Paroxysmal Sympathetic Hyperactivity with Dystonia Following Non-traumatic Bilateral Thalamic and Cerebellar Hemorrhage

Luca, Daniel G. Di; Mohney, Nathaniel; Kottapally, Mohan

doi:10.1007/s12028-019-00677-9

Cited by 6 publications

(5 citation statements)

References 4 publications

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“…Autonomic dysfunction and PSH can result from the impairment in the central autonomic regulatory centers, such as insular cortex, anterior cingulate and ventral prefrontal regions, as well as lower centers located in the amygdala, hypothalamus, thalamus, brainstem and spinal cord ( 12 , 27 , 28 ). Although structural lesions that increase the likelihood of autonomic instability or PSH have been identified ( 29 ), we did not detect any association between structural anomalies and PSH.…”

Section: Discussionmentioning

confidence: 99%

Characteristics and Outcomes of Paroxysmal Sympathetic Hyperactivity in Anti-NMDAR Encephalitis

Chen

Zhang

et al. 2022

Front. Immunol.

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BackgroundTo explore the clinical characteristics and prognosis of autonomic dysfunction and paroxysmal sympathetic hyperactivity (PSH), and evaluate the efficacy of drugs used to suppress PSH episode in anti-NMDAR encephalitis patients.MethodsPatients who met the diagnostic criteria of anti-NMDAR encephalitis were enrolled from January 2012 to August 2018 and followed up for 2 years. PSH was diagnosed according to the PSH-Assessment Measure. The demographics data, clinical features, auxiliary tests results, treatments, and outcomes were prospective collected and analyzed.ResultsA total of 132 anti-NMDAR encephalitis patients were enrolled, of which 27.3% and 9.1% experienced autonomic dysfunction and probable PSH respectively. Cardiac autonomic dysfunction was the most common subtype (77.8%). Patients with a higher incidence of ovarian teratoma, mechanical ventilation, neurological intensive care unit admission, and elevated glucose and NMDAR antibody titer in the CSF were more likely to exhibit autonomic dysfunction or PSH. Episodes of PSH can be suppressed by monotherapy in patients without prior sedative drug use with an efficacy of 90%. No significant difference was observed between the prognosis of patients with or without autonomic dysfunction, or between the PSH versus non-PSH groups after 6 months and even during long-term follow-up. However, patients with cardiac autonomic dysfunction had poor prognosis at 6 months.ConclusionPSH is a common clinical condition in patients with anti-NMDAR encephalitis, especially in severe cases, and can be effectively managed by several drug monotherapies. Despite necessitating longer hospital stay, autonomic dysfunction or PSH do not seem to compromise the neurological recovery of patients.

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Section: Discussionmentioning

confidence: 99%

Characteristics and Outcomes of Paroxysmal Sympathetic Hyperactivity in Anti-NMDAR Encephalitis

Chen

Zhang

et al. 2022

Front. Immunol.

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“…The remaining 5% is caused by brain tumor, encephalitis, hydrocephalus and unspecified causes. [2][3][4][5][6][7]11,12 Although pathophysiologic basis for PSH is incompletely understood, speculative explanations rest on "disconnection theory" and "excitation-inhibition ratio (EIR) model." Disconnection theory suggested a loss of inhibitory cortical centers control over caudal excitatory autonomic centers, while the EIR model proposed failure to modulate spinal cord excitatory sensory circuits by inhibitory centers within brainstem (the periaqueductal grey matter).…”

Section: Discussionmentioning

confidence: 99%

“…[6][7][8] Medical treatments for PSH include combinations of µ-opioid receptor agonist (morphine), non-selective ß-receptor blocker (propranolol), α 2 -receptor agonist (clonidine), GABA-receptor agonist (gabapentin), dopaminereceptor antagonist (bromocriptine) and benzodiazepines (diazepam) to abort or minimize PSH episodes via inhibition of sympathetic flow, afferent sensory process and effector end organ response. [6][7][8][11][12][13][14] Early diagnosis and optimized treatment is believed to shorten ICU stay, facilitate patient recovery and minimize physical disability. In conclusion, 'clinical scoring' was used to dignose PSH, since there was no any confirmatory test.…”

Section: Discussionmentioning

confidence: 99%

“…The remaining 5% is caused by brain tumor, encephalitis, hydrocephalus and unspecified causes. 2–7 , 11 , 12 …”

Section: Discussionmentioning

confidence: 99%

“…Almost all (95%) cases of PSH are caused by traumatic head injury, anoxia and stroke. [2][3][4][5][6][7]11,12 Since there is no confirmatory test, diagnosis of PSH is made using combination of "clinical features severity" (CFS) score and "diagnosis likelihood tool" (DLT) score, named as PSH-AM (assessment measure) score. The CFS score assesses presence and severity of clinical features, while the DLT measures the presence of compatible clinical parameters (frequency, duration, paroxysms and simultaneity of hyper-sympathetic episodes, antecedent cause, triggering factors, allodynia, excluding alternative causes, and response to treatment).…”

Section: Introductionmentioning

confidence: 99%

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<p>Diagnosis and Treatment of Paroxysmal Sympathetic Hyperactivity in Medical ICU, University of Gondar Hospital, Northwest Ethiopia: A Case Report</p>

Bekele

Mesfin

Hailu

et al. 2020

IMCRJ

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Background Paroxysmal sympathetic hyperactivity (PSH) is a neurologic syndrome characterized by paroxysmal and simultaneous occurrence of hypertension, hyperpyrexia, tachycardia, tachypnea, diaphoresis and dystonic posturing due to surge in sympathetic outflow after acquired brain injuries. Diagnosis of PSH is made using the paroxysmal sympathetic hyperactivity-assessment measure (PSH-AM) score, which comprises “clinical features severity” (CFS) score and “diagnosis likelihood tool” (DLT) score. Case presentation A 35-year-old woman diagnosed to have echo-proven chronic rheumatic heart disease for 25 years. Percutaneous balloon mitral valvotomy was done 6 weeks previously for severe mitral stenosis. Left atrial thrombus was detected after the procedure and anticoagulant (warfarin) was initiated. She presented with severe headache and repeated vomiting of 1 day duration on arrival to the hospital. She had frequent seizure attacks with subsequent loss of consciousness on third day of admission. Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made after CT-scan revealed acute subdural hematoma and ventricular bleeding. Then she was transferred to medical intensive care unit (ICU), intubated and put on mechanical ventilator. Anti-epileptic drugs, antibiotics, vitamin K and fresh frozen plasma were given. She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis and decerebrate posturing after 7 days of neurological insult. She had normal inter-ictal EEG tracing during cyclic autonomic surge. CFS score was 11 and DLT score was 10. In sum, PSH-AM score was 21, suggested “probable” diagnosis of PSH. Morphine, diazepam, propranolol and gabapentin were given in combination to treat PSH. Severity of autonomic storm started to improve on second week of ICU admission. On the third week of admission, her clinical condition deteriorated suddenly, she developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR). Conclusion 'Clinical scoring' was used used to diagnose PSH, since there was no any confirmatory test. Cocktail of drugs were required to treat catecholamine surge in PSH.

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

Liu

Wen

Zhu

et al. 2020

Autonomic Neuroscience

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Paroxysmal Sympathetic Hyperactivity with Dystonia Following Non-traumatic Bilateral Thalamic and Cerebellar Hemorrhage

Cited by 6 publications

References 4 publications

Characteristics and Outcomes of Paroxysmal Sympathetic Hyperactivity in Anti-NMDAR Encephalitis

Characteristics and Outcomes of Paroxysmal Sympathetic Hyperactivity in Anti-NMDAR Encephalitis

<p>Diagnosis and Treatment of Paroxysmal Sympathetic Hyperactivity in Medical ICU, University of Gondar Hospital, Northwest Ethiopia: A Case Report</p>

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

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