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Misdiagnosis of Serotonin Syndrome as Fibromyalgia and the Role of Physical Therapists

GM Alnwick, PT, DPT, is Staff Physical Therapist and Master Clinician, Genesis Rehabilitation Services, Gorham Outpatient Clinic, Gorham, NH. Mailing address: 4 Woodbound Rd, Gorham, NH 03581 (USA)

Address all correspondence to Dr Alnwick at: galnwick{at}ne.rr.com

Submitted July 23, 2006; Accepted February 15, 2008

	Abstract

 
Background and Purpose: With increased use of serotonergic medications, a condition triggered by serotonin excess within the brain and spinal cord has emerged and may be gaining prevalence. The purposes of this case report are to describe how to identify serotonin syndrome in a patient who is taking citalopram (a selective serotonin reuptake inhibitor) on the basis of signs and symptoms and to promote the ability of physical therapists to recognize such signs and symptoms.

Case Description: The patient was a 42-year-old woman referred for physical therapy with a diagnosis of fibromyalgia. The physical therapist recognized that the patient's symptoms did not resemble those of fibromyalgia and recommended referral to a neurologist for further diagnostic testing.

Outcomes: The patient was referred to a neurologist, who diagnosed serotonin syndrome related to the use of citalopram. The patient was weaned off citalopram and made a successful recovery, with scores on the Oswestry Disability Index decreasing from 70% to 28% at discharge from the physical therapy treatment and to 0% at the 6-month follow-up. The patient has since returned to her prior activity level, which includes skiing, motorcycle riding, and working at her consulting firm.

Discussion: This case report demonstrates how careful evaluation by the physical therapist indicated that signs and symptoms were not consistent with fibromyalgia, and further medical evaluation revealed the actual diagnosis of serotonin syndrome.

	Introduction

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

 
For physical therapists to become more autonomous practitioners and to meet the American Physical Therapy Association goal of Vision 2020,¹ careful examination and evaluation procedures must be used to question the referral diagnosis rather than to blindly proceed with treatment for fibromyalgia and other disorders of the neuromuscular and musculoskeletal systems. As explained in the Guide to Physical Therapist Practice,¹ physical therapists should engage in an examination process that includes taking a history, conducting a systems review, and performing tests and measures to identify potential and existing problems.¹ Throughout the examination, data are gathered to evaluate and to form clinical judgments.² These judgments may consist of formulating a treatment plan or suggesting referral to the proper medical care provider.

As physical therapists conduct their assessments, it is critical to investigate the presence of any signs or symptoms that may indicate the need for referral to the most appropriate health care professional. It is especially important to obtain a detailed history from any patient with a diagnosis of fibromyalgia, a syndrome of unknown etiology that is characterized by chronic widespread joint and muscle pain,³ or other chronic pain syndromes. If a detailed history is not obtained, then significant information, including medications, may be omitted, increasing the chances of misdiagnosis and inappropriate treatment.

With the increased use of serotonergic medications, a condition triggered by serotonin excess within the brain and spinal cord has emerged and may be gaining prevalence.⁴ Selective serotonin reuptake inhibitors (SSRIs), including citalopram, are used to treat depression. Although the exact mechanism of action of SSRIs is not fully understood, it is believed that they inhibit the reuptake of serotonin at the neuronal synapse.⁵ Citalopram was approved by the US Food and Drug Administration for the treatment of depression in adults in July 1998. It is administered orally, and peak concentrations in plasma are attained about 4 hours after dosing. Its half-life in an individual who is healthy is 35 hours. Indications for this medication include anxiety, depression, panic disorder, and posttraumatic stress disorder. Some contraindications are abrupt discontinuation, bipolar disorder, bleeding, use in children, driving or operating machinery, mania, and seizure disorders; a more extensive list of contraindications and reasons for precaution is shown in Appendix 1. Adverse reactions to citalopram⁵ are shown in Appendix 2. The use of SSRIs for the treatment of various psychiatric disorders is increasing; consequently, the incidence of reported side effects, such as extrapyramidal movement disorders like those seen in serotonin syndrome (SS), also is increasing.⁶

In order to comprehend SS, it is necessary to have an understanding of serotonin. The actions of serotonin in the peripheral nervous system include vasoconstriction via smooth muscle stimulation, platelet aggregation, uterine contraction, intestinal peristalsis, and bronchoconstriction. In the central nervous system, serotonin has effects on controlled behavior, attention, affect, pain perception, aggression, motor control, temperature control, sleep, appetite, and sexual function. Because serotonin is unable to cross the blood-brain barrier, it must be produced both centrally, within the brain stem, and peripherally, within the intestine.⁴

Serotonin syndrome is an iatrogenic disorder induced by pharmacologic treatment with serotonergic agents that increase serotonin activity.^4,7 It is thought to occur as a result of excess stimulationof the 5-hydroxytryptamine 1A (5-HT_1A) receptor and possibly the 5-hydroxytryptamine 2 (5-HT₂) receptor.^8–11 Serotonin syndrome may result from an excess of synaptic serotonin following the use of serotonergic agents alone or in combination with other serotonin-enhancing drugs.⁶ In most cases, SS has a rapid onset, within minutes to hours, although it can occur over a period of days, weeks, or even months after the start of treatment with various SSRIs.^4,12 The incidence of SS is, in large part, unknown. The variable and nonspecific nature of its presentation makes it difficult to diagnose; therefore, it has gone underreported.⁸ Signs and symptoms of SS may consist of mental status changes, with acute manifestations consisting of cognitive behavioral changes, neuromuscular excitability, autonomic instability, and pain.^4,8 Serotonin syndrome also appears to be dose related, with the dose of the medication affecting both the likelihood of developing SS and the severity of the clinical presentation.^4,12,13 Because the signs and symptoms may overlap those of other chronic pain syndromes, a diagnosis is made on clinical grounds.⁴

Serotonin syndrome is not detected by laboratory tests or diagnostic imaging. Sternbach¹⁴ has set forth diagnostic criteria for this syndrome:

1. At least 3 of the following clinical features should occur coincident with the addition of or increase in dosage of a known serotonergic agent: mental status changes (confusion, hypomania), agitation, myoclonus, hyperreflexia, diaphoresis, shivering, tremor, diarrhea, incoordination, and fever.
   
2. Other etiologies (infections, metabolic disorders, and substance abuse or withdrawal) need to be excluded.
   
3. A neuroleptic agent should not have been started or increased in dosage prior to the onset of the signs and symptoms listed above.
   

Mason et el⁸ and Chechani¹⁵ also discussed pain as a symptom of SS. Because SS is diagnosed on the basis of symptoms and signs, some patients may experience mild symptoms for weeks before progressing to a more severe form of the syndrome.¹² Therefore, the purposes of this report are to bring attention to some of the signs and symptoms of SS that may be overlooked if their onset is gradual and to promote the ability of physical therapists to identify such signs and symptoms in patients with SS.

	Case Description

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

 
Initial Evaluation

The initial physical therapy visit consisted of a thorough evaluation by use of a systems approach as described in the Guide to Physical Therapist Practice.¹ Two months prior to receiving the neurologist's diagnosis of SS, the patient's primary care physician (PCP) referred her for physical therapy with a diagnosis of fibromyalgia, identified by increasing pain and weakness. Her pain rating at the time of the initial evaluation was 8 of 10 and ranged from a low of 4 of 10 with rest to a high of 10 of 10 with increased activity on an 11-point (0–10) numeric pain scale, in which 0 represented "no pain" and 10 represented "the worst pain possible."^16,17 The numeric pain scale has been shown to have high test-retest reliability (intraclass correlation coefficient=.96) and a strong correlation (r=.85) with data collected using a visual analog scale.¹⁶ The patient reported that pain ranging from 4 of 10 to 10 of 10 was constant. There did not appear to be any relationship between time of day and intensity of pain, nor was there a specific pain pattern. The patient reported that pain increased with activity and did not diminish with any specific position. The application of a hot pack, however, did seem to provide a small amount of relief. The patient described her pain as throbbing throughout her extremities, with burning and a sense of tightness along the spine. With increased pain, she also had increased nausea, with or without vomiting. There were also signs of dizziness that did not appear to increase or decrease with the degree of pain. Prior to the initial evaluation, the patient had experienced many similar symptoms.

History of Course of Symptoms

Table 1 summarizes the time line of events.

Two years prior to diagnosis.
The patient began to have gastrointestinal tract problems consisting of increased bouts of nausea and vomiting with a slow and gradual onset. She also began to experience headaches that were bifrontal, with throbbing pain and hypersensitivity to light and sound. She had pain in her left shoulder, along her spine, and in many of her joints. She also experienced left-side weakness, muscle tightness, fluctuating temperature, insomnia, restlessness, and nervousness.

One year prior to diagnosis.
The patient had little to no appetite, bouts of diarrhea, and a sense of fullness and urgency with urination. She also experienced left-side muscle aching and spasms that caused her to have difficulty ambulating and to need a straight cane. The patient began to have mental symptoms, such as confusion and decreased memory. She also had dilated pupils, vertigo, and dysarthria.

Six months prior to diagnosis.
The patient experienced intermittent fatigue, bouts of increased sweating, episodes of feeling very cold, and nightmares. Mental symptoms, including confusion and decreased memory, were worsening. She complained of increased pain throughout her spine, joints, and extremities as well as left-sided weakness of the upper and lower extremities. She had decreased sensation in the lateral aspects of both hands.

The diagnostic criteria set forth by Sternbach,¹⁴ combined with the patient's history of taking an SSRI, suggested that the above symptoms were indeed relevant to SS.

Physical Examination

I performed a physical examination 2 months prior to the diagnosis of SS being made by her neurologist.

Vital signs.
Vital signs were not noted at the time of the initial visit.

Neurologic findings.
Deep tendon reflexes were grossly 2 in bilateral upper extremities (biceps, triceps, and brachioradialis). Patellar and Achilles tendon reflexes were unattainable bilaterally. Nystagmus of greater than 3 beats was observed bilaterally, along with increased dizziness with finger tracking. The patient had difficulty when she was asked to touch her finger to her nose and then to touch my finger. Sensation to light touch was within normal limits, except for hypersensitivity to very light touch in the entire right lower extremity.

Musculoskeletal findings.
Palpation revealed tenderness in a nonanatomic pattern throughout the patient's extremities and body. These findings did not coincide with the criteria for fibromyalgia.³ Because of the patient's increased pain level, a proper assessment of gross range of motion and strength (force-generating capacity) was not performed. The patient's roommate reported that she spent much of the night "jumping" and having muscle spasms with jerking motions in all parts of her body. This problem severely limited her ability to sleep for more than 2 hours at a time.

Cardiovascular, endocrinologic, and integumentary findings.
There were no significant findings for the cardiovascular, endocrinologic, and integumentary systems.

Gastrointestinal tract findings.
The patient reported gastrointestinal tract symptoms (nausea, vomiting, and difficulty with bowel and bladder functions).

Other findings.
At the time of the initial evaluation, the patient completed and scored 70% on the Oswestry Disability Index (ODI) questionnaire. The ODI is a reliable and valid tool¹⁹ designed to capture a patient's perceived disability through responses to a series of questions relating to activities of daily living and degree of pain experienced with a specific activity. Each section is designed to provide a percentage of disability. The higher the percentage, the greater the level of disability perceived by the patient.¹⁹

The patient's balance was poor, as demonstrated by her need to hold on to a table with both hands in order to remain in an upright position in response to light pressure placed upon her shoulders and torso by the therapist in various directions while she was sitting. Gait assessment demonstrated a severe antalgic gait with the use of a straight cane. The patient also exhibited decreased stride length and stance phase bilaterally with a step-to-gait pattern. She reported that there were times when her legs would "give out" without any apparent warning. This problem had led her to have several recent falls.

Medications

At the time of the initial evaluation, the patient reported taking the following medications: carisoprodol for muscle spasms, clonazepam (1 mg) nightly 4 or 5 times per week for anxiety, gabapentin (300 mg) 3 times per day for pain, and citalopram (20 mg) for anxiety and depression. She reported having taken carisoprodol, clonazepam, and gabapentin for several years and citalopram for the preceding 6 years. Before citalopram, she had taken sertraline hydrochloride (also an SSRI) and nefazodone.

Laboratory Results

The patient reported having had 2 cranial magnetic resonance imaging (MRI) scans and a computed tomography (CT) scan of the brain, which were read as normal. She had never had a spinal tap or an electroencephalogram.

Family History and Social Activity

The patient was a 42-year-old woman who was co-owner of a consulting firm. She enjoyed motorcycle riding, skiing, playing hockey, and working around her house and yard. She lived with her roommate and roommate's children in a 2-story house. At the time of her initial evaluation, she was unable to go up and down stairs and, therefore, had relocated to the first floor of the house. She reported that she had a very good support system at home and was able to get all the help she needed to perform many activities of daily living that she could not perform unassisted. She also reported a family history of cardiac disease, hypothyroidism, Guillain-Barrè syndrome, and depression. She had signed an informed consent form that was kept on file at the outpatient clinic that she attended. Requirements for the Health Insurance Portability and Accountability Act were upheld during the time of treatment management as well as during the preparation of this case report. The patient was very proactive in reporting her case so that others would not have to experience what she had experienced.

Diagnosis

In accordance with the Guide to Physical Therapist Practice, the physical therapy diagnosis pattern for this patient was that of "impaired muscle performance, 4C."¹ This conclusion was reached on the basis of a thorough evaluation and the inclusion and exclusion criteria set forth in the Guide to Physical Therapist Practice.¹ After the initial physical therapy evaluation was performed and the diagnosis was determined, given the wide array of neurologic symptoms and pain symptoms in a nonanatomic pattern, I recommended that the patient be referred to a neurologist by her PCP. Because the patient was reporting some relief through therapy, her PCP recommended that physical therapy consisting of passive range of motion and gentle manual techniques be continued until she saw the neurologist. An ODI questionnaire administered 31 days after the initial physical therapy evaluation validated the effectiveness of treatment and demonstrated that the patient was indeed showing improvement. At this time, she scored 62%; she had scored 70% at the initial evaluation (Tab. 2). With a minimal detectable change of 5 or 6 points and a minimal clinically important difference of 6 points,¹⁹ the change in the ODI questionnaire score from 70% to 62% is a clinically meaningful sign of improvement. I agreed that treatment should continue until the patient regressed, reached a plateau, or had met all goals.

Prognosis

If SS is detected early enough and treated appropriately, the prognosis is very good.¹¹ The prognosis described in the Guide to Physical Therapist Practice¹ notes that over the course of 2 to 6 months, the patient will demonstrate optimal muscle performance. The patient also should make a full recovery and return to premorbid status. The number of visits expected for this diagnosis ranges from 6 to 30, depending on factors that may affect the course of treatment.¹

Intervention

First intervention period.
Because of the amount of pain that the patient was experiencing at the time of the initial evaluation and her reports of nausea and dizziness and history of falls, I determined that she would not be able to tolerate any type of aggressive treatment or therapeutic exercise. Therefore, physical therapy treatment consisted of very gentle passive range-of-motion, myofascial, and massage techniques, energy conservation techniques, and relaxation techniques. These techniques have been shown to be effective for treating patients with chronic pain.^20–22

Second intervention period.
Initial treatment by the neurologist (June 18, 2004) consisted of tapering off and discontinuing citalopram, with an acute-episode rescue consisting of diazepam (5 mg), as needed. The patient also began taking a tricyclic antidepressant at a dose sufficient to restore normal sleep (25 mg, increasing to 50 mg after 1 week). She was advised to avoid clonazepam. After the second appointment with the neurologist (1 month after diagnosis was made), the medication regimen consisted of gabapentin (300 mg) 3 times per day and the continuation of nortriptyline (50 mg). Two months after her initial appointment with the neurologist, the gabapentin dosage was increased to 3 times per day, at doses of 600, 600, and 900 mg, because of an increase in pain. Diazepam was discontinued and clonazepam (1 mg, as needed) was resumed at this time, and nortriptyline (50 mg) was taken only at night. Three months later, the medication regimen consisted of the continuation of nortriptyline and gabapentin, and bupropion (150 mg) was introduced. This regimen was continued until the next appointment with the neurologist. Upon the patient's last reported visit with the neurologist 9 months later, her medication regimen consisted of gabapentin 3 times per day at doses of 600, 600, and 900 mg, nortriptyline at doses of 25 mg in the morning and 75 mg at night, and clonazepam (1 mg, as needed).

With the changes in medications, the patient was able to tolerate more aggressive treatment and physical therapy interventions. Range-of-motion activities gradually progressed from passive to active assistive and, finally, to active range of motion with resistance. Treatment also included a walking program on the treadmill and outside, a progressive-resistance exercise program, and instruction on a home exercise program addressing the core muscle group as well as the extremities.

	Outcomes

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

 
Within 2 weeks after withdrawal of the citalopram, the patient reported feeling less dizzy, experiencing less pain, and no longer needing her cane to ambulate. Her strength improved from the inability to tolerate any resistance to the ability to tolerate 4 to 4+ of 5 grossly in both upper and lower extremities. An ODI questionnaire was administered at the end of the treatment. At that time, the patient scored 28%; the change in scores is a clinically significant sign of improvement. Strength was grossly within normal limits, pain was rated as 0 to 1 of 10, and the patient was walking without any assistance or deviations. After the patient was discharged, she followed up approximately 6 months later to report that she had no residual effects, with the exception of some short-term memory difficulties. She has since returned to work; she has been able to tolerate her prior activity level, which includes skiing, motorcycle riding, cutting and splitting wood, and other hobbies and interests; and she scored 0% on a final ODI questionnaire.

	Discussion

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

 
The purposes of this case report were to bring attention to some of the signs and symptoms associated with an atypical presentation of SS, consisting of pain and a gradual onset, which may be misdiagnosed as fibromyalgia, and to promote the ability of physical therapists to identify such signs and symptoms in patients with SS. The patient described in this report had been referred for physical therapy with a diagnosis of fibromyalgia because of chronic pain. Her condition had been misdiagnosed for a little over 2 years. This case report describes the process by which the physical therapist was able to base decisions on a detailed history and clinical signs and symptoms that did not resemble fibromyalgia. This process resulted in a referral to a neurologist for further evaluation and, ultimately, a final diagnosis of SS by the neurologist.

Serotonin syndrome was originally described in animals pretreated with 1-tryptophan and given various monoamine oxidase inhibitors or other serotonin precursors in combination with drugs that increase their bioavailability. First described in humans in 1960,⁸ SS is thought to be induced by the combined activation of 5-HT_1A and 5-HT₂ receptors.²² Since then, numerous articles have been published on the topic.^{4,6–13,15,23,24} It is questionable as to why so many cases have been misdiagnosed, as with the patient described in this case report. However, in this particular case, the patient had a gradual onset rather than the typical acute onset seen in other SS cases. It is important not to overlook even minor, initial symptoms, because they can rapidly become severe.

The diagnosis of SS also is made difficult by the overlap of its symptoms with those of neuroleptic malignant syndrome and extrapyramidal disorders.⁶ In this case report, the patient with SS had been misdiagnosed as having fibromyalgia (Tab. 3). Fibromyalgia is a rheumatologic syndrome of unknown etiology. It is characterized by chronic widespread bilateral upper- and lower-body joint, muscle, and spinal pain. The American College of Rheumatology 1990 classification criteria for fibromyalgia include diffuse soft-tissue pain with a duration of at least 3 months and pain on palpation in at least 11 of 18 paired tender points.^3,25 The patient described in this case report did have diffuse soft tissue pain; however, she did exhibit a change in mental status, agitation, myoclonus, hyperreflexia, tremor, diarrhea, and incoordination. Although there was tenderness throughout the body, the treating therapist did not observe tenderness at the specified 11 of 18 tender points necessary for a diagnosis of fibromyalgia.³ The major symptomatology that led to the suggestion that the patient be referred to a neurologist was that of neurologic signs consisting of, but not limited to, nystagmus, reflex disturbances, difficulty with memory, sensory disturbances, and a history of falls, which are not symptoms of fibromyalgia.

Goldenberg and colleagues²⁵ reported that there was weak efficacy for the use of ultrasound, chiropractic care, and electrotherapy in patients with fibromyalgia. However, they did find strong efficacy for cardiovascular activity, patient education, and exercise therapy, all of which are within the scope of physical therapist practice.^1,25 Given the initial diagnosis of fibromyalgia and the symptoms of pain in this patient, it would have been appropriate to have referred this patient for physical therapy earlier. I am unaware of any evidence in the areas of physical therapy and the treatment of SS. Therefore, more research should be done on SS, the mechanisms of pain and muscle weakness caused by SSRIs (including citalopram), and their responses to physical therapy interventions. In general, for patients with this clinical presentation, it might be beneficial to refer them for physical therapy in order to obtain a full-systems-approach evaluation and begin conservative treatments.

Physical therapists usually are able to spend a considerable amount of time working closely with patients and are in a good position to identify symptoms that are either consistent or inconsistent with a patient's diagnosis. They can spend an hour to perform an initial evaluation and provide frequent follow-up appointments, 2 or 3 days per week for 4 to 8 weeks, depending on the diagnosis. This time spent with the patient allows the physical therapist to collect significantly more information and perform trials of various treatments, including modalities, exercise, and manual techniques, each of which allows the physical therapist to assess and reassess the patient's status. This information then can be added to the information collected by the physician, resulting in a more accurate diagnosis and enabling the best treatment possible. In this particular case, the treating therapist was able to collect significant information, including prior health status, time line of events leading up to current symptoms, and assessments of the musculoskeletal, neuromuscular, integumentary, and cardiopulmonary systems. The information collected from this patient led to her ultimate referral to a neurologist. Once the correct diagnosis was obtained, proper measures were taken. The patient was gradually weaned off citalopram and switched to a non-SSRI antidepressant. Over a period of weeks, she gradually improved, eventually becoming pain-free, and was able to return to her prior activity level with only minimal residual effects.

Serotonin syndrome can theoretically be the result of any drug or combination of drugs that has the net effect of increasing serotonergic neurotransmission.¹⁵ In this particular case, the trigger medication was citalopram.

Further research is warranted in the areas of physical therapy and SS. It would be beneficial for clinicians to become more aware of the potential side effects of commonly used medications and of the potential confusion of SS and fibromyalgia in professional (entry-level) education as well as clinical practice. This awareness would be especially useful in patients with unknown etiologies. Furthermore, obtaining a detailed history, using the most current research, and taking a systems approach would result in a more accurate diagnosis and allow for the most clinically relevant treatment.

	Appendix 1.

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

 

View larger version (19K): [in this window] [in a new window]   Appendix 1. Contraindications and Precautions for Citalopram5

	Appendix 2.

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

View larger version (22K): [in this window] [in a new window]   Appendix 2. Adverse Reactions to Citalopram5

	Footnotes

 
The author thanks the patient for her cooperation and willingness to share her story and Joyce Leclerc, Health Science Librarian, Androscoggin Valley Hospital, for her assistance in obtaining reference articles. The author also thanks Dr Heather Alnwick, Dr Maggie Moore-West (Franklin Pierce University), Dr Donald West (Medical Director of the Psychiatric Inpatient Program, Dartmouth Hitchcock Medical Center), Dr Tad Pfeffer (The University of Colorado at Boulder), Dr Anne Pfeffer, and Heidi Guinen, MSW, LCSW, for their suggestions.

	References

Top Abstract Introduction Case Description Outcomes Discussion Appendix 1. Appendix 2. References

 

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This Article Abstract Full Text (PDF) All Versions of this Article: ptj.20060208v1 88/6/757    most recent Submit a response Alert me when this article is cited Alert me when Rapid Responses are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Alnwick, G. M Search for Related Content PubMed PubMed Citation Articles by Alnwick, G. M Related Collections Coordination, Communication, and Documentation Pain Professional Issues Case Reports Diagnosis/Prognosis: Other Social Bookmarking                      What's this?