Applied Psychophysiology and Biofeedback, Vol. 31, No. 3, September 2006 (C ?2006)
Thermal Biofeedback for Primary Raynaud’s
Phenomenon: A Review of the Literature
Maria Katsamanis Karavidas,1,5Pei-Shan Tsai,2Carolyn Yucha,3
Angele McGrady,4and Paul M. Lehrer1
Published online: 3 October 2006
The clinical presentation of primary Raynaud’s phenomenon (RP) derives from various
pathogenic triggers. The use of thermal biofeedback (TBF) may be of benefit in reduc-
ing the severity and frequency of attacks. This article summarizes the relevant research
regarding the pathophysiology of primary RP and mechanism of TBF for RP. Systematic
reviews of the efficacy of TBF for RP and treatment guidelines for clinicians are provided.
The panel concludes that the level of evidence for TBF efficacy is categorized as Level
IV: efficacious. The rationale, based on three randomized controlled trials conducted in
independent laboratories, demonstrated “superiority or equivalence” of treatments that
include TBF. However, randomly controlled trials (RCT) with positive clinical outcomes
skills. Procedures for reviewing and rating of the levels of evidence of efficacy of studies
was based on the Template for Developing Guidelines for the Evaluation of the Clinical
Efficacy ofPsychophysiological Interventionsdeveloped bythejointtaskforceoftheAAPB
and the Society for Neuronal Regulation (SNR).
KEY WORDS: Thermal biofeedback; Primary Raynaud’s phenomenon.
Primary Raynaud’s Phenomenon
Raynaud’s phenomenon (RP) refers to recurrent, episodic vasoconstriction of the
digital arteries and arterioles (Block & Sequeira, 2001; Wigley, 2002). The ischemic phase
of RP presents clinically as demarcated pale (blanching) or cyanotic skin, limited to the
digits (Wigley, 2002). It typically starts in one or several digits after exposure to cold or
1University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, New
2Taipei Medical University, Taipei, Taiwan.
3University of Nevada, Las Vegas, NV.
4Medical College of Ohio, Toledo, OH.
5Address all correspondence to Maria Katsamanis Karavidas, University of Medicine and Dentistry of New
Jersey-Robert Wood Johnson Medical School, Piscataway, New Jersey; e-mail: email@example.com.
1090-0586/06/0900-0203/1 C ?2006 Springer Science+Business Media, Inc.
204 Karavidas, Tsai, Yucha, McGrady, and Lehrer
stress and may spread symmetrically to both hands. The attack usually ends with a rapid
reperfusion of the digits, manifested by erythematous skin (reactive hyperemia).
RP is classified as primary if there is no known cause, and secondary if an associated
disorder has been detected (Block & Sequeira, 2001). In practice, clinical criteria are used
for distinguishing patients with primary RP from those with secondary RP. The suggested
criteria for primary RP include: vasospastic attacks precipitated by cold or emotional
stress, the absence of a secondary cause, symmetric attacks, the absence of tissue necrosis,
ulceration, or gangrene; a negative test for antinuclear antibody; a normal erythrocyte
sedimentation rate; and normal nail fold capillaries (Allen & Brown, 1932; LeRoy &
Medsger, 1992). Secondary RP is associated with: onset after age 30 or 40 years; episodes
tissue disease; specific auto antibodies associated with underlying inflammatory disease;
and evidence of microvascular disease on microscopy of nail fold capillaries (Block &
Sequeira, 2001; Wigley, 2002). In addition to these clinical criteria, digital blood pressure
et al., 2000; Maricq, Valter, & Maricq, 1998). Freedman et al. (1988) used the criteria of
Allen and Brown (1932), while other studies, reviewed in this paper, diagnosed RP using a
structured interview assisted by color charts. In addition, inclusion criterion is at least two
medical treatments for primary RP. Initial management usually includes the avoidance of
(Coffman, 1991) for Raynaud’s phenomenon.
Prevalence rates of Raynaud’s phenomenon differ by gender (Gardner-Medwin,
Macdonald, Taylor, Riley, & Powell, 2001). A questionnaire study conducted in the United
States estimated a prevalence of 4.3% in women and 2.7% in men (Weinrich, Maricq, Keil,
to treatment where the disorder does occur (Robinson, Gagnon, Riley, & Price, 2003).
Current research suggests that a local abnormality at the digital microcirculation level
may be an underlying mechanism (Turton, Kent, & Kester, 1998). An overactivity of the
sympathetic nervous system (SNS) is less likely to be the primary abnormality of RP,
although early evidence supports the involvement of the SNS-mediated vascular tone in
the pathogenesis of the disease (Turton et al., 1998). Research on the pathophysiology of
Raynaud’s disease indicates that attacks are most probably caused by a hypersensitivity
of peripheral vascular α2-adrenergic receptors to cooling (Freedman, Moten, Migaly, &
Mayes, 1993). Additionally, peripheral vascular α1-adrenoceptors are hypersensitive in
Raynaud’s disease patients at baseline (Edwards, Phinney, Taylor, Keenan, & Porter, 1987;
Graafsma et al., 1991). Since vascular α1- and α2- adrenoceptors are hypersensitive in
Raynaud’s disease patients, normal catecholamine elevations that are produced by emo-
tional stress or by reflex cooling can also trigger the vasospastic attacks (Freedman et al.,
Jobe, Sampson, Roberts, and Kelly (1986) found that those with Raynaud’s disease
were no more emotionally unstable than a normal population. Anxiety scores, as measured
by the Institute for Personality and Ability Testing (IPAT) Anxiety Scale Questionnaire
(Cattell, 1957) did not differentiate Raynaud’s subjects (mean score of 24.1) from the
Thermal Biofeedback for Primary Raynaud’s Phenomenon 205
Personality Questionnaire did not differentiate Raynaud’s subjects (mean score of 7.13)
from normal subjects (mean score of 8.51).
Similarly, Freedman and Ianni (1983) randomly provided concurrent cognitive stress
management training to half of subjects in each of four treatment groups in the study
(because emotional stress has been implicated as a trigger for Raynaud’s attacks). The
addition of cognitive stress management did not significantly affect efficacy.
Behavioral treatment of RP has focused mainly on vasodilatation with or without
biofeedback (BF). Feedback-assisted vasodilatation refers to thermal biofeedback (TBF)
which teaches the skill of self-regulation of skin temperature (Schwartz & Sedlacek, 2003,
pp. 369–381). TBF therapy has been found to reduce both the frequency and severity of
vasospastic attacks (Taub & Stroebel, 1978; Sedlacek & Taub, 1996). The goal of TBF
therapy is to train subjects to control peripheral vasoconstrictor responses and to acquire
voluntary hand warming skills. It is hypothesized that, once learned, hand warming can
be produced without feedback. Ideally, trained individuals generate hand warming quickly
individuals are taught to vasodilate just prior to going outside in cold weather. Once
vasospasm has actually occurred, it is difficult to reverse with handwarming. A non-neural
beta-adrenergic mechanism as well as a reduction in alpha sympathetic nerve activity may
be involved in the vasodilatation produced by TBF (Freedman, Keegan, Migaly, Galloway,
& Mayes, 1991; Freedman et al., 1988). Other nonpharmacological therapies designed to
reduce emotional stress may also be helpful in preventing Raynaud’s attacks.
The aims of this review were: (1) to comprehensively examine the level of evidence
for efficacy of biofeedback treatment of RP in the published empirical literature; (2) to
rate treatment efficacy according to standard guidelines; and (3) to make recommendations
based on the findings.
MedLine and PsychInfo databases were searched for research articles published in
Raynaud’s phenomenon. Three search terms were used to identify potential studies. These
terms were “Raynaud’s,” “temperature,” and “biofeedback.” Studies were restricted to
treatment effect of TBF. We only reviewed papers describing randomized controlled trials
that did not include measurements of at least one of the following treatment outcomes were
excluded: symptom frequency, symptom intensity, and temperature response to cold.
conducted because few of the trials included the same comparisons and outcomes. A total
of ten studies (reported in 12 papers) were included. Efficacy of TBF for the COI refers
to “the determination of treatment effect derived from a systematic evaluation obtained
in a controlled clinical trial.” Rating of the levels of evidence of efficacy was based on
206Karavidas, Tsai, Yucha, McGrady, and Lehrer
the Template for Developing Guidelines for the Evaluation of the Clinical Efficacy of
Psychophysiological Interventions developed by the joint task force of the AAPB and the
Society for Neuronal Regulation (SNR) (La Vaque et al., 2002). Five levels of evidence
were defined: Level 1—Not empirically supported; Level 2—Possibly efficacious; Level
3—Probably efficacious; Level 4—Efficacious; and Level 5—Efficacious and specific. All
papers were evaluated by two independent reviewers who extracted data on study design,
in the scoring, a third rater was asked to categorize the study. This was required for only
one study; the third reviewer agreed with one of the original reviewers and the rating was
REVIEW OF BF TRIALS FOR RAYNAUD’S PHENOMENON
A total of ten studies of Raynaud’s phenomenon met inclusion criteria for review.
Seven were RCT’s (see Table IA), one a CCT (see Table IB), and two were FU studies
(see Table IC). Of the eight studies reviewed, seven were RCT’s. These studies all included
predominantly female participants. With the exception of one RCT (N=313), these studies
used a small sample size (N=12–39). One study did not report the age of the study partici-
study. Surwit, Pilon, and Fenton (1978) and three papers presented various aspects of a
single study of the Raynaud’s Treatment Study (RTS; Middaugh et al., 2001; Raynaud’s
Treatment Study Investigators, 2000; Thompson et al., 1999). A critical examination of
the reviewed studies highlighted three major shortcomings shared by the majority of the
published studies: (1) methodological flaws (e.g., outdoor temperature considered as a con-
TBF alone vs. control group). For example, in a study by Guglielmi, Roberts, and Patterson
(1982), the attack rates of TBF, EMG, and no-treatment control groups all dramatically
declined (93, 99, and 88%, respectively) as the outdoor temperature became warmer. Three
out of ten studies did not account for the seasonal effects element; (2) all-female sample
versus a mixed sample, and (3) inconsistencies as a result of gaps in reporting complete
demographic data and accurate subject information at baseline.
ADEQUACY OF THERMAL BIOFEEDBACK TRAINABILITY
The failure to detect a superior beneficial effect of TBF compared to other general
relaxation techniques on Raynaud’s symptomatology in some studies may be due to in-
effective TBF training. Subjects in some studies did not acquire the skill of voluntary
vasodilation when exposed to cold stress. Guglielmi et al. (1982) reported that less than
50% of TBF subjects in their study learned to produce finger temperature increases during
training. Similarly, Middaugh et al. (2001) reported that only 35% of TBF subjects met the
study criteria for increasing finger temperature. Keefe, Surwit, and Pilon (1980), trained
(1979) study achieved digital temperature responses after four weeks of training, results
did not persist at a 9-month follow-up.
Other studies document the effectiveness of training to produce a 2–4◦F increase in
hand warming. Freedman and Ianni (1983) demonstrated that temperature biofeedback
Thermal Biofeedback for Primary Raynaud’s Phenomenon 207
Table I. Summary of Studies Evaluating the Efficacy of TBF for Raynaud’s Phenomena
N; % Female; age range
Dosage (hours) ×
Surwit et al.
1. TBF + autogenic
No information regarding the degree of hand warming that
subjects were able to achieve
2. Autogenic training
Trained subjects demonstrated significant pre to post
improvement both in ability to maintain digital skin temperature during cold stress challenge and in the
number of attacks experienced. Trained subjectsdemonstrated a 32% decrease in number of attacks
compared to a decrease of 10% for the controls (n.s.)
3. Waiting-list control
Addition of TBF to autogenic training did not provide
Individual Laboratory or
Keefe et al.
1. TBF + autogenic
No information regarding the degree of hand warming that
subjects were able to achieve
2. Autogenic training
Number of attacks per day dropped in all subjects during
training & at 1-month follow-up. All subjects showed
significant improvement in ability to maintain skin
temperature in response to cold during training
3. Progressive relaxation
No significant differences between three treatment groups
TBF subjects achieved an average of .6◦C increase in
finger temperature during training. Significant
temperature increases (.65◦C) occurred during a
posttraining voluntary control test in those who received
TBF but not in those who received autogenic training orEMG BF; 66.8% reduction in frequency of attacks at
one-year follow-up in the TBF group; TBF under cold
stress significantly improved voluntary vasodilation at
follow-up & produced a significantly greater (92.5%)
reduction in symptom frequency. One half of the subjects
were assigned to receive concurrent cognitive stress
2. TBF under cold stress
3. Autogenic training4. EMG BF
208Karavidas, Tsai, Yucha, McGrady, and Lehrer
Table I. Continued.
N; % Female; age range
Dosage (hours) ×
Freedman et al.
mean = 42
5 × 5
Compared to the pretreatment month, subjects in the TBF
group showed a significant decline in attack rates at Year1 (81.3%) and Year 2 (80.5%) follow-up. The attack rateof the autogenic group did not change significantly at
Year 1 (32.3%) or Year 2 (26.3%)
2. Autogenic training
Jacobson et al.
1. TBF + relaxation
0.33 × 6
Both groups demonstrated finger temperature increases
during training. BF-RT subjects showed an average of
.5◦C increase in finger temperature per trial. RT subjects
showed an average of 1.4◦C increase in skin temperature
per trial. No information regarding the pre to post
change in attack rates was available. Both groups
demonstrated identical post-training outcomes in
self-rated improvement in symptom severity (slightly to
2. Relaxation alone (RT)
1 & 24
Guglielmi et al.
No information regarding the degree of hand warming that
subjects were able to achieve
2. EMG relaxation
Less than 50% of the TBF subjects learned to produce
finger temperature increases during training. All three
groups reported a decrease in number of attacks. TBFgroup showed 93% decrease in frequency of attacks
compared to 99% in the EMG group and 88% in the
no-treatment group. No significant differences were
found among the three groups
3. No-treatment control
mean = 45
2×5 or 1×10;
35% of the TBF subjects met the study criteria for
increasing finger temperature (1◦F above the last 3 min
of baseline, .5 above the last 3 min of baseline and93–94◦F or >94◦F). TBF did not reduce attacks
compared with control BF. Nifedipine-treated subjects
showed 56% fewer attacks than TBF group (p=0.08)
Thermal Biofeedback for Primary Raynaud’s Phenomenon 209
Table I. Continued.
N; % Female; age range
Dosage (hours) ×
Thompson et al.
2. Control BF (EMG)
Middaugh et al.
Jobe et al.
1. TBF + EMG BF +
1 × 8 EMG + 1
Subjects in the CC group showed an increase of 3.9◦C and
those in the TBF-RT group showed an increase of 4.1◦C
from pretest to posttest. No information regarding the
pre to post change in attack rates was available. Nodifferences between groups in severity & recovery from
attacks. Both groups increased the temperature response
to cold. The CC group had less pain during attacks at the
end of training & less severe attacks than BF group at
Keefe et al.
Same as above
Mean number of vasospastic attacks per day at follow-up
(1.2) were approximately equal to the number of attacks
at the end of training (1.3/day). n.s. There was a 42%
reduction in vasospastic attacks from the initial week
pre-treatment and a 29% reduction from the first week of
treatment to one-year followup. Training effect of
improving digital temperature responses during a cold
stress challenge was impaired
9 months after training as compared to 4 weeks after
Freedman et al.
Same as above
Symptom reduction persisted for 3 years post-training for
both TBF groups
210Karavidas, Tsai, Yucha, McGrady, and Lehrer
yielded significant temperature increases (0.65◦C) and Jacobson, Manschreck, and
Silverberg (1979) showed that combination treatment (TBF and relaxation) and relaxation
treatment alone produce increases in skin temperature (i.e., 0.5 and 1.4◦C respectively).
Classical-conditioning training yielded an increase of 3.9◦C temperature while the
combination training (TBF, EMG biofeedback and relaxation) showed a 4.1◦C increase
from pretest to posttest (Jobe et al., 1986).
The various TBF protocols reported in the literature also varied widely in intensity of
TBF training. The total hours of TBF training ranged between 2 and 23.5 hours held over
a 3- to 20-week period. One study (Keefe et al., 1980) adopted a group-approach to TBF
training while others (Freedman & Ianni, 1983, 1988; Jacobson et al., 1979; Guglielmi
et al., 1982; Middaugh et al., 2001; RTS Investigators, 2000; Surwit et al., 1978; Thompson
et al., 1999) used an individual approach.
Several studies did not report the degree of hand warming that subjects were able to
achieve and percentage of subjects who actually learned to produce temperature increases
(see Table I). Thus, we do not know whether training to criterion would have impacted the
COMPARISON GROUPS AND TREATMENT FORMATS
Experimental designs varied widely among the studies we reviewed. Four studies
(Guglielmi et al., 1982; Jacobson et al., 1979; Keefe et al., 1980; RTS, 2000) examined
the efficacy of TBF alone, and compared TBF effects to other relaxation techniques or
calcium-channel blocking agents. Others (Freedman & Ianni, 1983; Freedman, Ianni, &
Wenig, 1985; Jobe et al., 1986; Keefe et al., 1979) used a combination of relaxation
techniques and TBF. An intent-to-treat analysis approach was adopted by the RTS, but not
in the general population, they are less sensitive to efficacy in a population motivated to
learn and practice the technique.
Some studies examined the efficacy of TBF compared to an alternative treatment
group (e.g., autogenic training, progressive muscle relaxation, classical conditioning, EMG
BF, or a calcium channel blocking agent). Several studies used a no-treatment group. Few
studies included a placebo control. In one study, EMG BF was used as the control BF
condition. Six of the eight reviewed studies demonstrated that TBF did not provide a better
outcome to other types of relaxation techniques, classical conditioning, nonthermal BF
(e.g., EMG), or a calcium channel blocking agent but this does not show effectiveness for
Combining TBF with other treatment approaches make it difficult to assess whether
training under cold stress produced a significantly greater reduction in symptom frequency
than TBF alone, autogenic training, or EMG BF, suggesting that cold “challenge” may be
an important element in the TBF protocol. An optimal “dosage”or amount of TBF training
RP has not been determined.
Two studies (Guglielmi and the RTS) reported substantial problems in teaching
hand warming skills. In neither study were the therapeutic effects significant, compared
with a no-treatment control (Guglielmi data) or placebo control (RTS, either frontalis
Thermal Biofeedback for Primary Raynaud’s Phenomenon 211
EMG feedback or medication placebo). Guglielmi’s study (1) achieved >88% reduction
in attack rates in a no-treatment group as well as in two treatment groups; (2) had poor
success in training either EMG decreases or temperature increases; and (3) found that
attacks for no-treatment and treatment groups systematically declined across the 5 months
of the study from January to June, as environmental temperatures increased, indicating
that outdoor temperature effects may have been responsible for improvements in attack
SUPERIORITY OR EQUIVALENCE
Freedman and Ianni (1983) and Freedman et al. (1988) demonstrated that TBF pro-
duces greater reductions in symptom frequency than either autogenic training or EMG BF.
In contrast, other studies (Surwit et al., 1978; Keefe et al., 1980; Jobe et al., 1986; Jacobson
as various relaxation techniques.
IntheRTS, as nifedipine-treated group had better outcomes than one treated withTBF
(RTS Study Investigators, 2000). Guglielmi et al. (1982) reported decreases in symptom
suggest that TBF does not induce specific treatment effects. It is possible that simply
participating in a study produces symptom improvement and that favorable outcomes
resulted from subjects’ expectations of treatment effects. Thus, the improvement in self-
reported symptom severity/frequency might be due to nonspecific effects of the treatment
modality such as mood, decreased anxiety, etc.
Other controlled investigations have shown that Raynaud’s disease patients treated
with TBF resulted in significant reductions in symptom frequency, ranging from 67–92%,
and maintained for up to 3 years (Freedman & Ianni, 1983; Freedman et al., 1988). In
fact, many consider the two studies by Freedman et al. to be the best in the literature,
with a rigorous, well-controlled design, lengthy daily diary measures of attack rates, and
outcomes assessed annually for three years with careful attention to seasonal tempera-
tures. There were clear and statistically significant differences in favor of TBF, both in
hand warming and in reduction of attack rate. The study by Jobe et al. (1986) uniquely
compared a classical conditioning procedure (CC) with a TBF + EMG + relaxation
procedure. Both groups achieved substantial hand warming (group averages >3.9◦C) and
both groups made similar clinical improvements. The impact on attacks was measured
by self-rated improvements on a scale from 1 to 5 for 3 different aspects of attacks: at-
tack severity, attack painfulness, and time to recover from attacks (duration). Immediately
post training, the CC group seemed more improved than the TFB + EMG + relaxation
group (4.0 vs. 3.5, p < .05) with regard to pain, but the groups were similar in sever-
ity and recovery. At one year, the advantage was still with CC, but again for only one
of the three measures, this time for severity (4.83 vs. 3.63, p < .05); the groups were
now similar on pain and duration. From the raw data that was provided, it is evident
that both groups rated themselves as substantially improved, immediately post-training,
and at one-year follow-up, although there was some advantage to the CC group-on one
of three measures, with the groups equivalent on two of three measures at each time
212Karavidas, Tsai, Yucha, McGrady, and Lehrer
EFFICACY RATINGS OF BF FOR RAYNAUD’S DISORDERS
The following ratings, paraphrased here from the published guidelines, are from the
AAPB/SNR efficacy rating guidelines (La Vaque et al., 2002):
Level 1: Supported only by anecdotal reports and/or case studies in non-peer reviewed
venues. Not empirically supported.
Level 2: Possibly Efficacious: At least one study of sufficient statistical power with well
identified outcome measures, but lacking randomized assignment to a control condition
internal to the study.
trolled studies, and within subject and intra-subject replication studies that demonstrate
Level 4: Efficacious: A treatment for a particular condition of interest can only be rated as
“efficacious,” in the hierarchical rating system for evidence for treatment efficacy, when
the following six criteria are met:
2. The studies have been conducted on well-defined subjects with a specific prob-
lem for whom inclusion criteria are delineated in a reliable, operationally defined
3. The studies used valid and clearly specified outcome measures related to the prob-
lem being treated and,
4. The data are appropriately analyzed;
5. Diagnostic and treatment procedures are clearly defined in a manner that makes
replication by others possible; and
6. The superiority or equivalence of the investigational treatment has been shown in
at least two independent research settings.
Evidence of Level 5: Efficacious and Specific (the investigational treatment has
been shown to be statistically superior to credible sham therapy, pill, or alternative
bona fide treatment in at least two independent research settings).
The panel concludes that the level of evidence of efficacy for TBF is categorized as
Level IV: efficacious. There are RCT’s from three independent labs: Surwit et al. (1978),
Keefe et al. (1980) and Freedman et al. (1988) demonstrating “superiority or equivalence”
of treatments that include TBF. Certainly the criteria for Level III: Probably Efficacious are
met; the Freedman RCTs demonstrate specific effects plus four other RCTs demonstrate
efficacy. Level V: efficacious and specific, is not as yet reached because there is evidence
of specific effects in one research setting but not two. Thus, the case for specific effects
has not yet been made. As a caveat, however, all three RCT’s with positive results were
small studies. The one large RCT, the RCT trial, had negative results but did not achieve
Thermal Biofeedback for Primary Raynaud’s Phenomenon213
TBF is widely used by clinicians to treat RP. A typical TBF research study training
session includes a 10–15-min waiting or adaptation period, a 10–15-min baseline period,
a 15–20-min TBF training period, and a 10–20-min verbal review of the session. The
typical number of sessions of treatment reported in the studies reviewed is between 5 and
10, although some individuals may require 8 to16 sessions or even more to learn hand-
warming skills. Hand-warming skills are difficult to learn, but the acquisition of these skills
was administered to all participants to ensure the consistency of the training protocol. In
practice, however, patients are usually trained to a criterion level of mastery rather than
a set number of sessions to ensure the acquisition of the specific vasodilation response.
We recommend that future TBF training protocols include testing transfer of training and
generalization of vasodilation (or reduced vasoconstriction) response from the laboratory
to real-life situations. One or two TBF sessions should be conducted under cold stress
conditions. A no-feedback session during which subjects are to increase finger temperature
without feedback may also be useful. Home practice with or without feedback devices is
Optimally, the goal of any treatment modality for Raynaud’s disease is to reduce
the vasoconstriction response to cold and other stressors. To ensure an optimal beneficial
such as progressive muscle relaxation, frontalis EMG BF, or autogenic training can be
introduced before the actual TBF training. Guided imagery that is tailored to the individual
subject to increase relaxation and warming can also be incorporated into treatment plans.
training environment and instructor contact. In fact, many of the studies did not outline the
qualifications and training received by their own biofeedback technicians. It is possible that
the trainer characteristics rather than the intervention explained the varying “trainability.”
For example, Taub and School (1978) showed that an overly impersonal approach to TBF
training interferes with learning to warm the hands. This may explain the poor results
of two major studies (Guglielmi and RTS) that documented limited success in training
subjects with TBF. Guglielmi et al. (1982) indicated that, while the lab technician offered
support and encouragement to the subjects on their performance, the experimenter in the
adjacent room was given explicit instructions to limit his/her interactions to a simple
greeting when subject arrived for their weekly sessions. Subjects were offered “support
and encouragement” during training, but it is not clear the extent and detail of performance
feedback offered by lab technicians, or the interpersonal warmth between therapist and
patient. Both groups were asked to refrain from seeking additional information on the topic
of biofeedback. One can surmise that the research assistants themselves could therefore
provide only limited feedback to subjects since they themselves were restricted by the
research procedures. Limited feedback and an overly controlled environment could also
214Karavidas, Tsai, Yucha, McGrady, and Lehrer
have lead to a sterile learning environment. In the RTS study, where verbal coaching was
only provided after the biofeedback phase to the cohort 1 group (November–February
1993 and 1994) coaching resulted in a 32% increase in finger temperature. Since learning
was less than expected, participants in cohort 2 (November–February 1994–1995) were
coached during the feedback phase. The modification in feedback resulted in an additional
4% increase in finger temperature (n.s.). Overall, only 35% of the Raynaud’s subjects and
67% healthy individuals achieved study standards for “successful learning” (p < .001).
Perhaps excessive digital vasoconstriction, due to Raynaud’s disease, may override
in this population. Middaugh et al. (2001) found that gender, coping skills and anxiety were
significant predicators of trainability. It is more likely that the Raynaud’s population is
hypersensitive to sensations in their periphery and thus may harbor additional fears about
interventions further increasing pain. Failed interventions and lack of consensus from the
medical community of the pathology and role of anxiety are just some factors that can
contribute in making Raynaud’s patients less optimistic and open to the effectiveness of
TBF. Interpersonal warmth may be particularly important in allowing an anxious patient to
relax and is a key element in biofeedback training.
This paper systematically reviewed eight controlled clinical trials and two follow-up
studies that examined the efficacy of TBF for primary RP. The level of evidence of efficacy
for TBF was rated as Level IV: efficacious based on the AAPB/SNR criteria. Several study
limitations were noted in the studies reviewed. The panel recommends that future research
on TBF for RP should meet the following conditions:
1. Better specification of duration of the disease, since onset, gender and age of
participants, and medication status;
2. More consistent criteria for study outcomes;
3. Better specification of dosage, duration, and format of the TBF protocol;
4. Inclusion of strategies to control for placebo and/or nonspecific effects; and
5. Continued use of placebo and no treatment controls
6. Inclusion of learning criteria for TBF training.
7. Evaluation of maximally effective forms of treatment, including a personally warm
interaction with the therapist, with treatment elements and pacing of treatment
closely reflecting that used in clinical practice.
For clinical practice, treatment guidelines for use of TBF for primary RPT are as
1. Subjects should be trained to a predetermined criteria (i.e., voluntarily raising
temperature to 93◦F for at least 15 min [Sedlacek, 1979]) to ensure the acquisition
of the specific vasodilation response.
2. Include cold stress conditions in the training.
3. Include a no feedback session to facilitate the transfer of skills outside the labora-
4. Include home practice and applied practice in the natural environment.
Thermal Biofeedback for Primary Raynaud’s Phenomenon215
5. Consider a multiple treatment approach.
6. Address anxiety and comorbid emotional disorders that may complicate treatment.
Allen, E. V., & Brown, G. E. (1932). Raynaud’s disease: a critical review of minimal requisites for diagnosis.
American Journal of Medical Science, 183, 187–200.
Block, J. A., & Sequeira, W. (2001). Raynaud’s phenomenon. The Lancet, 357, 2042–2048.
Cattell, R. B. (1957). IPAT anxiety scale. Institute for Personality and Ability Testing, Champaign, IL.
Coffman, J. D. (1991). Raynaud’s phenomenon. Hypertension, 17, 593–602.
Freedman, R. R., & Ianni, P. (1983). Role of cold and emotional stress in Raynaud’s disease and scleroderma.
British Medical Journal, 287, 1499–1502.
Freedman, R. R., Ianni, P., & Wenig, P. (1985). Behavioral treatment of Raynaud’s disease: Long-term follow-up.
Journal of Consulting and Clinical Psychology, 53, 136.
vasodilating mechanism in temperature biofeedback. Psychosomatic Medicine, 50, 394–401.
Freedman, R. R., Moten, M., Migaly, P., & Mayes, M. (1993). Cold-induced potentiation of a2-adrenergic
vasoconstriction in idiopathic Raynaud’s disease. Arthritis and Rheumatism, 36, 685–690.
Gardner-Medwin, J. M., Macdonald, I. A., Taylor, J. Y., Riley, P. H., & Powell, R. J. (2001). Seasonal differences
in finger skin temperature and microvascular blood flow in healthy men and women are exaggerated in
women with primary Raynaud’s phenomenon. British journal of Clinical Pharmacology, 52, 17–23.
Graafsma, S. J., Wollersheim, H., Droste, H. T., ten Dam, M. A. G. J., van Tits, L. J. H., Reyenga, J., de Miranda,
J. F. R., & Thien, T. (1991). Adrenoreceptors on blood cells from patients with primary Raynaud’s phe-
nomenon. Clinical Science, 80, 325–331.
Guglielmi, R. S., Roberts, A. H., & Patterson, R. (1982). Skin temperature biofeedback for Raynaud’s disease: A
double-blind study. Biofeedback and Self-Regulation, 7, 99–120.
Jacobson, A. M., Manschreck, T. C., & Silverberg, E. (1979). Behavioral treatment for Raynaud’s disease: A
comparative study with long-term follow-up. American Journal of Psychiatry, 136, 844–846.
Jennings, J. R., Maricq, H. R., Canner, J., Thompson, B., Freedman, R. R., Wise, R., et al. (1999). A thermal vas-
cular test for distinguishing between patients with Raynaud’s phenomenon and healthy controls. Raynaud’s
Treatment Study Investigators. Health Psychology, 18, 421–426.
Jobe, J. B., Sampson, J. B., Roberts, D. E., & Kelly, J. A. (1986). Comparison of behavioral treatment for
Raynaud’s disease. Journal of Behavioral Medicine, 9, 89–96.
Keefe, F. J., Surwit, R. S., & Pilon, R. N. (1979). A 1-year follow-up of Raynaud’s patients treated with behavioral
therapy techniques. Journal of Behavioral Medicine, 2, 385–391.
Keefe, F. J., Surwit, R. S., & Pilon, R. N. (1980). Biofeedback, autogenic training, and progressive relaxation in
the treatment of Raynaud’s disease: A comparative study. Journal of Applied Behavior Analysis, 13, 3–11.
La Vaque, T. J., Corrydon, H., Trudeau, D., Monastra, V., Perry, J., Lehrer, P., et al. (2002). Template for
Psychophysiology and Biofeedback, 27(4), 273–281.
LeRoy, E. C., & Medsger, T. A. (1992). Raynaud’s phenomenon: A proposal for classification. Clinical and
Experimental Rheumatology, 10, 485–488.
Maricq, H. R., Jennings, J. R., Valter, I., Frederick, M., Thompson, B., Smith, E. A., et al. (2000). Evaluation
of treatment efficacy of Raynaud phenomenon by digital blood pressure response to cooling. Raynaud’s
Treatment Study Investigators. Vascular Medicine, 5, 135–140.
Maricq, H. R., Valter, I., & Maricq, J. G. (1998). An objective method to estimate the severity of Raynaud
phenomenon: Digital blood pressure response to cooling. Vascular Medicine, 3, 109–113.
Middaugh, S. J., Haythornthwaite, J. A., Thompson, B., Hill, R., Brown, K. M., Freedman, R. R., et al. (2001).
The Raynaud’s treatment study: Biofeedback protocols and acquisition of temperature biofeedback skills.
Applied Psychophysiology and Biofeedback, 26, 251–278.
Raynaud’s Treatment Study (RTS) Investigators. (2000). Comparison of sustained-release nifedipine and tem-
perature biofeedback for treatment of primary Raynaud phenomenon. Archives of Internal Medicine, 160,
Robinson, M. E., Gagnon, C. M., Riley, J. L., & Price, D. D. (2003). Altering gender role expectations: effects on
pain tolerance, pain threshold, and pain ratings. Journal of Pain, 4, 284–288.
therapies. In M. S. Schwartz, & F. Andrasik (Eds.), Biofeedback: a practitioner’s guide (3rd ed.). (pp. 369–
381). NY: The Guilford Press.
216Karavidas, Tsai, Yucha, McGrady, and Lehrer
Sedlacek, K. (1979). Biofeedback for Raynaud’s disease. Psychosomatics, 20, 535–541.
and Practice, 27, 548–553.
Simlan, A., Holligan, S., Brennan, P., & Maddison, P. (1990). Prevalence of symptoms of Raynaud’s phenomenon
in general practice. British Medical Journal, 301, 590–592.
Surwit, R. S., Pilon, R. N., & Fenton, C. H. (1978). Behavioral treatment of Raynaud’s disease. Journal of
Behavioral Medicine, 1, 323–335.
Taub, E., & School, P. J. (1978). Some methodological considerations in thermal biofeedback training. Behavior
Research Methods and Instrumentation, 10(5), 617–622.
Taub, E., & Stroebel, C. F. (1978). Biofeedback in the treatment of vasoconstrictive syndromes. Biofeedback and
Self Regulation, 3(4), 363–373.
Thompson, B., Geller, N. L., Hunsberger, S., Frederick, M., Hill, R., Jacob, R. G., et al. (1999). Behavioral and
pharmacological interventions: The Raynaud’s treatment study. Controlled Clinical Trials, 20, 52–63.
Turton, E. P. L., Kent, P. J., & Kester, R. C. (1998). The etiology of Raynaud’s phenomenon. Cardiovascular
Surgery, 6, 431–440.
Weinrich, M. C., Maricq, H. R., Keil, J. E., McGregor, A. R., & Diat, F. (1990). Prevalence of Raynaud’s
phenomenon in the adult population of South Carolina. Journal of Clinical Epidemiology, 43, 1343–1349.
Wigley, F. M. (2002). Raynaud’s phenomenon. New England Journal Medicine, 347, 1001