Prolonged facial pain has long been a source of frustration to the medical profession, both from the diagnostic and therapeutic standpoints. The difficulty arises not in the “typical” facial pain syndromes such as trigeminal neuralgia, migrainous neuralgia or post-herpetic neuralgia, nor with pain due to diseases of the teeth, throat, nose, eyes and ears, but in the deep, poorly localized vaguely described pain which does not adhere to a strict anatomical distribution. The latter symptom complex has been given many names, but in spite of this is a remarkably uniform syndrome. It is characterized by pain that is felt deep in the soft tissues or the bone, rather than in the superficial tissues as occurs so often in the typical neuralgias, is poorly localized and vaguely described. The pain may be felt in regions supplied by the fifth and ninth cranial nerves and the second and third cervical nerves. Its distribution does not conform to the peripheral distribution of these nerves, but may involve portions of the sensory supply of two or more of them and may cross the mid-line. In general the pain is constant and endures for long periods of weeks to years. It is unusual to find trigger zones or clear-cut precipitating factors, and the pain is rarely excruciating.

“The non-mathematician is seized by a mysterious shuddering when he hears of ‘four-dimensional’ things, by a feeling not unlike that awakened by thoughts of the occult. And yet there is no more commonplace statement than that the world in which we live is a four-dimensional space-time continuum. By this we mean that it is possible to describe the position of a point at rest by means of three numbers (co-ordinates) x, y, z, and that there is an indefinite number of points in the neighbourhood of this one, the position of which can be described by co-ordinates such as x1, y1, z1, which may be as near as we choose to the respective values of the co-ordinates x, y, z of the first point. In virtue of the latter property we speak of a ‘continuum’, and owing to the fact that there are three co-ordinates we speak of it as being ‘three-dimensional’.

Although there is now universal agreement that the reduction of food-intake is the central phenomenon in the syndrome of anorexia nervosa, the cause of the food refusal is still incompletely understood. One of the difficulties in elucidating the psychogenic roots of the anorexia is the fact that the patients themselves are unable to explain their thoughts and feelings. Conversations with them give the impression that one is speaking to a very young child who cannot or dare not express herself, so that the interviews are reduced to monosyllabic answers to questions and long periods of silence without relevation of pertinent material. After having spent much time with such patients in the past, we have since tried to obtain additional information from parents and other family members, neighbours and family doctors who knew the patients and their environment. Although we are well aware that this kind of information pertains more to outward behaviour than to “endopsychic” processes and therefore will probably be considered as of limited value by those who are interested in the so-called psychodynamics of the disease, we were able to formulate at least a tentative hypothesis that seemed to fit the life situation in our patients and bring them under a common denominator. From this hypothesis, which will be formulated below, a simple prediction followed as to how these patients should be treated. In the present paper we wish to formulate the hypothesis and present the preliminary results of a form of treatment, based on this prediction.

This study concerns a two-year follow-up of all the male alcoholics discharged from the Alcoholic Unit at Warlingham Park Hospital between January 1960 and October 1961.

In one of the outer suburbs of Sydney, along the jagged Pacific coastline, there is a high cliff known as “The Gap” which is notorious for the frequency with which it attracts, often fatally, the person with suicidal intent. Recently a young man entered a Sydney taxi-cab and asked to be driven to an address in the street which leads to this particular area. Having settled comfortably in the front seat he announced cheerfully to the driver, “Well, this is certainly going to be my last ride!” To his apparent surprise and annoyance, his cab promptly deposited him at the nearest police-station, from where he was removed, under considerable protest, to a psychiatric hospital for observation.

Obsessions may appear for the first time during the course of a depression without having been present before the onset of the depression. Such cases (hereinafter called “Gainers”) have been noted by Esquirol (1827), Prichard (1835), Marc (1840), Schüle (1886), Gordon (1925), Saunders (1932), Lewis (1934), Woolley (1937), Muncie and White (1937), Lion (1942), Stengel (1948), Terhune (1949), Sargant and Slater (1950), Pollitt (1956), Reda and Paretti (1958), and Skoog (1959). The frequency of this phenomenon, however, remains uncertain. Heilbronner (1912) described 22 cases of melancholia with obsessions of whom 18 were “Gainers”. Vurpas and Corman (1933) described 27 cases of depression with obsessions (two organically based) of whom 24 were “Gainers”.

The Sturge-Weber syndrome belongs to the relatively uncommon group of ailments known as heredodegenerative disorders. In 1879 Sturge described a case of epilepsy in a young girl who exhibited a congenital glaucoma and a facial angioma or naevus flammeus. Sturge speculated that the patient's convulsions were caused by a similar naevus formation in the brain. Kalischer (1897, 1901) discovered angiomatotic changes in the meninges, and later the typical calcium deposits corresponding to these angio-mata were found in X-ray examinations by Weber (1922), Dimitri (1923), and Krabbe (1934). The appellation of the Sturge-Weber syndrome varies, owing to the number of its investigators. Levison (1953) calls attention to this question of nomenclature.

One of the common clinical interests shared by physicians and psychiatrists is the genetically determined syndrome to which Klinefelter has given his name. Over the past few years positive identification has become possible through advances in cytogenetics, and more recently evidence has been accumulating which seems to indicate that a significant correlation may exist between Klinefelter's Syndrome and the development of other diseases, malignant disease in particular. Mental retardation is one of the most common symptoms found in the syndrome, so the psychiatrist is often in the best position to detect it. The case to be described here as well as having a few interesting facets of psychopathology may also provide more evidence of the pathological loading which the basic genetic abnormality seems to carry.

In the last decade, much physiological and biochemical information has been collected about the organic role played by the enzyme “true” cholinesterase in the transmission of nervous impulses (Crossland, 1957; Feldberg, 1957; Nachmansohn, 1959); but attempts to explain the function of pseudocholinesterase have been less consistent, and confined mainly to the effects of physical disease (Berry et al., 1954; Koster et al., 1943; Kunkel et al., 1947; McArdle, 1940) with one exception: Richter, (1942) discovered a significant relationship between raised pseudocholinesterase activity and neurotic anxiety or depression. Eysenck commented on this behavioural link (1947), but no further investigations appear to have been carried out in spite of the provocative theme. The possibility of other behavioural abnormalities being associated with an elevated pseudocholinesterase level therefore seemed to merit some attention.

Huntington's chorea is transmitted by a rare autosomal Mendelian dominant gene. Its hereditary transmission is facilitated by a late onset of the condition in many cases. Often the first signs are not seen until late in the reproductive period, so that it is not uncommon for a patient already to have produced a number of children before the diagnosis is made. On a theoretical basis, 50 per cent. of these offspring are at risk for carrying the gene and consequently for developing the condition themselves.

Since 1932 the amylobarbitone (amobarbital sodium, Amytal) interview has been used as a technique for diagnostic evaluation of patients with psychiatric illnesses (Lindemann, 1932). Amytal has also been used to make mute patients talk, as a sedative, a mood elevator, and as an agent in various other types of psychiatric treatment such as sleep therapy, abreaction, narcoanalysis (Horsley, 1936), narcosynthesis (Grinker et al., 1945), narcosuggestion, and narcoplexis (Brickner et al., 1950).

The deleterious effects of barbiturates on the vulnerable addictive personality have been well recognized for some years. The first warning came as far back as sixty-one years ago (Clarke, 1904) only a year after the introduction of the first barbiturate drug. Goodman and Gilman (1956) state that habituation to the barbiturates in the sense of psychic dependence is not infrequent, and point out the important fact that most persons addicted to barbiturates have some basic character disorder or psychoneurosis. These authors even go on to say that barbiturate addiction is a more serious public health and mental health problem than morphine addiction because it produces greater mental, emotional and neurological impairment, and because withdrawal entails real hazards.

Tegretol (carbamazepine; 5-carbamyl-5H-dibenz (b, f) azepine) has been under investigation since 1958 in the treatment of epilepsy on the continent of Europe, following the demonstration of its anticonvulsant properties in animals by Theobald and Kunz (1963). Clinical reports have been enthusiastic (Lorgé, 1963, Bonduelle et al., 1963). The present investigation was undertaken with a view to a more critical appraisal of this drug, avoiding the dangers of sudden alteration of anticonvulsant therapy in epileptic patients, documented by Schwab et al. (1959), while still maintaining the double-blind nature of the trial.