LETTERS

TO

THE

Am

EDITOR

renal

tubular cell, and is generally thought to clear within three weeks of discontinuation of lithium therapy (1-3). A case we reported in the medical literature (4) and another case report (5) indicate that nephrogenic diabetes insipidus secondary to lithium does not always clean rapidly and may, in fact, persist for up to 20 months after lithium has been discontinued. We are drawing

attention

to this

because,

to our

knowl-

edge, persistent lithium-induced nephrogenic diabetes insipidus has not been reported in the psychiatric literature. Awareness of its existence may be of considerable clinical value in the management of lithium-associated polyunic and polydipsic states that do not clear with termination of lithium therapy, especially in view ofthe recognized efficacy of thiazide diuretics in such circumstances.

REFERENCES

1. Angrist BM, Gershon 5, Levitan Si, et al: Lithium-induced diabetes insipidus-like syndrome. Compr Psychiatry 11:141-146, 1970 2. Lee RV, Jampol LM, Brown WV: Nephrogenic diabetes insipidus and lithium intoxication-complications of lithium carbonate therapy. N EngI J Med 284:93-94, 1971 3. Ramsey TA, Mendels J, Stokes JW, et al: Lithium carbonate and kidney function: a failure in renal concentrating ability. JAMA

219:1446-1449,

1972

4. Price TRP, Beisswenger PJ: Lithium and diabetes insipidus. Ann Intern Med 88:576-577, 1978 5. Simon NM, Garber E, Arieff AJ: Persistent nephrogenic diabetes insipidus after lithium carbonate. Ann Intern Med 86:446447, 1977

R.P.

TREVOR PAUL

I.

PRICE,

M.D.

M.D.

BEISSWENGER,

Hanover,

J Psychiatry

135:10, October

dive dyskinesia should carefully define the condition in order to obtain homogeneous populations. Factors such as response to neunoleptic withdrawal and reinstitution and nesponse to anticholinergics or to dopamine agonists such as amphetamines can help to identify relatively homogeneous subgroups of dyskinetic patients and perhaps to define tandive dyskinesia more precisely. The approach used by Dr. Asnis and associates lumps together patients with dyskinesias of various etiologies, which will retard any efforts to understand the pathophysiology underlying tardive dyskinesia. Moreover, calling these various dyskinesias ‘ ‘ tardive dyskinesia’ ‘ and claiming a 43% prevalence of tandive dyskinesia in psychiatric outpatients will alarm many psychiatrists unnecessarily. Certainly, psychiatrists should be aware of the possibility of tardive dyskinesia, but the dyskinesias discussed by the authors have no proven relationship to classically described tardive dyskinesia, which is often irreversible and hence of considerable concern. Finally, mention might be made of some of the difficulties involved in the use of videotapes as described in the article. The authors report excellent reliability, but this must be distinguished from validity. Their raters clearly agreed on whatever they were measuring, but there is no evidence that what they measured was tardive dyskinesia. Moreover, the person making the videotapes apparently was not blind to whether a patient was dyskinetic or not. Naturally, when videotaping a dyskinetic subject, one would attempt to demonstrate the dyskinesia as clearly as possible and would look for moments of dyskinesia to videotape. This would not be the case with control subjects, although some dyskinetic-like symptoms would be expected occasionally in normal controls. Therefore, the apparent distinction between dyskinetics and normals might be an artifact ofthe selective attention of the person doing the videotaping.

N.H. JEFFREY

A.

MATTES,

Forest

Tardive SIR:

nesia

M.D.,

Dyskinesia I consider in

the

associates

article

‘ ‘

Outpatients’

(December

A Survey ‘ by

1977

of Tardive Gregory M.

issue)

to be

DyskiAsnis,

Dr.

suffi-

ciently misleading as to require some discussion. The central issue is whether the condition the authors evaluated was in fact tandive dyskinesia. The bulk of the evidence indicates that it was not. Tardive dyskinesia, although not precisely defined, is generally considered to be a dyskinesia associated with longterm use of neuroleptics. Typically, it worsens on neunoleptic withdrawal, improves on reinstitution of neuroleptics, and is often worsened by anticholinergics. It must be distinguished from a variety of other dyskinesias, some drug-related, some not. The paper by Dr. Asnis and associates reports no association between years of neuroleptic use and the presence of dyskinesias (in fact, the dyskinetic group had nonsignificantly fewer years of use). This suggests that the dyskinesias involved were not tardive dyskinesia; if a dyskinesia results from long-term neunoleptic use, one would expect a correlation between presence ofdyskinesia and years of use. Similarly, the fact that age did not correlate with the presence ofdyskinesia and the trend (not statistically significant) suggesting that the use of antiparkinsonian agents was associated with a lower incidence of dyskinesia indicate that the condition under investigation was not tandive dyskinesia. This issue is of considerable importance. Studies of tan1248

M.D.

Hills, N. Y.

or Not?

Psychiatric

and

1978

Asnis SIR:

ed

Dr.

associated

Replies Mattes

suggests

findings

that for

tandive

there

are

dyskinesia,

commonly i.e.,

acceptyears

of

neuroleptic use, age, and concurrent use of antiparkinsonian medication. Because our survey did not support these associations, Dr. Mattes suggests that we were not evaluating tandive dyskinesia. However, the literature includes conflicting evidence on the role of these factors in tandive dyskinesia (1). The explanation ofthese controversial findings in the literature is far from clean, although diversity of study populations may have been a factor. In our study, we carefully reviewed recent medical history, physical examinations, laboratory assessments, and family history to rule out other causes ofdyskinesia. No cases of endocninopathy, heredodegenenative disease, or other medical illnesses could be identified that might have presented as a dyskinetic syndrome. I agree with Dr. Mattes that further studies are needed to understand the pathophysiology of tardive dyskinesia; this was not the intent of our survey. It is na#{239}ve to believe that various pharmacologic challenges will separate tandive dyskinesia from other dyskinesias. Within the syndrome of tardive dyskinesia, systematic evaluations with dopamine and acetylcholine agonists and antagonists have revealed varying responses, indicating a heterogeneous disorder (2). In terms of the evaluation process, Dr. Mattes suggests

Am

J Psychiatry

/35:10,

October

/978

the person who did the videotaping the raters, since he had already decided that

LETTERS

might have ‘tipped” whether the patient ‘

had dyskinesia. We doubt that this was the case. The technician who recorded the evaluation did not know which patients had dyskinesia and recorded every subject in a standandized way. Most dyskinetic patients had dyskinetic movements not only during the structured part of the exam but also during the 1- to 2-minute observation period, when only the patient was present and videotaped, and all raters concurred on dyskinesia during the latter period. The point is highlighted by the fact that one patient with tardive dyskinesia demonstrated dyskinetic symptoms only during the obsenvation period in which all three raters independently concurred. Finally, Dr. Mattes is concerned about psychiatrists being alarmed ‘ ‘ unnecessarily’ ‘ by our report. We found that 10% ofthe dyskinetic population, on 4% ofthe survey population, had moderately severe dyskinesia; the remaining cases of dyskinesia were ofminimal or mild severity. It has been sug-

gested that dyskinesia of possible recent onset tinuing 4). For

antipsychotic this reason,

of dyskinesia

of minimal on mild severity and may be readily reversed by discon-

medication on lowering the dosage (3, careful examinations to detect early signs

should

be a routine

part

of psychiatric

evalua-

tions of patients treated with neunoleptics. Until the clinician has more guidelines as to which patients are most vulnerable, every patient taking neuroleptic medication must be viewed as susceptible to tardive dyskinesia. Part of good patient care should be an ‘ ‘overconcern’ ‘ for the development ofthis syndrome.

REFERENCES

1. Mardsen CD, Tarsy D, Baldessarini Ri: Spontaneous and druginduced movement disorders in psychotic patients, in Psychiatnc Aspects of Neurologic Disease. Edited by Benson DF, Blumer D. New York, Grune & Stratton, 1975 2. Casey DE, Denny D: Pharmacological characterizations of tardive dyskinesia. Psychopharmacology 54:1-8, 1977 3 . American College of Neuropsychopharmacology-Food and Drug Administration Task Force: Neurological syndromes associated with antipsychotic drug use. Arch Gen Psychiatry 28:463-467,

1973

4. Quitkin F, Rifkin A, Gochfeld L, et al: Tardive dyskinesia: first signs reversible? Am i Psychiatry 134:84-87, 1977 GREGORY

Positive SIR:

Side

M. AsNI5, M.D. New York, N.Y.

of Lithium?

by Sahayl J. Nasr, M.D. , and Robert W. ‘ ‘Coincidental Improvement in Asthma Treatment’ ‘ (September 1977 issue) in association with the observations of Peter L. Putnam, M.D. (Letten to the Editor, March 1978 issue) concerning remission of dermatologic symptoms in two patients with eczematoid denmatitis treated with lithium prompted us to report another possible ‘ ‘positive’ ‘ side effect of lithium observed in two patients with seborrheic dermatitis.

Atkins, During

The

The

Effects

are

article

M.D. Lithium

,

on

dermatologic

pressive man cleared prophylactic lithium ing a 5-year follow-up. year-old schizophrenic

symptoms

of a 63-year

old

manic-dc-

completely 1 month after initiation of treatment and have not reappeared dunA similar effect was observed in a 32woman with severe seborrheic der-

TO

THE

EDITOR

matitis who was treated successfully with low doses of lithium for her premenstrual tension syndrome. It is worth noting that remission of both premenstrual and dermatologic symptoms was achieved with a lithium dose of only 300 mg/ day, for one week before expected day of menstruation.

We are currently a double-blind ium carbonate matitis.

pursuing

investigation on nonpsychotic

the issue

further

on the effect patients

G.N.

by conducting

of low doses with seborrheic

CHRISTODOULOU, AG.

M.D.

M.D. Greece

VARELTZIDES,

Athens,

Mental

Health

Services

of lithden-

in HMOs

SIR: In ‘ ‘The External Provision of Health Maintenance Organization Mental Health Services’ ‘ (June 1978 issue) David J. Muller, M.D. , offers unsubstantiated opinions about

HMOs. health

My

experience

services

(HCHP)

since

at

as a director the

1969 leads

Harvard

of integrated

Community

me to believe

that

Health

mental Plan

the comparison

of alternative

models must be addressed objectively. ‘quality,’ ‘ “flexibility,’ ‘ and “personal care” superior in Dr. Mullen’s clinic? He does not cite norms of staff training or experience, individual or group performance standards, supervisory practices, evaluation of treatment outcome, quality control mechanisms, on organized consumer input-features of many HMOs. Contract negotiations seem an insufficient substitute. Although I find many statements in the article objectionable, two oversimplifications require response. The first relates to cost: If “cost to the HMO” is less (no numbers are given), what about cost to the member? In stating, ‘ ‘ When the benefits are used up, there may be insufficient motivation to pay out of pocket and continue therapy.” and “The initial sessions may therefore have been wasted,’ ‘ Dr. Mullen ignores the vast literature demonstrating effectiveness of brief treatment. With staff motivation, treatment can be planned so that most patients can be treated within insurable limits. At HCHP, where extended psychotherapy is available, less than 1% of patients seen require treatment beyond the benefit limit of 20 sessions a year. A system using prepaid benefits to introduce patients to fee-for-service treatment will be inexpensive to the HMO and profitable to the clinic but expensive for the member. Capitation payments go farther iffewer “heads” show up. Current estimates suggest that l0%-15% of the population may require psychiatric services (I). A cost/benefit assessment should include numbers referred and seen, cancellations, and no-show rates. At HCHP, 12% of members who use health services in a year come to the mental health service. Combined cancellation and no-show rates are less than 10%, and over 82% of patients referred show up. Other internal services report similar experience (2). Comparison figures from Dr. Mullen would be of interest. The second area I would like to address is liaison. A number of authors have urged shared responsibility for mental health care (1). In a medical setting, where doctors and nurses see many psychological problems, this must include willingness to diagnose and treat common disturbances as well as readiness to refer when necessary. The notion that “at least monthly conferences’ ‘ with HMO physicians will adequately support such efforts is na#{239}ve.At HCHP, approximately 30% of medical patients receive a diagnosis of emo-

How

are

‘

1249