Paroxysmal Sympathetic Hyperactivity

2020 ◽  
Vol 40 (05) ◽  
pp. 485-491
Author(s):  
Rachael A. Scott ◽  
Alejandro A. Rabinstein

AbstractParoxysmal sympathetic hyperactivity (PSH) is a relatively common, but often unrecognized, complication of acute diffuse or multifocal brain diseases, most frequently encountered in young comatose patients with severe traumatic brain injury. It is presumed to be caused by loss of cortical inhibitory modulation of diencephalic and brain stem centers and possible additional maladaptive changes in the spinal cord that combine to produce exaggerated sympathetic responses to stimulation. The syndrome consists of repeated sudden episodes of tachycardia, tachypnea, hypertension, sweating, and sometimes fever and dystonic posturing. The diagnosis is clinical. Treatment includes reducing any external stimulation that can trigger the episodes, and starting abortive (e.g., intravenous morphine) and preventive medications (e.g., gabapentin, propranolol, clonidine). Prompt and adequate treatment of PSH may reduce the likelihood of secondary complications, such as dehydration, weight loss and malnutrition, and muscle contractures.

2015 ◽  
Vol 20 (4) ◽  
pp. 335-340
Author(s):  
Deborah S. Raithel ◽  
Kirsten H. Ohler ◽  
Isabel Porto ◽  
Alma R. Bicknese ◽  
Donna M. Kraus

Paroxysmal sympathetic hyperactivity (PSH) is a life-threatening condition characterized by hyperadrenergic activity and autonomic dysfunction. Also termed autonomic storms, PSH can occur after a variety of cerebral insults, most commonly traumatic brain injury. Limited pediatric literature is available, especially in patients with brain injury from hypoxia. No consensus exists for the terminology, diagnostic criteria, or treatment algorithm for PSH. Thus, the optimal management, including medication selection and dosing, remains unclear. We present the detailed treatment of a 9-year-old, African American male with hypoxic brain injury after pulseless arrest following status asthmaticus, who subsequently developed PSH. The patient began to experience episodes of tachycardia, hypertension, tachypnea, diaphoresis, rigidity, and dystonic posturing on hospital day 5. After ruling out other potential causes, a diagnosis of PSH was made. Episodes of PSH failed to respond to lorazepam or labetalol but were aborted successfully with morphine. Management of PSH after hypoxic brain injury required medications for acute treatment as well as for prevention of PSH. Morphine was found to be highly effective and safe for aborting the autonomic crises. Other agents more commonly described in the literature did not result in an adequate response and were associated with significant adverse effects. A combination of clonazepam, baclofen, and either propranolol or clonidine aided in reducing the frequency of episodes of PSH. We suggest using morphine for aborting severe episodes of PSH that do not respond to antihypertensive agents or benzodiazepines.


2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Min Li ◽  
Gang Zhu ◽  
Hao Guo ◽  
Shun Nan Ge ◽  
Guo Dong Gao ◽  
...  

AbstractBackgroundCerebral fat embolism (CFE) syndrome at high altitude was rare complicated with paroxysmal sympathetic hyperactivity (PSH) syndrome and septic shock. It is a challenge to differential diagnosis and treatment at high altitude.Case presentationThis case presents a CFE with PSH and septic shock of a 23-year-old man occurred at high altitude of 3800 m above sea level, transferred by airplane successfully and cured in the department of neurosurgery, Xi’an Tangdu Hospital.ConclusionsIt is key that CFE with PSH can be rapid diagnosed and treatment bundles of septic shock should be initiated as soon as possible. Early neurological rehabilitation played an important role for good outcome.


BJS Open ◽  
2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Stéphane Nguembu ◽  
Marco Meloni ◽  
Geneviève Endalle ◽  
Hugues Dokponou ◽  
Olaoluwa Ezekiel Dada ◽  
...  

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.


Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 613
Author(s):  
Katerina Stepankova ◽  
Pavla Jendelova ◽  
Lucia Machova Urdzikova

The spinal cord injury (SCI) is a medical and life-disrupting condition with devastating consequences for the physical, social, and professional welfare of patients, and there is no adequate treatment for it. At the same time, gene therapy has been studied as a promising approach for the treatment of neurological and neurodegenerative disorders by delivering remedial genes to the central nervous system (CNS), of which the spinal cord is a part. For gene therapy, multiple vectors have been introduced, including integrating lentiviral vectors and non-integrating adeno-associated virus (AAV) vectors. AAV vectors are a promising system for transgene delivery into the CNS due to their safety profile as well as long-term gene expression. Gene therapy mediated by AAV vectors shows potential for treating SCI by delivering certain genetic information to specific cell types. This review has focused on a potential treatment of SCI by gene therapy using AAV vectors.


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