Symptoms Of Paroxysmal Sympathetic Hyperactivity Research Articles

Ca lâm sàng: Cơn cường giao cảm kịch phát sau đột quỵ nhồi máu não cấp

Background: Paroxysmal sympathetic hyperactivity (PSH) may occur after acute ischemic stroke. The clinical presentation of PSH results from increased sympathetic overdrive, including transient paroxysms of tachycardia, hypertension, hyperventilation, hyperthermia, dystonic posturing, and excessive sweating. The exact pathophysiology of PSH, however, remains unclear, and no definitive treatment is available. Case presentation: Herein, the authors report a case of PSH in a female patient who experienced an acute ischemic stroke, for which a good clinical outcome. An 88-year-old woman was admitted to 108 Military Central Hospital. She had a Glasgow Coma Scale (GCS) score of 9 (M4V2E3), right hemiplegia, NIHSS score of 29. At admission, computed tomography revealed a reduction in the density of the left hemisphere, the blood supply area of the left middle cerebral artery (ASPECT 2 points). 12 days after ischemic stroke, the patient was diagnosed with PSH based on PSH-AM score (19 points). Morphine, gabapentin, and baclofen were administered; the drug effect was sufficient. 17 days poststroke, the patient gradually recovered from the adrenergic symptoms of PSH, and head computed tomography performed 12 days after stroke revealed improvement. Ultimately, the patient recovered with GCS score of 12 (M5V3E4), NIHSS score of 16, and lived at home. Conclusion: The outcome of the present case demonstrates that PSH can be reversed if it is identified early and before it becomes irreversible, that is, post the development of hypoxic encephalopathy or hemorrhagic transformation in ischemic stroke. * Keywords: Paroxysmal sympathetic hyperactivity; Acute ischemic stroke.

Effectiveness of Pharmacological Agents and Validation of Diagnostic Scales for the Management of Paroxysmal Sympathetic Hyperactivity in Hispanics.

The identification and treatment of paroxysmal sympathetic hyperactivity (PSH) still present a significant challenge. We assessed the efficacy of pharmacological agents in treating PSH symptoms and the validity of the diagnostic scales in a cohort of Hispanic patients. A retrospective chart review of cases from a single hospital was conducted in 464 records. Exclusion criteria included underlying conditions such as severe infection. Only nine patients remained in the cohort after examining their clinical records, corresponding to the following diagnoses: traumatic brain injury, subdural hemorrhage, anoxic or ischemic encephalopathy, pneumocephalus, and cerebral palsy. Using the PSH likelihood scale, six of the nine patients were identified with a score of 17 or higher, corresponding to a “probable” PSH, and three patients obtained a score between 8 and 16, corresponding to a “possible” PSH diagnosis. The top three classes of medications used were beta-blockers, antipyretics, and opioids. Benzodiazepines and neuromodulators were also frequently used in patients with trauma, but not in the ones with non-traumatic injuries. Interestingly, 75% of the patients have prescribed levothyroxine as a home medication after the PSH presentation. Medication administration did not follow a specific pattern, suggesting high variability in the management of PSH within our setting, requiring further research. Our results suggest that the pituitary axis might be involved in the progression of PSH. Establishing a specific medical code (e.g., ICD-10) describing PSH as a single entity is essential for appropriate identification and management.

Risk factors and clinical features of paroxysmal sympathetic hyperactivity after spontaneous intracerebral hemorrhage.

Paroxysmal sympathetic hyperactivity (PSH) is a rare complication of spontaneous intracerebral hemorrhage (ICH).We aimed to evaluate the risk factors and clinical features for PSH after ICH. From January 1, 2013 to April 1, 2018, patients with ICH were consecutively included in this observational study. Baseline characteristics were compared in patients with and without PSH. Multivariate logistic regression analysis was used to determine the risk factors associated with PSH development. Clinical features of patients with PSH were also analyzed. There were 548 patients with ICH included and a total of 15 (2.7%) patients were identified with PSH. In univariate analysis, PSH development was associated with the following: previous hemorrhagic stroke, pupils abnormity, admission Glasgow Coma Scale (GCS) score, hematoma volume, liver function abnormity, neutrophil count and early tracheostomy. Multivariate logistic regression analysis showed that a significantly increased risk of PSH was found in patients with previous hemorrhagic stroke (odds ratio [OR], 4.176; 95% confidence interval [CI], 1.111-15.698), admission GCS score (OR, 0.703; 95% CI, 0.548-0.902) and early tracheostomy (OR, 8.317; 95%CI, 1.755-39.412).The most common symptoms of PSH were hyperthermia (80%) and hyperhidrosis (80%).The median Intensive Care Unit stays and Glasgow Outcome Scale at discharge were 34 (19-46) and 2 (1.5-3), respectively. PSH is characterized by a cluster of symptoms and abnormal vital signs, which may lead to poor outcomes in ICH. The present study suggests that previous hemorrhagic stroke, admission GCS score and early tracheostomy may be the significant risk factors for PSH after ICH.

限局性脳梁血腫を伴った外傷性脳損傷の経過中にparoxysmal sympathetic hyperactivityを呈した1例(Paroxysmal sympathetic hyperactivity during follow–up for traumatic brain injury with hematoma localized in the corpus callosum: a case report)

要旨 paroxysmal sympathetic hyperactivity（PSH）は重症頭部外傷，低酸素脳症などに起こり，交感神経系が発作性に過活動になる病態である。また，鈍的頭部外傷による限局した脳梁血腫は稀有であるが，その経過においてPSHを呈した症例は我々の知る限りでは報告されていない。症例は16歳の男性で，ロードバイクで下り坂を走行中に対向の軽自動車と正面衝突し，救急搬送となった。第3病日の頭部CTにおいて，限局した脳梁血腫が顕在化した。第7病日から間欠的に40℃台の高熱，頻脈，頻呼吸，発汗，全身の震え，瞳孔散大などの交感神経亢進症状が出現した。第9病日より，PSHを疑いガバペンチン投与を開始。交感神経亢進症状は徐々に鎮静化した。その後，意識レベルは改善し，第54病日に独歩退院した。PSHは外傷性脳損傷（traumatic brain injury: TBI）における，集中治療室（intensive care unit: ICU）滞在期間長期化のリスク因子であり，PSHの病態において，大脳深部損傷との関連があるという報告もある。脳梁損傷のような大脳深部損傷に交感神経亢進症状が発作的に出現する場合はPSHを疑い，治療を早期に開始することが予後改善のために重要であり，治療法の1つとして，ガバペンチンが有効である可能性がある。

Influence of paroxysmal sympathetic hyperactivity (PSH) on the functional outcome of neurological early rehabilitation patients: a case control study

BackgroundParoxysmal Sympathetic Hyperactivity (PSH) is a frequently observed condition among critically ill patients on intensive care units. According to different studies, PSH is associated with worse recovery and increased mortality in acute-care facilities. In this monocentric, retrospective case-control study, we investigated whether this association also applies to post-acute neurological early rehabilitation.MethodsThe study included n = 387 patients, admitted to an intensive care or intermediate care unit within 1 year (2016). Among these, 97 patients showed clinical signs of PSH. For each patient with PSH, a patient without PSH was identified, controlling for age, gender, functional and respiratory status upon admission. However, for 25 patients with PSH, there was no suitable control patient fulfilling all defined matching criteria. Primary outcome was type of discharge, dichotomized into favorable (follow-up rehabilitation) and unfavorable outcome (all others). Secondary outcome measures were functional and respiratory status, number of secondary diagnoses, duration of treatment interruptions and length of stay at discharge.ResultsAbout 25% of neurological early rehabilitation patients showed clinical signs of PSH. A young age (OR = 0.94; CI = 0.91–0.97) and less severe PSH symptoms (OR = 0.79; CI = 0.69–0.90) were independent predictors of a favorable outcome. In addition, severity of PSH symptoms was associated with weaning duration, while the occurrence of PSH symptoms alone had no influence on most secondary outcome variables. The treatment on intermediate care units proved to be longer for patients with PSH symptoms, only.ConclusionsPatients with PSH represent a large group of neurological early rehabilitation patients. Overall, we did not find PSH-related differences in most of the examined outcome measures. However, severe PSH symptoms seem to be associated with poorer outcome and longer treatment on intermediate care units, in order to prevent possible complications.

Heart Rate Variability Among Children With Acquired Brain Injury.

ObjectiveTo find evidence of autonomic imbalance and present the heart rate variability (HRV) parameters that reflect the severity of paroxysmal sympathetic hyperactivity (PSH) in children with acquired brain injury (ABI).MethodsThirteen children with ABI were enrolled and age- and sex-matched children with cerebral palsy were selected as the control group (n=13). The following HRV parameters were calculated: time-domain indices including the mean heart rate, standard deviation of all average R-R intervals (SDNN), root mean square of the successive differences (RMSSD), physical stress index (PSI), approximate entropy (ApEn); successive R-R interval difference (SRD), and frequency domain indices including total power (TP), high frequency (HF), low frequency (LF), normalized HF, normalized LF, and LF/HF ratio.ResultsThere were significant differences between the ABI and control groups in the mean heart rate, RMSSD, PSI and all indices of the frequency domain analysis. The mean heart rate, PSI, normalized LF, and LF/HF ratio increased in the ABI group. The presence of PSH symptoms in the ABI group demonstrated a statistically significant decline of the SDNN, TP, ln TP.ConclusionThe differences in the HRV parameters and presence of PSH symptoms are noted among ABI children compared to an age- and sex-matched control group with cerebral palsy. Within the ABI group, the presence of PSH symptoms influenced the parameters of HRV such as SDNN, TP and ln TP.

症状変化を繰り返したparoxysmal sympathetic hyperactivityの1例(A case of paroxysmal sympathetic hyperactivity with fluctuation of symptoms)

要旨paroxysmal sympathetic hyperactivity（PSH）は重症頭部外傷など重症頭蓋内傷病後に発作的な交感神経過緊張症状を起こす病態である。発作の症候や強度の変化を繰り返す経過は報告されていない。症例は30代男性で重症頭部外傷に対する低体温療法終了後に高熱，頻脈，頻呼吸，大量発汗など発作的な交感神経過緊張症状と筋緊張亢進を認め，感染症を疑い治療したが，炎症反応陰性化後も含め10日にわたり症状が持続した。その後も第28病日からの5日間と第43病日からの3日間に典型的なPSH症状期を計3回繰り返し，間欠期は大量発汗と筋緊張のみが持続するという特異な経過をたどった。感染など鑑別すべき病態が否定され診断基準に合致したためPSHと診断した。PSHでは発作症状期と間欠期を繰り返し，間欠期には発作症状の一部のみが持続する経過がありうる。大量発汗など交感神経過緊張症状の一部が続く場合には他の病態を否定したのちにPSHを積極的に疑い診断，治療を試みるべきである。

Paroxysmal sympathetic hyperactivity in severe traumatic brain injury.

Paroxysmal sympathetic hyperactivity (PSH) is a less-known complication of traumatic brain injury (TBI). This study was done to assess the clinical features and outcome of patients who develop PSH following severe TBI. A prospective observational study was done on patients, admitted in the intensive care unit, for treatment of severe TBI. The clinical characteristics and outcome of patients, with and without PSH, was compared. At the time of discharge, patients were assessed with the Disability Rating Scale (DRS), and at 6months with the Glasgow Outcome Score Extended (GOSE). The incidence of PSH was 8% (29/343). Tachycardia, hypertension, and sweating were seen in all of the patients. Tachypnea was seen in 24 (82.8%), hyperthermia in 28 (96.6%), and posturing in 13 (44.8%) patients. Thirteen (44.8%) patients had all six symptoms of PSH. Follow-up data were available for 23 (79.3%) patients. At the end of 6months, 14 (60.9%) patients had died, seven (30.4%) were severely disabled, and two (8.7%) were moderately disabled. There was a significant correlation of GOSE with the number of symptoms of PSH (Spearman's rho = 0.502, p = 0.015). The patients with PSH had significantly higher DRS scores at discharge, 25.3 vs. 19.9, p < 0.001; higher mortality at 6months 60.9 vs. 30.4%, p < 0.001; and higher proportions with unfavorable outcome. Presence of PSH in patients with severe TBI was associated with prolonged hospital stay, poorer DRS at discharge, more deaths, and unfavorable outcome. The number of symptoms of PSH had a significant effect on outcome at 6months.

Pharmacologic Management of Paroxysmal Sympathetic Hyperactivity After Brain Injury.

Paroxysmal sympathetic hyperactivity (PSH) is a result of acute brain injury that has been well known for many decades. However, the evidence for management of PSH is almost entirely anecdotal in nature. We reviewed case reports or series of pharmacotherapy management of PSH. These studies mentioned treatment options, but few studies exist to guide treatment strategies. For many years, the syndrome was not clearly understood; therefore, the therapy has focused on control of symptoms. In 2014, a Steering Committee came together to develop a conceptual definition and produced a consensus set of diagnostic criteria. Although understanding the diagnostic criteria is very well needed in management of patients with PSH, pharmacologic management is also crucial. Data describing the drug choices, dosing, and duration of therapy are also sparse. Recognition of appropriate medications is important because PSH is associated with morbidity, longer hospitalization, delaying transfer to rehabilitation units, and increasing cost. In this review article, we discussed the common medications used in the treatment of PSH. Treatment should target symptom abortion, prevention of symptoms, and refractory treatment. Symptom-abortive medications are indicated to control discrete breakthrough episodes, using medications such as morphine and short-acting benzodiazepines. Other medications used for prevention of symptoms and refractory treatment include long-acting benzodiazepines, nonselective β-blockers, α2 agonists, opioids, and GABA agonists. The mechanisms by which these agents improve symptoms of PSH remain speculative. However, a combination of medications from different classes seems the most effective approach in managing PSH symptoms. There is wide variability in clinical practice with regard to drug choices, dosing, and duration of therapy. Future research needs to be conducted using the new PSH assessment measure to appropriately apply drug management.

Management of Severe Paroxysmal Sympathetic Hyperactivity Following Hypoxic Brain Injury.

Dear Editor, Paroxysmal sympathetic hyperactivity (PSH) is the autonomic dysfunction characterized by tachypnea, tachycardia, hypertension, hyperthermia, sweating and motor features such as dystonia. It is the leading cause of higher morbidity and mortality in an intensive care unit setting. The main etiologic factors of PSH are traumatic brain injury (79%), hypoxic ischemic encephalopathy (10%) and stroke (1, 2). Presence of hypoxia, diffuse axonal injury and younger age facilitates the development of PSH (3). Treatment of PSH is comprised of reducing sympathetic and motor hyperactivity. Opioids, gabapentin, benzodiazepines, bromocriptin, β-blockers and centrally acting α2-agonists are recommended (1, 4). We described our management for a case of severe PSH, which occurred after hypoxic brain injury, and orally administered baclofen is effective in motor symptoms of PSH, contrary to that reported before (1). A 19-year-old boy with a history of hypoxic brain injury due to cardiopulmonary resuscitation after a thoracic penetrating trauma was admitted to our intensive care unit. He was unconscious and the Glasgow Coma Score was 5/15; thus, informed consent was obtained from his parents. He experienced episodes of increased body temperature (>38.5°C), blood pressure (>140/90 mmHg), heart rate (>100 m−1) and respiration rate (>35 m−1) with decerebrate posturing and excessive sweating. Morphine 2 mg intravenous (IV), dexmedetomidine 1 μg kg−1 h−1 IV infusion and remifentanil 0.5 μg kg−1 h−1 IV infusion were administered during episodes; symptoms were controlled for a while, but not totally. On the other hand, blood, tracheal aspirate and urine sample cultures were collected and appropriate antibiotics were administered. Blood leukocyte count, CRP and procalcitonin values decreased following antibiotherapy; however, fever could not be controlled despite antipyretic therapy (such as paracetamol and metamizole). Moreover, liver enzymes were increased; therefore, antipyretic drugs were stopped and intravenous cooling was performed by the Alsius Coolgard 3000®, USA. Fever was controlled, but tachypnea, tachycardia, hypertension and extensor contractions were persistent. In PSH cases that were managed in our clinic before, we observed limited episodes, including one extremity or one half of the body on the opposite side of the lesion and one half of the head on the lesion side. In this case, episodes occurred in the whole body, including four extremities and the head. We used β-blocker propranolol (160 mg d−1) and α2-agonist clonidine (0.2 mg d−1); thus, the frequency and the intensity of sympathetic episodes were diminished. It is suggested that baclofen cannot cross the blood-brain barrier efficiently when administered orally (5). Although it has been reported that oral baclofen is ineffective to treat motor spasticity in PSH, we observed that the intensity of spasticity was reduced from the Modified Ashworth Scale (MAS) 5 to MAS 2 following oral baclofen therapy (90 mg d−1) (1, 5). In conclusion, β-blocker treatment is efficient in cases that present only sympathetic hyperactivity. In severe cases like our patient, β-blockers, centrally acting α2-agonists and gamma-amino butyric acid (GABA)-B agonist baclofen should be incorporated in PSH therapy. We emphasize that oral baclofen administration could be effective to treat spasticity, contrary to the earlier reports.

Propranolol for Paroxysmal Sympathetic Hyperactivity with Lateralizing Hyperhidrosis after Stroke.

Brain injury can lead to impaired cortical inhibition of the hypothalamus, resulting in increased sympathetic nervous system activation. Symptoms of paroxysmal sympathetic hyperactivity may include hyperthermia, tachycardia, tachypnea, vasodilation, and hyperhidrosis. We report the case of a 41-year-old man who suffered from a left middle cerebral artery stroke and subsequently developed central fever, contralateral temperature change, and hyperhidrosis. His symptoms abated with low-dose propranolol and then returned upon discontinuation. Restarting propranolol again stopped his symptoms. This represents the first report of propranolol being used for unilateral dysautonomia after stroke. Propranolol is a lipophilic nonselective beta-blocker which easily crosses the blood-brain barrier and may be used to treat paroxysmal sympathetic hyperactivity.

Paroxysmal Sympathetic Hyperactivity after Traumatic Brain Injury: Clinical and Prognostic Implications

A proportion of patients surviving severe traumatic brain injury (TBI) have symptoms suggestive of excessive sympathetic discharge, here termed paroxysmal sympathetic hyperactivity (PSH). The goals of this study were: (1) to describe the clinical associations and radiological findings of PSH, its incidence, and features in subjects with severe TBI in the intensive care unit (ICU); (2) to investigate the potential role of increased intracranial pressure in the pathogenesis of PSH; and (3) to determine the prognostic influence of PSH during the ICU stay, on discharge from the ICU, and at 12 months post-injury. A prospective cohort study was undertaken of all ICU admissions with severe TBI older than 14 years over an 18-month period. The PSH symptoms consisted of paroxysmal increases in blood pressure, respiratory rate, and heart rate; worsening level of consciousness; muscle rigidity; and hyperhidrosis. Subjects demonstrating PSH episodes were compared with a group of non-PSH consecutive subjects studied over the first 6 months of the study period. Data were recorded on the clinical variables associated with PSH episodes, early post-injury cerebral CT findings, and neurological status at 1 year. Of 179 severe TBI patients admitted over the study period, 18 (10.1%) experienced PSH. Injury severity-related variables (e.g., initial APACHE II score, admission coma level, and proportion with intracranial hypertension) were similar between the two groups. The PSH group had a longer ICU stay and a greater incidence of infectious complications. At 1 year post-injury, 20% of this group demonstrated ongoing PSH episodes. Over 18 months, 10.1% of admissions following severe TBI demonstrated PSH features in ICU. Subjects with PSH had a longer ICU stay and higher rate of complications, although this did not appear to compromise their long-term neurological recovery.