Clinical scoring scales for brain injury

The development of data processing techniques has enabled the establishment of large databanks on brain injury. Clinical features are described with clinical scoring scales, the main one being the Glasgow Coma Scale. Three types of patient response are analyzed: eye opening, oral answers, active muscular reaction. The advantages and disadvantages of each are presented. Others scales have been proposed but are not in common use. Several classifications have been established combining depth and length of coma. Post-traumatic amnesia, i.e. the period of time running from the injury to recovery of anterograde memory, constitutes the most important parameter in the classification of these injuries. Generally, three gravity grades are used: mild, moderate and severe brain injuries. Knowledge of the prognosis is essential for determining the most appropriate medical care and is directly related to the quality of the collected data. Five outcome categories can be described.     

Nutrition des traumatisés crâniens graves

Traumatic injury and severe brain injuries in particular, have systemic consequences affecting all major functions. As energy expenditure increases, energy needs are covered by gluconeogenesis from muscle protein even if they are modulated by the use of different drugs. A gradual erosion of protein reserves results in an acute state of malnutrition exacerbating the immunosuppression induced by trauma, and facilitates infection. Artificial nutrition may limit this process. Gastric feeding route should be initiated early and guided by a written protocol. Gastroparesis being one of the main causes of failure of this route, it must be quickly identified, before calorie deficit harms patients. Nasojejunal tube or parenteral nutrition must be then considered in order to cover nutritional requirements which correspond to about 20–25 kcal/kg per day during the initial phase, and up to 30 kcal/kg per day during the recovery period. Sepsis, agitation or autonomic dysfunction syndromes may increase nutritional requirements. Their evaluation can be improved by mathematical formulas or calorimetry in complex situations (obesity…). Despite the intensity of muscle catabolism, protein intake should be approximately 1.5 g/kg per day. Furthermore, trauma is associated with depletion of glutamine, some vitamins and trace elements including selenium. Supplementation of glutamine reduces infectious morbidity. It must be given at a sufficient dosage and may be associated with selenium. Finally, an adequate glycemic control is essential to avoid brain damage.     

Post-traumatic dysautonomic crises in intensive care unit: a French national assessment

Introduction

The dysautonomic crises (DC) after traumatic brain injury are an unknown syndrome whereas the first case was described more than 50 years ago. This work aimed to collect their support modalities in French neuro-intensive cares units.

Material and methods

French medical doctors, working in neuro-intensive care unit, were questioned by mail. The questionnaire developed point of prevalence, physiopathology, diagnosis, treatment, prognostic of DC and the existence of a support protocol in the department.

Results

There were 52 replies (40%) of 25 different hospitals. The DC were common or frequent for 77% of intensivists. The large majority (94%) reported a lack of knowledge about the physiopathology of the DC. The DC presented more often a therapeutic problem (28%) than a diagnostic problem (10%). The intensivists didn’t know if the DC impacted on the prognostic of the patients (33%). The preferred treatment for the DC was an association of alpha/beta blockers and neuroleptics (38%). The more used preventive treatment was alpha/beta blockers (33%). Only two departments had a support protocol.

Conclusion

Although DC were a common complication in neuro-intensive care unit, their support seems mainly empirical.     

A perceptual analysis of dysarthria following cranial trauma

INTRODUCTION: Dysarthria is a frequent cause of handicap for patients with traumatic brain injury. Clinical assessment and quantification of the disorder is necessary before treatment. METHODS: We report a perceptual analysis of speech in a population of 18 patients with traumatic brain injury, in comparison with 18 control subjects. Evaluation was provided with a 33-item clinical scale. RESULTS: Interjuge reliability was good. Speech analysis distinguished controls from patients. Main perceptual deviances were impairment of naturalness, prosodic and phonetic disturbances.     

Superior vena cava syndrome: cause of secondary raise of intracranial pressure after traumatic brain injury

A 41-year-old male is admitted for cranial trauma, having fallen from his own height. His state of extreme agitation imposes sedation, intubation and mechanical ventilation. A CT-scan reveals acute right hemispheric subdural haematoma, with discrete midline shift, and diffuse cerebral oedema. ICP-monitoring reveals severely increased intracranial pressure, which is responsive to routine medical neuroprotective treatment. Ten days after admission, sedation and neuroprotective treatment is gradually withdrawn. At the end of the second week, a secondary ascent in ICP is observed. The presence of a right subclavian central venous line, in combination with the strong inflammatory response and septic state of the patient, has caused bilateral thrombosis of subclavian and internal jugular veins. This superior vena cava syndrome (SVCS) impedes cerebral venous drainage, thus raising ICP. Within a few days of anticoagulant therapy, SVCS resolved. Impeded cerebral venous drainage is often forgotten or ignored as a cause of secondary elevated ICP. In face of persisting or recurring raised ICP and cerebral oedema, or apparition of communicant hydrocephalus, cerebral venous drainage should be investigated.     

Hierarchical strategy for treating elevated intracranial pressure in severe traumatic brain injury

The objective of the treatment of intracranial hypertension is to decrease intracranial pressure (ICP) while maintaining cerebral blood flow (CBF). Despite numerous treatments, none of them associates total efficiency and security. Systemic secondary cerebral injuries, which are responsible for cerebral ischemia, lead us to administer non specific treatments in order to optimize CBF and cerebral oxygenation. Thus, the goals are: 1) to maintain cerebral perfusion pressure> or =70 mmHg; 2) to control metabolic status by preventing hyperglycaemia, anaemia and hyperthermia; 3) to maintain normoxia and normocapnia (hypercapnia increases ICP and hypocapnia decreases CBF). Beside the neurosurgical evacuation of extra- and intraparenchymatous haematomas, osmotherapy and cerebrospinal fluid (CSF) evacuation are the two specific treatments of intracranial hypertension. Osmotherapy consists in an administration of a hypertonic solution which induces a decrease in cerebral water and finally in ICP. Mannitol (20%), which is the reference, associates osmotic and rheologic effects, and decreases CSF production too. Recent data conduct us to administer larger doses, between 0.7 and 1 g/kg in 15 minutes. Hypertonic saline solution associates osmotic effects and plasma volume loading. Thus, this solution is particularly appropriate in severe head injury with arterial hypotension. CBF evacuation decreases rapidly ICP without any major side-effect. Until now, there is no proof of a superior efficiency of a treatment for intracranial hypertension compared to another. Considering their mechanism of action, all of them are efficient but potentially dangerous too. Indeed, the choice between treatments depends on data which are issued from the multimodal monitoring. General non specific treatments are always necessary. Specific treatments are indicated if ICP is above 20-25 mmHg. Maintaining cerebral perfusion pressure represents the first therapeutic goal. If intracranial hypertension persists, evacuation of CBF or osmotherapy may be advocated. In case of refractory intracranial hypertension, it may be useful to deepen neurosedation. Controlled hypocapnia and barbiturates remain a third line therapy providing to monitor and maintain an appropriate CBF and cerebral oxygenation. Controlled hypothermia and decompressive craniectomy must be individually discussed.     

Quand faut-il décider d'un transfert en milieu neurochirurgical spécialisé ?

The annual incidence of severe head injury lies between 9 and 25/100000 inhabitants, depending on the criteria used for its definition. In most countries, the shortage in neurosurgical ICU beds makes it impossible to take in charge all patients with a severe brain injury. But the beneficial effect of a specialized neurosurgical ICU on outcome after brain injury has been demonstrated in several retrospective studies. Ideally, the best strategy is to admit the patients with a severe head injury directly in a neurosurgical centre. When this is not possible, the appropriate decision of a secondary transfer relies on the quality of the relationships between physicians in the community and the neurosurgical hospitals. Teleradiology is the best method to avoid unnecessary transportation or deleterious delays before transfer. In an era of decreasing medical budgets, technical improvements to enhance medical cooperation should be encouraged.     

Les troubles psychotiques post-traumatiques : un modèle physiopathologique de la schizophrénie

Traumatic Brain Injury (TBI) and later serious psychopathology have long been associated in the literature. Psychotic disorder following traumatic head injury is reported to occur in 0.7 to 9% of patients who sustain a head injury. This paper summarizes the recent literature about psychotic symptoms following TBI and try to articulate these psychotic disorders to a pathophysiological model of primary schizophrenia. Psychotic disorder due to a general medical condition (TBI) indicates that the hallucinations or delusions are the direct physical consequences of the medical condition. A contrario, schizophrenia-like psychosis is a secondary schizophreniform syndrom that must be differentiated from posttraumatic schizophrenia where the head trauma is an external factor furthering the onset of a primary psychosis. A dimensional approach could although take place for understanding pathophysiology. Head injury has been reported to increase the likelihood of the development of psychosis disorder due to TBI, schizophrenia-like psychosis and posttraumatic schizophrenia. While TBI is a major public health issue, schizophrenia following TBI is relatively rare and poorly studied. The onset of schizophrenia occurs most commonly from late adolescence to mid-adulthood, in an age group where head injury is more frequent. Even if early illness features of schizophrenia might increase exposure to TBI, posttraumatic schizophrenia could be the result of a gene-environment interaction. The pathophysiology research in psychotic disorders following TBI does not distinguish schizophrenia from other psychotic syndromes but have to consider a dimensional approach of these psychotic phenomena. Family history of schizophrenia and frontal or parietal lobe deficits was more common in patients with posttraumatic psychotic symptoms. Susceptibility to schizophrenia is believed to be due to multiple genetic and interacting factors and mild childhood head injury may play a role in the development and onset of schizophrenia in families with a strong genetic predisposition. The authors suggest hypotheses aimed at furthering the understanding of the physiologic mechanisms relating traumatic brain injuries to psychotic symptoms. Psychotic disorder following TBI, schizophrenia-like psychosis and posttraumatic schizophrenia are a potential interest to clinicians and neuroscientists, as it may provide clues to understanding primary psychotic disorders such as schizophrenia. Schizophrenia is a psychotic disorder commonly attributed to the interaction of genetic vulnerability and environmental events which implies that environmental factors modulate the effects of the genotype. Schizophrenia related to TBI could also be the result of a gene-environment interaction. Schizophrenia genes may increase exposure to head trauma (through agitation or cognitive impairment), with head trauma further increasing the risk for schizophrenia. Further studies are needed to articulate the links between secondary psychotic symptoms and primary schizophrenia in a structure/function paradigm. The new imaging techniques of magnetic resonance imaging, position emission tomography and single-photon emission computed tomography could aid in this sense.     

Anévrysme de la carotide intrasellaire simulant un adénome à prolactine

A 52-year-old woman with secondary amenorrhea presented with ophthalmoplegia, subarachnoidal bleeding. Pituitary function tests showed mild hyperprolactinemia and deficiencies of other functions of adenohypophysis. X-ray films of the skull showed enlarged sella turcica, and CT scan was interpreted as demonstrating pituitary tumour. Carotid arteriography led to diagnosis of intrasellar aneurysm of the right internal carotid, without any pituitary tumour. After embolisation of the aneurysm, followed, by a temporo-sylvian anastomosis, endocrine functions did not improve. The mechanism of hyperprolactinemia is discussed, probably due to pituitary ischemia. This case provides evidence of interest of further investigations before a transsphenoidal surgery in pituitary tumours, in particular if subarachnoidal bleeding occurs.