The best review of this question is Rick Strassman's "Adverse Reactions to Psychedelic Drugs: a Review of the Literature" in _J. Nerv and Mental Disease_ 172(10):577-595. He writes:
The most common adverse reaction is a temporary (less than 24 hours) episode of panic --the "bad trip". Symptoms include frightening illusions/ hallucinations (usually visual and/or auditory); overwhelming anxiety to the point of panic; aggression with possible violent acting-out behavior; depression with suicidcal ideations, gestures, or attempts; confusion; and fearfulness to the point of paranoid delusions.
Reactions that are prolonged (days to months) and/or require hospitalization are often referred to as "LSD psychosis," and include a heterogenous population and group of symptoms. Although there are no hard and fast rules, some trends have been noted in these patients. There is a tendency for people with poorer premorbid adjusment, a history of psychiatric illness and/or treatment, a greater number of exposure to psychedelic drugs (and correlatively, a great average total cumulative dosage taken over time), drug-taking in an unsupervised setting, a history of polydrug abuse, and self-therapeutic and/or peer-pressure-submission motive for drug use, to suffer these consequences.
In spite of the impressive degree of prior problems noted in many of these patients, there are occasional reports of severe and prolonged reactions occuring in basically well adjusted individuals. In the same vein, there are many instance of faily poorly adapted individuals who suffer _no_ ill effects from repeated psychedelic drug use. In fact, it has been hypothesized that some schizophrenics do not suffer adverse reactions because of their familiarity with such acute altered states. Another possibility is that there individuals may be "protected" by possible "down-regulation" of the receptors for LSD, bu the (over-)production of some endogenous compound. _Individual_ prediction of adverse reactions, therefore, is quite difficult...
Major "functional" psychosis vs. "LSD psychosis"
A diagnostic issue dealth with explicitly in only a few papers is that of LSD-precipitated major functional illnesses, e.g. affective disorders or schizophrenia. In other words, many of these so called LSD psychoses could be other illnesses that were triggered by the stress of a traumatic psychedelic drug experience. Some of the same methodological issues described earlier affect these studies, but they are, on the averagem better controlled, with more family and past psychiatric history available for comparison.
Hensala et al. compared LSD-using and non-LSD-using psychiatric inpatients. They found that this group of patients was generally of a younger age and contained more characteristically disordered individuals than the non- LSD-using group. Patients with specific diagnoses with or without LSD histories were not compared. Based on their observations, they concluded that LSD was basically just another drug of abuse in a population of frequently hospitalized individuals in the San Francisco area, and that it was unlikely that psychedelic use could be deemed etiological in the development of their psychiatric disorders.
Roy, Breakey et al., and Vardy and Kay have attempted to relate LSD use to the onset and revelopment of a schizophrenia-like syndrome. A few comments regarding this conceptual framework seem in order, before their findings are discussed. The major factor here is that of choosing schizophrenia, or in the Vardy and Kay study, schizophreniform disorders, as the comparison group. There is an implication here that LSD psychoses are comparable, phenomenologically, to schizophrenia-like disorders, and that LSD can "cause" the development of such disorders. The multiplicity of symptoms and syndromes described in the "adverse reaction" literature should make it clear that LSD can cause a number of reactions that can last for any amount of time--from minutes to, possibly, years. I believe what is being studied here is the question of the potential role of LSD in accelerating or precipitating the onset of an illness that was "programmed" to develop ultimately in a particular individual--in a manner comparable to the major physical or emotional stress that often precipitates a bona fide myocardial infarction in an individual with advanced coronary atheresclerosis. The stress did not _cause_ the heart disease; it was only the stimulus that accelerated the inexorable process to manifest illness.
In looking at the relevant studies, Breakey et al. found that schizophrenics who "used drugs" had an earlier onset of symptoms and hospitalization than non-drug-using schizophrenics, and had possibly better premorbid personal- ities than non-drug using patients (although Vardy and KAy have challenged this analysis of Breakey's data).
Bowers compared 12 first-admission patients with psychosis related to LSD use, requiring hospitalization and phenothiazines, to 26 patients hospital- ized and treated with phenothiazines with no history of drug use. Six of these controls had been previously hospitalized. Drug-induced psychotic patients were found to have better premorbib histories and prognostic indicators than the nondrug groups. There was no difference in rates of family history of psychiatric illness. However, several issues flaw this study. One is the poly-drug abusing nature of the "LSD-induced" psychotic patients, compared to the controls. The role of LSD, therefore, in causing or precipitating these symptomatic disorders, is open to dispute. The other is the lack of an adequate comparison control group, i.e. the controls were specified only as "psychotic," and did not necessarily match the LSD group in either symptoms or diagnostic classification. A follow-up study of the patients occured between 2 and 6 years later. One half did well and one half did poorly, although the lack of a control group for a follow-up in a similarly symptomatic control group makes interpretation of the data difficult.
Roy, in a somewhat different design, compared chronic schizophrenic patients (diagnosed according to DSM-III criteria) who had used LSD within the week preceding hospitalization, and found no difference in age of symptom onset or hospitalization compared to patients without a history of illicit drug use.
Vardy and Kay, in an elegant study with a 3- and 5- year follow-up period, demonstrated that patients hospitalized for a schizophrenic picture that developed within two weeks of LSD use (patients with other diagnoses were explicitly excluded form comparisons with non-drug-using schizophrenics) were "fundamentally similar to schizophrenics in geneology, phenomenology, and course of illness (165, p. 877). Pre- morbid adjustment, age of onset of symptoms and hospitalization, family history of psychosis or suicide, and most cognitive features were also equal between groups. Family histories of alcohol abuse were markedly great in the LSD group.
I believe these data, taken as a whole, limited as they are in terms of comparing subgroups (i.e. LSD-using vs. non-LSD-using) of "schizophrenia- like" disorders, point towar, at most, a possible precipitory role in the development of these disorders, in a non specific and not etiologically related manner.
Frequently Asked Questions about LSD
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