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.

Neurogenic pulmonary edema in subarachnoid hemorrhage: relevant clinical concepts

Background Subarachnoid hemorrhage (SAH) continues to be a condition that carries high rates of morbidity, mortality, and disability around the world. One of its complications is neurogenic pulmonary edema (NPE), which is mainly caused by sympathetic hyperactivity. Due to the complexity of the pathophysiological process and the unspecificity of the clinical presentation, it is little known by general practitioners, medical students and other health care workers not directly related to the neurological part, making the management of this chaotic condition difficult. This review aims to present recent evidence on clinical concepts relevant to the identification and management of NPE secondary to SAH. Main body of the abstract NPE is defined as a syndrome of acute onset following significant central nervous system (CNS) injury. Its etiology has been proposed to stem from the release of catecholamines that produce cardiopulmonary dysfunction, with this syndrome being associated with spinal cord injury, cerebrovascular disorders, traumatic brain injury, status epilepticus, and meningitis. NPE has long been considered a rare event; but it may occur more frequently, mainly in patients with SAH. There are two clinical presentations of NPE: the early form develops in the first hours/minutes after injury, while the late form presents 12–24 h after neurological injury. Clinical manifestations consist of non-specific signs of respiratory distress: dyspnea, tachypnea, hypoxia, pink expectoration, crackles on auscultation, which usually resolve within 24–48 h in 50% of patients. Unfortunately, there are no tools to make the specific diagnosis, so the diagnosis is by exclusion. The therapeutic approach consists of two interventions: treatment of the underlying neurological injury to reduce intracranial pressure and control sympathetic hyperactivity related to the lung injury, and supportive treatment for pulmonary edema. Short conclusion SAH is a severe condition that represents a risk to the life of the affected patient due to the possible complications that may develop. NPE is one of these complications, which due to the common manifestation of a respiratory syndrome, does not allow early and accurate diagnosis, being a diagnosis of exclusion. Therefore, in any case of CNS lesion with pulmonary involvement, NPE should be suspected immediately.

L-Theanine Protects Bladder Function by Suppressing Chronic Sympathetic Hyperactivity in Spontaneously Hypertensive Rat

Chronic sympathetic hyperactivity is known to affect metabolism and cause various organ damage including bladder dysfunction. In this study, we evaluated whether L-theanine, a major amino acid found in green tea, ameliorates bladder dysfunction induced by chronic sympathetic hyperactivity as a dietary component for daily consumption. Spontaneously hypertensive rats (SHRs), as an animal model of bladder dysfunction, were divided into SHR–water and SHR–theanine groups. After 6 weeks of oral administration, the sympathetic nervous system, bladder function, and oxidative stress of bladder tissue were evaluated. The mean blood pressure, serum noradrenaline level, and media-to-lumen ratio of small arteries in the suburothelium were significantly lower in the SHR–theanine than in the SHR–water group. Micturition interval was significantly longer, and bladder capacity was significantly higher in the SHR–theanine than in the SHR–water group. Bladder strip contractility was also higher in the SHR–theanine than in the SHR–water group. Western blotting of bladder showed that expression of malondialdehyde was significantly lower in the SHR–theanine than in the SHR–water group. These results suggested that orally administered L-theanine may contribute at least partly to the prevention of bladder dysfunctions by inhibiting chronic sympathetic hyperactivity and protecting bladder contractility.

Hypothyroidism Therapy

Hypothyroidism refers to the common pathological disorder of thyroid hormone deficiency. The successful therapy for hypothyroidism is levothyroxine (LT4) administration, which is the same as thyroxine but produced synthetically. Serum thyrotropin (TSH) normalization with LT4 replacement therapy in hypothyroidism is generally needed to restore a euthyroid state. The daily dose of thyroxine therapy depends on various factors, such as body weight, age, and severity. It also differs from hypothyroidism during pregnancy to congenital hypothyroidism. The presence of various comorbidities may exist such as myxoedema coma, coronary artery disease, obesity, anemia and COVID-19 which necessitate individualized treatment. LT4 intolerance manifested with sympathetic hyperactivity may appear during the first hours after the LT4 administration. It requires starting with very low doses of LT4 that should be increased gradually, and reaching normal TSH may take several months. The sympathetic hyperactivity may be attributable to the presence of uncorrected iron-deficiency anemia that worsens by the use of thyroid hormone.

Sympathetic hyperactivity in patients with hypertension: pathogenesis and treatment. Part II

The second part of the review considers different classes of drugs affecting blood pressure in increased activity of the sympathetic nervous system. Additional possibilities are discussed on how to reduce the negative effect of sympathetic hyperactivity on cardiovascular system and improve the prognosis.

Neuromodulation With Thoracic Dorsal Root Ganglion Stimulation Reduces Ventricular Arrhythmogenicity

Introduction: Sympathetic hyperactivity is strongly associated with ventricular arrhythmias and sudden cardiac death. Neuromodulation provides therapeutic options for ventricular arrhythmias by modulating cardiospinal reflexes and reducing sympathetic output at the level of the spinal cord. Dorsal root ganglion stimulation (DRGS) is a recent neuromodulatory approach; however, its role in reducing ventricular arrhythmias has not been evaluated. The aim of this study was to determine if DRGS can reduce cardiac sympathoexcitation and the indices for ventricular arrhythmogenicity induced by programmed ventricular extrastimulation. We evaluated the efficacy of thoracic DRGS at both low (20 Hz) and high (1 kHz) stimulation frequencies.Methods: Cardiac sympathoexcitation was induced in Yorkshire pigs (n = 8) with ventricular extrastimulation (S1/S2 pacing), before and after DRGS. A DRG-stimulating catheter was placed at the left T2 spinal level, and animals were randomized to receive low-frequency (20 Hz and 0.4 ms) or high-frequency (1 kHz and 0.03 ms) DRGS for 30 min. High-fidelity cardiac electrophysiological recordings were performed with an epicardial electrode array measuring the indices of ventricular arrhythmogenicity—activation recovery intervals (ARIs), electrical restitution curve (Smax), and Tpeak–Tend interval (Tp-Te interval).Results: Dorsal root ganglion stimulation, at both 20 Hz and 1 kHz, decreased S1/S2 pacing-induced ARI shortening (20 Hz DRGS −21±7 ms, Control −50±9 ms, P = 0.007; 1 kHz DRGS −13 ± 2 ms, Control −46 ± 8 ms, P = 0.001). DRGS also reduced arrhythmogenicity as measured by a decrease in Smax (20 Hz DRGS 0.5 ± 0.07, Control 0.7 ± 0.04, P = 0.006; 1 kHz DRGS 0.5 ± 0.04, Control 0.7 ± 0.03, P = 0.007), and a decrease in Tp-Te interval/QTc (20 Hz DRGS 2.7 ± 0.13, Control 3.3 ± 0.12, P = 0.001; 1 kHz DRGS 2.8 ± 0.08, Control; 3.1 ± 0.03, P = 0.007).Conclusions: In a porcine model, we show that thoracic DRGS decreased cardiac sympathoexcitation and indices associated with ventricular arrhythmogenicity during programmed ventricular extrastimulation. In addition, we demonstrate that both low-frequency and high-frequency DRGS can be effective neuromodulatory approaches for reducing cardiac excitability during sympathetic hyperactivity.