Private inpatient psychiatric care.
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Biomedical subjects
Publications and source records attributed to I Marks.
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Many fears, phobias and rituals seem to arise from prepared phylogenetic mechanisms which favor old over new evolutionary dangers and affect the rules of aversive learning which govern the acquisition of fear. Recent developments in several forms of aversive learning (sensitization, conditioning, extinction, observational learning) can improve them as paradigms of the acquisition, spread and maintenance of normal and clinical fears. The most reliable treatment for phobias and rituals is exposure, whose effects closely parallel the habituation of normal defensive responses and the extinction of conditioned fear and avoidance in animals. Habituation during exposure is usually slow and step by step, and generalizes little, but once attained tends to endure. Conditioned fear extinction and fear habituation have similar courses and may depend on similar neural processes. To be reduced, avoidance has to be prevented or the safety intervals that it heralds must be given up. Some phobias may result less from enhanced acquisition than from insufficient exposure to attain habituation. Finally, the review discusses the limits of habituation and the instability of fear extinction in relation to the long-term efficacy of exposure therapy.
DSM-3 obsessive-compulsive out-patients were randomly assigned to fluvoxamine with antiexposure (F), fluvoxamine with exposure (Fe), or placebo with exposure (Pe) for 24 weeks. Of 65 patients offered treatment 60 entered the trial, 50 reached week 8, 44 completed treatment to week 24, and 37 reached follow up to week 48. On average the patient had depressed mood (mean Hamilton depression rating scale = 19). Drop-out numbers, clinical status and behavioural measures were comparable across groups. Most F patients did not do antiexposure, but Fe and Pe patients complied in doing exposure. All three groups improved in rituals and depression from week 0 to week 24 and 48, with a slight but non-significant superiority for combined treatment up to week 24. At week 8 there was a drug between-group effect on rituals, but not on depression. At week 24 there was a drug between-group effect on depression, but not on rituals. The drug superiority was short-lived. At week 48 there was no between-group difference in rituals or depression. Depression was related to ritual outcome at week 24 in F, and tended to be so in Fe.
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We report a case of a man with recurrent depression and persistent second-person auditory hallucinations telling him to kill himself. Using an audiotape cassette and headphones the duration of the hallucinations decreased significantly. Helpfulness of the audiotape continued at 15 months follow-up.
Twelve heroin addicts and one methadone addicts began withdrawal from street opiates, under clonidine cover, in a general psychiatric ward. Ten (80%) of them completed it within 6 days. Clonidine doses used were lower than in similar studies and all patients were alert and mobile throughout withdrawal. Two other groups of opiate addicts, of similar age and sex, were withdrawn on standard methadone regimens. Clonidine and methadone withdrawal had similar acceptability and attrition rates. Self-reports of subjective discomfort were higher in the clonidine group without affecting compliance with treatment. Withdrawal under clonidine cover deserves further study, in view of the need for postwithdrawal treatment to prevent relapse to opiate use.
Of 57 patients with panic disorder with agoraphobia, more had their first panic in late spring and summer than in fall and winter, and in warm weather than in cold weather. In the month before the first panic 52% of the patients had prodromal depression or anxiety. Agoraphobic avoidance preceded the first panic in 23%, began within days after the first panic in 32% (without prodromal anxiety or depression in only 20%), and after more than one panic (1 week to 11 years later) in 41%. The site of the first panic was from the agoraphobic cluster (public places) in 81%, at work or school in 11%, and inside the home in 8%. Thirty-eight percent of patients were with a familiar adult at the time. Many features of the syndrome can be explained by an integrated model with several interacting factors contributing in varying degrees to the different routes by which it develops. To the learning and biological factors already suggested we add an evolutionary factor to explain why most first panics occur outside the home and mainly in public places. Certain extraterritorial cues constituting an agoraphobic cluster seem to be prepotent and prepared triggers or modifiers of fear during stress.
Twenty-three drug-free patients with agoraphobia and panic disorder (DSM-III criteria) had, at rest, lower mean end-tidal PCO2 (32 v. 36 mmHg) and higher mean heart rate (92 v. 83 bpm) than did 18 controls. During 5 min of listening to fear talk, only eight (35%) patients and three (16%) controls panicked, but panic was associated with marked physiological changes in only two patients and one control. Patients said that breathlessness began slightly more often before than after panic. In 59% of patients the symptoms from voluntary hyperventilation (VHV) were very similar or identical to those of their usual panics. Compared with the remainder, these patients felt more unpleasant during hyperventilation (HV); in such patients HV may aggravate somatic symptoms. Agoraphobics with panic differed from controls in having higher baseline arousal, but were not more reactive than controls to HV or fear talk.
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Natural human uneasiness about blood, injury, or deformity sometimes becomes a specific phobia, which can lead to serious disability if vital medical procedures are refused. Blood-injury phobia usually starts in childhood and is often familial. Unlike other phobic cues, which cause persistent tachycardia, blood-injury phobic cues evoke an initial rise in heart rate followed by vasovagal bradycardia and, frequently, syncope. Although blood-injury phobia may have an evolutionary, genetic, and physiological basis, it can be treated effectively by exposure. The tendency to faint early in exposure therapy can be reduced by lying down, tensing the muscles, or inducing anger.
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Five chronically disabled dysmorphophobic patients with disturbed bodily perception improved with systematic exposure to avoided situations that evoked dysmorphophobic discomfort, and refraining from behaviours which reduced that discomfort. As avoidance and anxiety improved with exposure, so did associated bodily delusions. Four of the patients had additional problems, for which three cases had drugs at some time. The encouraging pilot results warrant a controlled study of exposure for dysmorphophobic avoidance and anxiety.
In uncontrolled studies, several behavioural methods, including habit reversal, were said to be useful in writer's cramp. In this controlled study, 23 subjects with writer's cramp recruited from a neurology clinic were randomly allocated to five sessions over four weeks of either habit reversal training or a control treatment of relaxation training. Three subjects dropped out. Twenty patients (9 habit reversers, 11 controls) completed the trial up to three months follow-up. Outcome measures included observation of writing within the session, assessment of writing tasks completed at home, and blind ratings by an independent assessor. The results showed that habit reversal was no better than relaxation. Taking both treatments together, patients improved to three months follow-up on seven of nine measures, but remained substantially handicapped.