scholarly journals Stiff-person syndrome in a patient with comorbid bipolar and panic disorders: A case report and literature review

2020 ◽  
Vol 10 (3) ◽  
pp. 95-99
Author(s):  
Karishma Patel ◽  
Lauren Stummer ◽  
Krina Patel

Abstract Stiff-person syndrome (SPS) is a neurologic disorder characterized by muscle stiffness, rigidity, and muscle spasms, and it can increase a patient's risk for falls. It is recognized as a rare disease with limited clinical guidelines to manage the condition and its symptoms. Currently, there is even less clinical guidance for the management of common comorbid conditions in these patients. This patient case report aims to evaluate the efficacy of various medications for symptom management in a patient with SPS and comorbid psychiatric disorders, specifically bipolar I and panic disorder. Throughout the patient's course of treatment, various medications were trialed, including fluoxetine, hydroxyzine, valproic acid, propranolol, and clonazepam. Ultimately, fluoxetine, hydroxyzine, and propranolol were discontinued due to adverse drug reactions and incomplete symptom resolution. The patient's bipolar I disorder was adequately managed with valproic acid. Once the clonazepam was changed from as-needed to scheduled dosing, the patient's panic disorder and anxiety-triggered spasms were well controlled. The efficacy of benzodiazepines, specifically high doses of diazepam, in alleviating muscle spasms and anxiety in SPS has been demonstrated in the literature. Case reports including patients with SPS that are prescribed selective serotonin reuptake inhibitors provide controversial evidence as some studies report exacerbation of SPS symptoms with prolonged use. As this case report and literature review suggest, patients with SPS and comorbid panic disorder and anxiety-triggered spasms may benefit from the use of benzodiazepines. The use of other medication classes for the treatment of other comorbid psychiatric disorders in a patient with SPS is lacking evidence.

2002 ◽  
Vol 27 (4) ◽  
pp. 318-319 ◽  
Author(s):  
Emad L Zaki ◽  
James E Springate

2006 ◽  
Vol 134 (7-8) ◽  
pp. 267-272
Author(s):  
Milan Latas ◽  
Vladan Starcevic ◽  
Goran Trajkovic

Introduction. Besides numerous studies that examined various aspects of comorbidity in patients with panic disorder and agoraphobia and numerous studies that examined efficacy of different treatment modalities in these patients, there was no study that examined relationship of overall psychiatric comorbidity and treatment of patients with panic disorder and agoraphobia. Objective. The objective of the study was to establish the effect of psychiatric comorbidity on treatment efficiency of patients with panic disorder and agoraphobia. Method. The sample of the study consisted of 119 patients with primary diagnosis of panic disorder and agoraphobia. The therapy of patients was based on the use of individual integrative model of treatment, which incorporated psycho-pharmaceuticals (benzodiazepines and antidepressants) and cognitive- behavior therapy. Symptom severity was estimated by Panic and Agoraphobia Scale before and after the completion of treatment. Patients with comorbidity and patients without any comorbidity were compared by MANOVA and ANOVA with repeated measures. Results. The results of the study showed that 91% of patients met diagnostic criteria of comorbid psychiatric disorder and these patients had more severe clinical picture than patients without any comorbid disorder before the treatment. The results also showed that, after the completion of treatment, there was a significant reduction of all analyzed symptoms, that the effects of treatment were significantly better in patients with psychiatric comorbidity and that comorbid psychiatric disorders had no negative effect on the main goals of the treatment. Conclusion. Based on these results, it may be concluded that: in patients with panic disorder and agoraphobia and comorbid psychiatric disorders, the pharmacotherapy must be based on simultaneous use of antidepressants and benzodiazepines, while standard cognitive-behavior therapy of patients with panic disorder and agoraphobia must be modified in case of the existing comorbid psychiatric disorders.


2019 ◽  
Vol 2019 ◽  
pp. 1-3 ◽  
Author(s):  
L. M. Conners ◽  
A. Betcher ◽  
A. Shahinian ◽  
P. Janda

Stiff-person syndrome (SPS) is an uncommon neurological disorder characterized by significant rigidity and muscle spasms primarily affecting the truncal and proximal musculature. Furthermore, a wide-based gait with functional impairment is generally seen. High-dose benzodiazepines or baclofen are widely considered the optimal initial therapy; however, major adverse effects often preclude adequate dosing. Refractory cases may be treated with intravenous immunoglobulins (IVIG), plasma exchange, or B-cell depletion with rituximab, although these are also associated with major, sometimes fatal, adverse reactions. Several reports have validated the safety and utility of botulinum injections in this setting, yet botulinum remains markedly underutilized in this cohort. Below, a case report and review of the literature show botulinum can decrease pain and stiffness, improve gait and balance, and decrease dependence on powerful systemic treatments in this group.


2009 ◽  
Vol 2009 ◽  
pp. 1-3 ◽  
Author(s):  
Tina M. Gardner ◽  
Rehan Aziz ◽  
Sunanda Muralee ◽  
Rajesh R. Tampi

Valproic acid and its derivatives are now commonly used to treat various psychiatric disorders in the elderly. Data indicates that the elderly patients are more susceptible to developing neuropsychiatric complications when treated with these medications. In this report, we describe the case of a 66-year-old woman with early-onset, Alzheimer's type dementia, who developed myoclonus when treated with a valproic acid preparation for behavioral disturbances associated with the dementia.


2018 ◽  
Vol 8 (3) ◽  
pp. 148-154 ◽  
Author(s):  
Lauren M. Brown ◽  
Nicole Cupples ◽  
Troy A. Moore

Abstract Introduction: Hyperammonemia is a potential adverse effect of valproic acid (VPA) therapy, which is often asymptomatic but can lead to severe, life-threatening encephalopathy. Carnitine deficiency due to VPA is the proposed mechanism for hyperammonemia and the development of VPA-induced hyperammonemic encephalopathy (VHE). Levocarnitine, the active form of carnitine, has been suggested for treatment and prevention of VHE. Methods: Data was collected by chart review of 3 patients who received oral levocarnitine supplementation in the psychiatric setting for VPA-induced hyperammonemia. Review of the literature was performed through June 2017 using the following PubMed search terms: valproate, valproic acid, hyperammonemia, altered mental status, encephalopathy, and levocarnitine. Articles were included if they described use of levocarnitine in VPA-treated patients with psychiatric disorders. Results: One patient developed encephalopathy with resolution of symptoms after VPA discontinuation. Valproic acid was restarted with the addition of levocarnitine to prevent VHE reoccurrence. In the other 2 cases, levocarnitine was started prophylactically in patients who developed hyperammonemia without emergence of any clinical symptoms. Ammonia levels were reduced to normal in all cases, and no symptoms consistent with encephalopathy were reported. The literature search identified 6 additional cases with 5 of 6 reports supporting use of levocarnitine for decreased ammonia levels as well as an observational trial. Discussion: This literature review and case series illustrates successful use of levocarnitine supplementation for reduction of ammonia levels in the setting of VPA-induced hyperammonemia among patients with psychiatric disorders. However, clinical significance of ammonia reduction in asymptomatic patients is difficult to determine.


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