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J Am Dent Assoc, Vol 135, No 6, 771-778.
© 2004 American Dental Association
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DENTISTRY & MEDICINE

JADA Continuing Education

Panic disorder

Psychopathology, medical management and dental implications



ARTHUR H. FRIEDLANDER, D.D.S., STEPHEN R. MARDER, M.D., ERIC C. SUNG, D.D.S. and JOHN S. CHILD, M.D.


   ABSTRACT
TOP
 ABSTRACT
EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 TREATMENT
 OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
 CONCLUSION
 REFERENCES
 
Background. This article reviews the clinical features, epidemiology, pathophysiology, dental findings, and dental and medical management of the care of patients with panic disorder, or PD.

Types of Studies Reviewed. The authors conducted a MEDLINE search for the period 1998 through 2003, using the key term "panic disorder" to define the pathophysiology of the disorder, its epidemiology and dental implications. The articles they selected for further review included those published in peer-reviewed journals.

Results. PD is a common and debilitating psychiatric disease in which a person experiences sudden and unpredictable panic attacks, or PAs, with symptoms of overwhelming anxiety, chest pain, palpitations and shortness of breath. Persistent concern about having another attack and worry that it may indicate a heart attack or "going crazy" impairs the person’s social, family and working lives. Frequently accompanying the disorder is agoraphobia, depression and mitral valve prolapse, or MVP.

Clinical Implications. In patients with PD, the prevalence of dental disease may be extensive because of the xerostomic effects of psychiatric medications used to treat it. Dental treatment consists of preventive dental education and prescribing saliva substitutes and anticaries agents. Precautions must be taken when prescribing or administering analgesics, antibiotics or sedative agents that may have an adverse interaction with the psychiatric medications. Because there is a connection between PAs and MVP, the dentist needs to consult with the patient’s physician to determine the presence of MVP and whether there is associated mitral valve regurgitation. Patients with MVP and accompanying mitral valve regurgitation require prophylactic antibiotics when undergoing dental procedures known to cause a bacteremia and heightened risk of endocarditis.

Panic disorder, or PD, is a complex mental illness in which a person experiences recurrent and unexpected panic attacks, or PAs, which are not associated with any external event or situation. The attacks consist of intense apprehension and terror accompanied by physical symptoms, such as difficulty breathing, palpitations, chest pain, dizziness and sweating. The attacks have an abrupt onset and usually peak in intensity within 10 minutes. PAs often are accompanied by a sense of imminent danger and an urge to escape. The cluster of symptoms appears to be life-threatening. The episodes often result in calls to paramedics and visits to emergency departments. Persistent worry and concern about future attacks and their consequences, such as "having a fatal heart attack" or "going crazy" can distress people greatly, impair their outlook toward life and impair their ability to conduct a daily routine.1,2 With the passage of time, approximately one-third to one-half of people begin to have PAs in association with certain situations (for example, use of public transportation, driving a car across a bridge, or being in a crowded elevator or shopping mall) from which escape might be difficult or embarrassing. Consequently, people begin to avoid these situations or force themselves to enter into them, while experiencing intense anxiety or agoraphobia.

Dentistry, in concert with medicine, can offer patients with panic disorder the same treatments as patients without panic disorder.

Fifty to 60 percent of people with PD also frequently experience major depression at some time in their lives. Among people with both PD and depression, the onset of depression precedes the onset of PD in one-third of this population, while the onset of depression coincides with or follows the onset of PD in the remaining two-thirds.3 When PD and depression occur together, the symptoms of anxiety and depression are even more severe and result in almost 20 percent of these people’s attempting suicide.4,5

The diagnosis of PD is made after medical conditions that can exhibit paniclike symptoms have been ruled out.6 These include acute myocardial ischemia; hyperthyroidism; pheochromocytoma; excessive use of caffeine, stimulants, sympathomimetics found in nasal decongestants; and withdrawal from alcohol or sedative hypnotics. These conditions usually are excluded by medical history, physical examination, routine blood chemistries, thyroid function tests and electrocardiography.

In 2000, however, it was noted that a unique set of medical problems does occur more often in a subgroup of people with PD than in the general population. This cluster of medical problems includes bladder and kidney disorders (infections, stones, enuresis), hypothyroidism, migraine headaches and mitral valve prolapse, or MVP.7 The presence of MVP is of particular concern to dentists and their patients, because it heightens the risk of endocarditis in association with the performance of certain dental procedures.8 And it is for this reason that we believed that a review of recently published, peer-reviewed articles was germane. We conducted a MEDLINE search for the period 1998 through 2003, using the key term panic disorder to define the pathophysiology of the disorder, its epidemiology and dental implications.

Panic disorder often is a lifelong illness that remains only partially responsive to treatment.


   EPIDEMIOLOGY
TOP
 ABSTRACT
 EPIDEMIOLOGY
PATHOPHYSIOLOGY
 TREATMENT
 OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
 CONCLUSION
 REFERENCES
 
A literature review of epidemiologic studies in the United States indicated that PD usually begins in late adolescence or early adulthood.9 The lifetime prevalence of the illness is 2 percent for men and 5 percent for women, though the reasons for this sex-based difference in occurrence rates remain obscure.10,11 Women also appear to have a more severe form of the disease than do men.12

PD often is a lifelong illness that remains only partially responsive to treatment. Studies suggest that four to six years posttreatment, irrespective of therapeutic modality, only 30 percent of people are well, whereas 40 to 50 percent are improved but symptomatic, and the remaining 20 to 30 percent have symptoms that are the same or slightly worse.13,14 The persistent nature of the illness causes social and vocational impairment, which is costly to society. People with PD are more likely to become recipients of disability payments than are those with major depression, schizophrenia or alcohol dependence.15


   PATHOPHYSIOLOGY
TOP
 ABSTRACT
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
TREATMENT
 OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
 CONCLUSION
 REFERENCES
 
Most researchers believe that PD arises when genetically vulnerable people are subjected to environmental stresses, though the exact neurobiology of the illness remains unclear. A literature review of several studies noted that people with a first-degree relative having the disorder are up to 20 times more likely to develop the disorder than control subjects.16 Similarly, monozygotic (identical) twins have a significantly higher concordance (matching) rate for PD than do dizygotic (fraternal) twins.17 In 2003, researchers said that alterations in chromosome 13q are responsible for the cluster of medical problems including MVP that is seen frequently in a subgroup of people with PD.18

Imaging studies demonstrating abnormalities in cerebral blood flow and cerebral metabolism have led some researchers to believe that PD occurs when the amygdala—a component of the brain’s limbic system, which regulates mood and emotions—grossly misinterprets the significance of ambiguous bodily sensations (for example, "my rib pain is the onset of a heart attack") or innocuous environmental conditions (for example, "being in a warm stuffy room will lead to suffocation").19–22 Misconstruing a situation as an impending catastrophe, the amygdala initiates the "fear, fight or flight response." It does this by stimulating the parabrachial nucleus, causing an increase in respiratory rate, and by stimulating the locus ceruleus, causing an increase in norepinephrine release with a resultant increase in blood pressure and heart rate. The amygdala also stimulates the lateral and paraventricular nuclei of the hypothalamus, causing autonomic arousal (hypervigilance, exaggerated startle response) and an increase in plasma stress hormone (mainly cortisol) levels.23–25


   TREATMENT
TOP
 ABSTRACT
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 TREATMENT
OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
 CONCLUSION
 REFERENCES
 
The goal of treatment is the complete cessation of PAs. Their elimination relieves the patient of the associated anticipatory anxiety that is detrimental to the patient’s quality of life. Psychotherapy—specifically cognitive behavioral therapy, or CBT, and pharmacotherapy—have been shown to be equally effective in the treatment of PD. However, a rationale as to which modality should be offered any given patient has not been developed.26 A 1998 meta-analysis does show, however, that combining psychotherapy with antipanic medication is more efficacious than either treatment modality alone.27

CBT that consists of approximately 12 one-hour sessions over a course of three months educates patients about the disorder and teaches them to recognize and challenge their automatic, negative misinterpretation of ordinary physical sensations such as an ache in the chest. Thus informed, patients are able to realistically interpret the ache as being benign rather than as being the onset of a fatal heart attack. When patients are unafraid, their autonomic nervous systems are not stimulated, and PAs are obviated. Most therapists also gradually expose the patient to the situations that they fear most (regarding which they have phobias). Repeated and prolonged exposure results in desensitization and a dampening of the patient’s emotional and physiological responses. These activities also often are combined with breathing retraining, in which patients are taught how to regulate their respiratory rate during anxious moments, thereby avoiding hyperventilation.

After the acute phase of CBT, the frequency of the visits generally is decreased, and the visits eventually are discontinued within several months. CBT requires patients to do homework (for example, breathing exercises, and recording negative thoughts and irrational responses) or to confront feared situations; however, only 60 percent of patients are able to fully comply. Among those who do complete treatment, almost 70 percent respond with a decrease in the number of PAs and a lessening of both anticipatory worry and avoidance behaviors. These gains often are maintained over the long term and result in an overall improvement in function.28 The costs associated with multiple visits to a clinician, however, as well as a paucity of clinicians trained to provide CBT limits its applicability to many patients.29–31

Medications specifically for the treatment of PD have not been developed. However, selective serotonin reuptake inhibitor, or SSRI, antidepressants (Box 1Go) have proven to be relatively effective.32 These medications decrease the severity of PD (that is, the frequency of PAs, anticipatory anxiety, depression, agoraphobia) by preventing presynaptic neurons from reabsorbing (reuptaking) serotonin from the synaptic cleft—the space between two neurons—for recycling. This results in a heightened concentration of serotonin in the cleft and enhanced neuronal activity, which may inhibit the amygdala from stimulating the structures that give rise to a panic sensation.33 After an appropriate clinical response, patients usually take the medication for 12 to 18 months. When the medication is discontinued, however, 55 to 70 percent of patients relapse and need to start taking the drug again. Some patients need to continue taking the drug indefinitely.34 Adverse reactions to SSRIs include diarrhea, nausea, dizziness, insomnia, anxiety or agitation, tremor, headache and sexual dysfunction (for example, decreased libido, ejaculatory and erectile dysfunction, anorgasmia).35,36


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  		BOX 1 COMMONLY PRESCRIBED MEDICATIONS FOR PANIC DISORDER.

 
It usually takes six to eight weeks before patients begin to experience noticeable benefits from either CBT or SSRI therapy. Therefore, some patients with severe PAs or high levels of anticipatory anxiety require the simultaneous administration of benzodiazepines (Box 1Go) until the other therapy begins to work.37 Benzodiazepines rapidly calm patients by heightening activity at the receptors for the inhibitory neurotransmitter {gamma}-aminobutyric acid, or GABA.38 Adverse side effects of benzodiazepine therapy include sedation, fatigue, ataxia, slurred speech, memory impairment, weakness and physical dependence, especially in those people with histories of substance abuse.


   OROFACIAL CONSIDERATIONS
TOP
 ABSTRACT
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 TREATMENT
 OROFACIAL CONSIDERATIONS
DENTAL MANAGEMENT
 CONCLUSION
 REFERENCES
 
In a review of manufacturers’ U.S. Food and Drug Administration–approved package inserts that accompany each of the medications used to treat PD and an analysis of the current medical literature, we identified adverse orofacial reactions that may occur.

All the SSRIs have been shown to cause xerostomia (affecting approximately 15–25 percent of patients), dysgeusia (affecting 10–40 percent of patients), stomatitis and glossitis. Some of these medications also have been implicated as causing sialadenitis and gingivitis (Table 1Go). The majority of benzodiazepines have been reported to cause both xerostomia and sialorrhea and, in some instances, oral ulcerations and jaw pain (Table 2Go).39,40


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  		TABLE 1 ADVERSE OROFACIAL REACTIONS TO THE SELECTIVE SEROTONIN REUPTAKE INHIBITORS.*

 

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  		TABLE 2 ADVERSE OROFACIAL REACTIONS TO BENZODIAZEPINES.*

 

   DENTAL MANAGEMENT
TOP
 ABSTRACT
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 TREATMENT
 OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
CONCLUSION
 REFERENCES
 
Some patients receiving psychiatric treatment for PD may be reluctant to admit it because of the local or historical stigma associated with mental illness. To overcome such barriers and obtain the necessary information, dentists should display supportive, nonjudgmental attitudes and advise their patients that such information will be confidential and is indispensable to the provision of safe dental care.

Before treating a patient who is receiving psychiatric treatment, the dentist should consult the patient’s psychiatrist. The information he or she requests should include the patient’s current psychological status and current psychotropic medication regimen. The dentist also should ask the psychiatrist about the patient’s history of MVP and how best to obtain a consultation from an internist (or preferably a cardiologist) as to the extent of possible heart disease without unduly alarming the patient.

Studies have shown that between 8 and 33 percent of patients with PD have a diagnosis of MVP,41–46 whereas it is present in only about 2.5 percent of the general population.47,48 The diagnosis of MVP must be made with careful attention to auscultatory and echocardiographic details to avoid mislabeling otherwise normal people as having a disease.48,49 MVP refers to the billowing of one or both mitral leaflets more than 2 millimeters above their annular hinge points and into the left atrium as the pressure in the left ventricle rises during systole.49 It is postulated that the MVP develops in people with PD because of panic-induced, long-term exposure to high levels of circulating catecholamines, which results in an increase in the force of ventricular contraction and changes in the integrity of the mitral valve.50

The patient’s internist or cardiologist will need to be informed if invasive dental procedures are planned and will need to comment on the patient’s need for prophylactic antibiotics. To respond properly to this query, a comprehensive medical history and physical examination will need to be performed. The heart will need to be auscultated with a stethoscope for the presence of abnormal sounds and murmurs. A diagnosis of MVP is made when a systolic click is heard with physiological maneuvers (for example, standing-squatting, hand gripping) as the mitral valve leaflets billow into the left atrium. Patients with this form of MVP do not require prophylactic antibiotics. In some instances, however, an accompanying late systolic murmur—sometimes called a "pathological MVP"—also can be heard, and it is indicative of mitral valve regurgitation that results from the mitral valve’s not closing completely and permitting blood to flow backward from the left ventricle into the left atrium. Patients with this form of MVP require prophylactics before practitioners can perform certain dental procedures. It must be emphasized, however, that auscultation without the use of physiological maneuvers is not sufficient49 and that even when employing the maneuvers, clinicians will not hear the regurgitation sounds in a small subset of patients with pathological MVP.

To ensure that the findings on auscultation are completely accurate, the physician also may obtain an echocardiogram, which permits visualization of the heart valves and blood flow patterns about the valves.51,52 The additive value of echocardiography is demonstrated by the results of a 1998 study of more than 120 patients with PD.53 Auscultation revealed that 4 percent of patients had a midsystolic click and that 12 percent had a systolic murmur. When the evaluations were augmented with an echocardiogram, however, it was determined that 17 percent of the patients had MVP accompanied by mitral valve regurgitation.

If an internist or cardiologist has determined that a patient has developed MVP with mitral valve regurgitation, the patient is at risk of developing endocarditis54,55 from certain dental procedures and will need to receive preoperative antibiotic prophylaxis and an antiseptic mouthrinse.8 In general, prophylaxis is recommended for procedures associated with significant bleeding from hard or soft tissues such as extractions, periodontal surgery, scaling and root planing and professional teeth cleaning (Box 2Go). Patients who are not allergic to penicillin should be given 2 grams of amoxicillin one hour before the procedure. They also should be given 15 milliliters of chlorhexidine to rinse with for 30 seconds just before commencing dental treatment. Furthermore, because endocarditis may occur despite appropriate prophylaxis, patients must be warned to report back to the office if they develop unexplained fever, night chills, weakness, myalgia, arthralgia, lethargy or malaise after treatment.56–59


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  		BOX 2 DENTAL PROCEDURES FOR WHICH ENDOCARDITIS PROPHYLAXIS IS RECOMMENDED.*

 
Preventive dental education is paramount for these patients. They should receive instruction in proper toothbrushing and flossing methods that maximize dental plaque removal. Artificial salivary products should be prescribed for those with signs of xerostomia. Dental treatment should consist of subgingival scaling, root planing and curettage, caries control and dental restorations. Profound local anesthesia is mandatory to perform these procedures adequately in these often-anxious people.

Adverse interactions between some medications used in dentistry and SSRIs may occur because the antidepressants inhibit certain metabolic pathways. Specifically, SSRIs inhibit the cytochrome P-450 isoenzymes that are needed to metabolize codeine, erythromycin and carbamazepine adequately. These dental therapeutic agents, therefore, should be used cautiously and in reduced dosages. Antihistamines, muscles relaxants, ketoconazole and the opioid analgesics have been reported to enhance the sedative effects of the benzodiazepines and likewise should be used cautiously and in reduced dosages.60–62

Vicodin (Abbott Laboratories, Abbott Park, Ill.), a combination of acetaminophen and hydrocodone, also should be used cautiously in patients with PD. Case reports in the literature implicate the medication as causing patients with well-controlled PD to develop acute and dramatic exacerbations of panic symptoms.63 The mechanism for these adverse events remains in doubt, however, because, in most people, use of the medication is associated with an anxiolytic effect.


   CONCLUSION
TOP
 ABSTRACT
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 TREATMENT
 OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
 CONCLUSION
REFERENCES
 
Dentistry, in concert with medicine, can offer patients with PD the same treatments as patients without PD. We conducted this literature review to familiarize dentists with the manifestations of the illness and to encourage them to confidently offer patients with PD the full range of dental treatment options.



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  		Dr. Friedlander is associate chief of staff and the director of Graduate Medical Education, VA Greater Los Angeles Healthcare System; the director of Quality Assurance, Hospital Dental Service, University of California, Los Angeles Medical Center; and a professor, Oral and Maxillofacial Surgery, University of California at Los Angeles School of Dentistry. Address reprint requests to Dr. Friedlander at VA Greater Los Angeles Healthcare System, 11301 Wilshire Blvd., Los Angeles, Calif. 90073, e-mail "arthur.friedlander{at}med.va.gov". idiopathic mitral valve prolapse and panic disorder. Croat Med J 2000;41:410-6.

 


   FOOTNOTES
 

Dr. Marder is the director, Department of Veterans Affairs, VISN 22 Mental Illness Research Education and Clinical Center, Los Angeles; the chair of psychiatry, VA Greater Los Angeles Healthcare System; and a professor and the vice chair, Psychiatry and Behavioral Sciences, David Geffen School of Medicine, University of California, Los Angeles.


Dr. Sung is the director, Hospital Dentistry Residency, Medical Center at the University of California, Los Angeles; and a clinical associate professor, Hospital Dentistry, University of California, Los Angeles School of Dentistry.


Dr. Child is the director, Ahmanson/UCLA Adult Congenital Heart Disease Center; co-chief, Division of Cardiology; and Streisand professor of medicine, David Geffen School of Medicine, University of California, Los Angeles.


   REFERENCES
TOP
 ABSTRACT
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 TREATMENT
 OROFACIAL CONSIDERATIONS
 DENTAL MANAGEMENT
 CONCLUSION
 REFERENCES
 

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