Dermatological Manifestations of Postural Tachycardia Syndrome Are Common and Diverse.
Journal of clinical neurology
2016; 12 (1): 75-78
Postural tachycardia syndrome (POTS) is a syndrome of orthostatic intolerance in the setting of excessive tachycardia with orthostatic challenge, and these symptoms are relieved when recumbent. Apart from symptoms of orthostatic intolerance, there are many other comorbid conditions such as chronic headache, fibromyalgia, gastrointestinal disorders, and sleep disturbances. Dermatological manifestations of POTS are also common and range widely from livedo reticularis to Raynaud's phenomenon.Questionnaires were distributed to 26 patients with POTS who presented to the neurology clinic. They were asked to report on various characteristics of dermatological symptoms, with their answers recorded on a Likert rating scale. Symptoms were considered positive if patients answered with "strongly agree" or "agree", and negative if they answered with "neutral", "strongly disagree", or "disagree".The most commonly reported symptom was rash (77%). Raynaud's phenomenon was reported by over half of the patients, and about a quarter of patients reported livedo reticularis. The rash was most commonly found on the arms, legs, and trunk. Some patients reported that the rash could spread, and was likely to be pruritic or painful. Very few reported worsening of symptoms on standing.The results suggest that dermatological manifestations in POTS vary but are highly prevalent, and are therefore of important diagnostic and therapeutic significance for physicians and patients alike to gain a better understanding thereof. Further research exploring the underlying pathophysiology, incidence, and treatment strategies is necessary.
View details for DOI 10.3988/jcn.2016.12.1.75
View details for PubMedID 26610893
Gastrointestinal dysfunction in postural tachycardia syndrome
JOURNAL OF THE NEUROLOGICAL SCIENCES
2015; 359 (1-2): 193-196
Postural tachycardia syndrome (POTS) is a dysautonomia defined by an exaggerated increase in heart rate upon changing posture. It is associated with disturbances involving multiple organ systems, including neurologic, dermatologic, and gastrointestinal (GI) symptoms. Previous studies identified GI complaints in these patients and showed gastric emptying and electrical activity abnormalities. However, the full spectrum of GI symptoms and their impact on quality of life remains unclear.A 30-question survey of GI symptoms was collected from 28 patients with POTS seen in the Boston Medical Center Autonomic Clinic. Answers were recorded on a Likert rating scale. Symptoms were positive if patients answered "strongly agree" or "agree" and negative if they answered "strongly disagree" or "disagree." Responses were collected and analyzed.The most commonly reported GI symptoms were nausea (86%), irregular bowel movements (71%), abdominal pain (70%), and constipation (70%). Additionally, 82% of patients reported having GI symptoms more than once per week, and 71% reported having seen a GI specialist, and symptoms did not improve with changes in position. Twelve patients had undergone a gastric emptying study, and six of these patients reported receiving a diagnosis of gastroparesis or delayed gastric emptying.GI disturbances are common, frequent, and prolonged in patients with POTS, likely impacting quality of life. Given the importance of the enteric nervous system to normal GI functioning, the same autonomic impairment leading to POTS may result in abnormal gut motility and ultimately subjective GI discomfort.
View details for DOI 10.1016/j.jns.2015.10.052
View details for Web of Science ID 000367276200036
View details for PubMedID 26671111
A survey-based analysis of symptoms in patients with postural orthostatic tachycardia syndrome.
Proceedings (Baylor University. Medical Center)
2015; 28 (2): 157-159
Postural orthostatic tachycardia syndrome (POTS) is a type of dysautonomia seen most commonly in young women and children. It is defined as an increase in heart rate of 30 beats per minute (bpm) or more within 10 minutes of standing in adults, or by 40 bpm or more in children in the absence of orthostatic hypotension. In addition to typical autonomic symptoms, POTS patients report a wide range of subjective complaints in multiple organ systems, though the exact frequencies are unclear. To address the symptom frequency, we had 39 patients with POTS at our institution complete an intake form consisting of a list of 37 symptoms. The most frequently reported symptoms included palpitations, lightheadedness, and headache, although sleep disturbances, gastrointestinal complaints, sensitivity to temperature, and rash were also common.
View details for PubMedID 25829642
Prokineticin 2 is an endangering mediator of cerebral ischemic injury
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
2012; 109 (14): 5475-5480
Stroke causes brain dysfunction and neuron death, and the lack of effective therapies heightens the need for new therapeutic targets. Here we identify prokineticin 2 (PK2) as a mediator for cerebral ischemic injury. PK2 is a bioactive peptide initially discovered as a regulator of gastrointestinal motility. Multiple biological roles for PK2 have been discovered, including circadian rhythms, angiogenesis, and neurogenesis. However, the role of PK2 in neuropathology is unknown. Using primary cortical cultures, we found that PK2 mRNA is up-regulated by several pathological stressors, including hypoxia, reactive oxygen species, and excitotoxic glutamate. Glutamate-induced PK2 expression is dependent on NMDA receptor activation and extracellular calcium. Enriched neuronal culture studies revealed that neurons are the principal source of glutamate-induced PK2. Using in vivo models of stroke, we found that PK2 mRNA is induced in the ischemic cortex and striatum. Central delivery of PK2 worsens infarct volume, whereas PK2 receptor antagonist decreases infarct volume and central inflammation while improving functional outcome. Direct central inhibition of PK2 using RNAi also reduces infarct volume. These findings indicate that PK2 can be activated by pathological stimuli such as hypoxia-ischemia and excitotoxic glutamate and identify PK2 as a deleterious mediator for cerebral ischemia.
View details for DOI 10.1073/pnas.1113363109
View details for Web of Science ID 000302294700073
View details for PubMedID 22431614
View details for PubMedCentralID PMC3325724