Fever has long been recognized as one of the earliest clinical indicators of illness and remains a leading reason for seeking medical care worldwide. It is typically classified based on its duration and underlying etiology. In clinical settings, intractable fever is as common as acute fever, particularly in patients with brain injuries. Beyond infectious causes, stroke survivors often experience recurrent intractable fever due to central or neurogenic mechanisms. This study aims to retrospectively investigate the incidence and clinical characteristics of acute and intractable fever in patients undergoing stroke rehabilitation. It explores the associations between these characteristics and the different types of fever. Additionally, the study seeks to identify potential risk factors contributing to the development of intractable fever, aiming to guide clinical management and optimize treatment strategies for stroke-related fever. This study evaluated 1,065 stroke patients in the rehabilitation phase who were admitted to the Neurorehabilitation Center between January 1, 2023, and December 31, 2023. Of these, 230 febrile patients met the inclusion criteria and were included in the analysis, comprising 194 cases of acute fever and 36 cases of intractable fever. Medical records and clinical characteristics were collected, and the data from the two groups of febrile patients were analyzed using t-tests, Mann-Whitney U tests, and chi-square tests. Logistic regression analysis was performed to identify risk factors associated with intractable fever, while receiver operating characteristic (ROC) curves were used to assess the predictive performance of individual and combined risk factors. A p-value of less than 0.05 was considered statistically significant. 15.7% of patients experienced intractable fever, which was significantly associated with brainstem lesions (P < 0.05). Compared to patients with acute fever, those with intractable fever had higher NIHSS scores (33.3% vs. 15.5%, P < 0.05), a greater incidence of consciousness disorders (66.7% vs. 28.9%, P < 0.05), and a higher rate of tracheostomy (55.6% vs. 15.5%, P < 0.05). All patients received antibiotic treatment, and gabapentin was administered to 16 cases. Patients with brainstem lesions were less likely to be treated with gabapentin (37.5% vs. 90%, P < 0.05), while those with intracerebral hemorrhage were more likely to receive gabapentin (87.5% vs. 10%, P < 0.05). Logistic regression analysis revealed that consciousness disorders and tracheostomy status were significant risk factors for intractable fever (P = 0.047, OR 6.691, 95% CI 1.030-43.478; P = 0.021, OR 5.366, 95% CI 1.282-22.465). Brainstem lesions also significantly increased the risk (P = 0.002, OR 9.617, 95% CI 2.277-40.614). Although limited in scope, this retrospective study highlights the increased risk of intractable fever during stroke rehabilitation among patients with consciousness disorders, tracheostomy, and brainstem injuries. The key risk factors identified include higher NIHSS scores, impaired consciousness, tracheostomy status, and brainstem lesions.

Bromocriptine is a dopamine receptor agonist used for central hyperthermia with limited data. We describe our single-center experience utilizing bromocriptine for central hyperthermia, including the population treated, most common dosing regimens, adverse events, and discontinuation reasons.

A retrospective study was conducted screening patients who were admitted to intensive care units for acute neurological insults and administered bromocriptine for central hyperthermia between April 2016 and September 2022. Baseline characteristics, disease severity markers, and bromocriptine doses were collected. Body temperatures prior to the first dose of bromocriptine, at the time of dose, and after each dose were recorded. Co-administration of additional hyperthermia management therapies was noted.

Thirty patients were included. The most common diagnosis was traumatic brain injury (TBI) (N = 14). The most common reason for discontinuation was resolution of indication (N = 14). Discontinuation due to mild adverse effects occurred in four patients; hepatotoxicity was the most common. There was a paired mean difference of -0.37°C (p = 0.005) between temperatures before and after bromocriptine initiation.

Bromocriptine is a potential therapy for the management of central hyperthermia in patients with severe acute neurologic insults who have failed other therapies. Bromocriptine was well tolerated and associated with a low incidence of adverse events.

Intracerebral hemorrhage (ICH) accounts for 10-15% of all strokes and leaves most survivors with impairments. Fever, a rise in the thermoregulatory set point, complicates ICH. This review summarizes ICH fever studies and employs meta-analytic techniques to explore the relationship between fever and ICH. We discuss methodological considerations for future studies and provide an overview of mechanisms by which fever, and its treatment, may impact ICH. We searched the PubMed database using the following terms: ((fever OR hyperthermia) AND (intracerebral hemorrhage OR intraparenchymal hemorrhage OR intracerebral haemorrhage OR intraparenchymal haemorrhage)). Our search returned 727 studies, of which 21 were included in our final analysis, consisting of 19 clinical, and two preclinical, studies. We conducted a meta-analysis on the clinical data to quantify how fever is related to mortality, functional outcomes, and intraventricular hemorrhage. Analysis of clinical studies suggested that fever causes an increased risk of mortality but does not appear to be associated with poor outcomes among survivors, making it difficult to ascertain the extent of harm caused by post-ICH fever or the benefits of its treatment. Perhaps these inconsistencies stem from variable fever definitions, and temperature measurement and fever treatment protocols. Additionally, the lack of mechanistic data in clinical studies coupled with preclinical studies showing no harmful effects of moderate bouts of hyperthermia raise concerns about the direct contribution of hyperthermia and fever in post ICH outcome. Overall, the significance of temperature increases after ICH is unclear, making this an important area for future research.

Some patients present to the intensive care unit due to noninfectious pathologies resulting in fever, especially acute neurological injuries, including brain trauma and intracranial haemorrhage. The cause has been identified to be central hyperthermia characterized by a high core temperature and a poor response to antipyretics and antibiotics. However, no proper guidelines on how to treat central hyperthermia have been developed for clinical practice.

A 63-year-old woman was transferred to our hospital due to injury after a traffic accident. Eight hours after admission, her pupils enlarged bilaterally from 2.5 mm to 4.0 mm. She developed severe coma and underwent decompressive craniectomy. She was diagnosed with central hyperthermia after surgery and was prescribed bromocriptine. The standard dose of bromocriptine could not control her hyperpyrexia, and we prescribed 30 mg a day to control her temperature.

Bromocriptine may be effective in controlling central hyperthermia and have a dosage effect.

Different mechanisms explain thermoregulatory dysfunction following ischemic stroke, hemorrhagic stroke, and traumatic brain injury. Temperature instability following brain injury likely involves hypothalamic injury, pathologic changes in cerebral blood flow, metabolic derangement, and a neurogenic inflammatory response. Although targeted temperature management (TTM) exerts pleiotropic effects, the heterogeneity of brain injury has hindered identification of patient subsets most likely to benefit from TTM. Early optimism about TTM's role in brain injury has been tempered by the failure of successive clinical trials to show improved patient outcomes. However, given the deleterious effects of fever, aggressive fever management is still warranted in the critically ill neurologic patient.

Hyperthermia from a central cause is associated with increased morbidity and mortality. Dysfunction of brainstem thermoregulatory pathways may explain the intractable rise in temperature. Antipyretics, dantrolene, bromocriptine, and surface and intravascular cooling devices have been attempted for temperature control. We report the case of a 54-year-old woman with history of hypertension who presented with pontine hemorrhage with extension into the midbrain and medulla. On days 8-9 of her hospital admission, she developed intractable fever and expired the same day despite aggressive treatment of hypothermia, including antipyretics, ice lavage, cold fluid boluses, surface cooling, dantrolene, and bromocriptine. Hyperthermia from brainstem hemorrhage can be difficult to manage with current treatment options. Early recognition of those patients who may develop hyperthermia could lead to early intervention and possibly better outcomes. More evidence from prospective randomized controlled trials will elucidate the risk-benefit profile of achieving normothermia with aggressive fever control in these patients.

Central fever (CF) is defined as elevated temperature with no identifiable cause. We aimed to identify risk factors for developing CF among patients with spontaneous intracerebral hemorrhage (ICH) and to evaluate the impact of CF on outcome.

Patients included in our prospective stroke registry between 1/1/09 and 1/10/10 were studied. We identified patients with CF as those with a temperature ≥38.3°C without evidence for infection or drug fever. Patients with CF were compared to those without fever and those with infectious fever. Demographics, risk factors and imaging data as well as outcome parameters were reviewed.

We identified 95 patients with spontaneous ICH (median age 76, median admission NIHSS 9). CF was identified in 30 patients (32%), infectious etiology was found in 9 patients (9%) and the remaining patients did not develop fever. Baseline variables were similar between the groups except for intra-ventricular extension of the ICH (IVH) and larger ICH volumes that were more common in the CF group (OR = 4.667, 95% CI 1.658-13.135 and OR = 1.013/ml, 95% CI 1.004-1.021). Outcome analysis showed higher mortality rates (80% vs. 36%, p < 0.001) and lower rates of favorable functional outcome defined as a modified Rankin score ≤ 2 at 90 days (0% vs. 53%, p < 0.001) in the CF group.

The risk of CF is increased in patients with larger ICH and in those with IVH. CF negatively impacts outcome in patients with ICH.

A 39 year old man arrived at the hospital with semi-comatose state as a result of spontaneous intracerebral hemorrhage (ICH), intraventricular hemorrhage (IVH) and subarachnoid hemorrhage (SAH). For emergency craniectomy and hematoma removal, general anesthesia with desflurane and vecuronium was planned. Before the induction of anesthesia, the body temperature and end-tidal carbon dioxide (ETCO2) levels were 38.3degrees C and 38 mmHg, respectively. The body temperature and ETCO2 increased during surgery. After 2 hours of anesthesia, the temperature had increased to 41degrees C, despite bladder irrigation and body cooling. After 3 hours of anesthesia, the temperature reached 43.5degrees C and cardiac arrest developed. Cardiopulmonary resuscitation was attempted, but the patient expired.

Despite the recognized deleterious effects of hyperthermia on critically ill neurological patients, few investigations have studied hyperthermia after an ischemic stroke in the intensive care unit (ICU) setting.

Acute ischemic stroke patients admitted to the ICU were assigned to one of three groups: normothermia, mild hyperthermia (MH), or severe hyperthermia (SH). The etiology of hyperthermia was further divided into infectious and non-infectious groups.

Among the 150 patients included in the study, MH and SH were observed in 15 and 40 patients, respectively. Hyperthermia and the Glasgow coma scale (GCS) score were independently related to in-hospital mortality and increased length of stay in the ICU (ILOS, > or =4 days).

Infection (39 patients) was more prevalent in the SH group than in the MH group and was associated with greater ILOS.

Monitoring and managing infection and reducing body temperature may be important factors for determining the outcomes of patients with acute ischemic stroke admitted to the ICU.

The purpose of this project was to identify risk factors for fever among critically ill patients with acute new-onset stroke, treated in a neurological intensive care unit (NICU). The frequency and risk factors for fever in the stroke patients during the first 7 days after admission were retrospectively studied.

Fever was defined as a patient's axillary temperature >37.5 degrees C in two separate measurements or >37.8 degrees C in one single measurement. Multivariable logistic regressions were applied to analyse the risk factors for any fever, explained infectious fever and unexplained fever. One hundred and thirty-seven patients were included in the final analysis.

Febrile episodes occurred in 65% (89/137) of the patients; 48.9% of the fever were explained by infection (predominantly pneumonia or bronchitis), and 15.3% were unexplained despite a complete diagnostic evaluation. Significant risk factors for any fever included age 65 years or older, impaired consciousness, extremity paralysis (muscle force < or = grade 3), center venous catheterization and tracheal intubation. In addition to those risk factors, the length of the stay at NICU before the fever was also a significant risk factor for explained infectious fever. Brain midline shift and initial serum leucocyte count more than 12.0 x 10(9)/l were significant risk factors for unexplained fever.

These results suggest that critically ill and new-onset stroke patients treated in NICU often have fever. The risk factors for different types of fever vary considerably.

Temperature management in acute neurologic disorders has received considerable attention in the last 2 decades. Numerous trials of hypothermia have been performed in patients with head injury, stroke, and cardiac arrest. This article reviews the physiology of thermoregulation and mechanisms responsible for hyperpyrexia. Detrimental effects of fever and benefits of normalizing elevated temperature in experimental models are discussed. This article presents a detailed analysis of trials of induced hypothermia in patients with acute neurologic insults and describes methods of fever control.

An increasing amount of research is now being directed towards the medical treatment of patients who have suffered an intracerebral haemorrhage (ICH). Despite this, no routine drug treatment to date has been shown to be unequivocally effective in unselected patients.

Approaches to treatment are based upon our understanding of the pathophysiological sequelae following ICH. Strategies to reduce haematoma growth, subsequent oedema formation and perihaematoma ischaemia are key targets for further research. Whether these therapies become valuable tools for the future is as yet unclear. Until then, the mainstay of the medical management of ICH remains individualised care.

There is now a pressing need for large prospective randomised controlled trials to determine the effectiveness of pharmacological therapies for this condition.

Fever is a common occurrence in patients following brain and spinal cord injury (SCI). In intensive care units, large numbers of patients demonstrate febrile periods during the first several days after injury. Over the last several years, experimental studies have reported the detrimental effects of fever in various models of central nervous system (CNS) injury. Small elevations in temperature during or following an insult have been shown to worsen histopathological and behavioral outcome. Thus, the control of fever after brain or SCI may improve outcome if more effective strategies for monitoring and treating hyperthermia were developed. Because of the clinical importance of fever as a potential secondary injury mechanism, mechanisms underlying the detrimental effects of mild hyperthermia after injury have been evaluated. To this end, studies have shown that mild hyperthermia (>37 degrees C) can aggravate multiple pathomechanisms, including excitotoxicity, free radical generation, inflammation, apoptosis, and genetic responses to injury. Recent data indicate that gender differences also play a role in the consequences of secondary hyperthermia in animal models of brain injury. The observation that dissociations between brain and body temperature often occur in head-injured patients has again emphasized the importance of controlling temperature fluctuations after injury. Thus, increased emphasis on the ability to monitor CNS temperature and prevent periods of fever has gained increased attention in the clinical literature. Cooling blankets, body vests, and endovascular catheters have been shown to prevent elevations in body temperature in some patient populations. This chapter will summarize evidence regarding hyperthermia and CNS injury.

Temperature management in acute neurologic disorders has received considerable attention in the last 2 decades. Numerous trials of hypothermia have been performed in patients with head injury, stroke, and cardiac arrest. This article reviews the physiology of thermoregulation and mechanisms responsible for hyperpyrexia. Detrimental effects of fever and benefits of normalizing elevated temperature in experimental models are discussed. This article presents a detailed analysis of trails of induced hypothermia in patients with acute neurologic insults and describes methods of fever control.