[Craniocerebral injuries in childhood].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
To prevent cerebral vasospasm after aneurysmal subarachnoid haemorrhage, cisternal irrigation has been reported to be more effective when combined with continuous head-shaking (head-shaking method). The present study was conducted to evaluate the safety and preventative effect for vasospasm in patients treated with the head-shaking method. Six of 17 patients managed postoperatively by the original head-shaking procedure developed neurological deterioration related to the method: two had intracranial haematoma (one with acute interhemispheric subdural haematoma, and the other with cerebellar haemorrhage), two had acute brain swelling, and two failed to show abnormal findings on computed tomography. These pathological processes may be suitably referred to as "head-shaking syndrome". Delayed ischaemic neurological deficits associated with low-density lesions on computed tomography were demonstrated in five patients (29%). From these observations, the head-shaking method may not be as safe as described in the original articles, and is critically evaluated in terms of its preventative effect for cerebral vasospasm.
Ischaemic brain lesions still have a high prevalence in fatally head injured patients and are the single most important cause of secondary brain damage. The present study was undertaken to explore the acute phase of severely head injured patients in order to detect early ischaemia using Robertson's approach of estimating cerebral blood flow (CBF) from calculated arterio-jugular differences of oxygen (AVDO2), lactates (AVDL), and the lactate-oxygen index (LOI). Twenty-eight cases with severe head injury were included (Glasgow Coma Scale Score below or equal to 8). All patients but one had a non-missile head injury. All the patients had a diffuse brain injury according to the admission CT scan. ICP measured at the time of admission was below 20 mmHg in 17 cases (61%). All patients were evaluated with the ischaemia score (IS) devised in our center to evaluate risk factors for developing ischaemia. Mean time from injury to the first AVDO2/AVDL study was 23.9 +/- 9.9 hours. According to Robertson's criteria, 13 patients (46%) had a calculated LOI (-AVDL/AVDO2) value above or equal to 0.08 and therefore an ischaemia/infarction pattern in the first 24 hours after the accident. Of the 15 patients without the ischaemia/infarction pattern, in three cases the CBF was below the metabolic demands and therefore in a situation of compensated hypoperfusion. No patient in our series had hyperaemia. Comparing different variables in ischaemic and non-ischaemic patients, only arterial haemoglobin and ischaemia score (IS) was significantly different in both groups. The ischaemia score had mean of 4.3 +/- 1.7 in the ischaemic group and 2.7 +/- 1.4 in non-ischaemic patients (p = 0.01). It is concluded that ischaemia is highly prevalent in the early period after severe head injury. Factors potentially responsible of early ischaemia are discussed.
We studied the effect of contrast enhancement on magnetic resonance imaging (Gadolinium DTPA Magnetic Resonance) in 10 patients with a recent head injury. The use of contrast did not increase the number of traumatic lesions identified and we did not detect evidence of altered blood brain barrier permeability in any of the 7 patients, who had a total of 27 lesions, imaged between one and 4 days after injury. Enhancement was found in each of 3 patients imaged 6 or more days after injury. These findings suggest that traumatic cortical and intraparenchymal lesions are not associated with increased cerebrovascular permeability within the first 96 hours of a head injury.
The pre-operative and early postoperative CT scans of 120 patients who had surgery for acute extradural haematoma were reviewed, 88 cases (73%) had an extradural haematoma alone (Group 1) while 32 cases (27%) had an additional intradural abnormality (Group 2). The abnormalities were a subdural haematoma in eight, a haemorrhagic contusion in 16 and hemisphere swelling in eight. The two groups were compared with regard to the findings that an additional intradural abnormality is likely to be associated with an older age, an injury following a road traffic accident, a GCS less than 7 at operation, additional extracranial injuries and a poorer outcome. The increase in the percentage of patients who were unconscious from the onset and the decrease in those who were always conscious with a concomitant intradural damage was without statistical significance.
Treatment resistant intracranial hypertension after severe head injury has a very high mortality with conventional therapy such as hyperventilation and mannitol infusions. In this report, we describe the use of large doses of thiopental as a means of treating such swelling. From a consecutive series of 107 severe head injuries with a Glasgow Coma Score (GCS) of 6 or below, we selected all patients below 40 years age with a progressive increase in intracranial pressure (ICP) to 40 mm Hg. The first 16 patients (mean age 20 years, mean GCS 4.3) were treated with deep barbiturate coma and hypothermia (32-35 degrees Celsius) until stable lowering of ICP was achieved. The next 15 patients received conventional intensive care and were in other respects very similar to the barbiturate group (mean age 26, mean GCS 5.2). After 9-12 months the outcome was classified according to the Glasgow Outcome Scale (GOS). Therapy with barbiturate coma resulted in 6 good/moderate outcomes, 3 severe and 7 dead/vegetative. Conventional treatment resulted in 2 good/moderate outcomes and 13 dead/vegetative. This is a highly significant difference and cannot easily be explained by more severe injuries or complications in the conventional group. Superior control of ICP was achieved by large doses of thiopental and the final outcome was better.
In a retrospective series of 144 patients with cranial trauma admitted to the Department of Neurosurgery, 96 were initially examined by CT. The initial clinical assessment, operative findings, if any, and the clinical course were compared to the results of the primary CT scan. In patients presenting lateralizing deficits, 49% had lesions on the expected side, and 23% on the opposite side. Thirty-one per cent of brain stem affected patients had a supratentorial mass lesion requiring craniotomy. Three decerebrate patients who had died had an initially normal CT scan. Thirty craniotomies were performed on the basis of the CT scan, and six cases deviated from the expected, but no case showed a false positive indication for surgery. The final diagnosis was in accordance with the initial clinical diagnosis, and with the initial CT scan in 44% and 84%, respectively, of all cases.
Chronological changes in diffuse brain swelling and brain oedema were studied in repeated CT studies following a closed head injury. These findings were compared with changes in intracranial pressure (ICP). The grades of diffuse brain swelling were classified into mild, moderate and marked according to the CT findings. Planimetry of low density areas of brain oedema was carried out on repeated CT images. Diffuse brain swelling was recognized in 71% of patients shortly after the head injury and subsided within days 3-5. Brain oedema first appeared 24 hours post injury and did not reach its maximum size and distribution before days 5-8. Thus, these two events can be clearly separated. The intracranial pressure reflected the course of the brain swelling and was not very high during the presence of maximum oedema.
The authors have analysed the computerized tomography (CT) findings and their correlation with the clinical state, early and late outcome in children and adolescents with head injuries (HI). This study represents clinical and CT data of 82 consecutive HI patients under 18 years of age. Among them 51 (62%) were boys and 31 (38%) girls. The application of CT to the evaluation of the morphologic manifestations of HI in children has shown some differences in forms and mechanisms of injury and in outcome compared to adults. In the paediatric HI the most frequent finding was diffuse brain swelling with CT evidence of ventricular and cisternal compression or obliteration. Prognostically the most unfavourable findings were shearing injury, intracerebral and subdural haematomas combined with brain swelling and parenchymal damage. According to the Lidcombe impairment scale, outcome from severe paediatric HI was determined in the 3rd and 6th months, one year and 2 years after the injury. The outcome two years after severe HI varied to a great extent and was better in children than in adults. Although there was long-term disruption of the patient's quality of life, our data show that as there are no predictors of individual outcomes in child HI, no child should be excluded from early and long-term rehabilitation.
We investigated the pathophysiological and morphological responses of anaesthetized rats to fluid percussion brain injury generated by an original midline fluid percussion injury device. Following different grades of trauma, lCBF was measured continuously in the right parietal cortex through a burr hole using laser Doppler flowmeter, and physiological parameters were monitored. Pathological changes also were evaluated microscopically. During the first 2 hours following trauma, we found four patterns of cerebral circulatory responses. Little measurable pathophysiological response occurred after percussion pulses of less than 1.33 atmospheres (atm). In animals subjected to pulses of greater than 4.30 atm, lCBF increased synchronously with blood pressure, and then both parameters decreased continuously until death. In animals subjected to pulses of 1.53 to 2.33 atm, trauma produced a transient increase in lCBF with no synchronous rise in blood pressure. In animals subjected to pulses of 2.70 to 3.87 atm, lCBF increased synchronously with blood pressure immediately following the injury, but had decreased markedly by 60 seconds and remained below the pre-injury baseline. Blood pressure recovered to baseline within 4 minutes of the injury. The transient increase in lCBF occurred within 5 seconds following percussion pulses of greater than 1.53 atm and appeared to be independent of the rise in systemic blood pressure. Apnoea occurred in animals subjected to pulses of greater than 1.53 atm, and the duration of apnoea and mortality rate correlated with the magnitude of the applied injury. A power decrease in the electroencephalogram post-injury and a delay in its recovery, both depended on the magnitude of the injury with few regional differences in the beta-2 band power. The distribution and extent of blood-brain barrier disruption and small haemorrhages also correlated with the magnitude of the injury. The number of neurons decreased significantly in both hippocampi by 2 weeks following moderate trauma. The four patterns of lCBF changes demonstrated in the present study, as well as the other responses to injury, may be useful for studying graded models of various diffuse brain injuries.
Recent studies on prognostic variables and the intensive care of head injuries enabled us to select 64 patients and administer a standard treatment protocol to prevent secondary brain injury. All the patients were in coma with a flexor motor pattern as the best response between 6 and 24 hours after the accident and/or decompressive surgery. Continuous epidural intracranial pressure (ICP) monitoring was used in all patients to control the effect of positioning, analgetics, hyperventilation and osmotherapy. None of the patients with a normal initial ICP (15 mm Hg or less) developed an ICP increase leading to brain tamponade. A subsequent further rise to 40 mm Hg signified a very high risk of progression towards brain tamponade. The majority of the patients (71%) with a maximum ICP increase of less than 40 mm Hg had an acceptable recovery. After 6-12 months, the outcome in this series of patients was 48% with a good/moderate recovery, 14% with severe deficits and 38% dead/vegetative.
The effect of anti-inflammatory treatment on monocyte/macrophage infiltration, major histocompatibility complex molecules (MHC) class II expression and delayed oedema following experimental brain contusion was studied by immunohistochemistry and tissue-specific gravity measurement in 44 rats. Colchicine, chloroquine and dexamethasone administered once daily for five days after the trauma reduced inflammation and oedema. The difference was statistically significant with colchicine and dexamethasone. The findings comprise further evidence of a pathogenetically important inflammation after experimental contusion. It is probable that anti-inflammatory agents may prevent secondary neurological damage due to elevated intracranial pressure and cell to cell- or cytokine-mediated neuronal degeneration and demyelination.
As a reliable continuous monitoring of cerebral blood flow and/or cerebral oxygen metabolism is necessary to prevent secondary ischaemic events after severe head injury (SHI) the authors introduced brain tissue pO2 (ptiO2) monitoring and compared this new parameter with TCD-findings, cerebral perfusion pressure (CPP) and CO2-reactivity over time on 17 patients with a SHI. PtiO2 reflects the balance between the oxygen offered by the cerebral blood flow and the oxygen consumption by the brain tissue. According to TCD-CO2-reactivity PtiO2-CO2-reactivity was introduced. After initially (day 0) low mean values (ptiO2 7.7 +/- 2.6 mmHg, TCD 60.5 +/- 32.0 cm/sec and CPP 64.5 +/- 16.0 mmHg/, ptiO2 increased together with an increase in blood flow velocity of the middle cerebral artery and CPP. The relative hyperaemic phase on days 3 and 4 was followed by a decrease of all three parameters. Although TCD-CO2-reactivity was except for day 0 (1.4 +/- 1.5%), sufficient, ptiO2-CO2-reactivity sometimes showed so-called paradox reactions from day 0 till day 3, meaning an increase of ptiO2 on hyperventilation. Thereafter ptiO2-CO2-reactivity increased, increasing the risk of inducing ischaemia by hyperventilation. The authors concluded that ptiO2-monitoring might become an important tool in our treatment regime for patients requiring haemodynamic monitoring.
Autoregulation and CO2-reactivity can be impaired independently of each other in many brain insults, the so-called 'dissociated vasoparalysis'. The theoretical combination of preserved CO2-reactivity and impaired or abolished autoregulation can have many clinical implications in the daily management of brain injured patients. To optimize their treatment, a bedside assessment of autoregulation and CO2-reactivity is desirable. When cerebral metabolic rate of oxygen is constant, changes in arterio-jugular differences of oxygen (AVDO2) reflect changes in CBF. In these situations relative changes in AVDO2 can be viewed as inverse changes in CBF and used as an evaluation method of CO2-reactivity and autoregulation. In 39 consecutive severe head injury patients with a mean age of 28 +/- 17 years and a diffuse brain injury, cerebrovascular response to changes in pCO2 was tested in the acute phase after injury (18 +/- 8 hours). In 28 of those cases autoregulation was also assessed. A relative CBF value (1/AVDO2) was calculated from baseline AVDO2 and was expressed as 100%. Changes in 1/AVDO2 after inducing pCO2 changes give a good estimate of changes in global CBF. Two different indexes were calculated for CO2-reactivity: 1) absolute CO2-reactivity (CO2RABS) and 2) percentage reactivity (CO2R%). CO2R% was used to separate patients with impaired/abolished CO2-reactivity from those with preserved CO2-reactivity. Patients with CO2R% above 1% were considered in the intact CO2-reactivity group and patients in whom CO2R% was below or equal to 1% were included in the impaired/abolished CO2-reactivity group. Only five cases (12.8%) presented an impaired/abolished CO2-reactivity. AVDO2 response to induced hypertension was studied in a subset of 28 patients. Phenylephrine was used to increase MABP about 25%. All AVDO2 values were corrected for changes in pCO2. Patients with changes in 1/AVDO2 less than or equal to 20% were included in the intact autoregulation group. Patients with estimated CBF changes above 20% were classified as having an impaired autoregulation (impaired/abolished). In 12 patients (43%) autoregulation was intact. In the remaining 16 patients (57%) autoregulation was imparied. Of the 28 cases, CO2-reactivity was impaired in only five cases. All patients with an impaired CO2-reactivity also had an impaired autoregulation. Monitoring relative changes in AVDO2 permits a reliable study of CO2-reactivity and autoregulation at the bedside. Introducing these variables into the day-to-day management should be considered in treatment protocols.
Disorders in sexual function constitute one of the most prevalent and least discussed problems following head injury. The disorders are often the outcome of an interaction between the neurological sequelae, the psychological makeup of the individual, and the sociocultural context of the couple. In a study of 34 head-injured patients, only 13 reached their premorbid level of sexual functioning over a period of 1 year. Deviant behavior, total loss of sexual function, and sexual dysfunction were noted in the rest. Deviant behavior was consistently associated with frontal lobe damage. Otherwise, neurological indices of head injury in the dysfunctional group were not different from those of the clinically recovered group. Associated psychiatric disturbances, gender-role differences, the impact on the marital harmony of the couple, and the role of sociocultural beliefs in the etiology of the disorders are analyzed and discussed, with a particular emphasis on Indian culture.
Contrecoup fractures of the base of the skull are regarded as rare in the clinical literature. In our material (n = 171 falls on the same level and on or from stairs), the overall frequency of contrecoup fractures of the anterior cranial fossa in fatal cranio-cerebral trauma due to falls was 12%, as compared to 24% with occipital point of impact of the head. The relationships between the impact site on the head, form of fracture at the point of impact with involvement of the skull cap and/or the base of the skull, coup and contrecoup injuries of the brain, localization of contrecoup fractures in the anterior cranial fossa and the occurrence of monocle and spectacle haematomas display a major variability. Fractures occur in the form of simple fractures and as impression fractures (fracture fragments or fracture boundaries displaced to the inside). Clinical diagnosis is difficult because of the concealed position of the anterior skull base. Contrecoup fractures become of forensic medical significance when symptoms of a frontobasal injury occur for the first time after trauma which has occurred some time in the past and when the question arises as to the causal connection with the original trauma. In investigation of living persons, it may be difficult to decide whether haemorrhages in the region of the orbit and its vicinity result from a direct blunt force or derive from fractures of the base of the skull, especially contrecoup fractures.
Regional cerebral blood flow (rCBF) in anaesthetized pigs is investigated before and after an induced focal cerebral contusion. Mean intracranial pressure increased for a short period following the contusion and reduced perfusion pressure to 60% of control pressure. Forty five minutes later the mean intracranial pressure was still high and different from the control values. Global flow and cerebral production of CO2 increased concomitantly. In the cortical region where the contusion was visible macroscopically the rCBF diminished from 36.5 to 29.1 ml/min/100 g. In the rest of the grey matter the rCBF raised after the contusion with an increase away from the centre of the lesion. CBF of cortical grey matter in the region symmetrically to the contusion increased significantly more than in the traumatized hemisphere. White matter rCBF changed least in the region underlying the contusion, while an increase was observed away from the contusion and on the opposite side of the brain. The correlation between tension of CO2 in arterial blood and regional cerebral blood flow disappeared in the region of the contusion. The correlation between global metabolism and regional cerebral blood flow disappeared after the contusion in all regions. Local flow modulating factors influencing flow in the region of macroscopically visible injury has influence abating with distance from the centre of the injury together with a possible neuronally transmitted drive on flow in the opposite hemisphere.
Long term CT-investigations of nearly 6000 brain-traumatized patients undergoing rehabilitative measures in the past ten years, showed pathologic findings in 85-90%: 40% showed abnormalities of the ventricular system; 60% traumatic tissue lesions; and 15% abnormalities of the brain surface. Kind and frequency of occurrence of the ventricular changes found by CT were in similar to those found by pneumencephalography. Traumatic inner-hydrocephalus permagnus, which occurred in about 0.25% of our patients, is considered with regard to its rehabilitative meaning. Most traumatic defects were found in the frontal lobe (36%) or in the temporal lobe (46%). Presence and etiology of traumatic infarctions were shown in CT images in 3.5% of all traumatic cases. 25% of these were situated in the posterior area: 25% in the basal ganglia; 15% in the midcerebral artery region, and 30% were typical borderline area infarctions. Because of the frequent differences between CT-findings and neurologic or neuropsychologic symptoms, CT-findings are to be judged only in conjunction with the clinical picture. They should never serve as the only guide for the exaluation of traumatic brain defects, prescribing therapy or predicting outcome.