In 1962 William Sargant and his colleagues described the therapeutic value of phenelzine, a monoamine oxidase inhibitor (MAOI), in chronic anxiety disorders and in the same year Klein and Fink reported the treatment of similar conditions with imipramine, a tricyclic antidepressant. Subsequent research has confirmed these findings and demonstrated the range of similar drugs that are effective in anxiety disorders. At the time of these original observations about the drug treatment of anxiety, there were no psychological treatments of proven value but in the intervening years much progress has been made in developing behavioural and cognitive procedures. The progress in determining the mode of action of these pharmacological and psychological treatments is reviewed and the implications of the findings are considered in relation to research into the causes of the anxiety disorders and to the treatment of patients.

Standard auditory evoked potentials (AEP) were recorded in 50 schizophrenic patients and 47 normal controls. All patients were rated on the Brief Psychiatric Rating Scale (BPRS), the Scale for the Assessment of Negative Symptoms (SANS), the Scale for the Assessment of Positive Symptoms (SAPS), and the Positive and Negative Syndrome Scale (PANSS), and were classified in three groups (positive-type [n = 10], negative-type [n = 23]and mixed-type [n = 17]patients) according to the normative criteria suggested by Kay. The mean latencies of AEP components (N1, P2, N2) and mean peak-to-peak amplitudes (N1P2, P2N2) did not correlate with age, duration of illness, length of hospitalisation or neuroleptic dosage. The evoked response did not differ between the three groups of patients (positive, negative and mixed). There was only a trend (P = 0.075) to a longer N1 latency in the negative-type group and a shorter one in the positive-type group than in the mixed-type and the control groups. The latency of N1 component correlated significantly with negative symptoms of schizophrenia (SANS scores). This correlation was related to the severity of a depressive dimension of the disorder reflected by the “depressive factor” of BPRS or “affective flattening” and “avolition” subscales of SANS.

Anxiety and depression are often interlinked as demonstrated by clinical, epidemiological, psychopharmacological and even genetic studies. However, robust biochemical and electrophysiological evidence for linkage or separation of mood and anxiety disorders is scarce. Brain stem auditory evoked potentials (BASEP) can easily and non-invasivly be measured in psychiatric patients and reflect neurophysiological processes in the brain stem. The aim of the present study was to evaluate BASEP in drug-free patients suffering from panic disorder or major depression and to compare these to healthy controls. Patients (n = 26; panic = 16, depression = 10) were diagnosed according to Diagnostic and Statistical Manual (DSM)-III-R criteria assessed by the Hamilton Anxiety and Hamilton Depression Scales, and all underwent 3 weeks of medications washout. All subjects (n = 36) completed the study. N3 latency was decreased in the patient group (P < 0.05), N3-5 interval was lengthened (P < 0.05), the N3 latency correlated with anxiety scores and depression scores correlated with the N3 and N5 latency periods. In conclusion, our small sample demonstrated shared electrophysiological variables in panic disorder and depression, further supporting the concept of spectrum disorder.

A study of 128 consecutive patients with thromboembolic stroke in a rehabilitation hospital from July 1988 to September 1990 found a prevalence of major depression of 17%. The patient population was described according to the principles of the World Health Organization's (WHO) International Classification of Impairments, Disabilities and Handicaps (ICIDH) according to biological impairment, measured by computerized tomography (CT) scanning of the brain and side of hemiparesis and physical disability, measured by functional movement and activities of daily living. Handicap, referring to the interaction between disability and the environmental situation, often defined as the subjective disadvantage of being ill, was not measured in this study. A stroke index with four items was generated from the parameters describing biological impairment and physical disability. The psychiatric rating scales (the 17-item Hamilton Scale for Depression (HAM-D), the Melancholia Scale [MES]and the Newcastle Diagnostic Depression Scale), and the new stroke-index showed adequate coefficients of Cronbach's alpha and Loevinger, suggesting that these scales have both adequate item correlation and homogeneity (adequate hierarchical structure). The impairment disability index of stroke thus seems to be a meaningful measurement of the specific factors of this disease. There was no correlation between the stroke-index and the psychiatric rating scales measuring the emotional dimension of disability caused by the disease expressed as depression. The results suggest that the depression found among stroke patients is not a simple reaction to the physical disability of the stroke.

This was a metabolic study of bulimia nervosa required to design short-term cognitive-behavioural therapy (CBT) beginning with a brief admission to a psychiatric ward. The treatment produced significant improvements in eating behaviour and results are compared with those of previously published studies. The comparisons do not suggest that brief admission at the onset of therapy might enhance its effectiveness. In other respects, increase in normal meal intake was found to correlate significantly with decrease in hinging. This supports the notion that appropriate food intake at meal times should be an important issue in CBT for bulimia nervosa.

We studied DSM-IV catatonic features in 120 psychiatric inpatients with a main diagnosis of acute psychotic, affective or cognitive disorder. Individual catatonic features were highly intercorrelated, although diagnostically nonspecific. A single factor, accounting for 85% of the variance, was extracted and interpreted as representing both types (excited and retarded) of catatonic syndrome.

Cannabis has been reported to produce acute psychiatric reactions, among these panic anxiety and derealization, which are self-limited. We report on three patients who experienced an initial panic attack during cannabis intake. Anxiety attacks reoccurred after the cessation of intake. Two of these patients had a current depressive disorder, one of them had a single Grand Mal seizure before the onset. We suggest that cannabis may trigger the emergence of recurrent panic attacks and uncover latent panic disorders in vulnerable persons.