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This paper summarized the clinical experience of using the method of “returning fire to its origin” for treatment of paroxysmal sympathetic hyperactivity （PSH）. According to the causes and clinical characteristics of PSH， the author believes that the deficiency of kidney qi， and the loss of yin and yang are the basis of the pathogenesis of PSH. Fright causes qi to be chaotic as the triggering mechanism of PSH. The key mechanism of PSH is that the deficiency yang with upper manifestation， and the fire does not return to its origin. The treatment should be nourishing yin and astringing yang， by taking modified Yinhuo Decoction （引火汤） internally， and receiving warm moxibustion as the first choice externally with selected acupoints Guanyuan （CV 4）， Mingmen （GV 4）， and bilateral Yongquan （KI 1）； For prevention， attention should be paid to take care of stomach qi， support healthy qi， and cultivate original qi.
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Paroxysmal sympathetic hyperactivity (PSH) is a syndrome characterized by paroxysmal tachycardia, increased blood pressure, tachypnea, hyperthermia, profuse sweating, abnormal posture or dystonia. It occurs in diseases such as moderate to severe brain injury, cerebral hypoxia, hydrocephalus, brain tumor and encephalitis. At present, the etiology and pathogenesis are still unclear, and it is easy to be misdiagnosed as epilepsy clinically. This article reports a 43-year-old male patient with late-onset mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS) confirmed by genetic testing. During hospitalization, he suddenly developed episodic involuntary limb movements, profuse sweating, tachycardia, and arterial hypertension. He was initially diagnosed with symptomatic epilepsy, but long-term electroencephalogram monitoring showed no synchronized discharge, and he was given antiepileptic drugs. The treatment was also ineffective. Brain magnetic resonance imaging revealed a new lesion in the left insular and insular operculum. Dexmedetomidine, baclofen, and gabapentin were given to suppress sympathetic nerve excitability. Drugs were effective, so the diagnosis was corrected to PSH. There is no report of MELAS complicated with PSH in the previous literature. It is speculated that it may be related to the low clinical cognition of PSH. In this case, new lesions in the insula and insular operculum appeared during the onset of PSH, suggesting that may be related to the pathogenesis of PSH.
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Paroxysmal sympathetic hyperactivity (PSH) is mainly secondary to a variety of acquired brain injuries, with the highest incidence of traumatic brain injury. Multiple symptoms such as paroxysmal tachycardia, shortness of breath, hypertension, hyperthermia and dystonia can occur simultaneously and repeatedly. The pathophysiological mechanism of PSH is complex. At present, drug treatment is mainly used to control symptoms; however, the combined use of multiple drugs will bring different degrees of toxic and side effects to multiple organs such as liver, kidney and lung while inhibiting sympathetic excitement. This paper mainly reviews the recent advance in non-drug treatment of PSH after craniocerebral injury from 4 aspects: nutritional support, hyperbaric oxygen therapy, avoidance of adverse stimulation and family support to standardize the PSH comprehensive management, and reduce episodes in order to improve prognosis and provide reference for clinical treatment.
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Objective:To observe the clinical characteristics of paroxysmal sympathetic hyperactivity (PSH) in children with acute brain injury.Methods:The clinical characteristics, hospitalization data, hospitalization cost, and prognoses of 40 children with acute brain injury admitted to our hospital from June 2018 to June 2020 were retrospectively summarized. In addition, the differences of above data between children with PSH and children without PSH were comparatively analyzed.Results:Nine children were with PSH, with an incidence of 22.5%; five were with anti- N-methyl- D-aspartate receptor (NMDAR) encephalitis, two were with acute necrotizing encephalopathy, and two were with severe viral encephalitis. Thirty-one children were without PSH; five were with metabolic encephalopathy, 19 were with viral encephalitis, three were with anti-NMDAR encephalitis, one was with acute cerebral infarction, one was with primary central nervous system lymphoma, one was with acute necrotizing encephalopathy, and one was with severe closed head injury. The patients with PSH had significantly higher proportion of patients with anti-NMDAR encephalitis, significantly higher hospitalization cost, statistically longer duration of disorder of consciousness and hospital stays, and significantly lower Glasgow coma scale (GCS) scores at discharge than the patients without PSH ( P<0.05). Conclusion:PSH is common in children with acute brain injury; PSH can lead to a long period of disorders of consciousness, long hospital stays, high hospitalization cost, and poor prognosis, which causes an increase in family and social burdens.
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Objective@#To investigate the early diagnosis and treatment for burn complicated with severe paroxysmal sympathetic hyperactivity (PSH).@*Methods@#Medical records of patients with burn complicated with severe PSH, admitted to our department from April 2016 to March 2019 and meeting the inclusion criteria were analyzed retrospectively. There were 4 males and 1 female, aged 17 months to 39 years, with an average of (21±16) years. During occurrence of PSH, the vital signs of patients were routinely monitored and oxygen were given. Other treatment included central venous catheterization and infusion of electrolyte solution, infusion of plasma according to patients′ condition, use of opioid analgesics and benzodiazepine sedatives, physical cooling and drug cooling, and establishment or maintenance of artificial airway and use of ventilator. Heart rate was controlled below 120 beats per minute in adults and 140 beats per minute in children with comprehensive treatment dominated by analgesia and sedation. Besides, single or multiple vasoactive agents, even in large doses were used to maintain normal blood pressure of patients. The occurrence characteristics, time, and treatment outcome of PSH were analyzed.@*Results@#PSH happened rapidly, with a sharp increase in several minutes to dozens of minutes. Five patients were with symptoms such as high body temperature, shortness of breath, very fast heart rate, normal or elevated systolic blood pressure, hyperhidrosis, and dystonia at the onset. The symptoms occurred simultaneously or successively. According to the Clinical Feature Scale, the above-mentioned 6 indexes achieved the highest score of 3 points except of systolic blood pressure. Four patients showed dilated pupils and impaired consciousness. Among the patients, PSH occurred in the acute exudation stage in 3 patients, in the fluid reabsorption stage in 1 patient, and in the late repair stage in 1 patient. PSH of patients lasted for 3 hours to 12 days. The symptoms of 4 patients were effectively controlled, and 1 patient died of deterioration. No PSH occurred in the cured patients during follow-up of 3 to 14 months.@*Conclusions@#Burn complicated with PSH can occur at any time before wound repair and in patients with different injury conditions. The causes of PSH include sudden burn, persistent pain, fright and fear, strange environment, low blood volume, and other adverse stimuli, and PSH is more likely to occur in children with underdeveloped brain function. Intravenous infusion of analgesics sedatives, physical therapy and medication to lower body temperature, stabilizing blood pressure and respiration are effective measures to treat PSH. PSH should be distinguished from the common complications of burns, such as sepsis, cerebral edema, hyperpyretic convulsion, transfusion response, stress disorder, etc.
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Paroxysmal sympathetic hyperactivity (PSH) has a profound impact on the prognosis of patients suffering from brain injury, but the research on pathogenesis in relation to PSH is limited. In this paper, the etiologies of PSH, including traumatic brain injury, hypoxic brain injury, cerebrovascular-related brain injury, craniocerebral infection, anti-N-methyl-D-aspartate receptor encephalitis, and a number of rare etiological factors were reviewed. The epilepsy hypothesis, disconnection hypothesis and new-presented neuroendocrine hypothesis about the pathogenesis of PSH were introduced, so as to provide reference for further research on PSH.
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Paroxysmal sympathetic hyperactivity (PSH),which recognized in a subgroup of survivors of severe acquired brain injury,is a syndrome of simultaneous,paroxysmal transient increases in sympathetic (elevated heart rate,blood pressure,respiratory rate,temperature,sweating) and motor (posturing) activity.These symptoms are not specific and can occur in sepsis,epilepsy,malignant hyperthermia,hydrocephalus and many other complications,which is related to confused diagnosis and delayed treatment of PSH.In addition,Patients with PSH have prolonged ICU stays and added healthcare costs.This article discusses the pathophysiological mechanism,clinical diagnostic criteria,and current drug treament measures of PSH,so as to guide rapid diagnosis.
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Objective To discuss the clinical symptoms of severe traumatic cerebral injury patients with paroxysmal sympathetic hyperactivity (PSH). These patients were given positive and effective prevention and treatment to reduce complications in order to improve prognosis. Methods Twenty patients with PSH were selected from October 2010 to October 2014 and were analyzed by gender, age, diagnosis, clinical symptoms, laboratory and equipment inspection to summary the treatment experiences of such patients. Results Of the 20 patients,14 were males and 6 were females,with age of 22-65 (35.4±9.5) years. Sixteen patients underwent unilateral or bilateral intracranial hematoma and decompressive craniectomy,and 4 patients were given conservative treatment. PSH occurred in these patients within 1 week after cerebral injury or surgery. However, the elderly might occur in the course of a few weeks or even months later. Each patient' s seizure frequency and duration had no significant regular pattern. The frequency varied from one time in several days to several times one day. Seizure duration was generally less than half an hour. All of the patients underwent CT and MRI examinations and showed different parts of the brain injury. But the damage of the brain stem, corpus callosum, basal ganglia and lateral ventricles beside sympathetic overactivity could lead to the occurrence of PSH. Most of the patients had a good effect after active drug treatment and symptomatic therapy. Conclusions PSH often occurs in severe traumatic cerebral injury patients. The doctor should pay attention to PSH. Early active and effective prevention and treatment can improve the prognosis of patients with PSH.
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Objective To report secondary paroxysmal sympathetic hyperactivity in a patient with tuberculous meningitis and to review the diagnostic criteria, clinical features, possible pathogenesis and management of this condition. Methods The clinical data of a case with paroxysmal sympathetic hyperactivity secondary to tuberculous meningitis was retrospectively analyzed and related literature was reviewed. Results A 1-year-old boy was admitted to our institute with a history of lethargy and vomiting for 3 days. Neurological examination revealed abnormalities. A lumbar puncture revealed the evidence of meningitis. PPD test, T-SPOT.TB and radiological examination revealed tuberculous meningitis. Later, when stayed in the intensive care unit, he developed paroxysmal hypertension, sinus tachycardia, tachypnea, dystonia, and high fever. These episodes improved after administration of propranolol, benzodiazepines and artane. Conclusions Paroxysmal sympathetic hyperactivity is a rare manifestation of tuberculous meningitis, early recognition is very important for avoid misdiagnosis and overtreatment.
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Objective To study the clinical characteristics , treatment methods and prognosis of the paroxysmal sympathetic hyperactivity (PSH). Methods We comprehensively analyzed 48 patients diagnosed with PSH from the neurosurgery department of Changzheng Hospital in Shanghai using a prospective study design. The patients were divided into two groups according the treatments they received. In addition to general treatment and hyperbaric oxygen treatment , patients in group A were mainly given propranolol , gabapentin , and benzodiazepines combined therapy , and those in group B received hibernation therapy as controls. The clinical characters , case characteristic , and treatment effect after two weeks of treatment were recorded and compared. Glasgow Coma Scale (GCS) and Glasgow Outcome Scale (GOS) scores were used to evaluate the prognoses of patients after 12 months. Results The average age of the PSH patients was (27. 48+9. 62) years old , with the GCS score ' 8 at admission. The treatment group (group A) had a shorter hospitalization time ([206. 08 + 28. 57] d vs [223. 75 + 27. 74] d , P<0. 05) and a shorter episode time after two weeks7 treatment ([170. 08 + 79. 39] min vs [225. 63 + 105. 70] min , P< 0. 05) compared with the control group. Two patients in group A were lost in the 12 months follow-up. The GOS score of group A was significantly better than that of the control group (P<0. 05). The GCS scores were not significantly different between the 40 survived patients in the two groups (20 in each group). Conclusion PSH is commonly seen in young people suffering severe traumatic brain injury , who require early drug treatment. Propranolol combined with gabapentin treatment can improve the prognosis of patients , and t is superior to artificill hibernation by shortening hospitalization time and improving patient survival.