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Paroxysmal sympathetic hyperactivity

Paroxysmal sympathetic hyperactivity
Literature review current through: May 2024.
This topic last updated: Aug 03, 2022.

INTRODUCTION — Paroxysmal sympathetic hyperactivity (PSH) is a disorder in the regulation of autonomic function most commonly observed in patients with acute brain injury, most notably severe traumatic brain injury (TBI) [1,2]. It manifests with recurrent episodes of excessive sympathetic activity that start rapidly, are often induced by stimulation, and resolve spontaneously after a variable period of time or after administration of an abortive medication.

PSH is important to recognize because, if untreated, PSH can persist and worsen over time, potentially resulting in serious complications [3]. In addition, when PSH is unrecognized, unnecessary testing and treatments for other conditions may result [4].

This topic discusses the clinical features, diagnosis, and treatment of PSH. Other aspects of severe TBI are discussed separately. (See "Management of acute moderate and severe traumatic brain injury" and "Traumatic brain injury: Epidemiology, classification, and pathophysiology".)

TERMINOLOGY — PSH is defined as a clinical syndrome manifested by paroxysmal episodes of sympathetic activity that occur in patients with severe acute brain injury [5]. Core clinical features include tachycardia, hypertension, tachypnea, hyperthermia, sweating, and/or increased muscle tone with possible dystonic posturing.

The condition now known as PSH has previously been referred to as autonomic storms, sympathetic storms, hypothalamic dysregulation syndrome, dysautonomia, paroxysmal autonomic instability with dystonia, and even diencephalic autonomic epilepsy (mischaracterizing the diagnosis because PSH is not epileptic in nature) [6,7]. In 2014, an international panel was convened to define the syndrome, its preferred nomenclature, and its diagnostic criteria [5]. PSH was chosen as the most appropriate name because it conveyed the main characteristics of the syndrome (sudden, episodic manifestations of sympathetic excess) and reflected the current understanding of its pathophysiologic mechanism (pure sympathetic hyperactivity) [5,8].

PATHOPHYSIOLOGY — The pathophysiology of PSH is incompletely understood. It is hypothesized that acute injury to the brain produces a disconnection between cortical inhibitory areas and lower sympathetic centers in the diencephalon (especially the hypothalamus), brainstem, and spinal cord. In theory, this disruption of the descending inhibitory modulation leads to exaggerated sympathetic responses to internal or external stimuli [1] and also produces maladaptive changes at the level of the spinal cord resulting in increased excitatory interneuronal activity [9,10]. As a consequence, non-noxious stimuli elicit excessive spinal cord responses and are misperceived as noxious at higher levels of the neuraxis [9].

The specific locations of the lesions responsible for disrupting the central sympathetic network are not well known. Because autonomic control is regulated by multiple cortical areas and subcortical structures, it is unlikely that a single focal lesion is responsible for the development of PSH. In fact, patients with PSH typically have diffuse or multifocal brain injury. Topographic associations with PSH on neuroimaging studies have been noted with diffuse axonal injury [11,12] as well as with lesions affecting the periventricular white matter, corpus callosum, diencephalon, midbrain, and pons [13,14]. Research using diffusion tensor imaging magnetic resonance imaging (MRI) has suggested that disconnection of the white matter tracts involving the posterior corpus callosum and posterior limb of the internal capsule may contribute to the pathogenesis of PSH [15].

High circulating catecholamine concentrations and, to a lesser degree, concentrations of adrenal hormones have been documented during episodes of PSH in patients with severe traumatic brain injury (TBI) [16].

EPIDEMIOLOGY

Associated conditions — PSH is most commonly described after brain trauma but can also occur after nontraumatic forms of acute brain disease, including anoxic-ischemic coma after cardiac arrest and intracranial hemorrhage [4,6,17].

Less commonly reported associations include autoimmune encephalitis, ischemic stroke, hydrocephalus, and cerebral fat embolism syndrome [4,6,8,17-20]. In isolated cases, fulminant multiple sclerosis, bacterial and tubercular meningitis, viral encephalitis, thalamic and fourth ventricular tumor, hypoglycemia, vasculitis, and postpartum vasoconstriction have been reported as the underlying condition [4,6].

Similar nonepileptic episodes have also been described in patients with juvenile neuronal ceroid lipofuscinosis, Rett syndrome, and Down syndrome, but it is not clear that the episodes in these nonacute conditions share the same pathogenesis or respond to the same treatments [21,22].

Incidence and risk factors

Traumatic brain injury (TBI) – The frequency of PSH in patients with TBI has been variably reported. Among different case series, it has been reported to occur in 10 to 20 percent, rarely as high as 30 percent, of patients with severe TBI [3,6,8,11,23-27]. These differences may be explained by the type of population included, the time of the assessment, the diagnostic criteria utilized for the diagnosis, and the clinical setting (intensive care unit [ICU] versus rehabilitation unit).

PSH occurs in both moderate and severe TBI, and the severity of TBI does not clearly correlate with the risk of PSH, although an association is suggested in some series [28,29]. Some studies suggest that PSH is more common in the setting of diffuse axonal injury [23,29,30]; one case-control study also identified intraventricular hemorrhage/subarachnoid hemorrhage and complete cisternal effacement on initial neuroimaging to be risk factors for PSH [30].

The frequency of PSH is reported to be higher in younger compared with older adults with TBI [1,4,8,11,24,29,31]; however, in pediatric series, adolescents with severe brain trauma may have a greater risk of developing PSH than younger children [25].

Hypoxic ischemic injury – PSH may be more prevalent in patients with anoxic-ischemic brain injury, and is reported in 30 to 38 percent of patients in some series, although these types of brain injuries are less common than TBI [31]. PSH after global brain anoxia-ischemia or encephalitis appears to be more common in pediatric patients [1,18].

CLINICAL FEATURES — PSH typically occurs in unresponsive patients with severe traumatic brain injury (TBI) and is manifested by repeated episodes in which a combination of symptoms occurs, the most common of which are [4,5,32]:

Tachycardia, usually sinus tachycardia, is almost invariably present.

Hypertension, especially systolic hypertension, is often associated with elevated pulse pressures.

Tachypnea is associated with hyperpnea and respiratory alkalosis.

Other common symptoms are:

Diaphoresis can be particularly dramatic and can rapidly lead to dehydration.

Hyperthermia is an inconsistent feature [4], but body temperature can be very high when it occurs [8].

Dystonic posturing is only observed with the most severe episodes and can be mistaken for a tonic seizure. When posturing occurs with PSH, it is typically symmetric.

Parasympathetic signs (bradycardia, hypotension) are characteristically absent during the episode.

The episodes have a rapid onset. They are most often triggered by external stimulation, such as endotracheal tube suctioning, loud noises, repositioning, and urinary retention, but they can also occur without apparent trigger [16].

The duration of each episode varies depending on its severity and the timing and efficacy of abortive treatment. When untreated, episodes can last for up to 20 to 30 minutes.

PSH may present in the acute care setting, as early as within the first day after brain injury, or may first be identified later during rehabilitation [4,6,11,18,25,28,33]. In one critical care series, the peak prevalence of PSH signs and symptoms occurred between days 9 and 13 [25]. A later timing of presentation may reflect a delay in clinical manifestations perhaps due to opiate or sedation administration during the acute hospitalization, a failure to recognize the syndrome during the acute hospitalization, or a delayed onset.

DIAGNOSIS — PSH is a clinical diagnosis. No test can confirm the diagnosis. Testing is indicated to exclude alternative diagnoses when deemed necessary, as discussed below. (See 'Differential diagnosis' below.)

A PSH Assessment Measure has been proposed to assist in the diagnosis of PSH (table 1) [5]. It consists of two components: a Clinical Feature Scale (to categorize the severity of the sympathetic signs for each episode) and a Diagnostic Likelihood Tool (to determine the presence of characteristics that increase the diagnostic certainty of PSH across episodes). The combination of these two components results in a score that reflects the confidence in the diagnosis of PSH as unlikely, possible, or probable. The Clinical Feature Scale is also used to monitor the severity of episodes over time, which in turn increases confidence in the diagnosis.

These tools have been validated in adult as well as pediatric populations, and there is some evidence that they may reduce the chances of misdiagnosis and favorably impact hospital length of stay and costs of hospitalization [11,25,34].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of PSH includes serious, even life-threatening neurologic and systemic complications [4,35]. However, PSH can usually be reliably recognized by experienced clinicians, thus avoiding expensive and potentially hazardous testing for alternative diagnoses. When testing is deemed appropriate, it should proceed expeditiously to avoid unnecessary and potentially harmful therapies and to allow early initiation of appropriate therapy [4].

The most commonly considered differential diagnoses include the following:

Pulmonary embolism (PE) is also associated with sudden onset of tachypnea and tachycardia. Also potentially life-threatening, it is important to promptly exclude PE, as acute anticoagulation can be dangerous in patients with hemorrhagic contusions or intracranial hematomas after traumatic brain injury (TBI).

The absence of severe hypoxia in PSH is a useful discriminating feature. Computed tomography (CT) angiography of the chest may be required to exclude PE in patients with PSH before a pattern of episodes is established. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism", section on 'Computed tomography pulmonary angiography'.)

Sepsis may complicate acute traumatic injury. While both sepsis and PSH can produce tachycardia, tachypnea, and elevated body temperature, sepsis is more typically associated with hypotension rather than the hypertension that is characteristic of PSH.

It may be appropriate to obtain cultures and initiate broad-spectrum antibiotics until infection is confirmed or excluded. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Symptoms and signs'.)

Elevated intracranial pressure and impending herniation are often suspected in this setting, although the Cushing triad (bradycardia, respiratory depression, and hypertension) classically associated with increased intracranial pressure is distinct from tachycardia and tachypnea that occur with PSH. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Clinical manifestations'.)

Emergency brain imaging, typically with noncontrast head CT, may be justified with the first episode of PSH when the likelihood of these complications is deemed high.

Tonic seizures can resemble PSH episodes, and both can be associated with tachycardia and hypertension. However, profuse diaphoresis and sustained tachypnea are not as often seen with seizures.

Electroencephalography (EEG) monitoring may be helpful if the diagnosis is uncertain. (See "Video and ambulatory EEG monitoring in the diagnosis of seizures and epilepsy".)

Acute painful episodes can produce symptoms similar to PSH and can also be a trigger for PSH. Clinicians should consider undiagnosed painful conditions (eg, fracture, painful spasticity, cholelithiasis, deep venous thrombosis, nephrolithiasis, constipation, and urinary retention) as possible alternative diagnoses as well as potential triggers for PSH to be mitigated, particularly if there is no identified trigger for PSH episodes [28].

Alcohol withdrawal can produce hypersympathetic signs and should also be included in the differential diagnosis. Tremor, agitation, and less paroxysmal onset are discriminating features.

TREATMENT — The treatment of PSH should include general care measures and pharmacologic therapy with abortive and preventive medications.

General and supportive care — Supportive measures in the acute setting include the following:

Reducing stimulation, especially those stimuli observed to trigger symptoms, can limit the occurrence of PSH episodes [36]. Sedation is appropriate, but not to the point that the patient can no longer be examined reliably. (See "Management of acute moderate and severe traumatic brain injury", section on 'Sedation and analgesia'.)

Hyperthermia should be treated with pharmacologic and mechanical measures, though it tends to be refractory and is most effectively controlled by treating the PSH itself. (See "Management of acute moderate and severe traumatic brain injury", section on 'Temperature management'.)

Hyperventilation during the episode (and the resulting hypocapnia) can be mitigated by ensuring that the patient is not receiving unnecessary pressure support and by aborting the episode as soon as possible.

Episodic tachycardia and hypertension are best addressed with a combination of abortive and preventive medications, as discussed below. Use of psychoactive medications typically prescribed for agitation is discouraged [26].

Over time, patients with PSH can develop dehydration, electrolyte imbalances, and contractures. Heterotopic ossification is another potential late complication. These complications are preventable with adequate monitoring and intervention (including intensive physiotherapy once limb mobilization no longer triggers PSH episodes) [37].

In addition, the increased metabolic demand created by the episodes of PSH requires adjustment of caloric intake (guided by indirect calorimetry) to prevent the development of malnutrition [37,38].

Other aspects of management in patients with severe traumatic brain injury (TBI) are presented separately. (See "Management of acute moderate and severe traumatic brain injury".)

Pharmacologic therapy — Episodes of PSH are treated with a combination of abortive and preventive medications [28,39,40]. The goal is to decrease the frequency and severity of episodes. Uncurtailed, episodes of increased sympathetic activity could pose a risk for end-organ damage (most notably in this setting, intracerebral hemorrhage).

The table shows a list of available options (table 2). Some medications, such as beta blockers and clonidine, can be used both as abortive and preventive drugs [39,41]. Others are best used as abortive only, such as morphine [39,41], or as preventive only, such as gabapentin [42].

The published evidence supporting specific pharmacologic interventions in PSH is limited to small cases series [1,5,8,23,43,44]. In our experience, these medications can be effective in reducing the frequency and severity of the episodes.

We often use intravenous morphine (starting dose 2 mg) to abort the episodes that last longer than a few minutes, along with gabapentin (starting dose 100 to 300 mg thrice daily) with a noncardioselective beta blocker (eg, propranolol, at a starting dose of 10 mg thrice daily) and/or clonidine at a starting dose of 0.1 mg twice daily to prevent recurrent episodes [1,4]. Frequent dose titrations of medications are often necessary over the initial days before good control is achieved. The use of these agents is frequently limited by hypotension. Benzodiazepines and baclofen can be helpful adjuncts in these cases; bromocriptine has also been reported to be useful as a preventive drug. Antidopaminergic drugs should be avoided. Dantrolene, a potent muscle relaxant, should be reserved for patients with refractory posturing resulting in muscle contractures.

Pharmacologic treatment should ideally be initiated in the intensive care unit (ICU) and maintained at least through the initial rehabilitation phase, and tapered slowly as symptoms resolve.

Although treatment, especially when promptly initiated, usually achieves adequate control of PSH, recalcitrant cases may occur. Refractoriness is more common among patients with anoxic brain injury and very severe diffuse axonal injury [1,4]. Intrathecal baclofen has been reported to be effective in one case series of patients with refractory PSH [45].

PROGNOSIS

Clinical course — The duration of the paroxysmal phase is variable [1]. According to one case series, the average duration of symptoms is between 18 to 162 days, with most cases resolving within a year [46].

In one study, sympathetic over-responsiveness to nociceptive stimuli was evident by testing several years after brain injury in patients who had otherwise recovered from clinically evident PSH [10]. The clinical significance of this observation is uncertain.

Outcomes and complications — In many but not all studies of adult patients with traumatic brain injury (TBI), PSH is associated with worse long-term functional outcomes [1,3,6,11,24,26,30,46-49]. PSH is also associated with worse prognosis in some studies of children [18,25,50] and in patients with anoxic brain injury [47]. More frequent and more severe episodes appear to worsen outcome [3,17,49]. Improvement of PSH over time in patients with acquired brain injury and disorders of consciousness is associated with greater chances of recovery of awareness [49]. The available data are insufficient to determine whether the association of PSH with worse functional outcomes is because PSH is a surrogate of more severe brain injury or due to a direct impact of PSH itself on prognosis. Some clinicians have noted residual dystonia and spasticity in many patients who have had PSH; however, other patients have recovered without sequelae. Furthermore, the risks of some delayed complications are increased with PSH, such as pronounced weight loss [38], joint swelling from heterotopic ossification [51], and muscle contractures; these may hamper rehabilitation efforts and impact functional outcomes.

In the short term, patients with PSH often have longer lengths of hospital stay [3,11,18,25,26,31,43,52], higher rates of tracheostomy and/or longer ventilator dependence [17,43], and a greater need for enteral feeding [50]. Infectious complications may also be more common in patients with PSH [24,43,51].

SUMMARY AND RECOMMENDATIONS

Definition – Paroxysmal sympathetic hyperactivity (PSH) is a serious but treatable complication of acute brain injuries, most commonly seen in adult patients with severe brain trauma. (See 'Terminology' above and 'Epidemiology' above.)

Clinical features – The clinical syndrome of PSH consists of recurrent episodes of tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, and dystonic posturing. The episodes have a rapid onset and are most often triggered by external stimulation. (See 'Clinical features' above.)

Diagnosis – The diagnosis of PSH is based upon the clinical features and setting. We suggest using the PSH Assessment Measure (table 1) to assist in the clinical diagnosis of PSH. (See 'Diagnosis' above.)

Differential diagnosis – The differential diagnosis includes intracranial hypertension, seizures, sepsis, and pulmonary embolism (PE). These can often be distinguished clinically, but sometimes evaluation is required until a pattern of episodes is established. (See 'Differential diagnosis' above.)

Supportive care – Minimizing stimulation may reduce the frequency and severity of episodes. Patients may also require adjustment of hydration, electrolyte replacement, and caloric intake to meet the increased losses from heightened metabolic demand. (See 'General and supportive care' above.)

Pharmacologic therapy – Pharmacologic interventions appear useful to abort and/or prevent or mitigate the PSH episodes.

We suggest intravenous morphine as needed along with gabapentin and clonidine, dosing titrated to effect (Grade 2C). Dosing and alternative therapies are provided in the table (table 2). The evidence supporting these interventions is largely anecdotal. PSH episodes may recur over several weeks, sometimes longer. (See 'Pharmacologic therapy' above and 'Clinical course' above.)

Outcomes – PSH is associated with worse prognosis for recovery in patients with severe traumatic brain injury (TBI), and also a higher likelihood of complications including tracheostomy, longer hospital stay, infections, and weight loss. (See 'Prognosis' above.)

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