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The study was designed to determine the effects of two protocols of sedation, medetomidine and medetomidine-butorphanol, on cerebral blood flow (CBF) by transcranial color-coded Duplex ultrasonography in healthy dogs. Transcranial Doppler ultrasonographic examination was performed in 20 dogs before and 20 min after sedation with either medetomidine (group 1) or medetomidine-butorphanol (group 2). The left and right middle cerebral arteries (LMCA and RMCA) were evaluated using the temporal windows, and the basilar artery (BA) was studied through the suboccipital window. Peak systolic velocity (PSV), mean velocity (MV), end diastolic velocity (EDV), resistance index (RI), and pulsatility index (PI) were measured for each vessel. Blood pressure (BP) and heart rate (HR) were also recorded before and after sedation in both groups. Statistically significant differences were found for PSV, MV and EDV when RMCA and LMCA were interrogated before and after sedation. PSV, RI and PI were found to be statistically significantly different when the study was performed on the BA. These results should be taken in account when a transcranial Doppler is performed in dogs sedated with the mentioned protocols and it might suggest some degree of neuroprotection.

S100B is a calcium-binding protein released into the blood from astroglial cells due to brain injury. Some authors have described a correlation between S100B serum concentration and severity of brain damage. There is not much information about the accuracy of urinary S100B for predicting outcome after severe traumatic brain injury (TBI). 55 patients with severe TBI were included in the study. Blood and urine samples were drawn to determine S100B levels on admission and on the subsequent 24, 48, 72 and 96 h. S100B concentrations (serum and urine) were significantly higher in patients who were dead a month after the accident compared to survivors. ROC-analysis showed that S100B at 24h post-severe TBI is a useful tool for predicting mortality (serum: AUC 0.958, urine: AUC 0.778). The best cut-offs for S100B were 0.461 μg/L and 0.025 μg/L (serum and urine respectively), with a sensitivity of 90% for both measurements and a specificity of 88.4% (serum) and 62.8% (urine). We can state that the determination of S100B levels both in urine and serum acts as a sensitive and an effective biomarker for the early prediction of mortality after severe TBI.

This study tested the hypothesis that S100β is a useful screening tool for detecting intracranial lesion (IL) in patients with a normal level of consciousness after traumatic brain injury (TBI).One hundred and forty-three post-TBI patients without a decrease in consciousness (GCS = 15) and with at least one neurological symptom (e.g. transitory loss of consciousness, amnesia, headache, dizziness or vomiting) were prospectively included. A blood sample was drawn at 6-hours post-TBI. A routine CT scan was obtained within 24 hours post-injury. Diagnostic properties of S100β for IL prediction in CT scan findings were tested using ROC-analysis.A total of 15 patients (10.5%) had IL. Serum levels were significantly higher in these patients. Significant differences were found between S100β levels and CT scan findings (p = 0.007). ROC-analysis showed that S100β is a useful tool for detecting the presence of IL in CT scans (p = 0.007). In this series, the best cut-off for S100β is 0.130 µg L(-1), with 100% sensitivity and 32.81% specificity.Within the first 6 hours post-TBI, serum S100β seems to be an effective biochemical indicator of IL in patients without a decrease in consciousness. These results indicate that higher S100β cut-off values substantially improve the clinical relevance of this protein.

Changes in blood flow in the arteries of the canine skull base following compression of the ipsilateral carotid artery were evaluated. Forty healthy conscious dogs were evaluated during examination in lateral recumbency. Using the temporal window, the rostral, middle and caudal cerebral arteries were evaluated. The basilar artery was studied through the suboccipital window. Following compression, the pulse Doppler signal was reduced or inverted when interrogating the rostral or middle cerebral artery, and no change was observed when the caudal cerebral artery or basilar artery was evaluated.

The purpose of this study was to establish the relationship between the hemodynamic response of prefrontal cortex (PFC) and individual differences in cognitive control, as measured by a color-word interference task. Twenty-five healthy volunteers were observed through functional near infrared spectroscopy (fNIRS) while performing a modified Stroop paradigm. Mean concentration levels of oxygenated hemoglobin (oxy-Hb) were correlated with behavioral performance in the conflict task. Those with shorter reaction times had higher levels of oxy-Hb concentration in superior dorsolateral PFC. Our results are the first to show a positive correlation between behavioral performance and oxy-Hb levels in superior dorsolateral PFC in a cognitive conflict task. These results suggest that the availability of oxygen in the superior PFC, possibly linked to an increase in metabolism, may be related to attention level and effectiveness of cognitive control.

The aim of this study was to ascertain the role of clinical variables and neuromonitoring data as predictors of brain death (BD) after severe traumatic brain injury (TBI).This prospective observational study involved severe TBI patients admitted to the intensive care unit between October 2009 and May 2011. The following variables were recorded: gender, age, reference Glasgow Coma Scale after resuscitation, pupillary reactivity, prehospital hypotension and desaturation, injury severity score, computed tomography (CT) findings, intracranial hypertension, and low brain tissue oxygenation (Pti02) levels (16 mm Hg), as well as the final result of BD.Among 61 patients (86.9% males) who met the inclusion criteria, the average age was 37.69 ± 16.44 years. Traffic accidents were the main cause of TBI (62.3%). The patients at risk of progressing to BD (14.8% of the entire cohort) were those with a mass lesion on CT (odds ratio [OR] 33.6; 95% confidence interval [CI]: 3.75-300.30; P = .002), altered pupillary reaction at admission (OR 25.5; 95% CI: 2.27-285.65; P = .009), as well low Pti02 levels on admission (OR 20.41; 95% CI: 3.52-118.33; P.001) and during the first 24 hours of neuromonitoring (OR 20; 95% CI: 2.90-137.83; P.001). Multivariate logistic regression showed that a low Pti02 level on admission was the best independent predictor for BD (OR 20.41; 95% CI: 3.53-118.33; P = .001).Clinical variables and neuromonitoring information may identify TBI patients at risk of deterioration to BD.

The present study was designed to determine how traumatic brain injury affect executive functioning, to know whether different treatments in the acute phase improve this functioning, and to check whether the severity of the neurocognitive impairment is detected by the Glasgow Outcome Scale (GOS). Ability for problem solving and executive functioning within 2 years after Traumatic Brain Injury (TBI) was examined in 35 conscious survivors. Two groups were formed. One group consisted of 13 patients who needed neurosurgery. The other group was made up of 22 patients without neurosurgical treatment. All were treated in the Neurosurgical Intensive Care Unit and in the Rehabilitation Service. The following variables were registered: Secondary Lesions, Glasgow Coma Scale (GCS), CT, subacute CT, and Glasgow Outcome Scale. Neuropsychological tests administered were Wisconsin Card Sorting Test (WCST) and the Tower of Hanoi/Sevilla. Comparing both groups' test performance (man Whitney U) we found that a severe traumatic brain injury, whatever the treatment applied in the acute phase, impairs the executive functioning of the patients; this impairment is related to acute pathophysiological events. The neurosurgical intervention does not improve the executive functioning. The Glasgow Outcome Scale does not detect more than 25% of the patients with severe impairment. It is suggested that the Tower of Hanoi/Sevilla could be a good tool to evaluate the executive functioning routinely in TBI patients as outcome. It also suggested that mild TBI patients must be referred for a complete neuropsychological examination.

Secondary brain insults predominantly due to hypotension are frequent among patients with fatal traumatic brain injury. We assessed the correlation between different systemic secondary brain insults and brain death in 404 patients admitted to our intensive care unit (ICU) after severe traumatic brain injury. We collated data on hypoxemia and hypotension prior to as well as the occurrence of hypoxemia, hypotension, shock, anemia, hyperglycemia, and hyperthermia within the first 24 hours after ICU admission. We also considered both the presence of extracranial injuries and the category of traumatic brain injury using computerized tomography. The 59 patients (14.6%) who developed brain death, were significantly older than patients without a fatal neurological outcome (46.1 +/- 22 vs 29.5 +/- 14.9 years; P < .0001). Intracranial mass lesions, whether surgically evacuated were more frequent among brain-dead patients. The systemic secondary brain insults significantly associated with brain death were hypoxemia, hypotension, shock, anemia, and hyperglycemia within the first 24 hours after ICU admission. After multivariate analysis, the factors that independently predicted brain death were the occurrence of shock (odds ratio [OR], 6.74; 95% confidence interval [CI], 2.85-15.84; P = .001) and older age (OR, 1.05; 95% CI, 1.03-1.07; P = .003). In conclusion, early shock seems to be the major systemic secondary brain insult associated with brain death in patients with severe traumatic brain injury. Prevention of or correction of shock might help to either decrease the occurrence of a fatal neurological outcome or in brain-dead patients to preserve organs in better condition for procurement.

Despite the use of well-accepted protocols for donor maintenance, the severe electrolytic disorders are not infrequent with deleterious consequences to the organs. The objective of our survey was to determine the incidence of episodes of electrolyte disorders among brain-dead patients (despite of rigid protocols of maintenance) and the rate of anaerobic metabolism in these patients (suggestive of an occult systemic hypoperfusion). The study group of 50 brain-dead patients underwent therapy to maintain normal arterial pressure, urine output, and body temperature. Standard monitoring for brain-dead patients was followed, except for a frequent evaluation of electrolytes, including glucose, sodium, potassium, phosphorus, osmolality, base excess, and lactate plasma levels. Our results demonstrate that with frequent determinations of electrolytes, despite following strict protocols of maintenance, there was a high incidence of hyperglycemia, hypophosphotemia, hypokaemia, and hyperosmolality. Interesting findings were the high incidence of elevated lactate, and the relationship between lactate levels and bases deficit as well as hypernatremia. It can be concluded that, even following rigid protocols, the maintenance of brain-dead patients demands a close evaluation of electrolyte levels. Our results also suggest that the inclusion in the monitoring protocol of anerobic metabolism data including lactate levels can help to avoid occult ischemia of organs, and consequently improve their quality for transplantation.

Despite improvements in the process of organ donation and transplants, the number of organ donors is progressively declining in developed countries. Therefore, the early detection of patients at risk for brain death (BD) is a priority for transplant teams seeking more efficient identification of potential donors. In the extensive literature on S100B as a biomarker for traumatic brain injury (TBI), no evidence appears to exist on its prognostic capacity as a predictor of BD after severe TBI. The objective of this study is to assess the value of including acute S100B levels in standard clinical data as an early screening tool for BD after severe TBI. This prospective study included patients with severe TBI (Glasgow Coma Scale score [GCS] ≤ 8) admitted to our Neurocritical Care Unit over a 30 month period. We collected the following clinical variables: age, gender, GCS score, pupillary alterations at admission, hypotension and pre-hospital desaturation, CT scan results, isolated TBI or other related injuries, Injury Severity Score (ISS), serum S100B levels at admission and 24 h post-admission, and a final diagnosis regarding BD. Of the 140 patients studied, 11.4% developed BD and showed significantly higher S100B concentrations (p

Introduction Circulating cell-free DNA levels are increased after trauma injury. This increase is higher since the first hours after trauma and may be related with primary outcome. A sensitive and reliable biomarker for patients at higher risk is needed to identify these patients to initiate early intervention. In this way, circulating DNA may be a possible biological marker after severe TBI. Materials and methods We investigated DNA plasma concentrations after severe traumatic brain injury and during the next 96 h in the Intensive Care Unit (ICU) by real time PCR. 65 patients suffering severe TBI were included in the study. Results Cell-free DNA levels were considerably higher in patients samples compared with voluntary control ones. After the following four days we observed a 51% decrease during the first 24 h and a 71% fall from 48 h. TBI population was stratified for the primary outcome (survivors/non-survivor) and DNA levels decrease ratio was calculated for the first 48 h. A higher decrease in the survivors from 0 h to 24 h compared with the non-survivors was found. A cut-off point of 1.95 ratio was established for the detection of the highest proportions of patients after the TBI that will not survive after the injury with a sensitivity of 70% and specificity of 66%. Conclusions In summary we showed that severe TBI is associated with elevated cf-DNA levels and we propose that cf-DNA decrease during the first 24 h may predict patient outcome.

We report the use of transcranial Doppler ultrasonography in a dog with hepatic encephalopathy secondary to a congenital portosystemic shunt. A severe increase in the pulsatility index was measured in the right middle cerebral artery, left middle cerebral artery, and basilar artery. These values returned to normal following medical stabilization of the patient and resolution of the neurologic signs. Transcranial Doppler ultrasonography appears to have value for monitoring the status of intracranial hypertension in patients with hepatic encephalopathy.

Purpose: Early identification and treatment of intracranial haematomas in patients sustaining traumatic brain injury is fundamental to successful treatment. This pilot study evaluates the Infrascanner as a handheld medical screening tool for detection, in situ, of brain haematomas in patients with head injury. Methods: This study included 35 TBI patients aged 17–76 (M ¼ 47.6), admitted to the neurosurgical intensive care unit and observation unit of a University Hospital in a Level 1 trauma centre. The Infrascanner TM NIRS device uses near infrared light measurements to calculate optical density in brain regions. Results: Results show Infrascanner sensitivity at 89.5% and specificity at 81.2%. PPV was 85% and NPV 86.7%. The device detected 90% of extra-axial, 88.9% of intra-axial and 93.3% of non-surgical haematomas (less than 25 mL). PPV for this classification was 82.3%; 87.5% sensitivity was found when the Infrascanner exam was performed within 12 hours post-trauma, whereas after 12 hours post-trauma, exams had 90.1% sensitivity. Conclusions: This study demonstrates that the Infrascanner is useful in initial examinations and screenings of patients with head injury as an adjunct to a CT scan or when it is not available and may allow earlier treatment and reduce secondary injury caused by present and delayed haematomas.

Insonation of Circle of Willis by transcranial Doppler duplex color sonography is described in 30 healthy dogs with 15 weighing33 lb and 15 weighing33 lb. Imaging was via a temporal window to explore the rostral, middle, and caudal cerebral arteries on both the left and right-hand sides; and through an suboccipital window to study the basilar artery. Normal mean values of the peak systolic velocity (PSV), end diastolic velocity, mean velocity, resistance index (RI), and pulsatility index (PI) were characterized and compared with those obtained in previous studies. There was significant differences in the PSV, RI, and PI in the rostral cerebral artery between dogs weighing33 vs.33 lb. Mean PSV was higher in weighing over 33 lb, whereas the mean resistive index and mean PI were lower in these dogs.

Una de las causas principales de lesion cerebral secundaria es la hipoxia cerebral, fundamentalmente de origen isquemico. No obstante, la oxigenacion tisular cerebral depende de multiples variables fisiologicas y la hipoxia cerebral puede ser originada por una alteracion de cualquiera de ellas. Aunque han sido desarrollados varios metodos de monitorizacion continua de la oxigenacion cerebral en pacientes neurocriticos, la medicion directa y continua de la presion de oxigeno en el tejido cerebral (PtiO2) es una realidad en el manejo de pacientes neurocriticos desde los ultimos anos. Esta tecnica destaca por su fiabilidad y valor de la informacion que proporciona. En el presente articulo se expone una revision de los aspectos mas relevantes de la monitorizacion de la PtiO2 y se propone un protocolo para su interpretacion. Este algoritmo pretende facilitar la identificacion de diferentes tipos de hipoxia cerebral y la correcta eleccion terapeutica en el complejo proceso de toma de decisiones en pacientes neurologicos criticos en riesgo de hipoxia cerebral.

Introduction Higher and lower cerebral perfusion pressure (CPP) thresholds have been proposed to improve brain tissue oxygen pressure (PtiO2) and outcome. We study the distribution of hypoxic PtiO2 samples at different CPP thresholds, using prospective multimodality monitoring in patients with severe traumatic brain injury.

Objective: To report new strategies in the treatment of persistent memory deficits following traumatic brain injury (TBI) using a combination of pharmacology and neuropsychological training. Study design: Two studies were carried out. The first study measured the regional cerebral blood flow (rCBF) of seven Patients with TBI with very severe memory deficits, once while resting and once one hour after the administration of citicholine (CDPc). In the second study, two groups of five patients of the same characteristics underwent an ecological neuropsychological memory rehabilitation program; during which time, one group was administered a placebo (Group A), and the other received CDPc (1~g/d v.o.) (Group B). Results: The results of Experiment 1 showed a hypoperfusion of the inferior left temporal cerebral blood flow during rest state while an induced normalization was observed after administration of the drug. Results of Experiment 2 showed no improvements in Group A's neuropsychological functions, while memory, learning processes and verbal fluency of Group B improved significantly after treatment. Conclusions: CDP-choline seems to be a drug with special affinity for cerebral areas associated with memory acting just where needed, normalizing blood flow in the hypoperfused left temporo-basal region, and making neuropsychological training effective. In general, data suggests that cognitive rehabilitation would follow the principle of first restoring and maintaining cerebral blood flow in the lesional site and then exercising function. In this study on memory rehabilitation, memory recuperation was made possible by first normalizing blood flow at the lesional site and at the same time applying neuropsychological training.