Mr. E is a 68-year-old Caucasian man referred by a pulmonologist after a series of sleep studies were done and were noncontributory in explaining the etiology of his sleep disorder. Thyroid studies, complete blood count with differential, and comprehensive panel were all unremarkable. His chief complaint at the time of initial evaluation was one of sleep disturbance with frequent awakening. He had difficulty initiating and maintaining sleep.
Mr. E denied any history of inpatient or outpatient psychiatric treatment. However, he reported a concussion to his head and injury at the age of 22 after he was involved in a motor vehicle accident. He denied any flashbacks, emotional numbing, or avoidance behaviors. He described limited symptoms and full-blown panic attacks with discrete episodes of feelings of anxiety, nausea, muscle tension, and headache, which would remit in 10 minutes, starting soon after that accident. He was seen in the emergency department at the time of the accident, and a computed tomography scan of the head was unremarkable, with no evidence of subdural hematoma or fracture.
Mr. E did not seek any treatment for his panic attacks. Subsequently, he reports having developed a sleep disturbance with frequent awakening. He describes his sleep as being interrupted by panic attacks. He also developed abdominal discomfort and nausea, for which he had upper gastrointestinal series including endoscopy done. The results were noncontributory.
His personal history is significant for the fact that he is a retired machinist and was employed for 28 years by one employer. He has been married for 40 years. He says he is constantly fixing things around the house and “feels wired.”
Medical history at the time of the initial evaluation was significant for a diagnosis type 2 diabetes, and treatment with diet and exercise and glyburide was recommended. His primary care physician was treating his insomnia with 15 mg of temazepam, but Mr. E reported no improvement on that. He was then prescribed 10 mg of zolpidem, with no clinical improvement. He also took 4 mg of doxazosin once a day for benign hypertrophy of the prostate.
In addition, Mr. E had a triple coronary artery bypass grafting surgery 3 months prior to this psychiatric assessment. Following the surgery, he recalls an exacerbation of the panic disorder, but he did not seek treatment at that time. He denies any family history of psychiatric disorder.
Mr. E presented casually but very neatly groomed with restricted range of affect, speaking in a soft monotone with careful trepidation prior to any utterance. He described discrete episodes of anxiety with tingling in the arms, cold sweats, lightheadedness, and tight band across the abdomen with palpitations lasting 10 minutes. He also complained of fatigue and tiredness from not having restful sleep. However, he denied depression and anhedonia. He described panic attacks disturbing his sleep. He denied suicidal ideation, feelings of hopelessness or helplessness, delusions and hallucinations, or obsessions and compulsions. He said his thoughts were full of anticipatory anxiety, fearfulness of dying from the palpitations, and tightness of the chest. His memory and cognition were fair, with a Mini-Mental State Exam score of 28/30. Insight and judgment also were fair. He was interested in understanding the nature of his psychiatric disorder and motivated to seek treatment.
The following options could be considered:
Begin psychopharmacologic treatment with either a selective serotonin reuptake inhibitor (SSRI) or a benzodiazapine.
Begin cognitive-behavior therapy (CBT).
Begin combined psychopharmacologic treatment and cognitive-behavior psychotherapy.
Refer the patient to his primary care physician for management.
In this case, Option 3 was chosen. Mr. E was followed as an out-patient on a weekly basis and started on 12.5 mg of sertraline orally once daily, 0.25 mg of alprazolam orally twice per day, and 50 mg trazodone orally at bedtime. While taking trazodone, he complained of sleep disturbance and called the office every day complaining of insomnia. Trazodone was discontinued 2 days later, and 10 mg of zolpidem orally at bedtime was prescribed. This was well tolerated initially, but after 4 weeks of treatment, he complained of pain in the leg. Zolpidem was discontinued, with alleviation of the pain in the legs, and sertraline was increased to 25 mg. However, Mr. E complained of diarrhea on 25 mg of sertraline and refused to continue the medication at a lower dose. He said the anxiety and panic attacks were intolerable and insisted on wanting to discontinue the medication. He was then started on 10 mg of paroxetine orally once daily but complained of sweating and flushing of the face. The dose of paroxetine was reduced to 5 mg.
Clonazepam was started 3 weeks after Mr. E was first seen. Alprazolam was discontinued 8 days after it was first initiated because he complained of nausea. Trazodone was restarted 4 weeks after the initial evaluation. After about 8 to 10 weeks of treatment, Mr. E reported complete remission of symptoms and was stabilized on 5 mg of paroxetine per day, 0.25 mg of clonazepam twice per day, and 50 mg of trazodone at bedtime each night. Mr. E was maintained on this dose and then followed by his primary care physician for 8 years.
Mr. E also was seen for 10 sessions of CBT on a weekly basis for 45 minutes each. Behavioral techniques such as breathing retraining, visual imagery, progressive muscular relaxation, and systemic desensitization were introduced. His personality traits were significant for an obsessive-compulsive style in his maintaining a diary of his symptoms. He had a ritualistic and very self-disciplined style of living. He had no history of drug or alcohol abuse or dependence. He always was on time for his appointments and very respectful in his manner of communication. He had a good sense of humor, was active in the community, and had good interpersonal relationships.
Subsequently, with no identifiable psychosocial stressors, when Mr. E was 76, he experienced an exacerbation of his panic disorder, with his anxiety worse in the morning hours. The maintenance dose of the three medications was evaluated by his primary care physician, who clinically titrated the dose of paroxetine and increased it to 20 mg. Alprazolam was restarted at a dose of 0.25 mg orally twice per day. However, Mr. E complained of daytime sedation with 20 mg of paroxetine. He was again referred for psychiatric treatment.
On re-evaluation, his Mini-Mental State Exam score was 28/30. He was coping with the psychosocial stressor of being the primary caregiver for his wife who had developed Alzheimer's-type dementia with functional decline. His mood was anxious, and his affect was restricted. He appeared to be uptight in his manner.
Mr. E said he had been dieting and exercising; his blood glucose was well controlled, and he did not need any oral antidiabetic medication for his type 2 diabetes. He reported tightness in the head and back of his neck, palpitations, and tingling numbness in the arms. He continued taking trazodone but could tolerate only 25 mg for insomnia.
Due to his complaints of daytime sedation, paroxetine was reduced to 10 mg, and alprazolam was titrated from 0.25 mg to 0.125 mg. Attempts were made to switch him to 0.5 mg of extended-release alprazolam at bed-time, but he complained of excessive sweating, so it was discontinued.
Because Mr. E had been introduced to behavioral therapy in the past, he was seen for ego-supportive eclectic psychotherapy only, the session lasting for 30 minutes on a weekly basis, primarily to discuss all the medication-related questions. Treatment was continued with 5 mg of paroxetine per day, 25 mg of trazodone per day, and 0.125 mg of alprazolam three times per day, with complete remission of symptoms in 10 weeks.
Mr. E stated that the medication had been able to ameliorate his symptoms completely, and he acknowledged the importance of the biological method of treating his anxiety disorder. However, he had used the behavioral techniques he had learned, including breathing retraining, visual imagery, and progressive muscular relaxation, throughout the maintenance phase of his treatment, over the course of 8 years.
Patients with panic disorder commonly present to their primary care doctors, or in other medical settings, reflecting the high use of medical services by patients with panic disorder, even when compared with those with other psychiatric disorders.1,2 Mr. E had a series of sleep studies and numerous medical tests prior to being referred to a psychiatrist for an evaluation. He had been resistant to seeking a psychiatric evaluation despite the efforts and recommendation made by his primary care physician on several occasions.
The initial onset of Mr. E's panic attacks was triggered at the age of 22 by a motor vehicle accident, with a re-exacerbation of panic attacks and limited symptom attacks after his open heart surgery. Faravelli3 found a high proportion of patients experienced a major life event (eg, death or severe illness, either personally or of a relative, within 2 months) prior to the onset of the panic. Longitudinal studies have found that men with anxiety symptoms, and specifically phobic anxiety, have a threefold increase in the risk of coronary heart disease, with a four- to sixfold increased risk of sudden cardiac death.4,5
Some anxious geriatric patients, who already tend to overemphasize somatic symptoms, may find gastrointestinal distress commonly associated with SSRI use intolerable. Older patients therefore should initially be given these medications in very small daily doses.6 Mr. E had gastrointestinal distress, including diarrhea, even at a very low dose of sertraline, so the medication had to be discontinued.
Treatment of patients with panic disorder with SSRIs such as paroxetine has been associated with a significant improvement in heart rate and rhythm, which could theoretically reduce the mortality rate due to sudden cardiac death. These changes with treatment may be due to alterations in autonomic activity.7
The efficacy of CBT in patients with panic disorder with or without agoraphobia has been demonstrated in many controlled studies.8 With Mr. E, this modality of treatment was combined with psychopharmacologic intervention during the first course of treatment. During the subsequent course of treatment 8 years later, an eclectic approach with ego-supportive psychotherapy focusing on the medication related issues was used because he had already been introduced to the behavioral techniques. He was adept at this and stated that he had used the techniques throughout the maintenance phase of treatment. This case highlights the importance of combining psychopharmacologic management with individual psychotherapy to improve the clinical outcome in patients diagnosed with panic disorder.
Editor's Note: This monthly presentation describes a case of a psychiatric disorder, discusses past treatment attempts, offers options for continuing treatment, and explains the reasons the solution was selected. Submissions of interesting psychiatric case reports are being accepted for this department. Please e-mail
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This case is presented by Ajanta Vinekar, MD, clinical assistant profesor, Department of Psychiatry, Robert Wood Johnson Medical School, New Brunswick, NJ, and Somerset Medical Center, Somerville, NJ.
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