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Fibromyalgia caused by serotonin syndrome?


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http://www.ptjournal.net/content/

88/6/757.abstract

serotonin syndrome misdiagnosed as fibro

this is a must read

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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

Gregory M Alnwick

+ Author Affiliations

http://ptjournal.apta.org/content/88/6/757.full

 

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@ne.rr.com

 

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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.

 

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-HT1A) 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:

 

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.

 

Other etiologies (infections, metabolic disorders, and substance abuse or withdrawal) need to be excluded.

 

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.

 

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Case Description

 

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.

 

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Table 1.

Time Line of Events

 

Four years prior to diagnosis.

The patient had been taking citalopram (20 mg per day) since 1998 for the treatment of depression that was related to abuse that she had experienced as a child. She began to experience symptoms approximately 2 years after starting citalopram. Because of dizziness, she was considered to have Ménière disease, an idiopathic syndrome of endolymphatic hydrops.18 The American Academy of Otolaryngology head and neck surgery criteria for Ménière disease are the triad of vertigo, hearing loss, and tinnitus.18

 

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.

 

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Table 2.

Oswestry Disability Index Questionnaire Results

 

The neurologic examination provided a medical diagnosis of SSRI-induced neurologic syndrome, or SS secondary to the use of citalopram. The findings from the neurologist report were as follows: pulse was 96 beats per minute; respiration rate was 22 breaths per minute and nonlabored; cardiovascular status was within normal limits; cognitive status was generally normal; cranial nerves showed normal funduscopy findings; eye movements, visual fields, pupil reactivity, and facial strength were equal bilaterally and normal; facial sensation was vaguely and reproducibly decreased in response to all modalities; hearing was within normal limits; the palate and tongue were at the midline; muscles showed unremarkable bulk and normal symmetric tone; there was significant left hemiparesis, without asymmetry; reflexes were 1 to 2+; and sensory examination findings were normal. There was a hemiparetic gait with the use of a straight cane and a high-frequency, low-amplitude tremor with adoption. The tremor was not noted with use of a cane. In addition, the patient had pain with swallowing, coughing, some choking, frequent headaches, swollen lymph nodes, neck pain, pain with breathing, wheezing, heart palpitations, pain with urination, blood in the urine, swelling in the feet and ankles, and frequent bouts of diarrhea and constipation with blood in the stool. The differential diagnosis consisted of Ménière disease, multiple sclerosis, pneumonia, other infection process, carbon monoxide poisoning, and gastroesophageal reflex disease. The impression was that of an extreme case of SS related to citalopram.

 

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.

 

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Outcomes

 

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.

 

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Discussion

 

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-HT1A 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.

 

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Table 3.

Comparison of Signs and Symptoms of Serotonin Syndrome14 and Fibromyalgia9,25

 

The criteria described above can aid in the diagnosis of SS. However, it is important to rule out other, similar disorders and to understand that SS can have pain as a primary symptom and can have a gradual onset rather than an acute onset. At present, there is no gold standard that would confirm or reject this syndrome. The patient described in this case report did have the majority of symptoms required to make a diagnosis of SS, as set forth by Sternbach.14 Prior to being diagnosed with SS, the patient had been examined by several physicians, including rheumatologists, psychiatrists, and numerous PCPs. All of them had missed the diagnosis of SS. After having this disorder for more than 4 years, the patient was eventually referred for physical therapy. It was the physical therapist who, after obtaining a detailed history and performing a physical examination, realized that the symptoms exceeded those of fibromyalgia and suggested that the patient be referred to a neurologist, who also obtained a detailed history, performed an examination, and diagnosed her with SS.

 

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.

 

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Appendix 1.

 

 

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Appendix 1.

Contraindications and Precautions for Citalopram5

 

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Appendix 2.

 

 

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Appendix 2.

Adverse Reactions to Citalopram5

 

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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.

Received July 23, 2006.

Accepted February 15, 2008.

Physical Therapy

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References

 

↵ Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001;81:9–746. Medline

↵ Fritz JM, Wainner RS. Examining diagnostic tests: an evidence-based perspective. Phys Ther. 2001;81:1546–1564. Abstract/FREE Full Text

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↵ Laine K, Anttila M, Heinonen E, et al. Lack of adverse interactions between concomitantly administered selegiline and citalopram. Clin Neuropharmacol. 1997;20:419–433. Medline

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McDaniel WW. Serotonin syndrome: early management with cyprohepatadine. Ann Pharmacother. 2001;35:870–873. Abstract

↵ Birmes P, Coppin D, Schmitt L, Lauque D. Serotonin syndrome: a brief review. CMAJ. 2003;168:1439–1442. FREE Full Text

↵ Manos GH. Possible serotonin syndrome associated with buspirone added to fluoxetine. Ann Pharmacother. 2000;34:871–874. Abstract

↵ Mackay FJ, Dunn NR, Mann RD. Antidepressants and the serotonin syndrome in general practice. Br J Gen Pract. 1999;49:871–874. Medline

↵ Sternbach H. The serotonin syndrome. Am J Psychiatry. 1991;148:705–713. Abstract/FREE Full Text

↵ Chechani V. Serotonin syndrome presenting as hypotonic coma and apnea: potentially fatal complications of selective serotonin receptor inhibitor therapy. Crit Care Med. 2002;30:473–476. CrossRefMedline

↵ Cleland JA, Venzke JW. Dermatomyositis: evolution of a diagnosis. Phys Ther. 2003;83:932–945. Abstract/FREE Full Text

↵ Ludenberg T, Lund I, Dahlin L, et al. Reliability and responsiveness of three different pain assessments. J Rehabil Med. 2001;33:279–283. CrossRefMedline

↵ Havia M, Kentala E. Progression of symptoms of dizziness in Ménière's disease. Arch Otolaryngol Head Neck Surg. 2004;130:431–435. Abstract/FREE Full Text

↵ Resnik L, Dobrzykowski E. Guide to outcome measurement for patients with low back pain syndromes. J Orthop Sports Phys Ther. 2003;33:307–318. Medline

↵ Plews-Ogan M, Owens JE, Goodman M, et al. Brief report: a pilot study evaluating mindfulness-based stress reduction and massage for the management of chronic pain. J Gen Intern Med. 2005;20:1136–1138. CrossRefMedline

Hsieh LL, Kuo CH, Lee LH, et al. Treatment of low back pain by acupressure and physical therapy: randomised controlled trial. BMJ [serial online]. 2006;332;696–700. Available at: www.bmj.com. Accessed April 14, 2006. Abstract/FREE Full Text

↵ Astin JA, Shapiro SL, Eisenberg DM, Forys KL. Mind body medicine: state of the science, implications for practice. J Am Board Fam Pract. 2003;16:131–147. CrossRefMedline

↵ Avarello TP, Cottone S. Serotonin syndrome: a reported case. Neurol Sci. 2002;23:S55–S56. CrossRefMedline

↵ Tomaselli G, Modestin J. Repetition of serotonin syndrome after reexposure to SSRI: a case report. Pharmacopsychiatry. 2004;37:236–238. CrossRefMedline

↵ Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA [serial online]. 2004;292:2388–2395. Available at: www.jama.com. Accessed May 10, 2006. Abstract/FREE Full Text

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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As you can see by this above report serotonin syndrome does not always put one in hospital is desperate shape as this woman was walking around seeing therapists.

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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  • Administrator

Thanks, btdt. Interesting article.

 

The woman may not have been suffering from serotonin syndrome but an adverse effect of citalpram -- a diagnostic error. Still, she had an iatrogenic condition caused by the medication.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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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.

Are you suspecting the therapist or the neurologist made the diagnostic error or the person who said she had fibro?

Seems to me the proof was in the pudding the treatment for serotonin syndrome worked it was diagnosed by a neurologist so I am thinking you suspect the neurologist is wrong. I so with I had my old computer that died an untimely death it was newer than this one. On that computer I had saved information about serotonin syndrome NOT being a life or death issue but having many degrees and the need for doctors to get cracking as they were failing patients by not diagnosing them correctly. It was a scientific article.

 

It opens old wounds of not getting care I needed as you may recall I was sure I had ss and still am I know I am bull headed but hey that is what has kept me alive this long.

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

Link to post
Share on other sites
  • Administrator

....

Are you suspecting the therapist or the neurologist made the diagnostic error or the person who said she had fibro?

Seems to me the proof was in the pudding the treatment for serotonin syndrome worked....

 

Correct. From the article, neurologist's reasoning was SSRIs increase serotonin, the woman was taking an SSRI, therefore her symptoms were serotonin syndrome.

 

That doesn't make a whole lot of sense. Yes, SSRIs can cause serotonin syndrome but symptoms usually involve severe disorientation, not fibro-like pain. Disorientation is not mentioned as a symptom.

 

SSRIs also cause adverse effects, such as paresthesia. This seems to me a more reasonable explanation for her symptoms, which were misdiagnosed as fibromyalgia.

 

Discontinuing citalopram would also have eliminated the adverse effect it caused.

 

Yes, I believe the neurologist was incorrect. Just because this was published as a scientific paper doesn't mean it's anywhere near truth -- we know that from many, many other scientific papers.

 

What this demonstrates is that particular neurologist didn't know jack about SSRI adverse effects. No surprise there. At least the physical therapist was alert and the woman is now all right.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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Share on other sites

 

....

Are you suspecting the therapist or the neurologist made the diagnostic error or the person who said she had fibro?

Seems to me the proof was in the pudding the treatment for serotonin syndrome worked....

 

Correct. From the article, neurologist's reasoning was SSRIs increase serotonin, the woman was taking an SSRI, therefore her symptoms were serotonin syndrome.

 

That doesn't make a whole lot of sense. Yes, SSRIs can cause serotonin syndrome but symptoms usually involve severe disorientation, not fibro-like pain. Disorientation is not mentioned as a symptom.

 

SSRIs also cause adverse effects, such as paresthesia. This seems to me a more reasonable explanation for her symptoms, which were misdiagnosed as fibromyalgia.

 

Discontinuing citalopram would also have eliminated the adverse effect it caused.

 

Yes, I believe the neurologist was incorrect. Just because this was published as a scientific paper doesn't mean it's anywhere near truth -- we know that from many, many other scientific papers.

 

What this demonstrates is that particular neurologist didn't know jack about SSRI adverse effects. No surprise there. At least the physical therapist was alert and the woman is now all right.

 

Are you joking????

 

Paresthesia

An altered sensation often described as burning, tingling, or pin pricks.

 

Her symptoms are not even close to Paresthesia I am glad your not my doctor. Here are her symptoms I have condensed them so they are easy to digest. I know it is a long article maybe that is the problem here.

 

I might add that all the symptoms she had I had the neurologist thought I had ms too that is how close we were this neurologists alternative diagnosis was also MS.

 

These were her symptoms

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.

 

Four years prior to diagnosis.

The patient had been taking citalopram (20 mg per day) since 1998 for the treatment of depression that was related to abuse that she had experienced as a child. She began to experience symptoms approximately 2 years after starting citalopram. Because of dizziness, she was considered to have Ménière disease, an idiopathic syndrome of endolymphatic hydrops.18 The American Academy of Otolaryngology head and neck surgery criteria for Ménière disease are the triad of vertigo, hearing loss, and tinnitus.18

 

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.

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).

Her drug history

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.

What the neurologist found

There was a hemiparetic gait with the use of a straight cane and a high-frequency, low-amplitude tremor with adoption. The tremor was not noted with use of a cane. In addition, the patient had pain with swallowing, coughing, some choking, frequent headaches, swollen lymph nodes, neck pain, pain with breathing, wheezing, heart palpitations, pain with urination, blood in the urine, swelling in the feet and ankles, and frequent bouts of diarrhea and constipation with blood in the stool. The differential diagnosis consisted of Ménière disease, multiple sclerosis, pneumonia, other infection process, carbon monoxide poisoning, and gastroesophageal reflex disease. The impression was that of an extreme case of SS related to citalopram.

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.

Since the treatment worked he for sure picked the right treatment so he is not too stupid I think he picked the right disorder too.

 

http://www.nejm.org/doi/full/10.1056/NEJMra041867

 

Three features of the serotonin syndrome are critical to an understanding of the disorder. First, the serotonin syndrome is not an idiopathic drug reaction; it is a predictable consequence of excess serotonergic agonism of central nervous system (CNS) receptors and peripheral serotonergic receptors.1,2 Second, excess serotonin produces a spectrum of clinical findings.3 Third, clinical manifestations of the serotonin syndrome range from barely perceptible to lethal.

 

New rules for diagnosing ss

The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity

 

 

Background:There are difficulties with the diagnosis of serotonin toxicity, particularly with the use of Sternbach’s criteria. 

Aim:To improve the criteria for diagnosing clinically significant serotonin toxicity. 

Design:Retrospective analysis of prospectively collected data 

Methods: We studied all patients admitted to the Hunter Area Toxicology Service (HATS) following an overdose of a serotonergic drug from January 1987 to November 2002 (n = 2222). Main outcomes were: diagnosis of serotonin toxicity by a clinical toxicologist, fulfilment of Sternbach’s criteria and treatment with a serotonin receptor (5-HT2A) antagonist. A learning dataset of 473 selective serotonin reuptake inhibitor (SSRI)-alone overdoses was used to determine individual clinical features predictive of serotonin toxicity by univariate analysis. Decision rules using CART analysis were developed, and tested on the dataset of all serotonergic overdose admissions.

Results:Numerous clinical features were associated with serotonin toxicity, but only clonus (inducible, spontaneous or ocular), agitation, diaphoresis, tremor and hyperreflexia were needed for accurate prediction of serotonin toxicity as diagnosed by a clinical toxicologist. Although the learning dataset did not include patients with life-threatening serotonin toxicity, hypertonicity and maximum temperature  > 38°C were universal in such patients; these features were therefore added. Using these seven clinical features, decision rules (the Hunter Serotonin Toxicity Criteria) were developed. These new criteria were simpler, more sensitive (84% vs. 75%) and more specific (97% vs. 96%) than Sternbach’s criteria.

Discussion:These redefined criteria for serotonin toxicity should be more sensitive to serotonin toxicity and less likely to yield false positives. 

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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  • Administrator

Enough, btdt. She had been taking Celexa 20mg for many years. Serotonin syndrome doesn't work like that.

 

Quitting the drug resolved whatever deleterious effect it had on her, no matter what you call it.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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Enough, btdt. She had been taking Celexa 20mg for many years. Serotonin syndrome doesn't work like that.

 

Quitting the drug resolved whatever deleterious effect it had on her, no matter what you call it.

 

Enough???

I say what I think is that a problem.

 

You did not address the new diagnostic criteria for chronic and or mild serotonin syndrome apparently it has been under recognized if this has not been an issue for you that is fine but maybe just maybe it has been an issue for others and maybe it should be addressed.

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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Share on other sites

Enough, btdt. She had been taking Celexa 20mg for many years. Serotonin syndrome doesn't work like that.

 

Quitting the drug resolved whatever deleterious effect it had on her, no matter what you call it.

 

How many times can the same thing be said over and over. Altostrata is not a medical doctor nor does she claim to be. This is what she believes to be the case, and after reading the majority of this thread, so do I. I also agree that this is enough.

 

 

Charter Member 2011

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  • 2 years later...

 

....

Are you suspecting the therapist or the neurologist made the diagnostic error or the person who said she had fibro?

Seems to me the proof was in the pudding the treatment for serotonin syndrome worked....

Correct. From the article, neurologist's reasoning was SSRIs increase serotonin, the woman was taking an SSRI, therefore her symptoms were serotonin syndrome.

 

That doesn't make a whole lot of sense. Yes, SSRIs can cause serotonin syndrome but symptoms usually involve severe disorientation, not fibro-like pain. Disorientation is not mentioned as a symptom.

 

SSRIs also cause adverse effects, such as paresthesia. This seems to me a more reasonable explanation for her symptoms, which were misdiagnosed as fibromyalgia.

 

Discontinuing citalopram would also have eliminated the adverse effect it caused.

 

Yes, I believe the neurologist was incorrect. Just because this was published as a scientific paper doesn't mean it's anywhere near truth -- we know that from many, many other scientific papers.

 

What this demonstrates is that particular neurologist didn't know jack about SSRI adverse effects. No surprise there. At least the physical therapist was alert and the woman is now all right.

 

I do believe the new diagnostics for ss do include something along these lines..."Yes, SSRIs can cause serotonin syndrome but symptoms usually involve severe disorientation, not fibro-like pain. Disorientation is not mentioned as a symptom."  I would have to look it up to be sure. 

 

"Discontinuing citalopram would also have eliminated the adverse effect it caused."

When I had an adverse reaction to prozac after 2 wks use 25 years ago he stopping prozac did not stop the reaction which played out much like a withdrawal reaction in symptoms and timeline it was not gone two years later and pain was a big part of it... so much so I was sent to a pain clinic and once there put on another antidepressant this time a tycylic. once again for pain... leading to more ssir snri... over time. 

 

Seems to me given all the things we know we still don't know everything about these drugs there may be a lot left to learn yet.  

 

Just a little something to back up the new perspective tho this is not it...

 

"Prakash S et al. – Serotonin syndrome (SS) is a drug–induced constellation of various clinical features that result from excess central serotonergic tone. The clinical features range from barely perceptible to life–threatening conditions. Physicians should consider the diagnosis of SS in patients with new onset or worsening headache after the addition of serotonergic drugs, especially in the presence of objective signs on examination suggestive of the disorder such as tremor, fever, hyperreflexia, diaphoresis or tachycardia."

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

Link to post
Share on other sites

 

 

....

Are you suspecting the therapist or the neurologist made the diagnostic error or the person who said she had fibro?

Seems to me the proof was in the pudding the treatment for serotonin syndrome worked....

Correct. From the article, neurologist's reasoning was SSRIs increase serotonin, the woman was taking an SSRI, therefore her symptoms were serotonin syndrome.

 

That doesn't make a whole lot of sense. Yes, SSRIs can cause serotonin syndrome but symptoms usually involve severe disorientation, not fibro-like pain. Disorientation is not mentioned as a symptom.

 

SSRIs also cause adverse effects, such as paresthesia. This seems to me a more reasonable explanation for her symptoms, which were misdiagnosed as fibromyalgia.

 

Discontinuing citalopram would also have eliminated the adverse effect it caused.

 

Yes, I believe the neurologist was incorrect. Just because this was published as a scientific paper doesn't mean it's anywhere near truth -- we know that from many, many other scientific papers.

 

What this demonstrates is that particular neurologist didn't know jack about SSRI adverse effects. No surprise there. At least the physical therapist was alert and the woman is now all right.

 

I do believe the new diagnostics for ss do include something along these lines..."Yes, SSRIs can cause serotonin syndrome but symptoms usually involve severe disorientation, not fibro-like pain. Disorientation is not mentioned as a symptom."  I would have to look it up to be sure. 

 

"Discontinuing citalopram would also have eliminated the adverse effect it caused."

When I had an adverse reaction to prozac after 2 wks use 25 years ago he stopping prozac did not stop the reaction which played out much like a withdrawal reaction in symptoms and timeline it was not gone two years later and pain was a big part of it... so much so I was sent to a pain clinic and once there put on another antidepressant this time a tycylic. once again for pain... leading to more ssir snri... over time. 

 

Seems to me given all the things we know we still don't know everything about these drugs there may be a lot left to learn yet.  

 

Just a little something to back up the new perspective tho this is not it...

 

"Prakash S et al. – Serotonin syndrome (SS) is a drug–induced constellation of various clinical features that result from excess central serotonergic tone. The clinical features range from barely perceptible to life–threatening conditions. Physicians should consider the diagnosis of SS in patients with new onset or worsening headache after the addition of serotonergic drugs, especially in the presence of objective signs on examination suggestive of the disorder such as tremor, fever, hyperreflexia, diaphoresis or tachycardia."

 

The first time I came off ssri after 2 years, just following my doctors too fast tapering schedule, I developed "fibromyalgia" after 1 year 4 months off the med. I was diagnosed "fibromyalgia," and put back on the ssri for the pain. It didn't take the pain completely away. I think I am like btdt in that respect.

This is my second time coming off ssri, again I followed by doctors too fast tapering schedule, as I knew nothing of withdrawal and only discovered it too late to reinstate and taper slower. Since discovering about withdrawal and how much diet can effect withdrawal, I discover eating sugars and carbs dramatically increase the amount of pain I'm in. I change my diet and avoid my doctor no matter what.

 

The body is complex, the meds affect it in so many different ways.

There is a saying from Buddha "believe nothing, no matter where you read it, or who said it - even if I (Buddha) have said it - unless it agrees with your own reason and common sense."

I think this site is good because we can compare and contrast our withdrawal experiences. Sometimes I think altostrata can come accross as too authoritative in her comments because of the wording. We are all on similar path, but not identical path, so some things may be the same or different in our experience of withdrawal.

01/2006 Put on Prozac for anxiety and panic attacks 08/2008 Came off Zoloft after tapering don't remember taper, lost weight, felt like had cold constantly, very panicky, pain everywhere (misdiagnosed fibromyalgia), head funny.05/2010 put back on Zoloft03/2012 came completely off Zoloft followed Dr standard taper- no appetite, lost weight (0.5 stone), flu-like feelings constantly, pain everywhere, head funny, nausea, very panicky, very strong emotions etc Lost 1 stone.04/2013 improving. actually put on some weight and hungry most of the time. Still burning pain joints, stomach upset, headache/feel faint and emotions very strong. Chest very painful too.01/2014 improving still. Gained weight!! Still hungry. Still headache/feel faint and strong emotions and chest/shoulder muscles painful. Periods irregular and very painful. Very tired. Joints burn only if eat refined sugars. Started eating fruits again.03/2014 2 years off. Now intolerances developed to nuts and soya. Permanently hungry, Emotions strong but started healing psychological reasons I was put on antidepressants with therapist. Shoulder pain bad, heady often, very tired.06/2014 flu-like symptoms returned, many intolerances, stomach painful, skin crawling feeling, muscles painful, very emotional. :-((

09/2016 over 4.5 years off, no real changes in symptoms, still much pain, headiness, heart weird, digestion bad, hormones unbalanced, nausea yet very hungry, tired, flu like symptoms etc etc.

<p>taking - vit C, probiotics and digestive enzymesI have Aspergers Syndrome.

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Very sorry if I come across as too authoritative. I have limited time to respond and have to compact 9 years of study into the short posts I can manage.

 

Any kind of nervous system disruption can contribute to fibromyalgia, I suppose. Fibromyalgia is thought to have an autonomic component. Many people have fibromyalgia-like pain as part of withdrawal syndrome. I experienced this for about 2 years myself.

 

Withdrawal syndrome is very different from serotonin syndrome. Serotonin syndrome is caused by an overdose of serotonergic drugs; it occurs while you're on the drugs, not after you're off them.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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  • 10 months later...

Wow. Just started reading this topic. Im sure most of u agree that some of these realizations are in retrospect b/c of being so consumed with struggling to deal with daily life as a result of SS and AD/AP. Some things are crystal clear + others a total blur. Approx 2004 I was between meds & docs and had begun major difficulties with fatigue. I assumed it was bc I was back to work after my husband's + mother's deaths. I figured i'd do a process of elimination + talk to my family dr. He of course blamed it on my weight + no excercise. I was extremely active + frankly, my weight had gone up since my hysterectomy 10 years b4. I'd even dropped 25 lbs from my depression since my losses. He knew this, but u get the drift. My asthma dr retested my allergies + sleep apnea and they had actually improved. My thyroid was fine (always been hypo), my job was great (at the time), and I was starting to enjoy life again. Anyhow, the fatigue was getting worse + I started with uber aches + pain. I was 45-46 and wondered maybe arthritis & weight. I started researching gastric bypass (after 10 years of dieting) plus my gyno couldnt find any evidence of hormonal probs. I had excellent med ins + started seeing a rheumatologist- recommended by a friend with lupus. Also started a new psych, since my old one had retired- suggested by my pcp bc he felt my issues could be behavioral. Wtf?? Yeah, I dont get that either but I was trusting. Now I had been prozac-free approx 4-5 years, xanax-free 3 yrs, + buspar-free 2 yrs. Other meds since early 90's, but when I have opportunity I will add my history to signature. But I digress...like, if I knew then what I know now. Ugh! So the new pdoc (turned quack - i've mentioned in prev topics) put me on paxil bc my symps were from clinical depression, tho I felt fine, and my ADD was a stressor. He later added ritalin, which I hadnt taken in yrs, but he's the expert...right? Well, back to point - the rheumo doc really got to work + did tests i'd never heard of. He was a bit uneasy about quack's rx-ing but didnt interfere at that point. Fast forward, since all results were good (a little arthritis + slight spinal stenosis - all normal for my age + history) and I was 10 yrs past my hep B + "inactive", he hesitantly diag'd me with fibromyalgia. He put me on anti-inflams + pain patches but didnt recommend extra meds for fatigue bc I was on ritalin (later switched to adderall). He was + is so caring and thorough that if he werent around I dont wanna think where i'd be. Ok, im off track BUT there it is! Fibro diagnosis! Now I go back to finally getting gastric bypass. I was very fortunate & successful bc it is serious surgery and I was in excellent physical shape. Long story short, i'd reached my goal weight of 150 (pre-hysterect) + got to ideal of 140 per my body/height. Gastro doc warned me not to go under 135 and I was back to normal diet + exercise. Anyhow, I went back to pcp and said "there u go, im not a tub anymore - so why is my fatigue worse than ever?" So he said it was narcolepsy + gave me rx for that (dont recall name). Stopped that after a month + he got frustrated, saying it was bc of my depression & fibro. Omg! Did he blow me off? I then decided I would only see him for when i'd get a cold. Meanwhile, pdoc had increased my rx doses until near end of 2006 - when ALL my probs were increasing. I was on 60 mg paxil, 90 mg adderall, and a few other meds in my history. My rheumo was very alarmed + made many attempts to contact pdoc. He felt this was bad in general, but worse for me since i've always been drug-sensitive. They had spoken in the past but was getting nowhere now. Thats when things were going downhill socially & professionally, etc. And this guy was (and still is) highly recommended by ppl + pros in my area. Odd thing is.. he stopped accepting ins. for his psych practice, yet continued for his family m.d. end of it. Then opened a new location outside my area. So I had to hike for appts and pay cash but I assumed I was getting premium care + continued. By now I was up to 80 mg paxil + 120 adderall plus APs + bipo meds that were destroying me. He convinced me it would help my fibro, mdd, bipo, ptsd, add, et al. Then my gastro became alarmed bc I was now 125 lbs...10 below my limit. I was too muddled to care and couldnt SEE the bad signs. He contacted the rheumo bc he had no luck with pdoc. Rheumo insisted I come in + have a pow-wow, where he saw I lost 10 more lbs. He explained that these changes were a result of over-medicating and NOT the fibro. That fibro reaches a peak, which i'd already had. A dr cannot retract a diag but he was close. They also cannot bad-mouth a colleague but emphasized the correlation of my mental & physical changes, and that pdoc never even attempted to return his calls or emails. I couldnt concentrate but it somehow sunk in. It was also confirmed by a concerned co-worker's psychologist husband who actually thought I was on street drugs + did a mini-intervention. It really hit home, but the damage was done. I was still pro AD but realized I had to lose this dr + his over-med routine. The rest is history in other posts, but my point is....was there ever really fibromyalgia?? I've asked the rheumo bc he's been so honest + supportive throughout and he says its hard to tell. Especially since fibro is elusive in itself and there are no definitive tests, even now (10 yrs on). Or it could be a combo, in my case. Its subjective bc of the common pre-existing symps + conditions. I agree since most of mine came b4 i'd even heard of ADs. The biggest being severe endometriosis, then lesser such as; past stress + trauma (physical & mental) and childhood joint probs. Anyway, dont want to bore u with more. Plus alot was explained by posts prior to mine in this thread. Its just that when I reached this topic it was like a building sized litebulb went off. Like holy crap! I've been denser than a tropical forest. Or maybe the fog has lifted temporarily, as it does occasionally. So I wonder...are most cases of this disease actually the seratonin syndrome or the withdrawal thereafter? I'm not saying all cases - that wouldnt be fair. I'll be visiting the rheumo in 2 weeks so I shall ask him if he's aware of any statistics regarding this. I'd like to see if its the egg or the chicken -or- the fibro or the post AD. Thanks for listening :-) If anyone is still awake or headache-free, chime in as to whether u too have had the fibro diag. This could be interesting.

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Interesting history you have PityKitty some of it I can identify with for sure being too dense to know your dense ya I had that and coined the previous term for the state... I also have "awakenings"  times I think clearly, but they pass. 

I checked you status and found you are new and I have not read your other posts as I have been sick lately and washed out by it trying to regain my energy.  This is the only post I have read that said a neurologist dx ss rather after the patient was sent there by a physio therapist. 

 

I have seen plenty of physio therapists in my life none noticed if my problem was the same as this persons or not... maybe this person just had a very well trained physio therapist. 

I am sure I posted the links I found it on a physio therapist site. 

hopefully I will catch up with things here soon 

wishing you well peace to you... 

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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  • 1 month later...

I was reading about ganglion cysts today as I am told I have them in my back.  That lead me to other things as googling often does.  I did a search on ganglion and fibro to see if this was part of fibro.  That search lead me to this page. 

http://brain.oxfordjournals.org/content/136/9/e246

 

It talks of fibro being a neurological disorder related it to sodium "Sodium channels play a pivotal role in this hyperexcitability."

There are some people who have issues with sodium related to antidepressants that we already know. 

A teaser from the site not sure how much of it I can put here... will try this see if I get trouble...

"Among neuropathic pain syndromes, we proposed that fibromyalgia pain is sympathetically maintained based on the following issues: (i) the high frequency of physical or psychological trauma as a triggering event; (ii) diverse heart rate variability studies showing that patients with fibromyalgia have changes consistent with ongoing sympathetic hyperactivity (Lerma et al., 2011); and (iii) a double-blind study showing that norepinephrine injections rekindle fibromyalgia pain (Martinez-Lavin et al., 2002).

Based on animal models of sympathetic pain, we focused our attention on dorsal root ganglia as potential sympathetic–nociceptive short-circuit sites in cases of fibromyalgia. Dorsal root ganglia contain the sensory fibres cell bodies. Trauma and/or infection trigger sympathetic sprouting within dorsal root ganglia through nerve growth factor over-expression. Such aberrant neuroplasticity enables catecholamines and sympathetic traffic to induce sensory neuron firing. Sodium channels play a pivotal role in this hyperexcitability. A sodium channel isoform (NaV1.7) encoded in gene SCN9A of chromosome 2q24.3 is predominantly expressed in the dorsal root ganglia pain-sensing neurons and sympathetic ganglia neurons and their fine-diameter axons.

In a pilot study, we described a particular SCN9A sodium channel gene variant (rs6754031 GG genotype) associated with severe fibromyalgia (Vargas-Alarcon et al., 2012). On the other hand, Faberet al. (2012) reported that a gain of function mutations in sodium channel NaV1.7, which render dorsal root ganglion neurons hyperexcitable, are present in a substantial proportion (28.6%; 8 of 28) of patients meeting strict criteria for small fibre neuropathy (Faber et al., 2012). This preliminary information raises the possibility that some cases of fibromyalgia and small fibre neuropathy may have underlying dorsal root ganglia sodium channelopathy.

The Üçeyler et al. (2013) study reinforces our proposal of fibromyalgia as sympathetically maintained neuropathic pain syndrome. Sympathetic dysfunction provides a coherent explanation for the multiple non-pain related fibromyalgia symptoms (Martinez-Lavin, 2012)."

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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Very interesting b/c I also have 1 g.cyst on my back + 1 on my shoulder. Also several in hands + wrists when I was young. Sorry i've been absent, lots going on. Thanks for ur thoughts + info. My doc wasnt aware of specific statistics on what I mentioned @fibro, but will check for me. He re-emphasized the individuality of fibro symptoms and agrees with the chicken/egg idea (ssri's or fibro). He's going to check some of his patient files, now he's curious. I'll find out in march. I'll check in asap, but if im behind I wish everyone happy holidays. Take care..

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  • 1 year later...

note to self look up dorsal root ganglion movement disorders and multiple chemical sensitivities.... too tired now. 

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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  • 2 weeks later...

 

How to cure fibro.... the man in this video states that pain causes the stomach to shut down and decreases serotonin causing depression... it seems to make sense to me.  He is also preaching to the choir in me at least about how drugs do not cure fibro...but do cause other problems.

He does say ADs are the hardest drugs to get off of and says suicide increases when taking ADs.  #1 way to heal fibro is to heal the gut...

 

how to heal the gut will be the next one I watch.

 

 Here's a video that explains all the dietary and lifestyle changes necessary for optimal health and healing:

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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  • 1 year later...
On 8/25/2011 at 7:14 AM, btdt said:

sorry that link did not work here

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

Gregory M Alnwick

+ Author Affiliations

http://ptjournal.apta.org/content/88/6/757.full

 

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@ne.rr.com

 

Next Section

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.

 

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-HT1A) 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:

 

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.

 

Other etiologies (infections, metabolic disorders, and substance abuse or withdrawal) need to be excluded.

 

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.

 

Previous Section

Next Section

Case Description

 

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.

 

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Table 1.

Time Line of Events

 

Four years prior to diagnosis.

The patient had been taking citalopram (20 mg per day) since 1998 for the treatment of depression that was related to abuse that she had experienced as a child. She began to experience symptoms approximately 2 years after starting citalopram. Because of dizziness, she was considered to have Ménière disease, an idiopathic syndrome of endolymphatic hydrops.18 The American Academy of Otolaryngology head and neck surgery criteria for Ménière disease are the triad of vertigo, hearing loss, and tinnitus.18

 

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.

 

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Table 2.

Oswestry Disability Index Questionnaire Results

 

The neurologic examination provided a medical diagnosis of SSRI-induced neurologic syndrome, or SS secondary to the use of citalopram. The findings from the neurologist report were as follows: pulse was 96 beats per minute; respiration rate was 22 breaths per minute and nonlabored; cardiovascular status was within normal limits; cognitive status was generally normal; cranial nerves showed normal funduscopy findings; eye movements, visual fields, pupil reactivity, and facial strength were equal bilaterally and normal; facial sensation was vaguely and reproducibly decreased in response to all modalities; hearing was within normal limits; the palate and tongue were at the midline; muscles showed unremarkable bulk and normal symmetric tone; there was significant left hemiparesis, without asymmetry; reflexes were 1 to 2+; and sensory examination findings were normal. There was a hemiparetic gait with the use of a straight cane and a high-frequency, low-amplitude tremor with adoption. The tremor was not noted with use of a cane. In addition, the patient had pain with swallowing, coughing, some choking, frequent headaches, swollen lymph nodes, neck pain, pain with breathing, wheezing, heart palpitations, pain with urination, blood in the urine, swelling in the feet and ankles, and frequent bouts of diarrhea and constipation with blood in the stool. The differential diagnosis consisted of Ménière disease, multiple sclerosis, pneumonia, other infection process, carbon monoxide poisoning, and gastroesophageal reflex disease. The impression was that of an extreme case of SS related to citalopram.

 

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.

 

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Outcomes

 

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.

 

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Discussion

 

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-HT1A 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.

 

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Table 3.

Comparison of Signs and Symptoms of Serotonin Syndrome14 and Fibromyalgia9,25

 

The criteria described above can aid in the diagnosis of SS. However, it is important to rule out other, similar disorders and to understand that SS can have pain as a primary symptom and can have a gradual onset rather than an acute onset. At present, there is no gold standard that would confirm or reject this syndrome. The patient described in this case report did have the majority of symptoms required to make a diagnosis of SS, as set forth by Sternbach.14 Prior to being diagnosed with SS, the patient had been examined by several physicians, including rheumatologists, psychiatrists, and numerous PCPs. All of them had missed the diagnosis of SS. After having this disorder for more than 4 years, the patient was eventually referred for physical therapy. It was the physical therapist who, after obtaining a detailed history and performing a physical examination, realized that the symptoms exceeded those of fibromyalgia and suggested that the patient be referred to a neurologist, who also obtained a detailed history, performed an examination, and diagnosed her with SS.

 

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.

 

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Appendix 1.

 

 

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Appendix 1.

Contraindications and Precautions for Citalopram5

 

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Appendix 2.

 

 

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Appendix 2.

Adverse Reactions to Citalopram5

 

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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.

Received July 23, 2006.

Accepted February 15, 2008.

Physical Therapy

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References

 

↵ Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001;81:9–746. Medline

↵ Fritz JM, Wainner RS. Examining diagnostic tests: an evidence-based perspective. Phys Ther. 2001;81:1546–1564. Abstract/FREE Full Text

↵ Namiaparampil DE, Shmerling RH. A review of fibromyalgia. Am J Manag Care. 2004;10:794–800. Medline

↵ Ener RA, Meglathery SB, Van Decker WA, Gallagher RM. Serotonin syndrome and other serotonergic disorders. Pain Med. 2003;4:63–74. CrossRefMedline

↵ Clinical pharmacology. Monographs: citalopram page. Available at: http://www.clinicalpharmacology.com/apps/default.asp?entry=11&rNum=507. Accessed March 11, 2005.

↵ Fisher AA, Davis MW. Serotonin syndrome caused by selective serotonin reuptake-inhibitors-metoclopramide interaction. Ann Pharmacother. 2002;36:67–71. Abstract

↵ Laine K, Anttila M, Heinonen E, et al. Lack of adverse interactions between concomitantly administered selegiline and citalopram. Clin Neuropharmacol. 1997;20:419–433. Medline

↵ Mason PJ, Morris VA, Balcezak TJ. Serotonin syndrome presentation of 2 cases and review of the literature. Medicine. 2000;79:201–209. CrossRefMedline

↵ Chan BS, Graudins A, Whyte IM, et al. Serotonin syndrome resulting from drug interactions. Med J Aust. 1998;169:523–525. Medline

McDaniel WW. Serotonin syndrome: early management with cyprohepatadine. Ann Pharmacother. 2001;35:870–873. Abstract

↵ Birmes P, Coppin D, Schmitt L, Lauque D. Serotonin syndrome: a brief review. CMAJ. 2003;168:1439–1442. FREE Full Text

↵ Manos GH. Possible serotonin syndrome associated with buspirone added to fluoxetine. Ann Pharmacother. 2000;34:871–874. Abstract

↵ Mackay FJ, Dunn NR, Mann RD. Antidepressants and the serotonin syndrome in general practice. Br J Gen Pract. 1999;49:871–874. Medline

↵ Sternbach H. The serotonin syndrome. Am J Psychiatry. 1991;148:705–713. Abstract/FREE Full Text

↵ Chechani V. Serotonin syndrome presenting as hypotonic coma and apnea: potentially fatal complications of selective serotonin receptor inhibitor therapy. Crit Care Med. 2002;30:473–476. CrossRefMedline

↵ Cleland JA, Venzke JW. Dermatomyositis: evolution of a diagnosis. Phys Ther. 2003;83:932–945. Abstract/FREE Full Text

↵ Ludenberg T, Lund I, Dahlin L, et al. Reliability and responsiveness of three different pain assessments. J Rehabil Med. 2001;33:279–283. CrossRefMedline

↵ Havia M, Kentala E. Progression of symptoms of dizziness in Ménière's disease. Arch Otolaryngol Head Neck Surg. 2004;130:431–435. Abstract/FREE Full Text

↵ Resnik L, Dobrzykowski E. Guide to outcome measurement for patients with low back pain syndromes. J Orthop Sports Phys Ther. 2003;33:307–318. Medline

↵ Plews-Ogan M, Owens JE, Goodman M, et al. Brief report: a pilot study evaluating mindfulness-based stress reduction and massage for the management of chronic pain. J Gen Intern Med. 2005;20:1136–1138. CrossRefMedline

Hsieh LL, Kuo CH, Lee LH, et al. Treatment of low back pain by acupressure and physical therapy: randomised controlled trial. BMJ [serial online]. 2006;332;696–700. Available at: www.bmj.com. Accessed April 14, 2006. Abstract/FREE Full Text

↵ Astin JA, Shapiro SL, Eisenberg DM, Forys KL. Mind body medicine: state of the science, implications for practice. J Am Board Fam Pract. 2003;16:131–147. CrossRefMedline

↵ Avarello TP, Cottone S. Serotonin syndrome: a reported case. Neurol Sci. 2002;23:S55–S56. CrossRefMedline

↵ Tomaselli G, Modestin J. Repetition of serotonin syndrome after reexposure to SSRI: a case report. Pharmacopsychiatry. 2004;37:236–238. CrossRefMedline

↵ Goldenberg DL, Burckhardt C, Crofford L. Management of fibromyalgia syndrome. JAMA [serial online]. 2004;292:2388–2395. Available at: www.jama.com. Accessed May 10, 2006. Abstract/FREE Full Text

Is it possible to get serotonin syndrome on reinstatement of a low dose after being in withdrawal for a number of months I wonder?

1999:  Paroxetine (20mg). Age 16. 2007-2008: Fluoxetine (Prozac) for 1.5 years (age 25) Citalopram 20mg 2002-2005, 2009: Escitalopram (20mg), 2 weeks, (age 26) (adverse manic reaction)/*Valium 5mg/Temazepam 10mg 2010: Mirtazipine (Remeron)( do not remember dosage) 2010, 5 months.                     

2010-2017: Citalopram (20mg) (age 27 to 34) 2016: i.1st Sept- 31st Oct Citalopram 10mg , ii.1st November 2017-30th November 2017, Citalopram 5mg iii.1st December 2017- 4th February 2018, Citalopram 0mg, iv.5th February 2018- March 2018 Citalopram 5mg (10mg every other day) 28th February- tried titration of 5mg ( some adverse effects)

2018: 1st March 2018- 1st June Citalopram 10 mg (tablet form) /started titration 8mg , then 7 mg.2018: June 15th- 10th July Citalopram 10 mg pill every other day 2018: 10th July - 13th Sept Citalopram- 0mg  (CBD oil first month of 0mg, passiflora on and off) 2018 13th Sept Citalopram  2mg ,  approx 16th Sept 4mg , approx 25th Sept 6mg held.  2019: 11 Feb 19: 7mg (instant bad rxn) 12 Feb 19 6mg held 1 May 19 5.4mg held 5 Oct 19 5.36mg 22 Oct 19 5.29mg 30 Oct 19 5.23mg 4/NOV/19 5.18mg 12 Nov 19 5.08mg 20 Nov 19 4.77mg

(Herbal/Supplements since 1st September: Omega Fish Oil 1200mg, 663mg of EPA- 2 tablets a day, magnesium and magnesium bath salts)

I did not die, and yet I lost life’s breath
- Dante
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On 10/21/2016 at 2:07 AM, btdt said:

note to self look up dorsal root ganglion movement disorders and multiple chemical sensitivities.... too tired now. 

too stupid today wonder what excuse I will have next time...

WARNING THIS WILL BE LONG
Had a car accident in 85
Codeine was the pain med when I was release from hosp continuous use till 89
Given PROZAC by a specialist to help with nerve pain in my leg 89-90 not sure which year
Was not told a thing about it being a psych med thought it was a pain killer no info about psych side effects I went nuts had hallucinations. As I had a head injury and was diagnosed with a concussion in 85 I was sent to a head injury clinic in 1990 five years after the accident. I don't think they knew I had been on prozac I did not think it a big deal and never did finish the bottle of pills. I had tests of course lots of them. Was put into a pain clinic and given amitriptyline which stopped the withdrawal but had many side effects. But I could sleep something I had not done in a very long time the pain lessened. My mother got cancer in 94 they switched my meds to Zoloft to help deal with this pressure as I was her main care giver she died in 96. I stopped zoloft in 96 had withdrawal was put on paxil went nutty quit it ct put on resperidol quit it ct had withdrawal was put on Effexor... 2years later celexa was added 20mg then increased to 40mg huge personality change went wild. Did too fast taper off Celexa 05 as I felt unwell for a long time prior... quit Effexor 150mg ct 07 found ****** 8 months into withdrawal learned some things was banned from there in 08 have kept learning since. there is really not enough room here to put my history but I have a lot of opinions about a lot of things especially any of the drugs mentioned above.
One thing I would like to add here is this tidbit ALL OPIATES INCREASE SEROTONIN it is not a huge jump to being in chronic pain to being put on an ssri/snri and opiates will affect your antidepressants and your thinking.

As I do not update much I will put my quit date Nov. 17 2007 I quit Effexor cold turkey. 

http://survivingantidepressants.org/index.php?/topic/1096-introducing-myself-btdt/

There is a crack in everything ..That's how the light gets in :)

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