Purpose This study aimed to investigate the diagnostic value of somatosensory evoked potentials (SEPs) in patients with paroxysmal sympathetic hyperactivity (PSH) and to identify independent predictors of the condition. Methods A retrospective cohort study was conducted on 123 patients with prolonged disorders of consciousness (PDOC) admitted to the Critical Care Rehabilitation Department of Nanjing Jiangning Hospital between August 2022 and August 2024. Patients were classified into PSH-positive (PSH+) and PSH-negative (PSH−) groups according to the Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM). Demographic, clinical, and SEPs parameters were collected. Univariate and multivariate logistic regression analyses were employed to examine the association between these variables and PSH. The predictive performance was evaluated using receiver operating characteristic (ROC) curve analysis. Results A total of 123 patients with prolonged disorders of consciousness were enrolled in the study. Among these, 34 patients (27.64%) were classified into the PSH + group and 89 patients (72.36%) into the PSH − group. Multivariate logistic regression analysis identified younger age (OR = 0.96, 95% CI: 0.92–0.99, p = 0.02), male patient (OR = 0.28, 95% CI: 0.09–0.75, p = 0.02), and reduced N20-P25 amplitude (OR = 0.34, 95% CI: 0.13–0.70, p = 0.01) as independent predictors of PSH. Using a cut-off value of 1.19 μV for the N20-P25 amplitude, the area under the curve (AUC) for discriminating PSH was 0.811 (95% CI: 0.71–0.912), yielding a sensitivity of 79.7% and a specificity of 75%. The combination of these three predictors improved the AUC to 0.846 (95% CI: 0.75–0.942). After adjusting for potential confounders, partial correlation analysis demonstrated a significant negative correlation between N20-P25 amplitude and PSH-AM score (adj. r = −0.30, p = 0.003). Conclusion A reduced N20-P25 amplitude may serve as an independent and objective electrophysiological biomarker for the early prediction of PSH. In combination with younger age and male patient, it contributes to the identification of high-risk populations and offers valuable guidance for clinical management.

Paroxysmal sympathetic hyperactivity (PSH) is a severe complication of acquired brain injuries (ABIs), characterized by sudden autonomic surges that exacerbate clinical outcomes. Its pathophysiology remains debated, and early biomarkers are lacking. This study aims to investigate autonomic changes preceding PSH and assess the feasibility of predictive modeling using heart rate variability (HRV). Continuous electrocardiogram (ECG) recordings were obtained from six male patients with disorders of consciousness (DoC), including unresponsive wakefulness syndrome and minimally conscious state. A total of 24 PSH episodes and 24 matched control (noPSH) events were analyzed. HRV metrics, including entropy measures and power spectral density (PSD), were evaluated. A support vector machine (SVM) classifier was implemented to differentiate PSH from control events and to predict PSH onset. PSH events were associated with significant heart rate increases, reduced entropy-based complexity, and decreased PSD in both low-frequency (LF) and high-frequency (HF) bands. An increased very-low-frequency (VLF)/(LF + HF) ratio suggested potential involvement of the renin-angiotensin-aldosterone system (RAAS) in PSH pathogenesis. The SVM classifier achieved perfect classification during the event. In addition, 10 min prior to onset, the model reached 67% sensitivity, 100% specificity, and 83% balanced accuracy. HRV analysis reveals distinct autonomic signatures preceding PSH and suggests, as a working hypothesis, that dysregulation of the RAAS may play a role. However, VLF power is influenced by multiple mechanisms and cannot be considered a specific or exclusive marker of RAAS activity. SVM-based predictive modeling offers a promising tool for PSH detection, providing a basis for investigating autonomic/neuroendocrine regulation, includingRAAS.

Fronto-limbic disconnection correlates with paroxysmal sympathetic hyperactivity following traumatic brain injury: An indirect disconnection-symptom mapping study

Clinical features of paroxysmal sympathetic hyperactivity in brain tumor: a retrospective case series study and literature review.

Paroxysmal sympathetic hyperactivity (PSH) is most commonly associated with traumatic brain injury. PSH in CNS infections has been quoted variably due to extremely low numbers of its occurrences. With this article, we document a case report of a patient admitted with PSH secondary to tubercular meningitis (TBM), with an attempt to highlight the burden of disease. The pathophysiology of PSH is yet to be clearly understood and clinical presentation is ambiguous leading to a delay in identification and, therefore, a delay in management. Despite using the diagnostic tool, PSH forms a diagnosis of exclusion. Management involves supportive care, pharmacological therapy and, surgical intervention for raised ICP. Detailed analysis of the handful of known cases showcases the grave morbidity this condition carries. An 11-year-old female child diagnosed with TBM underwent ventriculoperitoneal shunt surgery and was stable in the immediate post-operative period. After 3days, the patient developed episodes of high-grade fever with diaphoresis, tachycardia and hypertension, which continued to deteriorate despite aggressive management. Her PSH-Assessment Measure (PSH-AM) score was 26 (probable). Unfortunately, the patient eventually succumbed to the disease. In decreasing order, the manifestations were tachycardia (100%), tachypnea, dystonia, hyperthermia, hypertension and diaphoresis, with a predilection in males of pediatric age. Keeping a low threshold for diagnosis and early detection is essential for reducing long-term neurological sequelae. Our case report is the 7th case in the literature of PSH in TBM (unrelated to hydrocephalus) and the 15th case of PSH in TBM including those where hydrocephalus played a role.

Paroxysmal sympathetic hyperactivity in children: An updated narrative review.

Extensive miliaria crystallina secondary to paroxysmal sympathetic hyperactivity in a hospitalized trauma patient

Neuropsychiatric syndromes are characterized by disturbances in cognition, emotions, behavior, and represent the complex intersection between neurology and psychiatry, particularly in the critically ill. Despite this vulnerability in critically ill patients and the implications of the high level of care required in critical care settings, intensivists often face difficulty in the prompt recognition and management of neuropsychiatric syndromes. This in part may be reflective of the several overlapping and nonspecific clinical features (i.e. agitation, altered mentation, motor findings, autonomic instability, clonus), disparate definitions of encephalopathy within the literature, precipitating risk factors, lack of clearly defined diagnostic tests or laboratory findings, and shared secondary complications when diagnosis is delayed or missed. Agitation is often the most readily identifiable presenting symptom of neuropsychiatric syndromes in critically ill patients, largely due to its disruptive impact on patient care, both patient and staff safety, potential to delay in time to extubation, and risk of worsening patient outcomes.In this analytic review, neuropsychiatric syndromes that can present with agitation were identified and further appraised upon reviewing randomized controlled trials, meta-analyses, and systematic reviews from the PubMed database spanning from 1995 to 2024. In total 507 articles were identified using relevant search terminology, article titles were subsequently screened for relevance, followed by screening of abstracts. Neuropsychiatric syndromes included within this review were selected based upon diagnostic complexity, overlapping clinical features, and highlighted based upon prevalence within the literature: Serotonin syndrome, neuroleptic malignant syndrome, catatonia, and paroxysmal sympathetic hyperactivity. We highlight these distinct syndromes and propose a clinical heuristic-based decision tree to accompany clinical decision making for the intensivist from a psychiatrist's lens.

Patients with traumatic brain injury (TBI) may develop paroxysmal sympathetic hyperactivity (PSH), a syndrome manifesting as cyclic increases in vital signs and motor activity. Previous studies show propranolol mitigating sympathetic symptoms and negative outcomes, but few reports assess its effect on body temperature. The purpose of this study was to determine if propranolol attenuates hyperthermia secondary to PSH in patients with TBI. This study evaluated febrile patients with TBI treated with propranolol. The primary outcome was the difference in maximum (Tmax), minimum (Tmin), and average (Tavg) daily temperatures and temperature variability (Tvar). Secondary outcomes included similar evaluation of heart rate (HR) and mean arterial pressure (MAP), differences in a modified clinical features scale (mCFS), and number of infectious work-ups before and after propranolol initiation. Data were collected one day before, the day of, and 3 days after propranolol initiation. Repeated measures analysis of variance (ANOVA) was used to evaluate vital sign differences among days of therapy. Post-hoc Tukey's tests were performed to identify between-day differences if they existed. Fifty-nine patients were included. The majority were male (76.3%) and had a severe TBI (78.0%). Tmax, Tmin, Tavg, and Tvar were all not different between Day -1 and Day 3. Tmax decreased from 38.6 ± 0.11°C on Day 0 (the day of propranolol initiation) to 38.3 ± 0.14°C on Day 3 (P = 0.22). Maximum and average HRs were significantly decreased after propranolol initiation on Day 3 (P < 0.001) and on Days 2 (P = 0.04) and 3 (P = 0.01), respectively. Changes in MAP were not statistically significant. The mCFS and number of infectious work-ups were significantly lower after propranolol initiation. Temperature was not significantly decreased after propranolol initiation in patients with TBI and hyperthermia; however, HR and mCFS were significantly lower. Larger studies are needed to characterize the effect of propranolol on temperature in patients with PSH.

In this study, we enrolled patients with acute brain injury (ABI) to examine the relationship between paroxysmal sympathetic hyperactivity (PSH) and volume status, right heart function, and pulmonary edema, and their impact on prognosis. Thirty patients with ABI were prospectively enrolled. A correlation analysis between Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM) score and clinical indicators was performed using Pearson's or Spearman correlation coefficient. Receiver operating characteristic (ROC) curves were used to assess the prediction of 6-month Glasgow Outcome Scale Extended (GOSE) score. Inferior vena cava (IVC) diameter was evaluated as a marker of intravascular volume status, and its correlation with 6-month GOSE score in ABI patients was analyzed. There was no statistically significant difference in PSH-AM over time in patients with ABI (P = 0.791). The PSH-AM scores on Days 3 (R = 0.474, P = 0.08) and 5 (R = 0.460, P = 0.011) were positively correlated with pulmonary edema score. Early diastolic velocity (EDV) on Days 3 (R = -0.429, P = 0.018) and 5 (R = -0.452, P = 0.012) was negatively correlated with pulmonary edema score. Ejection time (ET) on Day 5 was positively correlated with inferior vena cava (IVC) (R = -0.381, P = 0.038). The ability to assess the 6-month GOSE score and the ROC curve (AUC) was observed for IVC on Day 1 (AUC = 0.785± 0.120, 95% confidence interval 0.550-1.000, P = 0.012). IVC diameter assessed on day 1 is a useful indicator of neurological prognosis in patients with ABI. There was no statistically significant difference in PSH over time in patients with ABI. Regarding the study's sample size and potential operator bias in IVC diameter measurement, the findings require validation in larger, multicenter studies with standardized measurement protocols.

Paroxysmal sympathetic hyperactivity (PSH) causes paroxysms of increased sympathetic hyperactivity in the setting of acquired brain injury. Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological syndrome characterised by cortical/subcortical vasogenic oedema in multiple brain areas. Patients present with seizures, encephalopathy and headaches. In this article, we report a patient who presented in status epilepticus with a hypertensive peak and decreased level of consciousness. Brain imaging showed diffuse hyperintensities with beading intracranial vessels. Then, the patient improved spontaneously without receiving any treatment except supportive management. Repeated brain imaging showed resolution of the abnormalities. A diagnosis of PRES was made. During her stay, she developed episodes of diffuse body rigidity associated with hypertension, tachycardia and diaphoresis, triggered by non-noxious stimuli suggestive of PSH. She received clonidine with significant improvement. This case illustrates the need to keep a high index of suspicion for PSH in cases of acquired diffuse brain injuries, such as PRES.

JOURNAL/mgres/04.03/01612956-202603000-00002/figure1/v/2025-06-28T140100Z/r/image-tiff Paroxysmal sympathetic hyperactivity syndrome (PSH) is common in patients with severe craniocerebral injuries. Carbon monoxide poisoning (ACOP) may lead to secondary PSH, and hyperbaric oxygen (HBO) is an important treatment method for ACOP that can promote the dissociation of carboxyhemoglobin and reduce the long-term sequelae of ACOP. To explore the risk factors and clinical characteristics of PSH secondary to acute ACOP and to investigate the efficacy of HBO treatment, a retrospective analysis was performed on patients with moderate to severe ACOP admitted to the Hyperbaric Oxygen Department of Beijing Chaoyang Hospital, Capital Medical University, from January 1, 2018 to December 31, 2024. Three patients developed PSH during hospitalization and were classified into the PSH group, while the remaining 50 patients were in the non-PSH group. Univariate Fisher's exact test indicated that a coma duration of more than 72 hours was related to the occurrence of PSH after ACOP, and irregular HBO treatment after onset might be associated with the occurrence of PSH after ACOP. All three PSH patients developed paroxysmal postural or dystonic disorders after onset, accompanied by sympathetic excitation manifestations such as increased heart rate, respiratory rate, elevated blood pressure, and fever. Antiepileptic drugs had poor effects, and the attacks were effectively controlled after HBO treatment combined with adjusted drug therapy. The results indicate that for patients with severe carbon monoxide poisoning, especially those with a long coma duration or irregular HBO treatment after onset, if epileptic seizures occur during the disease course and are accompanied by sympathetic excitation manifestations, the possibility of PSH should be considered. Regular HBO treatment is of great significance for controlling the onset of symptoms.

Introduction: Neurocysticercosis, a parasitic infection caused by Taenia solium larvae, is a prevalent health challenge in regions with poor sanitation and among individuals migrating from endemic areas. This case report discusses the complexities of neurocysticercosis management. Main symptoms and clinical findings: A 23-year-old male with neurocysticercosis-related hydrocephalus and paroxysmal sympathetic hyperactivity (PSH), presented with altered mental status, headaches, and neurological deterioration. MRI findings revealed numerous cystic lesions and characteristic findings indicative of neurocysticercosis, with subsequent CT imaging identifying progressive hydrocephalus. Main diagnoses, therapeutic interventions, and outcomes: Neurocysticercosis with hydrocephalus and PSH was diagnosed. This necessitated the placement of a ventriculoperitoneal shunt and external ventricular drain. Despite initial improvement with antiparasitic and corticosteroid therapy, the patient’s clinical course was complicated by seizures and autonomic dysregulation. PSH was suspected due to episodes of tachycardia and diaphoresis, requiring intensified anticonvulsant therapy and sedative management with propofol. Treatment adjustments included dual antiparasitic therapy (albendazole and praziquantel) and rigorous intracranial pressure management. Conclusion: This case highlights the complexities of neurocysticercosis management, particularly when complicated by hydrocephalus and PSH, emphasising the need for early recognition and dynamic treatment modifications. As neurocysticercosis increasingly affects non-endemic regions, healthcare systems must be equipped to recognise and treat its severe manifestations, with broader public health efforts focusing on prevention in endemic areas and among migrant populations. Key Points 1. This case report explores the intensive care management of a young patient with neurocysticercosis, complicated by low-pressure hydrocephalus and paroxysmal sympathetic hyperactivity. 2. The case highlights the delicate balance of cerebrospinal fluid diversion, timing of antiparasitic therapy, and autonomic stabilisation in a critically ill patient with central nervous system infection. 3. This emphasises the need for greater clinician awareness of low-pressure hydrocephalus and paroxysmal sympathetic hyperactivity, two under-recognised but serious complications that require timely, nuanced, and multidisciplinary care to improve outcomes.

BackgroundIn severe traumatic brain injury (TBI), sedatives are often used to control intracranial pressure (ICP), to reduce brain metabolism, to allow for other treatments such as mechanical ventilation or targeted temperature management, or to control paroxysmal sympathetic hyperactivity. Prolonged sedation is often necessary. The most commonly used sedatives in TBI are propofol and midazolam, often in combination, but both have significant side effects when used at high doses for several days. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, provides sedation and analgesia with minimal respiratory depression or haemodynamic instability. However, ketamine carries a US Food and Drug Administration (FDA) precaution regarding its use in patients with pre-anaesthetic elevated cerebrospinal fluid pressure, which discourages its use in TBI patients. Several observational studies and two large meta-analyses do not suggest that the use of ketamine as an induction agent or sedative in sedated and mechanically ventilated TBI patients would increase the ICP. Off-label use of ketamine for this indication is increasing worldwide. To date, no prospective randomized clinical trial (RCT) has demonstrated the safety of ketamine in TBI patients.MethodsThe Brain Injury and Ketamine (BIKe) study is a prospective multicentre double-blind placebo-controlled RCT, to evaluate the safety, and effect on therapeutic intensity to reduce ICP, of ketamine as an adjunct to a standard sedation regimen in patients with severe TBI. Adult TBI patients, admitted to the intensive care unit (ICU), requiring sedation and ICP monitoring within 72 h of admission, will be randomized to ketamine or placebo. The study drug will be started within 6 h of randomization. The dose of the investigational medicinal product (IMP) is 1 mg/kg/h, by continuous infusion. The IMP will be stopped when the last ICP control sedative is discontinued. Data collection will stop when the patient is discharged from the ICU. All patients will be followed for 6 months post-trauma. The study is powered for the safety endpoint of detecting a clinically relevant increase of two episodes in the median number of episodes of high intracranial pressure episodes per ICU stay. A total of 100 patients are required to meet these objectives. We hypothesize a clinically relevant reduction in the therapeutic intensity level (TIL) score of at least 3 points.DiscussionThis study is the first prospective RCT to investigate the safety of ketamine as an adjunct to a standard sedation regimen in TBI patients.Trial registrationClinicalTrials.gov NCT05097261. Registered on October 28, 2021.

Currently, there is no generally accepted method for elimination of centrogenic hyperthermic reactions. In paroxysmal sympathetic hyperactivity, body temperature should be maintained in a safe normothermic range for at least the first few days. The potential benefits of treatment may result from three primary goals: elimination of triggering factors, mitigation of excessive sympathetic overload, and supportive therapy. Treatment involves reducing any external stimulation that can trigger paroxysmal episodes. Because fever is caused by a prostaglandin-induced shift in the hypothalamic “set point”, conventional nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis, but centrogenic hyperthermic reactions are mostly resistant to antipyretic therapy. Physical cooling is used when medical treatment is ineffective. Endovascular cooling methods are more effective than external ones. Monotherapy for paroxysmal sympathetic hyperactivity is usually ineffective, so the possibility of using several drugs with different mechanisms of action should be considered. The use of moderate doses of several drug classes provides synergistic efficacy, reducing the toxicity of individual drugs. Multimodal treatment regimens are more effective than monotherapy. The lack of a generally accepted technique for elimination of centrogenic hyperthermic reactions requires further multicenter studies and the creation of appropriate clinical guidelines.

BackgroundParoxysmal sympathetic hyperactivity (PSH) is a severe dysregulation of the sympathetic nervous system, often resulting from traumatic brain injury (TBI). With a prevalence of 10–30% in TBI patients, PSH poses diagnostic and therapeutic challenges. This study reviews advancements in diagnosis, management, and outcomes associated with PSH.MethodsA comprehensive literature review of studies published in the past decade was conducted using PubMed, Scopus, Web of Science, and the Cochrane Library. Keywords included PSH, diagnostic criteria, treatment strategies, and clinical outcomes.ResultsThe PSH Assessment Measure (PSH-AM), combining the clinical feature scale and diagnosis likelihood tool, enhances early detection and differentiates PSH from similar conditions. Acute management using opioids and benzodiazepines proved effective, while beta-blockers and alpha-2 agonists reduced episodic recurrence. Despite improved diagnostic accuracy, challenges persist, such as overlapping symptoms and difficulty quantifying autonomic dysfunction. PSH is associated with prolonged hospital stays and poorer neurological outcomes, emphasizing the importance of timely intervention.ConclusionAccurate diagnosis using tools like PSH-AM is essential for mitigating PSH-related complications. Future research should explore biomarkers and personalized therapies to refine diagnosis and optimize long-term outcomes through multicenter trials.

Paroxysmal sympathetic hyperactivity (PSH) is characterized by episodes of excessive sympathetic activity and is associated with poor outcomes in brain injuries, yet its impact on severe intracerebral hemorrhage (ICH) remains unclear. This study investigates the association between PSH and clinical outcomes in patients with severe ICH. We conducted a prospective observational cohort study of patients with severe ICH from January 2018 to December 2022. Severe ICH was defined as ICH with a Glasgow Coma Scale score ≤ 8 on admission, indicating significant neurological impairment. Patients were assessed for PSH using the PSH-Assessment Measure, and categorized into probable, possible, and unlikely PSH groups. Propensity score matching was used to adjust for baseline differences among three groups. The primary outcome was the 90-day mortality rate. Secondary outcomes included a favorable functional outcome at 90days, defined by a modified Rankin Scale score of 0-2. Statistical analyses were performed using Cox proportional hazards regression and Kaplan-Meier survival analysis. After propensity score matching, 177 patients (59 in each group) were analyzed. The 90-day mortality rate was significantly higher (P < 0.01) in the probable PSH group (67.8%), compared with possible (47.5%) and unlikely PSH groups (35.6%). The Kaplan-Meier survival curve further illustrates a significantly increased risk of 90-day mortality in the probable PSH group (Log rank test P < 0.01). Multivariate Cox proportional hazards regression analysis confirmed that, after adjusting for confounders, the presence of probable PSH (hazard ratio 3.86, 95% confidence interval 2.17-6.87; P < 0.01) was independently associated with a higher risk of 90-day mortality. Functional outcomes at 90days were poorer in the probable PSH group. Probable PSH is significantly associated with worse outcomes in severe ICH, underscoring the importance of early recognition and targeted management strategies.

IntroductionParoxysmal Sympathetic Hyperactivity (PSH) is an under-recognized condition in pediatric patients, particularly those with non-traumatic brain injuries, often leading to delayed diagnosis and suboptimal management. The condition features episodic increases in sympathetic nervous system activity, which creates significant diagnostic and therapeutic challenges. This study aims to comprehensively characterize the clinical presentation, diagnostic challenges, and treatment outcomes of pediatric PSH in a tertiary care setting. Additionally, we investigate factors contributing to delayed diagnosis and assess the impact of various clinical and management variables on patient outcomes.MethodsThis retrospective cohort study was conducted at King Abdullah Specialist Children’s Hospital (KASCH), Riyadh, Saudi Arabia, encompassing 42 pediatric patients diagnosed with PSH between 2016 and 2023. We extracted comprehensive data from patient records, including demographic profiles, clinical presentations, diagnostic findings, and treatment outcomes. Statistical analyses were employed to identify factors influencing mortality and clinical improvement, including univariate and multivariate regression.ResultsThe cohort had a mean age of 6.53 years, with PSH onset typically around 4.19 years. The majority (88.1%) of PSH cases stemmed from non-traumatic causes, notably hypoxic-ischemic encephalopathy (31%). Key clinical features included fever, tachycardia, and dystonia, with a significant rate of initial misdiagnosis (69%). Healthcare providers frequently administer gabapentin as a preventive medication, while they commonly use benzodiazepines for abortive therapy. Clonidine use was associated with a statistically significant reduction in mortality (P < 0.05), whereas delayed diagnosis correlated with poorer clinical outcomes.ConclusionsPSH in pediatric patients predominantly arises from non-traumatic brain injuries, presenting with nonspecific symptoms that often lead to misdiagnosis. This study underscores the importance of early and accurate diagnosis in improving patient outcomes. Clonidine shows potential as a life-saving intervention in this context. These findings highlight the need for further research to refine diagnostic criteria and optimize treatment strategies for pediatric PSH.

Paroxysmal Sympathetic Hyperactivity, Generalized Dystonia, and Rigidity as Sequelae Following Hydrocephalus (P7-3.010)

Paroxysmal sympathetic hyperexcitation (PSH) refers to a clinical syndrome characterized by a sudden increase in sympathetic excitability caused by severe brain injury. This study aims to investigate the effectiveness and practicality of combining transcranial direct current stimulation (tDCS) with medication to treat PSH and employ non-linear electroencephalography (EEG) to assess changes in cortical activation post-intervention. 40 PSH patients were randomly assigned to receive either active tDCS or sham tDCS treatment over an 8-week period. The tDCS stimulation targeted the prefrontal area, left frontal-temporal-parietal cortex, right frontal-temporal-parietal cortex, and left dorsolateral prefrontal cortex. Both patient groups also underwent medication and other conventional therapies. The Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM), Coma Recovery Scale-Revised (CRS-R), medication dosage, and approximate entropy (ApEn) index were assessed before and after treatment. The active tDCS group exhibited more substantial improvements in changes of PSH-AM, changes of CRS-R, and medication reduction ratios compared to the sham tDCS group after the treatment. After treatment and during follow-up, a significantly greater number of patients in the active tDCS group demonstrated clinically important differences compared to the sham tDCS group. The active tDCS group showed significantly higher ApEn indices in the less affected frontal lobe compared to the control group. No significant differences in ApEn indices were noted in the sham tDCS group before and after treatment. Regression analysis revealed that the group (active tDCS/sham tDCS) was the primary factor associated with improving PSH-AM. Therefore, we believe that in patients with PSH, combining tDCS with medication therapy demonstrated superior clinical efficacy compared to medication therapy alone. Electrophysiological results also indicated enhanced cortical excitability. Therefore, this single-center pilot study suggests that multi-target, multi-session tDCS combined with medication may be an effective treatment protocol for PSH.