THE RELATION TO MANIC DEFENSE 与躁狂防御的关系 I would like to add a comment about manic states and the manic defense in general. Manic states are generally regarded as manifestations of manic-depressive psychosis, but they may be found in other pathological states such as schizophrenia or the schizoaffective disorders, as well as in organic states. Manic states are usually associated with either antecedent or consequent depressive states, but there are also manic states which may show a persistent or intermittent pattern without marked depressive accompaniments. Such patients may also suffer from persecutory delusions. The manic state is accompanied with psychomotor activity, elation of mood, ease of distractibility, and often delusions that have a marked omnipotent or omniscient quality to them. Manics often show an exaggerated sense of self-esteem and self-confidence and not infrequently try to act out the grandiose delusions which they develop. 我想补充一点关于躁狂状态和躁狂防御的评论。躁狂状态通常被认为是躁郁型精神病的表现，但也可能出现在其他病理状态，如精神分裂症或分裂情感性精神障碍，以及器质性状态。躁狂状态通常与前抑郁状态或后抑郁状态相关，但也有躁狂状态可能表现为持续性或间歇性的模式，没有明显的抑郁伴随。这样的病人也会有被害妄想症。躁狂状态伴随着精神运动活动、情绪高涨、注意力不集中，常常伴有明显的无所不能或无所不知的错觉。躁狂者经常表现出一种夸张的自尊和自信，并经常试图将他们产生的夸大妄想表现出来。 The manic defense, like the paranoid defense, is regarded as a response to an underlying state of depression, usually related to a preoccupation with real or fantasized loss. Part of the manic defense involves a tendency for the underlying conflict to be externalized, so that aggressive drive derivatives may be attributed to external objects, thus allowing the patient to interact with the object in aggressive or competitive or destructive ways. It is noteworthy that in manic states the cathexis of object representations remains virtually intact. Freeman (1971) has drawn attention to some differences in the defensive organization of manic as opposed to schizophrenic states. He writes: 躁狂防御，像偏执狂防御，被认为是对潜在抑郁状态的一种反应，通常与对真实或幻想的损失的先占观念有关。部分躁狂防御涉及到潜在冲突外化的趋势，因此攻击驱力的衍生物可能被归因于外部的物体，因此允许病人以攻击性的、竞争性的或破坏性的方式与客体互动。值得注意的是，在躁狂状态下，客体表征的精神投入几乎完好无损。Freeman(1971)注意到躁狂的防御组织与精神分裂状态的不同。他写道: Externalization is much more in evidence in mania than in schizophrenia.　Projection, which you so frequently find in schizophrenia, is rare in mania.　Projection, involving as it does a distortion of the drive with respect to its aim and object, results in a passive experience of the barred drive representation.　The very essence of mania is overactivity and a passive experiencing of drive expression is quite foreign to the condition.... Patients suffering from mania only feel themselves to be persecuted when they are confined and prevented from carrying through their intentions. This may give the impression of a　"persecutory" element in their thinking. The view taken here is that when the defense of projection operates, the corresponding phenomena(persecutory delusions, etc.) will only make an appearance in phases of illness that are not characterized by psychomotor overactivity,i.e, when the drive representations are blocked from an outlet to the external world. It is the cases which show psychomotor overactivity alternating with persecutory delusions that puzzle the clinical psychiatrist who then cannot decide whether he is confronted with a case of mania, schizophrenia, or paranoid psychosis(p.485). 外化在躁狂中比在精神分裂症中更明显。在精神分裂症中经常发现的投射，在躁狂症中很少见。投射，由于涉及到驱力对于它的目标和客体的扭曲，导致了被禁止的驱力表现的被动体验。躁狂的本质是过度活跃，对驱力表达的被动体验与这种情况完全不同……患有狂躁症的患者只有在他们被限制和被阻止实现他们的意图时才会觉得自己被迫害。这可能会给予他们的思想里一种“被害”的感觉。这里的观点是，当投射防御起作用时，相应的现象(被害妄想症等)只会在疾病的阶段出现，该阶段不以精神运动过度(即当驱力表示从外部世界的出口被阻塞时)为特征。临床精神病学家对那些表现出精神运动过度活动与被害妄想症交替出现的病例感到困惑，无法判断自己是面临着躁狂、精神分裂症还是偏执型精神病(p.485)。 It should be noted that the manic defense shares with the paranoid defense the dimensions of grandiosity and the tendency to externalization of aggression. Freeman suggests that the externalizing of projective defenses form an alternative to hypermanic overactivity in serving defensive objectives. The suggestion is well taken and may reflect the availability of alternate routes of energy discharge, either through motoric hyperactivity or through channels of cognitive reconstruction. One can speculate here on genetic patterns which might influence the pathology in the direction of either manic or paranoid defenses. We have no clear purchase on the question, but it provides an intriguing speculation. 值得注意的是，狂躁防御与偏执防御具有夸大的维度和外化攻击性的倾向。弗里曼认为，投射性防御的外部化形成了一种为防御目标服务的超躁狂过度活动的替代。这个建议被很好地采纳了，它可能反映了能量释放的代替路径的可得性，要么通过肌肉运动过度活动，要么通过认知重建的通道。我们可以推测遗传模式可能会影响病理方向(狂躁或偏执防御)。我们对这个问题没有明确的看法，但它提供了一个耐人寻味的推测。 We can wonder, for example, whether in the family backgrounds of manic patients there might not have been a persistent pattern of defense against the depressive affect through the use of external activity rather than, as is so often the case in paranoid families, of the utilization of rationalizing and blaming processes as a way of defending against similar depressive affects. Our suggestion is that it is the family context which provides the matrix of learning of defensive patterns and the reinforcement of them by a variety of interactional and internalizing devices. We shall see more of this in reference to the genesis of paranoia, but the question as to the differential influences in the genesis of mania seem to this writer at least to be relevant. 我们可以怀疑,例如,是否在躁狂患者的家庭背景里不存在一个持久的防御模式来对抗抑郁情感，除了通过使用外部活动，而不是利用合理化和指责过程作为一种防御类似抑郁的情感，后者在偏执家庭中非常常见。我们的建议是，正是家庭环境提供了防御模式的学习环境，并通过各种相互作用和内化的手段来强化它们。关于偏执的发生，我们将会看到更多这样的内容，但是其在躁狂起源中的不同影响在该作者看来至少是相关的。 In any case it seems that in cases of manic-depressive psychosis several factors are related to a relatively poor prognosis. A recent study suggests that the poor prognosis is associated with the female sex, and with the occurrence of either manic or paranoid manifestations. Prognosis is relatively good in patients who experience recurrent depressive episodes without associated manic attacks(Shobe and Brion,1971). We might suggest in this conjunction that the paranoid defense is a viable alternative to manic defense, even in clearly diagnosed cases of manic-depressive psychosis.　Carlson and Goodwin(1973) have recently demonstrated that the presence of paranoid symptomatology does not indicate the presence of a schizophrenic process and does not rule out a diagnosis of affective disorder. 无论如何，似乎在躁郁性精神病病例中，有几个因素与较差的预后有关。最近的一项研究表明，预后不良与女性有关，并与躁狂或偏执症状的发生有关。复发性抑郁发作而无相关躁狂发作的患者预后相对较好(Shobe and Brion,1971)。在这个结合中，我们可能会建议，偏执防御是躁狂防御的一个可行的替代，即使在明确诊断的躁狂抑郁症的病例里。卡尔森和古德温(1973)最近证明，偏执症状的存在并不意味着精神分裂症过程的存在，也不排除诊断为情感性障碍。 If the alternation or substitution between manic and paranoid defenses is understandable on dynamic grounds—in terms of its relation to and defensive avoidance of underlying depressive elements—the relationship between manic and paranoid defenses may not be altogether indefensible on more strictly biological or biochemical grounds. A recent careful study of the "switching process" in manic-depressive illness by Bunney et al.(1972) has indicated that specific neurotransmitter catecholamines—specifically dopamine and/or norepinephrine—are functionally increased in specific brain areas prior to the switch from depression into mania. They speculate that the specific switching mechanisms which are involved include a genetically transmitted defect which involves specific mechanisms which must be activated, and that the activation process is somehow reversible. 如果躁狂防御和偏执防御之间的交替或替代在动力学基础上是可以理解的——就其与潜在抑郁因素的关系和防御规避而言——躁狂防御和偏执防御之间的关系在更严格的生物学或生物化学基础上可能不是完全站不住脚的。Bunney等人(1972)最近对躁狂抑郁症的“转换过程”进行了仔细的研究，结果表明，在从抑郁转变为躁狂之前，特定的神经递质儿茶酚胺——尤其是多巴胺和/或去甲肾上腺素——在特定的大脑区域功能上有所增加。他们推测，其中涉及的特定开关机制包括一种基因上的传递缺陷，这种缺陷涉及必须被激活的特定机制，而激活过程在某种程度上是可逆的。 The genetic abnormality is thought to affect a mechanism which regulates the amount of functional neurotransmitter—most probably norepinephrine—at the synaptic cleft, perhaps by interference with norepinephrine transport across neural membranes. The switching process can be activated by a number of chemically active agents, not only the tricyclic antidepressants but also the amphetamines. We are reminded here that considerations of amphetamine psychosis suggested that the effects of the amphetamines on the central nervous system were probably medicated by the effect of dopamine and norepinephrine on specific activating systems. It may be that the release of these specific neurotransmitter agents in the central nervous system, by whatever underlying genetic or pharmacologic agency this is achieved, increases the activity in central nervous system structures which may underlie and give rise to both manic and paranoid manifestations. The further question would seem to remain as yet indeterminate—that is, whether the choice of alternative, whether manic or paranoid, is a result of central nervous system effects(the activation of specific and alternate neuronal systems) or whether the alternative is a function of more specifically psychological determinants. These possibilities indeed need not be exclusive. 这种基因异常被认为影响了一种调节突触间隙的功能性神经递质(很可能是去甲肾上腺素)数量的机制，这种机制可能是通过干扰去甲肾上腺素在神经膜上的传输来实现的。转换过程可以被许多化学活性物质激活，不仅是三环类抗抑郁药，还有安非他明。这里提醒我们，从安非他明精神病的角度考虑，安非他明对中枢神经系统的影响可能是通过多巴胺和去甲肾上腺素对特定激活系统的作用来治疗的。可能是这些特定的神经递质在中枢神经系统的释放，通过任何潜在的遗传或药理作用的实现，增加了中枢神经系统结构的活性，这可能导致躁狂和偏执的表现。进一步的问题似乎仍然是不确定的，也就是说，是选择替代，是狂躁还是偏执，是中枢神经系统效应的结果(特定的和替代的神经系统的激活)，还是选择是更具体的心理决定因素的功能。这些可能性确实不需要是排他的。