Line 1. The cognitive-perceptual symptoms found in
patients with PD include stress-related state phenomena such as
derealization, depersonalization and illusions, as well as more chronic
trait characteristics including suspiciousness and odd or eccentric
thinking. It is important to recall that similar symptoms may have differing
etiologies and severity’s among diverse PD categories (as well as among
Axis I disorders). For example, referential thinking and paranoid ideation
appear related to a mild thought disorder trait in Cluster A patients but
may be reactive to acute depressive moods among Cluster B patients.
Line 2. Low-dose neuroleptics (NP) are the treatment
of first choice for acute presentations of anger and hostility,
suspiciousness, referential thinking, paranoid ideation, illusions,
derealization, and depersonalization. This recommendation is supported at
the highest ("A") level by randomized, double-blind controlled
studies, and open label trials involving a wide variety of neuroleptics.
These studies have been conducted primarily in borderline and schizotypal
patients, in both inpatient and outpatient settings (Cowdry &: Gardner,
1988; Goldberg et al., 1986; Soloff, 1986); and in adult and adolescent
populations (Kutcher, Papatheodorou, Reiter, &; Gardner, 1995).
Low-dose neuroleptics appear to have a broad spectrum
of efficacy in acute use, with effects against symptom severity of depressed
mood and impulsively, as well as against anger-hostility and psychoticism.
(Cowdry &; Gardner, 1988; Soloff et al., 1986b, 1989).
Line 3. Treatment effects appear within days to 2
weeks. Patients with primary cognitive symptoms respond the best, while
patients with a depressive presentation (and secondary mood-congruent
cognitive distortions) do less well and should be considered for treatments
defined for affective dysregulation.
Line 4. Duration of treatment has been arbitrarily
defined by the length of treatment trials, which are generally 4-6 weeks in
acute inpatient studies and up to 12 weeks in outpatient settings. Prolonged
use of narcoleptic medication in patients with PD has been associated with
progressive noncompliance and dropout. In one continuation study of BPD
subjects treated with haloperidol up to 22 weeks, 87.5% failed to complete
the study, compared to a 58.1% attrition on placebo. Borderline patients
progressively endorsed more depressive complaints and difficulties with side
effects as the duration of the trial proceeded beyond acute treatment (12
weeks) (Kelly, Soloff, Cornelius, George, & Lis, 1992). An apparent
exception to the acute treatment strategy in the PD patient is a long-term
study of depot flupenthixol directed against the parasuicidal behaviors of
patients selected for repeated suicidal efforts and PD (principally
histrionic and borderline) (Montgomery & Montgomery, 1982). Efficacy
against recurrent parasuicidal behaviors was reported at 4-, 5-, and K-month
follow-ups for patients receiving the depot narcoleptic monthly compared to
the injected placebo. Attrition from this depot trial was low, at 19%
overall (22.2% flupenthixol vs. 15.8% placebo injection). There is currently
no research support for the use of narcoleptic medication as long-term
maintenance therapy in the PD population. The risk of tardive dyskinesia
must be weighed carefully against perceived prophylactic benefit if
maintenance strategies are considered.
Line 5. If response to a low-dose narcoleptic is
suboptimal after a "fair trial'' of 4-6 weeks, the dose should be
increased into the ''low'' range suitable for treating Axis I disorders and
continued for a second trial period of 4-6 weeks.
Lines 6, 7, 8. A suboptimal response at
this point should prompt re-review of the etiology of the
cognitive-perceptual symptoms. If the symptom presentation is truly part of
a nonaffective syndrome, as in the case of a Cluster A personality disorder,
atypical neuroleptics may be considered. While there are no double-blind,
randomized, placebo-controlled studies of atypical neuroleptics in the PD
population at this time, open label trials (Frankenburg & Zanarini,
1993) and case studies (Chengappa, Baker, & Sirri. 1995) have been
published supporting the use of clozapine for patients with BPD and severe,
refractory, psychotic symptoms "of an atypical nature,'' or severe
self-mutilation. In these studies, clozapine was used for patients who had
failed previous neuroleptic trials. Therefore the level of research support
for this decision is "C.'' There is no published literature available
on the treatment of personality disorder patients with risperidol,
olanzapine, or more recent additions to the atypical narcoleptic family of
medications. Line 7. Cognitive-perceptual distortions often present as
mood-congruent symptoms with an affective etiology, although this is not
always apparent on initial evaluation. The need to treat hostility and
paranoid ideation rapidly argues for the use of low-dose neuroleptics at the
start of this algorithm. Where an "affective'' cluster PD is present, a
monoamine oxidase inhibitor (MAOI) or selective serotonin reuptake inhibitor
(SSRI) antidepressant may be added to the low-dose neuroleptic regimen. This
strategy is analogous to the treatment of Axis I affective disorders with
psychotic content, where it is generally advisable to begin treatment with a
neuroleptic before, or at least concurrently with, an antidepressant. (The
use of MAOI and SSRI antidepressants for affective dysregulation in the PD
patient is discussed later.) In addition to their indication for depressed
mood. both MAOI and SSRI antidepressants have some research support for
efficacy against irritability and anger in the PD patient, findings
supported for each drug class by two or more controlled studies, warranting
an "A'' level of support for this recommendation. (Cowdry &
Gardner, 1988; Cornelius, Soloff. Perel, & Ulrich, 1990; Cornelius,
Soloff, Perel, & Ulrich, 1993; Kavoussi, Liu, & Coccaro, 1994;
Markovitz, Calabrese, Schulz, & Meltzer, 19919 Markovitz, 1995; Norden
1989; Salzman et al., 1995; Soloff et al., 1993).
