Paroxysmal Sympathetic Hyperactivity in Patients Victims of Traumatic Brain Injury. Literature Review

The present literature review aims to present the physiology of paroxysmal sympathetic hyperactivity (PSH) as well as its clinical course, conceptualizing them, and establishing its diagnosis and treatment. Paroxysmal sympathetic hyperactivity is a rare syndrome, which often presents after an acute traumatic brain injury. Characterized by a hyperactivity of the sympathetic nervous system, when diagnosed in its pure form, its symptomatologic presentation is through tachycardia, tachypnea, hyperthermia, hypertension, dystonia, and sialorrhea. The treatment of PSH is basically pharmacological, using central nervous system suppressors; however, the nonmedication approach is closely associated with a reduction in external stimuli, such as visual and auditory stimuli. Mismanagement can lead to the development of serious cardiovascular and diencephalic complications, and the need for neurosurgeons and neurointensivists to know about PSH is evident in order to provide a fast and accurate treatment of this syndrome.

Cerebral Vasospasm: Mechanisms, Pathomorphology, Diagnostics, Treatment

Cerebral vessels constriction is one of the leading causes of mortality and disability in patients with acute cerebral circulatory disorders. The most dangerous type of acute cerebrovascular disease accompanied by high mortality is ruptured cerebral aneurysms with subarachnoidal hemorrhage (SAH). Following a constriction of the cerebral vessels on the background of SAH is the reason for brain ischemia. This chapter will focus on the mechanisms of formation of cerebral vascular spasm, pathomorphological aspects of the cerebral vessels constriction, and the stages of vascular spasm—the development of constrictive-stenotic arteriopathy, contractural degeneration of smooth muscle cells, and endothelial damage. We will cover classifications of cerebral vessels constriction by prevalence and severity, modern methods of clinical and instrumental diagnostics and treatment including paroxysmal sympathetic hyperactivity syndrome associated with the development of secondary complications, a longer stay of the patients in the ICU, higher disability and mortality.

Etiologies and Mechanisms of Ischemic Stroke Associated with Sexual Intercourse: A Literature Review

<b><i>Background:</i></b> Exposure to some special events, also called stroke triggers, can precipitate the onset of ischemic stroke (IS). Previous studies have presented preliminary hypotheses about sexual intercourse as a trigger of IS in predisposed individuals, but the mechanisms of IS associated with sexual intercourse are still not well defined. This literature review summarizes the etiologies and mechanisms of IS associated with sexual intercourse. Further studies on stroke triggers are warranted, and early recognition and appropriate preventive strategies directed against the short-term risks posed by stroke triggers may complement the long-term risk factor reduction approach. <b><i>Methods:</i></b> Articles were selected from PubMed (1946–2021) and Web of Science Core Collection (1990–2021) using the following search terms: ischemic stroke, ischaemic stroke, stroke, cerebral infarction, cerebral ischemia, cerebral embolism, embolism, sexual intercourse, sexual activity, intercourse, coitus, coition, and coital. <b><i>Results:</i></b> A total of 20 studies, which included 26 patients with IS associated with sexual intercourse, were included. This literature review found that IS associated with sexual intercourse is not rare but has not received enough attention, and paradoxical embolization and postcoital arterial dissection are common etiologies. Other etiologies include drug usage (such as sexual adjuvant drugs and illicit drugs), paroxysmal sympathetic hyperactivity, and reversible cerebral vasoconstriction syndrome. <b><i>Discussion/Conclusion:</i></b> Sexual intercourse should be considered an important trigger for IS. Clinicians should be aware that IS associated with sexual intercourse is not subjective but may be a warning sign of multiple etiologies and mechanisms.

Paroxysmal Sympathetic Hyperactivity in Moderate-to-Severe Traumatic Brain Injury and the Role of Beta-Blockers: A Scoping Review

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. Methods. We searched MEDLINE, ResearchGate, and Google Scholar, for keywords related to PSH and the role of beta-blockers in moderate-to-severe TBI on September 23, 2020. Two authors blindly screened the articles found with Rayyan. Both resolved their conflicts by mutual consent. If no solution was found, a third author was consulted. Simple descriptive data analysis was performed and the results were presented both in a narrative and tabular form. Results. Of the 19 items found, 10 met the criteria for inclusion. 50% were systematic reviews without meta-analysis, 40% were observational studies, and 10% were experimental studies. Propranolol was the main beta-blocker found in 80% of the studies and was the only molecule used in the treatment of paroxysmal sympathetic hyperactivity in 40% of the included studies. Only two studies evaluated and showed a significant association between beta-blockers and mortality rate (5.1% vs. 10.8%; P = 0.03 ), (3% vs. 15%; P = 0.002 ), respectively. Conclusion. Propranolol is the beta-blocker that has been shown to be effective in reducing the length of stay and mortality rate in moderate-severe traumatic brain injury patients with PSH. However, further studies are needed to precisely define the terms and conditions of its use.