Paroxysmal Sympathetic Storm Research Articles

P88 Paroxysmal sympathetic storm and the role of beta-blockers in traumatic brain injury: a scoping review protocol

IntroductionMost 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.MethodWe 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.ResultsThe 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.ConclusionAt 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.

Diencephalic Storms From Leptomeningeal Metastases and Leukoencephalopathy

Diencephalic storms or paroxysmal sympathetic storms are characterized by episodic hyperhidrosis, hypertension, tachypnea, tachycardia, and abnormal posturing. These have been reported to occur in patients with hydrocephalus, intracranial tumors, and hypoxic, ischemic, or traumatic brain injury. They can be easily misdiagnosed as seizures, uncontrolled pheochromocytoma, drug withdrawal, thyroid storm, hypertensive crises, and sepsis or anxiety attacks. The most effective treatment to control these symptoms is yet to be identified. We present 2 individuals exhibiting these sympathetic surges; one whose symptoms were controlled with phenobarbital and the other with clonidine and oxycodone. Palliative medicine physicians should be made aware of this unusual complication.

21-Year-Old Man With Chest Pain, Respiratory Distress, and Altered Mental Status

21-Year-Old Man With Chest Pain, Respiratory Distress, and Altered Mental Status

Morphine-Sensitive Paroxysmal Sympathetic Storm in Pontine Intracerebral Hemorrhage

Paroxysmal sympathetic storm (PSS) is a rare complication of severe traumatic brain injury or cerebrovascular disease. Various medications have been tried in patients with PSS, but the clinical responses of the patients were variable. We report a classic case of PSS after spontaneous pontine hemorrhage in which the patient's fluctuating blood pressure and body temperature were dramatically stabilized using morphine.

Susceptibility weighted imaging in a patient with paroxysmal sympathetic storms

Susceptibility weighted imaging in a patient with paroxysmal sympathetic storms

A combined clinical and MRI approach for outcome assessment of traumatic head injured comatose patients

Traumatic brain injury (TBI) is associated with substantial consumption of health care resources. No clinical or paraclinical examination can reliably predict neurological evolution. In this study, we evaluated the ability of a combined clinical and MRI approach to predict outcome. This prospective study took place between June 2001 and March 2005 in a Neurosurgical Intensive Care Unit in Paris, France. Inclusion criteria were TBI patients still mechanically ventilated and without clinical signs of awareness after 2 weeks. Four clinical signs were assessed after cessation of sedation: grasping, yawning, chewing and paroxysmal sympathetic storm. FLAIR and T2* acquisitions on MRI were used in order to localize brain lesions. Statistically linked regions (clusters) were defined. Outcome was assessed at one year by Glasgow Outcome Scale (GOS). 73 patients were included: 41 had poor outcome (GOS 1-3) and 32 had good outcome (GOS 4-5). Lesions in the clusters "right upper pons and right lower midbrain"," hypothalamus and basal forebrain","left parietal, left temporal, left occipital lobes and left insula" and the presence of grasping or chewing were associated with poor outcome in multivariate analysis. This combined clinical and MRI approach gives a much better prediction than MRI approach only (P < 0.009), with an area under the ROC curve of 0.94 (95 % CI, 0.89-1.00). These data suggest that MRI associated with clinical assessment improves outcome prediction in severe TBI patients.

The excitatory:inhibitory ratio model (EIR model): An integrative explanation of acute autonomic overactivity syndromes

Numerous medical conditions present with acute and severe autonomic and muscular overactivity. These syndromes include Neuroleptic Malignant Syndrome, Serotonin Syndrome, Dysautonomia (or paroxysmal sympathetic storms) following acquired brain injury, Autonomic Dysreflexia, Parkinsonian-Hyperpyrexia Syndrome, Malignant Catatonia, intrathecal baclofen withdrawal, Malignant Hyperthermia, Stiff Man Syndrome and Irukandji Syndrome. In their worst forms, each of these syndromes are relatively rare, are treated by different medical specialties and show widely varying pathophysiology. Most are considered to be medical emergencies and share significant mortality rates. Previous authors have noted similarities between some of these conditions, prompting the suggestion that a single common mechanism may underlie their clinical presentation. However, the development of such an integrative model has not occurred. This paper presents a short review of the clinical syndromes, grouped by the location of pathology and mechanism of action. From this background, an integrative framework termed the excitatory:inhibitory ratio (EIR) model is presented. The EIR model consists of two inter-related networks operating at spinal and brainstem levels. The model is evaluated against pre-clinical scientific research, known pathways, each disorder's pathophysiology (where this is known) and variable severity, and used to explain the reasons behind the efficacy of current treatment regimes. Circumstantial evidence for an expanded aetiology for Malignant Hyperthermia is provided and generic treatment strategies for a number of other conditions are suggested. Finally, minor modifications to this model provide a basis to begin to explain less severe, regional "overlap" syndromes.

Paroxysmal sympathetic surge associated with gamma hydroxybutyrate

Gamma hydroxybutyrate is increasingly being used recreationally in the United Kingdom. We present a case of gamma hydroxybutyrate overdose associated with paroxysmal sympathetic storm, a phenomenon usually confined to patients who have sustained traumatic brain injury.

Paroxysmal Sympathetic Storm

Paroxysmal sympathetic storm (PSS) is a rare syndrome characterized by episodic hypertension, hyperhydrosis, hyperthermia, tachycardia, tachypnea, and extensor posturing. This article describes two cases of PSS: one following traumatic brain injury and the other following cardiac arrest. The first responded to labetalol, morphine, and codeine, whereas the second responded to labetalol. These observations underscore the importance of central opioid receptors and nonselective beta-adrenergic antagonists in modulating catecholamine pathways.

Acute hypothalamic instability in traumatic brain injury: A case report

Thorley RR, Wertsch JJ, Klingbeil GE. Acute hypothalamic instability in traumatic brain injury: a case report. Arch Phys Med Rehabil 2001;82:246-9. Acute hypothalamic instability occurs in patients with traumatic brain injury (TBI). It usually occurs in the form of autonomic dysfunction syndrome (also known as diencephalic seizures or paroxysmal sympathetic storms); however, there are other causes of acute hypothalamic instability of which the clinician must be aware. Neuroleptic malignant syndrome, malignant hyperthermia, autonomic dysfunction syndrome, and lethal catatonia are all syndromes that clinically present as signs and symptoms of acute hypothalamic instability. Because of the lethal potential of these syndromes, clinicians who care for patients with TBI must be aware of the various syndromes, their clinical presentation, and their treatment. We present a case of life-threatening acute hypothalamic instability in a patient with TBI.

Paroxysmal sympathetic storms ("diencephalic seizures") after severe diffuse axonal head injury.

Paroxysmal sympathetic storms ("diencephalic seizures") after severe diffuse axonal head injury.

Paroxysmal Sympathetic Storms (“Diencephalic Seizures”) After Severe Diffuse Axonal Head Injury

We describe a patient with a severe traumatic head injury who exhibited paroxysmal sympathetic storms, similar to those described in "diencephalic seizures." No epileptiform activity was evident on electroencephalography, and therapeutic levels of anticonvulsants failed to alter the spells; however, use of morphine sulfate abolished them. The features of this and several previously reported cases refute the primary roles of the diencephalon and seizures in this syndrome. Rather, in the setting of already compromised autonomic neuronal integrity, subtle fluctuations in intraventricular pressure or activation of reflexes triggered from muscle mechanoreceptors or chemoreceptors during episodes of hypertonia are more likely. "Paroxysmal sympathetic storms," a more appropriate descriptive term for these phenomena, should be recognized; thus, unnecessary diagnostic evaluations can be minimized, and appropriate therapy can be initiated.