Auxéméry Y
Service de psychiatrie et de psychologie clinique, hôpital d'instruction des armées Legouest, Metz cedex, France.
Encephale. 2012 Sep;38(4):329-35. doi: 10.1016/j.encep.2011.07.003. Epub 2011 Aug 31.
Blast injuries are psychologically and physically devastating. Notably, primary blast injury occurs as a direct effect of changes in atmospheric pressure caused by a blast wave. The combat-related traumatic brain injuries (TBI) resulting from exposure to explosions is highly prevalent among military personnel who have served in current wars. Traumatic brain injury is a common cause of neurological damage and disability among civilians and servicemen. Most patients with TBI suffer a mild traumatic brain injury with transient loss of consciousness. A controversial issue in the field of head injury is the outcome of concussion.
Most individuals with such injuries are not admitted to emergency units and receive a variable degree of medical attention. Nevertheless, cranial traumas vary in their mechanisms (blast, fall, road accident, bullet-induced craniocerebral injury) and in their gravity (from minor to severe). The majority of subjects suffering concussion have been exposed to explosion or blast injuries, which have caused minor cranial trauma. Although some authors refuse to accept the reality of post-concussion syndrome (PCS) and confuse it with masked depression, somatic illnesses or post-traumatic stress, we have raised the question again of its existence, without denying the intricate links with other psychiatric or neurological disorders. Although the mortality rate is negligible, the traumatic sequel after mild traumatic brain injury is clear. A difference in initial somatic severity is noted between the serious somatic consequences of a severe cranial trauma compared with the apparently benign consequences of a minor cranial trauma. However, the long-term consequences of the two types of impacts are far from negligible: PCS is a source of morbidity. The prognosis for minor cranial traumas is benign at vital level but a number of patients will develop long-term complaints, which contrast with the negativity of the clinical examination and complementary explorations. The origin of these symptoms questions their organic and psychological aetiologies, which are potentially associated or intricately linked. After a cerebral concussion patients report a cluster of symptoms referred to as postconcussive.
Post-concussion syndrome lies within the confines of somatic symptoms (headaches, dizziness, and fatigue), cognitive symptoms (memory and concentration problems) and affective symptoms (irritability, emotional lability, depression, anxiety, trouble sleeping). The nosographical entity of post-concussion syndrome is still in the process of elaboration following the input of new research intended to determine a cluster of specific symptoms. The persistent post-concussion syndrome is believed to be due to the psychological effects of the injury, biological factors, or a combination of both. Considered in isolation, the symptoms of post-concussion syndrome are non-specific and come together with other diagnostic frameworks such as characterised depressive episodes and post-traumatic stress. Post-concussion syndrome is not specific to concussion but can be present in subjects without any previous cranial trauma.
Blast trauma can thus be understood as experiencing a shockwave on the brain and as a psycho-traumatic event. The major methodological problem of the studies is the quantification of the functional symptoms present in different nosographical frameworks, which are often co-morbid. Post-traumatic stress disorder is one of several psychiatric disorders that may increase suffering and disability among people with mild traumatic brain injury; in addition mood disorders also seem to be frequent psychiatric complications among these patients. Psychotic disorders after TBI have been associated with several brain regions. The establishment of a causative relationship between TBI and psychiatric disorders is interesting in terms of our understanding of these possible sequelae of TBI. The grey substance of the grey nuclei of the base can also be altered by a scissoring mechanism of the perforating arteries. A cortical contusion through impression of the cortex on the contours of the cranium is frequent. The most common type of injury is traumatic axonal injury. Cerebral lesions that are secondary to TBI associate cell deaths through the mechanisms of apoptosis and necrosis concerning the nerve and glial cells. The scientific objective is to discover an anatomoclinical correlation between the symptoms of post-concussion syndrome and objectifiable brain damage. The predictive value of serum concentrations of the specific serum markers S-100B and neurone specific enolase has been established.
Cerebral imaging will allow the mechanisms concerned in cranial trauma to be better understood and thus may allow these mechanisms to be linked with co-morbid post-traumatic psychiatric disorders such as depression. The pyschopathological approach provides supplementary enlightenment where neuroimaging studies struggle to establish precise anatomoclinical correlations between neurotraumatic lesions, state of post-traumatic stress, and PCS. Moving away from a purely scientific view to focus on subjectivity, PCS can establish itself in subjects with no history of head trauma thus showing purely psychic suffering. Is the former name of "subjective post-head injury syndrome" no longer pertinent since the neurobiological affections can be objectified? Yet, the latter does not necessarily explain the somatic symptoms. Beyond any opposition of a psychic or somatic causality, it shows the complexity of this interaction. Admittedly, looking for a neuropathological affection is particularly cardinal to propose an aetiological model and objectify the lesions, which should be documented using a forensic approach. However, within the context of treatment, this theoretical division of the brain and the mind becomes less operative: the psychotherapeutic support will on the contrary back the indivisibility of the subject, he/she, who faced the "clatter".
爆炸伤会对心理和身体造成极大破坏。值得注意的是,原发性爆炸伤是爆炸波引起的气压变化的直接后果。在参与当前战争的军事人员中,因接触爆炸而导致的与战斗相关的创伤性脑损伤(TBI)极为普遍。创伤性脑损伤是平民和军人神经损伤及残疾的常见原因。大多数TBI患者为轻度创伤性脑损伤,伴有短暂意识丧失。头部损伤领域一个有争议的问题是脑震荡的后果。
大多数此类伤者未被送往急诊单位,接受的医疗关注程度不一。然而,颅脑创伤的机制(爆炸、跌倒、道路事故、子弹所致颅脑损伤)和严重程度(从轻微到严重)各不相同。大多数遭受脑震荡的受试者曾接触爆炸或爆炸伤,这些导致了轻度颅脑创伤。尽管一些作者拒绝承认脑震荡后综合征(PCS)的存在,并将其与隐匿性抑郁症、躯体疾病或创伤后应激混淆,但我们再次提出了其是否存在的问题,同时并不否认其与其他精神或神经疾病的复杂联系。尽管死亡率可忽略不计,但轻度创伤性脑损伤后的创伤后遗症是明显的。严重颅脑创伤的严重躯体后果与轻度颅脑创伤看似良性的后果相比,初始躯体严重程度存在差异。然而,这两种类型撞击的长期后果远非可忽略不计:PCS是发病的一个原因。轻度颅脑创伤在生命体征方面预后良好,但一些患者会出现长期不适,这与临床检查及辅助检查结果的阴性形成对比。这些症状的根源对其器质性和心理性病因提出了质疑,这两种病因可能相互关联或紧密相连。脑震荡后,患者会报告一系列称为脑震荡后症状的症状。
脑震荡后综合征包括躯体症状(头痛、头晕和疲劳)、认知症状(记忆和注意力问题)和情感症状(易怒、情绪不稳定、抑郁、焦虑、睡眠障碍)。随着旨在确定一组特定症状的新研究的开展,脑震荡后综合征的疾病分类实体仍在完善过程中。持续性脑震荡后综合征被认为是由损伤的心理影响、生物学因素或两者共同作用所致。单独来看,脑震荡后综合征的症状不具有特异性,且与其他诊断框架如典型抑郁发作和创伤后应激同时出现。脑震荡后综合征并非脑震荡所特有,也可出现在既往无颅脑创伤的个体中。
爆炸伤可被理解为大脑受到冲击波影响以及一种心理创伤事件。这些研究的主要方法学问题是量化存在于不同疾病分类框架中的功能症状,这些症状往往合并存在。创伤后应激障碍是几种可能增加轻度创伤性脑损伤患者痛苦和残疾的精神障碍之一;此外,情绪障碍似乎也是这些患者中常见的精神并发症。TBI后的精神障碍与多个脑区有关。就我们对TBI这些可能后遗症的理解而言,确定TBI与精神障碍之间的因果关系很有意义。基底节灰质也可因穿通动脉的剪切机制而改变。因颅骨轮廓对皮质的压迫导致的皮质挫伤很常见。最常见的损伤类型是创伤性轴索损伤。TBI继发的脑损伤通过涉及神经和胶质细胞的凋亡和坏死机制导致细胞死亡。科学目标是发现脑震荡后综合征症状与可客观化的脑损伤之间的解剖临床相关性。已确定了特定血清标志物S - 100B和神经元特异性烯醇化酶血清浓度的预测价值。
脑成像将有助于更好地理解颅脑创伤所涉及的机制,从而可能将这些机制与创伤后共病的精神障碍如抑郁症联系起来。在神经影像学研究难以在神经创伤性病变、创伤后应激状态和PCS之间建立精确的解剖临床相关性时,精神病理学方法提供了补充性的启示。从纯粹科学的观点转向关注主观性,PCS可出现在无头部创伤史的个体中,从而显示出纯粹的精神痛苦。既然神经生物学影响可以客观化,那么“主观头部损伤后综合征”这个旧名称是否不再适用?然而,后者并不一定能解释躯体症状。除了精神或躯体因果关系的任何对立之外,它显示了这种相互作用的复杂性。诚然,寻找神经病理学影响对于提出病因模型和客观化病变尤为重要,这应该采用法医方法进行记录。然而,在治疗背景下,这种大脑与心理的理论划分变得不那么有效:相反,心理治疗支持将支持个体的不可分割性,即面对“冲击”的他/她。