Cardiac neurotransmission imaging with 123I-meta-iodobenzylguanidine in postural tachycardia syndrome

Haensch, Carl-Albrecht; Lerch, H; Schlemmer, Hans; Jigalin, Anna; Isenmann, Stefan

doi:10.1136/jnnp.2008.168484

Cited by 24 publications

(20 citation statements)

References 34 publications

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“…In this study,11 the investigators found reduced cardiac MIBG accumulation in four of 20 patients with POTS. They propose that this finding implies cardiac denervation.…”

supporting

confidence: 48%

“…In this issue, Haensch and colleagues11 use the radionuclide 123 I-MIBG ( 123 I-meta-idobenzylguanidine) to study the neuronal uptake of norepinephrine (NE) in 20 patients with well characterised POTS ( see page ). The focus of this scintigraphic study is the synaptic junction; it utilises 123 I-MIBG as a substrate and false neurotransmitter that shares characteristics (uptake, storage and release) with NE, the major neurotransmitter of the sympathetic nervous system.…”

mentioning

confidence: 99%

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Beyond postural tachycardia syndrome

Mustafa

Robertson

2010

Journal of Neurology, Neurosurgery & Psychiatry

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“…In this study,11 the investigators found reduced cardiac MIBG accumulation in four of 20 patients with POTS. They propose that this finding implies cardiac denervation.…”

supporting

confidence: 48%

mentioning

confidence: 99%

Beyond postural tachycardia syndrome

Mustafa

Robertson

2010

Journal of Neurology, Neurosurgery & Psychiatry

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“…8,16 Reduced myocardial meta-iodobenzylguanidine uptake has been reported in patients with POTS. 19 However, the relationship between this finding and peripheral adrenergic denervation of the lower limb is still undetermined. The frequent onset after a viral illness and the presence of a ganglionic acetylcholine receptor antibody in 14% of patients suggest an auto-…”

Section: Pots As a Syndrome Of Orthostatic Intolerancementioning

confidence: 99%

Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder

Benarroch

2012

Mayo Clinic Proceedings

308

354

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Postural tachycardia syndrome (POTS) is defined by a heart rate increment of 30 beats/min or more within 10 minutes of standing or head-up tilt in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. POTS manifests with symptoms of cerebral hypoperfusion and excessive sympathoexcitation. The pathophysiology of POTS is heterogeneous and includes impaired sympathetically mediated vasoconstriction, excessive sympathetic drive, volume dysregulation, and deconditioning. POTS is frequently included in the differential diagnosis of chronic unexplained symptoms, such as inappropriate sinus tachycardia, chronic fatigue, chronic dizziness, or unexplained spells in otherwise healthy young individuals. Many patients with POTS also report symptoms not attributable to orthostatic intolerance, including those of functional gastrointestinal or bladder disorders, chronic headache, fibromyalgia, and sleep disturbances. In many of these cases, cognitive and behavioral factors, somatic hypervigilance associated with anxiety, depression, and behavioral amplification contribute to symptom chronicity. The aims of evaluation in patients with POTS are to exclude cardiac causes of inappropriate tachycardia; elucidate, if possible, the most likely pathophysiologic basis of postural intolerance; assess for the presence of treatable autonomic neuropathies; exclude endocrine causes of a hyperadrenergic state; evaluate for cardiovascular deconditioning; and determine the contribution of emotional and behavioral factors to the patient's symptoms. Management of POTS includes avoidance of precipitating factors, volume expansion, physical countermaneuvers, exercise training, pharmacotherapy (fludrocortisone, midodrine, ␤-blockers, and/or pyridostigmine), and behavioral-cognitive therapy. A literature search of PubMed for articles published from January 1, 1990, to June 15, 2012, was performed using the following terms (or combination of terms): POTS; postural tachycardia syndrome, orthostatic; orthostatic; syncope; sympathetic; baroreceptors; vestibulosympathetic; hypovolemia; visceral pain; chronic fatigue; deconditioning; headache; Chiari malformation; Ehlers-Danlos; emotion; amygdala; insula; anterior cingulate; periaqueductal gray; fludrocortisone; midodrine; propranolol; ␤-adrenergic; and pyridostigmine. Studies were limited to those published in English. Other articles were identified from bibliographies of the retrieved articles. 1,2 According to current criteria for adults, 3 POTS is defined by a heart rate increment of 30 beats/min or more within 10 minutes of standing or head-up tilt (HUT) in the absence of orthostatic hypotension; the standing heart rate is often 120 beats/min or higher. These criteria may not be applicable for individuals with low resting heart rate. For individuals aged 12 to 19 years, the required increment is at least 40 beats/min.3 The orthostatic tachycardia may be accompanied by symptoms of cerebral hypoperfusion and sympathetic hyperactivity that are reliev...

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“…36 A recently published study reported that POTS might be a manifestation of autonomic cardiac neuropathy. 37 POTS has been reported associated with trauma, 38 Lyme disease, 39 electrocution, 40 multiple sclerosis, 41 and mitochondrial cytopathy 42 and also after ablation of slow pathway for atrioventricular (AV) node reentrant tachycardia. 43 Breath-holding spells The breath-holding spells group of disorders is usually seen in children and are broadly subdivided into 2 groups.…”

Section: Dysautonomic Syncopementioning

confidence: 99%