programs and have called for re-evaluation of the scientific validity of this UL. Case reports cannot establish causality, but they can reveal patterns in the timing of the onset and treatment of patients with pernicious anemia. These patterns can be compared with secular trends of usual medical practice for the treatment of pernicious anemia and with the changes in usage of folic acid preparations, including recommended therapeutic dosage and precautions for its usage surrounding the synthesis of folic acid in 1945 and vitamin B12 in 1948. Folic acid package inserts, early editions of hematology textbooks, and international expert reports provide valuable historical information. The recommended therapeutic daily dosage for folic acid of 5-20 mg was unchanged from 1946 through to 1971. The likely cause of the neurological problems encountered is the development of vitamin B12 neuropathy when pernicious anemia was treated with high-dosage folic acid before vitamin B12 was widely available in the early 1950s. Thus, the historical record does not provide compelling evidence that folic acid can potentially cause neurologic complications among those with low vitamin B12 status and lends support for reconsidering the basis for the UL of folic acid.

Jules Dejerine and the peripheral nervous system.

Jules Dejerine (1849-1917) was a French neurologist who contributed to the description of numerous neurologic conditions ranging from neurovascular pathology to neuromuscular disorders. A considerable body of his research was devoted to the peripheral nervous system. In this area, the eponymous Dejerine-Sottas syndrome refers to a form of infantile hereditary neuropathy. Dejerine also contributed to the description of many other disorders of the peripheral nervous system and was even a precursor in the study of acquired neuropathies (as well as acute inflammatory neuropathies, before the first description of the Guillain-Barré syndrome) and in the field of radicular pathology. In this centennial year of his death, we emphasize the variety and originality of Dejerine's opus on diseases of the peripheral nervous system.

Renaut Corpuscles or Peripheral Nerve Infarcts? A Historical Overview.

Renaut corpuscles are cylindrical hyaline structures that arise from the peripheral nerve perineurium and project into the endoneurium. Despite their earlier accurate description in the French and German literature, Kernohan and Woltman (1938) reported very similar structures as "nerve infarcts" in a case series of vasculitic neuropathy. Krücke (1955) deserves credit for discovering this error and further explaining how peripheral nerves react differently (from brain parenchyma) to ischemia. We tried to elucidate the reason why Kernohan and Woltman, and others, made this scientific error by describing the historical evolution of our understanding of the structure and function of Renaut corpuscles.

Multiple Crush Concept Applied to Multiple Nerves in Leprous Neuropathy.

There is a large reservoir of leprosy patients, no longer contagious, due to multidrug therapy, who are considered cured and are becoming increasingly disabled due to progressive chronic nerve entrapment in the upper and lower extremities. After a review of the history of understanding leprous neuropathy, an approach is outlined based on the approach taken to relieve pain and restore sensation that prevents ulcers and amputations in diabetics with neuropathy and superimposed nerve compressions. The results of the first application of this approach in an indigenous area for leprosy, Guayaquil, Ecuador, is discussed with implications for international care of this neglected patient population.

The first radiographic image of a peripheral nerve disorder? Lipomatous macrodactyly (unrecognized lipomatosis of nerve).

Lipomatosis of nerves (LN) involves benign fibro-fatty infiltration and is often associated with territorial overgrowth of soft tissue and bone; this distinctive disease pattern can be visualized on plain radiographs. We recently discovered a case (presented by Sir Robert Jones in 1898 to the Pathological Society of London) that indirectly represents a historical landmark in the imaging of peripheral nerves. The clinical findings and image, with obvious soft tissue and bone overgrowth, are pathognomonic for LN, making this one of the earliest radiological observations of a peripheral nerve lesion.

King George III and porphyria: a clinical re-examination of the historical evidence.

The diagnosis that George III suffered from acute porphyria has gained widespread acceptance,but re-examination of the evidence suggests it is unlikely that he had porphyria.The porphyria diagnosis was advanced by Ida Macalpine and Richard Hunter, whose clinical symptomatology and historical methodology were flawed.They highlighted selected symptoms, while ignoring, dismissing or suppressing counter-evidence.Their claims about peripheral neuropathy, cataracts, vocal hoarseness and abdominal pains are re-evaluated; and it is also demonstrated that evidence of discoloured urine is exceedingly weak. Macalpine and Hunter believed that mental illnesses were primarily caused by physical diseases, and their diagnosis of George III formed part of a wider agenda to promote controversial views about past, contemporary and future methods in psychiatry.

Historical perspective: neurological advances from studies of war injuries and illnesses.

Early in the 20th century during the Russo-Japanese War and World War I (WWI), some of the most important, lasting contributions to clinical neurology were descriptive clinical studies, especially those concerning war-related peripheral nerve disorders (eg, Hoffmann-Tinel sign, Guillain-Barré-Strohl syndrome [GBS]) and occipital bullet wounds (eg, the retinal projection on the cortex by Inouye and later by Holmes and Lister, and the functional partitioning of visual processes in the occipital cortex by Riddoch), but there were also other important descriptive studies concerning war-related aphasia, cerebellar injuries, and spinal cord injuries (eg, cerebellar injuries by Holmes, and autonomic dysreflexia by Head and Riddoch). Later progress, during and shortly after World War II (WWII), included major progress in understanding the pathophysiology of traumatic brain injuries by Denny-Brown, Russell, and Holbourn, pioneering accident injury studies by Cairns and Holbourn, promulgation of helmets to prevent motorcycle injuries by Cairns, development of comprehensive multidisciplinary neurorehabilitation by Rusk, and development of spinal cord injury care by Munro, Guttman, and Bors. These studies and developments were possible only because of the large number of cases that allowed individual physicians the opportunity to collect, collate, and synthesize observations of numerous cases in a short span of time. Such studies also required dedicated, disciplined, and knowledgeable investigators who made the most out of their opportunities to systematically assess large numbers of seriously ill and injured soldiers under stressful and often overtly dangerous situations.

Chapter 1: Peripheral nerve repair and regeneration research: a historical note.

Although the most significant advances in nerve repair and regeneration have been acquired over the last few decades, the study of nerve repair and regeneration potential dates back to ancient times namely to Galen in the second century A.D. This brief historical note outlines the milestones which have guided us to our present knowledge. In particular, we focus on the nineteenth century and the first decades of the twentieth century, an age in which the fathers of neurosurgery and neurobiology established the basis for most of the nerve repair and regeneration concepts used today. Finally, we shine a light on the most current history to show how recent pressure to use modern interdisciplinary and translational approach represents a sort of rediscovery of the scientific habits of the fathers of modern biomedicine, who used to carry out research from an integrated and broad point of view rather than from a super-specialized and specific one as it is often used today.

Peripheral nerve disorders and treatment strategies according to Avicenna in his medical treatise, Canon of medicine.

The written transmission of knowledge has played a great part in the advancement of medicine, and historical documents hold the key to a full exploration of the history of medicine. Some fields, including disciplines that deal with peripheral nerve disorders, have received little benefit from such valuable material. In particular, peripheral nerve surgery lacks perspectives from historical data. For many years, physicians have obtained positive results in the surgical treatment of peripheral nerve diseases. Relevant documents reveal that the first author who described the surgical repair of damaged peripheral nerves was Avicenna, a leading figure of the medieval era who lived in the Middle East. In his primary medical work, the Canon, he provides a description, albeit sketchy, of a suture procedure for peripheral nerve transection. This treatise influenced physicians for several centuries. In this presentation, we analyze excerpts from the Canon that concern peripheral nerve disorders and strategies for their management.