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Objective: To quantify the occurrence of high intracranial pressure (HICP) refractory to conventional medical therapy after traumatic brain injury (TBI) and to describe the use of more aggressive therapies (profound hyperventilation, barbiturates, decompressive craniectomy).Design: Prospective study of 407 consecutive TBI patientsSetting: Three neurosurgical intensive care units (ICU).Measurements and Results: Intracranial pressure (ICP) was studied during the first week after TBI; 153 patients had at least 1 day of ICP>20 mmHg. Early surgery was necessary for 221 cases, and standard medical therapy [sedation, mannitol, cerebrospinal fluid (CSF) withdrawal, PaCO2 30-35 mmHg] was used in 135 patients. Reinforced treatment (PaCO2 25-29 mmHg, induced arterial hypertension, muscle relaxants) was used in 179 cases (44%), and second-tier therapies in 80 (20%). Surgical decompression and/or barbiturates were used in 28 of 407 cases (7%). Six-month outcome was recorded in 367 cases using the Glasgow outcome scale (GOS). The outcome was favorable (good recovery or moderate disability) in 195 cases (53%) and unfavorable (all the other categories) in 172 (47%). HICP was associated with worse outcome. Outcome for cases who had received second-tier therapies was significantly worse (43% favorable at 6 months, p=0.03).Conclusions: HICP is frequent and is associated with worse outcome. ICP was controlled by early surgery and first-tier therapies in the majority of cases. Profound hyperventilation, surgical decompression and barbiturates were used in various combinations in a minority of cases. The indications for surgical decompression and/or barbiturates seem restricted to less than 10% of severe TBI. [ABSTRACT FROM AUTHOR]

Objective: Rubinstein-Taybi syndrome (RSTS) is a rare congenital disorder (1:125.000) characterized by growth retardation, psychomotor developmental delay, microcephaly and dysmorphic features. In 25% of patients seizures have been described, and in about 66% a wide range of EEG abnormalities, but studies on neurological features are scant and dated. The aim of this study is to describe the electroclinical phenotype of twenty-three patients with RSTS, and to try to correlate electroclinical features with neuroradiological, cognitive and genetic features., Patients and Methods: Electroclinical features of twenty-three patients with RSTS (age between18months and 20years) were analyzed. Sleep and awake EEG was performed in twenty-one patients, and brain MRI in nineteen patients. All subjects received cognitive evaluation., Results: EEG abnormalities were observed in 76% (16/21) of patients. A peculiar pattern prevalent in sleep, characterized by slow monomorphic activity on posterior regions was also observed in 33% (7/21) of patients. Almost no patient presented seizures. Eighty-four percentage of patients had brain MRI abnormalities, involving corpus callosum and/or posterior periventricular white matter. Average General Quotient (GQ) was 52, while average IQ was 55, corresponding to mild Intellectual Disability. The homogeneous electroclinical pattern was observed mainly in patients with more severe neuroradiologic findings and moderate Intellectual Disability/Developmental Disability (ID/DD). No genotype-phenotype correlations were found., Conclusion: The specific electroclinical and neuroradiological features described may be part of a characteristic RSTS phenotype. Wider and longitudinal studies are needed to verify its significance and impact on diagnosis, prognosis and clinical management of RSTS patients., (Copyright © 2015 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.)

Traumatic brain injury (TBI) in children is frequent, sometimes lethal, and may have life-long consequences in survivors. Prevention at school and in sports, including both kids and families, is of paramount importance. Scarce data are available in terms of epidemiology, physiopathology, management and prognosis. This non-systematic review suggests that rational organization of rescue and transport to designated hospitals, linked with early diagnosis/removal of surgical masses and comprehensive monitoring and intensive care, offer the best chances for reducing mortality and morbidity in severe cases. After the acute phase rehabilitation and families play a fundamental role.

This review focuses on the potential application of hypothermia in adults suffering traumatic brain injury (TBI). Hypothermia is neuroprotective, reducing the damaging effects of trauma to the brain in a variety of experimental situations, such as brain ischemia and brain injury, but it has failed to demonstrate outcome improvement in a major controlled, randomized trial. The evidence for the use of hypothermia as a protective procedure is scarce and contradictory. However, evidence does suggest that hypothermia is effective in reducing intracranial hypertension after head injury. Since hypothermia has important side effects, further work is necessary before introducing this procedure into clinical practice for TBI.

Intubation, which requires sedation and myorelaxants, may lead to inaccurate neurological evaluation of severely head-injured patients. Aims of this study were to describe the early clinical evolution of traumatic brain injured (TBI) patients admitted to intensive care unit (ICU), to identify cases of over-estimated neurological severity, and to quantify the risk factors for this over-estimation. A total of 753 TBI patients consecutively admitted to ICU of three academic neurosurgical hospitals (NSH) were assessed. Cases whose severity was potentially over-estimated were identified by four criteria and indicated as "mistakenly severe" (MS): (1) no surgical intracranial masses; (2) could not follow commands at neurological assessment; (3) were dismissed from the ICU in < or =3 days to a regular ward; and (4) had regained the ability to obey commands. A total of 675 patients were intubated and/or sedated-paralyzed at the post-stabilization evaluation. In all, 304 patients had surgically treated intracranial masses. Among the 449 non-surgical cases, 58 patients fulfilling the criteria for MS were identified. The main features distinguishing MS from truly severe cases were younger age, higher Glasgow Coma Scale (GCS) score at all time points, Marshall classification of Computerized Tomographic (CT) scan mostly Diffuse Injury I and II, fewer pupillary abnormalities, and a lower frequency of hypoxia, hypotension, and extra-cranial injuries. In a certain proportion of non-surgical TBI patients, mostly intubated and sedated, neurological examination is difficult and severity can be over-estimated. Risk factors for this inaccurate evaluation can be identified, and clinical decisions should be based on further examination.

This study investigated AJDO2 (arterio-jugular difference of oxygen content) in a large sample of severely head-injured patients to identify its pattern during the first days after injury and to describe the relationship of AJDO2 with acute neurological severity and with outcome 6 mo after trauma. In 229 comatose head-injured patients, we monitored intracranial pressure, cerebral perfusion pressure, and AJDO2. Outcome was defined 6 mo after injury. Jugular hemoglobin oxygen saturation (SjO2) averaged 68%. The mean AJDO2 was 4.24 vol% (SD, 1.3 vol%). There were 80 measurements (4.6%) with SjO2 <55% and 304 (17.6%) with saturation >75%. AJDO2 was higher than 8.7 vol% in 8 measurements (0.4%) and was lower than 3.9 vol% in 718 (42%) measurements. AJDO2 was higher during the first tests and decreased steadily over the next few days. Cases with a favorable outcome had a higher mean AJDO2 (4.3 vol%; SD, 0.3 vol%) than patients with severe disability or vegetative status (3.8 vol%; SD, 1.3 vol%) and patients who died (3.6 vol%; SD, 1 vol%). This difference was significant (P < 0.001). We conclude that low levels of AJDO2 are correlated with a poor prognosis, whereas normal or high levels of AJDO2 are predictive of better results.

Objective: To investigate the possibility of artificially decreasing intra-abdominal pressure (IAP) by applying continuous negative pressure around the abdomen., Material and Methods: We investigated the effects of negative extra-abdominal pressure (NEXAP) on IAP and central venous pressure (CVP) in 30 patients admitted to our intensive care unit (age 57+/-17 years, BMI 26.1+/-4.0 kg/m2, SAPS II 41.8+/-17.0). Patients with severe hemodynamic instability and/or those admitted following a laparotomy were not studied. Measurements included bladder pressure as an estimate of IAP, CVP, invasive mean arterial pressure (MAP) and heart rate (HR). In five patients extensive hemodynamic measurements were also taken using a Swan-Ganz catheter. Following measurements at baseline (Basal), NEXAP (Life Care - Nev 100, Respironics) was applied on the abdomen, in random order, at a pressure equal to IAP (NEXAP0), 5 cmH(2)O (NEXAP-5) or 10 cmH(2)O (NEXAP-10) more negative than NEXAP0., Results: Basal IAP ranged from 4 to 22 mmHg. NEXAP decreased IAP from 8.7+/-4.3 mmHg to 6+/-4.2 (Basal vs NEXAP0 p<0.001). There was a further decrease of IAP when more negative pressure was applied: 4.3+/-3.2 mmHg, 3.8+/-3.7 mmHg (NEXAP-5 and NEXAP-10 vs NEXAP0, respectively, p<0.001). Similarly, CVP decreased from 9.3+/-3.4 mmHg to 7.5+/-3.8 (Basal vs NEXAP-10, p<0.001). The lower the IAP when NEXAP was applied, the lower the CVP (r2=0.778, p<0.001, multiple linear regression). When measured, cardiac output did not significantly change with NEXAP., Conclusions: Negative extra-abdominal pressure may be applied in critically ill patients to decrease intra-abdominal pressure non-invasively.

Adequate early assessment of brain damage is essential. Location, extension and severity of structural damage affect brain function and ultimately determine the outcome. The extent of functional impairment, and the morphology of intracranial lesions, require specific treatment, often a combination of medical and surgical interventions. Brain damage usually evolves over time, and repeated assessments are necessary. Clinical evaluation is often biased by concomitant sedation and/or anesthesia, but remains necessary. A revision of the literature is presented. Brain damage is assessed combining clinical and instrumental data. Clinical examination is performed assessing the 3 components of the Glasgow Coma Scale. Spontaneous or stimulated (pain stimulus) eye opening, verbal and motor responses are observed after hemodynamic and respiratory stabilisation. Unfortunately a significant proportion of patients can not be properly examined for several reasons: eye opening can be altered by palpebral and facial injuries, verbal response can be impaired by maxillo-facial injuries or by endotracheal intubation, and motor response remains the most consistent parameter. Sedation, analgesia and myorelaxants, however, can profoundly diminish or abolish the motor response to maximal stimulation, so that examination should be performed after clearance of drugs. Often alcohol or other substances can further impair the neurological performances. Pupils diameter and reactivity to light should be observed, excluding pharmacologic effects (as dilation due to catecholamines) and direct ocular or orbital damage. The CT scan is necessary for disclosing surgical masses and for identifying the extent of diffuse damage and the location of focal lesions. These data should be combined with additional functional exploration, as provided by cerebral extraction of oxygen and electrophysiologic data. Early estimation of cerebral damage is complex and prone to mistakes. Accurate, repeated evaluations, based on the combination of clinical observation and imaging, are necessary.