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In this paper we discuss the history of hysteria from the Babylonian and Assyrian texts through to the situation as it appears to us at the end of the 19th century. We note the shifting emphasis on causation, earlier ideas being linked to uterine theories, later speculations moving to the brain, and then the mind. We note the persistence of the condition referred to as hysteria over the millennia and the fascination that the condition has held for physicians, neurologists, and psychiatrists since the origins of known medical texts.

Background: Through Edward Reynolds' collaboration with Samuel Alexander Kinnier Wilson's (SAKW) son, James, on Babylonian neurology and psychiatry, and his contact with James' nephew, Jim, grandson of SAKW, a remarkable film of patients with movement disorders, made by SAKW in the mid-1920s, has come to light. Methods/Results: The 20-min silent film with captions by SAKW includes patients with senile tremor, Parkinson's disease and postencephalitic parkinsonism, hemiballismus, Huntington's chorea, Sydenham's chorea, hysterical palsy and tremor, multiple sclerosis, and progressive lenticular degeneration. Most of the patients are filmed in the square outside the National Hospital. The British Film Institute dates the film to 1924 and the captions to 1925. The case records of 6 of the 14 patients, who were admitted to the National Hospital, Queen Square, under the care of Dr. SAKW have been identified and summarized. Discussion: SAKW may have been stimulated and facilitated to make this film through his personal contact with Charlie Chaplin with whom he stayed at his Californian estate, probably in the summer of 1924. The first films of neurological patients were made in Europe and USA at the beginning of the 20th century, although most have perished. This may be one of the oldest examples from UK. It is also notable for the inclusion of Wilson's disease and a brief shot of SAKW himself. © 2011 Movement Disorder Society

In this paper we discuss the history of hysteria from the Babylonian and Assyrian texts through to the situation as it appears to us at the end of the 19th century. We note the shifting emphasis on causation, earlier ideas being linked to uterine theories, later speculations moving to the brain, and then the mind. We note the persistence of the condition referred to as hysteria over the millennia and the fascination that the condition has held for physicians, neurologists, and psychiatrists since the origins of known medical texts.

Between 1945 and 1959 it was convincingly documented that folic acid can precipitate or aggravate the neurological and haematological consequences of vitamin B12 deficiency by increasing the demand for vitamin B12. Since then there has been much misunderstanding of the issues, mainly by advocates of folic acid fortification who have been inclined to minimise or even dismiss the risks by misinterpreting the evidence as only a 'masking' of the anaemia of pernicious anaemia. Recent studies in the era of fortification are rediscovering the risks to the nervous system, especially cognitive function, of excess folate in the presence of vitamin B12 deficiency. I have reviewed the Reports of four Expert Advisory Committees in Europe and the USA, which suggest that the safe upper tolerable limit (UL) for folic acid is 1 mg in adults. These reports are unsound and there is already evidence of neurological harm from long-term exposure to doses of folic acid between 0.5 and 1 mg in the presence of vitamin B12 deficiency. There is an urgent need to review the safe UL for folic acid and to consider the addition of vitamin B12 to folic acid fortification policies.

Summary: Purpose: To consider the origins of our understanding of the electrical basis of epilepsy in the light of the Lumleian lectures to the Royal College of Physicians in London for 1849, “On the pathology and treatment of convulsive diseases,” by Robert Bentley Todd (1809–1860). Methods: I have reviewed Todd's neglected Lumleian lectures and his observations and concepts of the electrical basis of epilepsy in relation to the influence of Michael Faraday (1791–1867), his contemporary in London, and in relation to later nineteenth century writings on the subject by Jackson, Ferrier, and Hitzig, all of whom overlooked Todd's lectures. Results: Todd was a clinical scientist as well as Professor of Physiology and Morbid Anatomy, with a special interest in the nervous system, at King's College, where he came into contact with Michael Faraday, the greatest electrical scientist of all time, at the nearby Royal Institution. On the basis of his own clinical and experimental studies and his cutting-edge knowledge of neuroanatomy, neurophysiology, neuropathology, and electrical science, Todd brilliantly developed his concepts of the electrical basis of brain activity and of epilepsy in particular. With his microscope, he perceived each nerve vesicle and its related fibres (neurone in later terminology) as distinct entities for the generation of nervous polarity (force) and its transmission in the white nerve fibres throughout the nervous system by unknown molecular mechanisms. In epilepsy, an increase in electrical tension, especially in the grey matter of the hemispheres, led to periodic, sudden explosive discharges, based on Faraday's concept of disruptive discharges. Conclusions: Todd was the United Kingdom's first outstanding neurologist and neuroscientist before these disciplines existed. Influenced by Faraday, he proposed and confirmed the electrical basis of nervous discharges in epilepsy more than 20 years ahead of Jackson, Ferrier, and Hitzig, who did not refer to his priority, although Ferrier also worked at King's College, and Jackson also gave his own famous Lumleian lectures on the same subject in 1890. Todd deserves the credit for laying the foundations of our modern understanding of epilepsy.

The United Kingdom's (UK) National Health Service is a universal service that delivers health care that is largely free at the point of contact, the costs offset by general taxation and an employment tax. One great strength of the system is its delivery of primary care. Each patient has an assigned general practitioner who is responsible for the overall management of his or her ongoing health care, including the prescribing of medications and assigning of appropriate referrals for any specialist services. Recently introduced changes in national budgeting are likely to cause general practitioners to play a more direct role in the purchase of patient services from providers of secondary or specialist care. Physician demographics. It is estimated there are 155,000 doctors in the UK, of whom 23% are primary care physicians. Neurology remains a small specialty in the UK with approximately 270 adult neurologists and 38 pediatric neurologists. On average, there is one adult neurologist per 200,000 to 250,000 individuals. Recently, however, the specialty has been expanding rapidly. The specialty of epileptology is not well established. There are perhaps a dozen or more neurologists in the UK who claim a special interest or expertise in epilepsy. Epilepsy services, however, are often provided by neuropsychiatrists or clinical pharmacologists. Epilepsy care. In outlining the pattern of care for patients with epilepsy, the descriptions that follow will draw on data derived from an unselected prevalent population of people with epilepsy in the Mersey Region of the UK.1 Thirty-six randomly selected general practices were contacted after a stratification for size and geographical location; 31 practices agreed to participate. Patients who had a history of seizures in the previous 2 years or who took antiepileptic drugs (AEDs) because of a history of epilepsy were identified. Of the total practice population of approximately 170,000 people, …

The metabolism of folic acid and the metabolism of vitamin B12 are intimately linked such that deficiency of either vitamin leads to an identical megaloblastic anemia. The neurologic manifestations of folate deficiency overlap with those of vitamin B12 deficiency and include cognitive impairment, dementia, depression, and, less commonly, peripheral neuropathy and subacute combined degeneration of the spinal cord. In both deficiency states there is often dissociation between the neuropsychiatric and the hematologic complications. There is a similar overlap and dissociation between neurologic and hematologic manifestations of inborn errors of folate and vitamin B12 metabolism. Low folate and raised homocysteine levels are risk factors for dementia, including Alzheimer's disease, and depression. Even when folate deficiency is secondary to psychiatric illness due to apathy or poor diet it may eventually aggravate the underlying disorder in a vicious circle effect. Clinical responses to treatment with folates are usually slow over weeks and months, probably due to the efficient blood-brain barrier mechanism for the vitamin, perhaps in turn related to the experimentally demonstrated excitatory properties of folate derivatives. The inappropriate administration of folic acid in the presence of vitamin B12 deficiency may lead to both neurologic and, later, hematologic relapse. Impaired maternal folate intake and status increases the risk of neural tube defects. Periconceptual prophylactic administration of the vitamin reduces, but does not eliminate the risk of neural tube defects even in the absence of folate deficiency. Folates and vitamin B12 have fundamental roles in central nervous system function at all ages, especially in purine, thymidine, neucleotide, and DNA synthesis, genomic and nongenomic methylation and, therefore, in tissue growth, differentiation and repair. There is interest in the potential role of both vitamins in the prevention of disorders of central nervous system development, mood, dementia, including Alzheimer's disease, and aging.

Recent studies have shown that most newly diagnosed epileptic patients can be satisfactorily treated with a single antiepileptic drug. We therefore undertook a prospective randomised pragmatic trial of the comparative efficacy and toxicity of four major antiepileptic drugs, utilised as monotherapy in newly diagnosed epileptic patients. Between 1981 and 1987 243 adult patients aged 16 years or over, newly referred to two district general hospitals with a minimum of two previously untreated tonic-clonic or partial with or without secondary generalised seizures were randomly allocated to treatment with phenobarbitone, phenytoin, carbamazepine, or sodium valproate. The protocol was designed to conform with standard clinical practice. Efficacy was assessed by time to first seizure after the start of treatment and time to enter one year remission. The overall outcome with all of the four drugs was good with 27% remaining seizure free and 75% entering one year of remission by three years of follow up. No significant differences between the four drugs were found for either measure of efficacy at one, two, or three years of follow up. The overall incidence of unacceptable side effects, necessitating withdrawal of the randomised drug, was 10%. For the individual drugs phenobarbitone (22%) was more likely to be withdrawn than phenytoin (3%), carbamazepine (11%), and sodium valproate (5%). In patients with newly diagnosed tonic-clonic or partial with or without secondary generalised seizures, the choice of drug will be more influenced by considerations of toxicity and costs.

Background The history of obsessive compulsive, phobic and psychopathic behaviour can be traced to the 17th century AD. Methods and results We draw attention to these behaviours in a Babylonian cuneiform medical text known as Shurpu . These three categories were united in the Babylonian mind around the concept of the māmīt ‘oath’ idea, the behaviour habits being so unbreakable it appeared that the subject had sworn an oath to do or not to do the action involved. The behavioural accounts were entirely objective, including what we would call immature, antisocial and criminal behaviour, and obsessional categories of contamination, aggression, orderliness of objects, sex and religion. They do not include subjective descriptions of obsessional thoughts, ruminations or the subject9s attitude to their own behaviour, which are more modern fields of enquiry. Conclusions The Babylonians had no understanding of brain or psychological function but they were remarkable describers of medical disease and behaviour. Although they had both physical and supernatural theories of many medical disorders and behaviours, they had an open mind on these particular behaviours which they regarded as a ‘mystery’ yet to be ‘resolved’. We are not aware of comparable accounts of these behaviours in ancient Egyptian or classical medicine. These Babylonian descriptions extend the history of these disorders to the first half of the second millennium BC.

Ten patients who developed a major depressive episode in association with vigabatrin treatment for intractable epilepsy are reported. The depression usually occurred early in the course of treatment, but when delayed followed a recent increase in dose. Depressive symptoms occurred at doses varying between 1.5 g and 4 g a day, often but not always when patients were experiencing a decrease in their seizure frequency. Most patients had a history of affective disturbance, sometimes in association with other GABAergic drugs. The observations support a possible role for GABAergic mechanisms in the biology of mood disorders.

Summary John Hughlings Jackson is widely credited with the first electrical theory of epilepsy (1873), which was confirmed by the experimental studies of Hitzig and Ferrier. His views are summarised in his famous Lumleian lectures to the Royal College of Physicians in 1890. Robert Bentley Todd, however, had earlier developed an electrical theory of epilepsy, which he presented in his own brilliant Lumleian lectures to the Royal College of Physicians in 1849. Todd was influenced by the electrical discoveries of his contemporary, Michael Faraday, and thought of the brain as having battery like properties that led to the sudden discharge of electrical energy (nervous force) in epilepsy. Unlike Hughlings Jackson, Todd was an anatomist and physiologist as well as a physician, and he did his own electrical experiments in rabbits to prove his theory, something Hughlings Jackson, who relied on Ferrier for scientific and experimental support, could never have done. There is no mention of Todd's Lumleian lectures in Hughlings Jackson's later lectures and writings, nor in those of Hitzig or Ferrier. Todd's remarkable observations and lectures, and his electrical theory of epilepsy deserve to be drawn to the attention of the medical and scientific community.

Through Edward Reynolds' collaboration with Samuel Alexander Kinnier Wilson's (SAKW) son, James, on Babylonian neurology and psychiatry, and his contact with James' nephew, Jim, grandson of SAKW, a remarkable film of patients with movement disorders, made by SAKW in the mid-1920s, has come to light.The 20-min silent film with captions by SAKW includes patients with senile tremor, Parkinson's disease and postencephalitic parkinsonism, hemiballismus, Huntington's chorea, Sydenham's chorea, hysterical palsy and tremor, multiple sclerosis, and progressive lenticular degeneration. Most of the patients are filmed in the square outside the National Hospital. The British Film Institute dates the film to 1924 and the captions to 1925. The case records of 6 of the 14 patients, who were admitted to the National Hospital, Queen Square, under the care of Dr. SAKW have been identified and summarized.SAKW may have been stimulated and facilitated to make this film through his personal contact with Charlie Chaplin with whom he stayed at his Californian estate, probably in the summer of 1924. The first films of neurological patients were made in Europe and USA at the beginning of the 20th century, although most have perished. This may be one of the oldest examples from UK. It is also notable for the inclusion of Wilson's disease and a brief shot of SAKW himself.

• We describe 10 patients with a previously unreported, to our knowledge, association of multiple sclerosis and unusual vitamin B 12 deficiency. The clinical features and the age at presentation were typical of multiple sclerosis, with eight cases occurring before age 40 years, which is a rare age for vitamin B 12 deficiency. Nine patients had hematologic abnormalities, but only two were anemic. All six patients examined had low erythrocyte cobalamin levels. Only two patients had pernicious anemia; in the remaining patients the vitamin B 12 deficiency was unexplained. A vitamin B 12 binding and/or transport is suspected. The nature of the association of multiple sclerosis and vitamin B 12 deficiency is unclear but is likely to be more than coincidental. Further studies of vitamin B 12 metabolism, binding, and transport in multiple sclerosis are indicated, as these cases may offer a clue to the understanding of a still mysterious neurologic disorder.

Summary Robert Bentley Todd (1809–60) was the UK's first eminent neurologist and neuroscientist. An anatomist, physiologist, and clinical scientist with an interest in the nervous system, he was the first to confirm the electrical basis of brain activity in the 1840s. He was influenced by his contemporary, Michael Faraday at the Royal Institution, and by two colleagues at King's College, John Daniell and Charles Wheatstone, who were also working at the cutting edge of electrical science. Todd conceived of nervous polarity (force) generated in nervous centres and compared this with the polar force of voltaic electricity developed in the galvanic battery. He brilliantly foresaw each nerve vesicle (cell) and its related fibres (ie, neuron) as a distinct apparatus for the development and transmission of nervous polarity. Epilepsy was the result of periodic unnatural development of nervous force leading to the "disruptive discharge" described by Faraday. Faraday, who studied animal electricity in the Gymnotus (electric eel), and Todd saw nervous polarity as a higher form of interchangeable energy.

Is the subjective experience of epilepsy and its treatment in different social and cultural settings important in understanding, managing, supporting, researching, and preventing the disorder? Undoubtedly, as it is with other acute and chronic disorders. But as the authors of this book emphasise, epilepsy is a special case with its universality, ubiquity, variability, consciousness-interrupting paroxysms, misunderstanding, social impact, and historical legacy. Eds Steven C Schachter, Lisa Francesca Andermann Lippincott Williams & Wilkins, …

SummaryProposals by psychiatrists to reclassify conversion disorder in DSM-5 and ICD-11 are proving difficult and controversial. Patients with conversion disorder usually present initially to neurologists, who often use different concepts and terminology. History and clinical practice suggest that the way forward is to seek agreed principles and a common understanding between the two disciplines, preferably in a single universal classification.

It is widely acknowledged that SA Kinnier Wilson's (SAKW) two volume textbook of Neurology published posthumously in 1940,1 3 years after his death, is among the greatest single author works on the subject in any language. SAKW was fluent in French and German and his knowledge of neurological and psychiatric developments in both languages, as well as his own, became encyclopaedic, reinforced by his founding and editing of the Journal of Neurology and Psychopathology , now the Journal of Neurology, Neurosurgery and Psychiatry , from 1920 onwards.2 The difficult but ultimately successful task of editing and publishing this valuable but unfinished book fell on his brother-in-law, Ninian Bruce, a distinguished Edinburgh physician with an interest in neurology. The second volume ends rather inconclusively with chapters on motor, occupational, sensory and reflex neuroses. SAKW was the last neurologist to use the term ‘neuroses’ in its original neurological sense of a disorder of nervous system function without local pathology.3 A glaring omission from the book is any chapter on hysteria, long a subject of interest to neurologists but enhanced by increasing experience and literature related to World War I.4–7 A chapter on the psychoneurosis, hysteria, would have been the next logical chapter, all the more so as I have become aware that SAKW wrote extensively on the subject, which was obviously of great interest to him. Through my contact with SAKW's son, James Kinnier Wilson, I have in my possession a reprint of a thorough but overlooked review of hysteria published by SAKW in Encyclopaedia Medica in 1919,8 which with some updating could have formed the basis of a chapter in his later textbook. SAKW also wrote on the subject before9 and after 1919, notably his Presidential …

It is becoming clear that folic acid affects mood and cognitive function, especially in older people. Edward Reynolds draws together the evidence Folic acid is important for functioning of the nervous system at all ages.1–4 In the fetus the relation between maternal folate status and the risk of neural tube defects is well established: clinical trials have shown that periconceptual preventive treatment with 400 μg or higher of folic acid significantly reduces the risks of such defects.4 In neonates, infants, children, and adolescents, inborn errors of folate transport and metabolism are associated with a variety of overlapping syndromes which are influenced by age of clinical presentation. These include developmental delay, cognitive deterioration, motor and gait abnormalities, behavioural or psychiatric symptoms, seizures, signs of demyelination or failure of myelination, and vascular changes seen on magnetic resonance imaging or postmortem examination.4 Less commonly, subacute combined degeneration and peripheral neuropathy may also occur. In adult patients presenting with megaloblastic anaemia due to folate deficiency, approximately two thirds have neuropsychiatric disorders which overlap considerably with those associated with anaemia due to vitamin B-12 deficiency. 2 5 However, depression is commoner in patients with folate deficiency, and subacute combined degeneration with peripheral neuropathy is more frequent in those with vitamin B-12 deficiency. The degree of anaemia is poorly correlated with the presence of neuropsychiatric disorders, but if these anaemias were left untreated nearly all patients would eventually develop neuropsychiatric complications.2 Over the past 35 years numerous studies have shown a high incidence of folate deficiency correlated with mental symptoms, especially depression and cognitive decline in epileptic, neurological, psychiatric, geriatric, and psychogeriatric populations. 3 4 Furthermore, recent studies in elderly people suggest a link between folic acid, homocysteine, ageing, depression, and dementia, including Alzheimer's disease and vascular disease. 4 6 …

During three decades of neurological practice I have witnessed a remarkable change in attitudes to the benefits and risks of folic acid therapy in nervous system disorders. In the 1960s all that was known and taught was that folic acid was harmful to the nervous system, especially in precipitating or exacerbating the neurological complications of vitamin B12 deficiency. So deeply held was this view that the possibility of neuropsychological benefits from this vitamin was initially viewed with considerable scepticism.1

Samuel Alexander Kinnier Wilson (1878–1937) and Sir Charles Sherrington (1857–1952) were two of the most distinguished figures in 20th century neurology and neuroscience. Kinnier Wilson is best remembered now for the disease that bears his name1 and for his scholarly and influential textbook which was first published posthumously in 1940.2 In 1920, he also founded and edited the Journal of Neurology and Psychopathology , which evolved into the present Journal of Neurology, Neurosurgery and Psychiatry . Sherrington was the outstanding neurophysiologist of the first half of the 20th century, famous for his studies of the reflex and integrative functions of the nervous system and for his philosophical and poetic contributions.3 4 Through my contact with Kinnier Wilson’s son, James, with whom I collaborated on Babylonian neurology,5 6 two documents have come to light which confirm a warm professional relationship between Kinnier Wilson and Sherrington late in their respective academic careers. Figure 1 is a letter from ED (later …

John Hughlings Jackson (1835–1911) was the most influential clinical neurologist of the nineteenth, and probably also the twentieth, century, certainly in the English-speaking world. When he died in 1911 eight of his colleagues at the National and London hospitals eulogized him in the British Medical Journal and the word “genius” appears several times. William Gowers, a neurological giant himself, elsewhere referred to him as “the master”. The Second International Neurological Congress, which was held in London in 1935, coincided with the centenary of his birth and was therefore dedicated to Hughlings Jackson. In their 1998 biography the Critchleys refer to him as “the father of English neurology”.

The second International Neurological Congress, held in London in 1935, coincided with the centenary of the birth of John Hughlings Jackson (1835–1911). Samuel Alexander Kinnier Wilson (1878–1937), who was the Secretary-General of the Congress, had been one of Jackson’s last house physicians at The National Hospital, Queen Square, between 1904 and when Jackson retired in 1906.1 Kinnier Wilson went on in 1912 to describe the hepatolenticular disorder that now bears his name.2 Prior to the 1935 Congress, Kinnier Wilson wrote a centenary appreciation of Hughlings Jackson in the Lancet in which he made it clear that the year and the place of the Congress “have been chosen to do honour to that great man”.3 Jackson’s genius consisted in ( a ) his power of combining the little and the great, of uniting an unsurpassed faculty of detailed clinical observation with a philosophical breadth of thought and imagination, for example his minute analysis of focal motor seizures (Jacksonian epilepsy) and his concept of the motor cortex, and ( b ) in discovering unities amid heterogeneous diversities. As …

• Subacute combined degeneration of the spinal cord due to vitamin B 12 deficiency invariably has been associated with a low serum vitamin B 12 level. We describe a young man who presented with a unique syndrome of subacute combined degeneration associated with high serum vitamin B 12 level, low red blood cell vitamin B 12 level, and an abnormal plasma vitamin B 12 -binding protein. Uptake of cobalamin by his leukocytes in vitro was inhibited by his own but not by normal control plasma. Intensive hydroxocobalamin (vitamin B 12 ) treatment was associated with clinical and electrophysiologic recovery accompanied by normalization of mean corpuscular volume, red blood cell vitamin B 12 level, plasma homocysteine, and urinary methylmalonic acid. The subacute combined degeneration was probably precipitated by treatment with folic acid as the significance of his high serum vitamin B 12 level was not apparent when he first presented with megaloblastic anemia 3 years earlier. To our knowledge, this is the first example of neurologic disease associated with high serum vitamin B 12 level and provides further evidence that sometimes a serum vitamin B 12 level may not be a reliable guide to vitamin B 12 deficiency.

The editorial by Kendell ([2001][1]) independently reflects the view of Baker & Menken ([2001][2]) that it is time to abandon the term ‘mental illness’. All three authors emphasise that an important reason for so doing is that the term is stigmatising and undermining of the care and treatment of

We have previously described 10 patients with multiple sclerosis (MS) and unusual vitamin B12 deficiency. We have therefore studied vitamin B12 metabolism in 29 consecutive cases of MS, 17 neurological controls, and 31 normal subjects. Patients with MS had significantly lower serum vitamin B12 levels and significantly higher unsaturated R-binder capacities than neurological and normal controls, and they were significantly macrocytic compared with normal controls. Nine patients with MS had serum vitamin B12 levels less than 147 pmol/L and, in the absence of anemia, this subgroup was significantly macrocytic and had significantly lower red blood cell folate levels than neurological and normal controls. Nine patients with MS had raised plasma unsaturated R-binder capacities, including three patients with very high values. There is a significant association between MS and disturbed vitamin B12 metabolism. Vitamin B12 deficiency should always be looked for in patients with MS. The cause of the vitamin B12 disorder and the nature of the overlap with MS deserve further investigation. Coexisting vitamin B12 deficiency might aggravate MS or impair recovery from MS.

Clinical experience with gamma-vinyl GABA (GVG, vigabatrin) has accumulated mainly in Europe, where the drug has been licensed in several countries since 1989. Short-term efficacy studies in adolescent and adult patients with intractable drug-resistant epilepsy have shown that approximately 50% exhibit a reduction in seizure frequency of one-half or more but rarely complete seizure control. The best results are in patients with partial seizures with or without secondarily generalization. GVG responders have been followed for periods of up to 5 years, and overall 10-20% may exhibit subsequent seizure breakthrough, as probably occurs with any drug in such chronic patients. The most common side effect is drowsiness. Reversible behavior disorders, psychoses, and depression rarely occur in predisposed individuals. No new long-term side effects have been reported but vigilance is necessary. Studies of GVG as a first-line drug in newly diagnosed epileptic patients are proceeding.

In the 19th century the triumphs of neuropathology and the clinico-anatomical method led to the evolution of neurology as a separate ‘organically’ based discipline associated with the concept of functional localisation. At the same time the growth of psychodynamic psychiatry contributed to the progressive separation of the two disciplines, with neuropsychiatry sitting uneasily in the middle. Psychiatrists are now showing increasing interest in the structure and function of the nervous system, but are having difficulty in integrating their findings into ‘functional’ diseases. This may be because disorder of function in the nervous system is much more complex than previously envisaged. The function of the nervous system is profoundly affected by psychological and social factors. The view that neurology is wholly ‘organic’ and synonymous with structural disease of the nervous system is fallacious. Neurological patients have complex dynamic disorders of function in the nervous system whether or not structural disease is present.

Red cell folate and vitamin B12 estimations were performed on 243 successively admitted in-patients at a District General Hospital Psychiatric Unit and 42 out-patients (29 attending a lithium clinic). Patients were classified into five diagnostic groups. The mean ages of the manic and schizophrenic patients were lower than of the depressed or euthymic patients but age was not correlated with red cell folate or serum B12 levels in any group. There were 89 (31%) patients with red cell folate below 200 ng/ml and 35 (12%) with concentrations below 150 ng/ml. Significantly more of these low-folate patients were in-patients than out-patients. The mean red cell folate in the depressed patients was significantly lower than in the euthymic, manic and schizophrenic groups. Alcoholics had a similar mean red cell folate to depressed patients which was not quite significantly lower than the other groups. The mean serum B12 level in the alcoholics was, however, significantly raised. There were no significant differences in red cell folate or serum B12 between lithium-treated and untreated euthymic patients. The highest proportions of values below 200 ng/ml and 150 ng/ml were found in depressed and alcoholic patients. Endogenous depressives had the highest percentage of values below 150 ng/ml (folate-deficient) of all psychiatric groups and alcoholic patients. The significance of these findings is discussed.

Twenty-seven patients with multiple sclerosis had mild but significant macrocytosis when compared with an individually matched neurological control group and the normal laboratory reference range. The cause of the macrocytosis is unknown, but our recent clinical observations implicate a possible disturbance in vitamin B12 metabolism, binding or transport.

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